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    The Truth about Antidepressants.-Withdrawal Side Effects
     
     
    This is a massive subject, and I am living a very difficult life at this time which is interfering with my writing. So, I have to rough this out. This report is based mainly upon information I gathered during a study of antidepressants I did in 2008/09. This was the study that netted the classified documents from GSK
    This is the first section of this report.
    I will do this report one section at a time, and the steps will be:
    1. Testimonies of people destroyed by antidepressants
    2. The chemistry of the various antidpressants, and which dangerous substances in everyday life they deliver directly to the brain – Yes, you heard that right, there are several that do nothing more than deliver modeling glue and other nasty aromatic hydrocarbons straight to your brain, and KEEP THEM THERE. Several would be replaced well by a gasoline inhaler attached to a backpack that you carry with you – (pill form is easier though) and others, like Prozac, are derived from fluoride. Antidepressants deliver a very stable but FILTHY high until you fry, and the hydrocarbon based ones cause exactly the same damage you get from working in a paint booth without a respirator.[U1] I HAVE PROOF.
    3. The visible physical damage antidepressants cause and how and why it occurs, including osteo porosis, calcification of the brain, brain shrinkage, destruction of white matter, corkscrewed axons, liver and other organ damage, and some interesting ancedotes related to this.
     
    4. The motivation for attempting to destroy the entire population of a nation with these substances, and an expose of the corruption in the FDA, the medical community, the Jewish connection, the banker/Rothchild/Rockefeller/facist connection, the future slave state, how the research SSRI’s are based on was done in Russia and imported to America in the form of Prozac, and the proposed finalization of the destruction of Western civilization which “antidepressants” will play a central role in.
    5. A detailed exposure of why antidepressants destroy bonding relationships, and make it impossible for anyone to fall permanently in love genuinely, with a little side attachment explaining the reasons for why specific brands destroy sex in different ways. – I actually have the line by line answers for EACH BRAND, and which part of the brain they ruin to often permanently destroy sex in different ways. Different brands destroy different pathways, but all are effective in wrecking sex.
    6. How they get away with hurting so many people under the supposed cover of doing good, and the methods put in place to avoid being sued, imprisoned, and hung. What WE need to do to forever expose this scam, and make sure they are sued, imprisoned, and hung. I have the answer to EXACTLY how we can blow this open and hang them.–
    Prescribed Deletion – testimonies of the destroyed.
    These are the words of those who have been destroyed by antidepressants. If you are among them, STOP listening to your P-doc telling you it never happens; the reality is that they ALL know it happens and they are lying to you. View this chart, and READ THE RESULTS THAT FOLLOW.
    These are testimonies of people destroyed by antidepressants.
    – – – – – –
    “Whoever said that they lost most their ability to love; MAN, that is the thing I miss the most. I was a very, very, very passionate person prior to celexa. I was passionate about everything, my marriage, my job, my country. I couldn’t hear our national anthem without stopping and feeling the hairs on the back of my neck stand straight up. 14 years in the Army National guard, I was very into my career with them too. I was passionate about running, about my relationship with (and this will probably sound wierd) my dog. I miss all of these things. I hope they all come back to me. They were very much the bricks in the foundation of my life and I feel like they are gone. When I say I want the old me back, I mean the person who was passionate, the person who loved and was loved. The driven person who saw what he wanted and went out and got it. That was all taken from me with the introduction of Celexa in my life. I just want it back.”
    – – – – – –
    “I’ve been in an extremely peculiar state for the past 8 months after stopping Wellbutrin/buproprion. I have literally lost everything inside of me and no longer have a sense of “inner being”. My personality has been completely erased, along with the inner psyche I’ve spent a lifetime building. When I attempt to “look inside”, it is impossible because there is literally nothing there. Everything that made up my specific sense of personal being is gone, including my hopes, fears, dreams, goals, opinions, values, morals, likes/dislikes, and most strikingly, all emotions and feelings.—I have no feelings associated with past events, and no emotional connections with anything in the world. Specific emotions that defined my personal sense of being are no longer there. People, places, things and events that I thought were etched in my soul as having significance no longer mean a thing. Absolutely nothing, I can’t stress this enough.–I am unable to look backward or forward, have no sense of past accomplishments and no desire for future ones. The strangest thing is, I cannot feel anything toward being in this state, as that part of me is gone too. It’s like a recursive erasure of everything I ever was, am, and will be.–It doesn’t feel like life is a conscious experience that I am having anymore, as there is no inner construct within me to absorb an experience on any level. I see, hear, touch, and smell, yet each of these is so devoid of emotional content that they don’t coalesce into anything meaningful I can call a human consciousness. My sense of being has been replaced by a constant void of nothingness that is unchanging, 24/7, I feel nothing towards the nothingness. It is not like feeling empty inside, there is no inside to feel empty within.—Getting to this state was a long process that started with gradually losing my emotions. This started when I decided to withdraw from the antidepressant Wellbutrin/Bupropion which I’d been on a high dosage of for 5 years. Strangely, going back on it did not help, but made things worse. When I stopped and started the drug a second time, I experienced one tremendous day of improvement followed by a seizure while sleeping, and woke up in a confused state. After this I regressed and felt completely dead inside.–This waking up in a confused state happened 2 more times, once in May 2010 and once in September 2010. Both of these were preceded by sudden improvements. But upon waking I felt like I had lost a basic part of my self. Not just feelings, but the core of my being. What I felt to be the complete and final destruction of my inner being happened on September 7th, 2010, and there hasn’t been a change since (it has now been 8 months).—“I tell you, I never had a problem before celexa. I just want to be back to me. I want to no longer be the pitiful creature it made me. I want to be me. The old me. I want myself back. Life isn’t worth living with this new person holding my thoughts and feelings hostage. I have been off Celexa since last year. I JUST WANT ME BACK.”—“I have been on 0 mgs for almost a year, and my emotional state has yet to come back to normal. (normal me). I have been from Psyc doc to Psyc doc (never needed before celexa) to try to figure it out. They point the problem back to me. I found out by reading around the Internet, and buying the book “Prozac: Panacea or Pandora” by doctor Ann Blake Tracy, and I found out that several people, if not all people, who go off these drugs experience exactly what I have experienced. When Natalie wrote what she wrote, you can go back to some of my earlier posts and the withdrawal effects are written down almost verbatim. These are bad for our brains, they change our personalities. I want my life back, and don’t want even my worst enemy to experience what I have been through. These people have no love for their fellow man[U2]. We need to, no matter how emotionally messed up we are, we need to band together and prevent them (a commercial for Cymbalta just came on the tv, made my blood boil) from prescribing them to ANYONE. Depression hurts said the commercial, I never knew depression till after celexa. I have been through hell, therefore hell exists.”
    – – – – – –
    “What I don’t understand is how a drug could completely erase me as a human being. What I’m experiencing is not depression, anhedonia, or flat affect, but a permanent change in my consciousness that literally destroyed my humanity. All the parts that made up my being are literally gone. I don’t understand how this is even possible, or what (if anything) I can do to change it.”
    – – – – – –
    “I’m 25 yrs old. I used to be a bodybuilder, avid fisherman, used to drag race, and enjoy the great outdoors. USED TO. I was on effexor for about 3 yrs, 75mgs. I decided I wanted to stop taking it, I felt fine. Im 25 I said and I can deal with lifes problems. I told my doc if I may discontinue the drug he said sure, if you want to. Doctor didn’t even ask me if I wanted to wean off, I suggested him to give me the 35mgs, but he gave me only a weeks worth. I have never in life felt so sick. I would not wish this on anyone, not even my enemy. The first 3 months were hell. dizziness, nausea, fatigue, bad memory, brain zaps, you name it I had it. I couldnt even walk sometimes. I fought and fought and it is now 7 months that I am clean off this horrible so called drug. To this day, 7 MONTHS later, I am left with weakness, bad memory, and horrible coordination. I can no longer workout, all my muscles went down, I have no energy to do what I liked to do in my life. I cannot function or remember things at work. I am useless. If it wasn’t my cousins place, I would have been fired along time ago. I am not depressed, I don’t have panic attacks. In my opinion, Effexor has left me permanent damage. I have been through more tests than you can think of. blood tests upon blood tests for every disease known to man. This drug has changed my life for the worse and everynight i cry, because I feel that this medicine has severly left me damaged. My doctor has no idea what to do[U3].”
    – – – – – –
    “I was prescribed Zoloft 25-50mgs 9 years ago while I was in college.
    Before I begin with the nightmare, let me stress I WAS NOT SICK when I started this drug. I had anxiety (situational )and was a little tired. That is it. Other than these issues, I was as healthy as a horse, never been in the hospital, rarely if ever needed to go to the doctor. I was very active and on the go. Well, Zoloft worked immediately, what can I say. I loved it. Loved it loved it loved it. I thought it was a gift from God, saved me and my college career. I wasn’t as shy as I had been. I felt more social. But then I found I could not get off without severe head pain and brain zaps. So, I stayed on it. Every few months I would think about going off again, but the symptoms I would get kept me on it, and very afraid to come off. So, I stayed on it for 8 long years. (I forgot to mention I gained 25 pounds within the first 3 months on it. That was another reason I wanted off). After 8 years, I’d had enough. I felt like I no longer needed it, I had been long out of college and the original situations that gave me anxiety were long gone. So, at my doctors advice, I tapered over about 3-4 weeks. Then my life was shattered. Completely shattered. I was told the withdrawal would only last a week or two at most, so I rode it out. It never went away and only kept getting worse. So, I gave up and tried to go back on. I couldn’t take the symptoms anymore. But my body was having none of that. Strangely, now when I took Zoloft, my body and brain reacted badly, as if it were rejecting it. I got a fever and felt like I was dying. I had no choice but to get off again. I was given other SSRI’s, but none of them helped either, and all of them made me worse. I no longer tolerated meds like I did prior to Zoloft. I kid you not, here I am 3 YEARS later and still very ill, and it all began when getting off Zoloft. Here is what I suffer 24/7….. severe head pain and pressure brain zaps/ electrical zaps shooting through brain down to toes burning in extremities and brain severe fatigue and weakness dizziness/vertigo severe depression ( never was depressed, ever, until coming off Zoloft ) severe anxiety panic attacks…BAAAAD daily crying jags skin eruptions and bone and muscle pain burning tongue insomnia
    digestive pain cramping on right side under rib cage hair loss
    sensitivities to food and medications previously tolerated well
    extremely sensitive to vitamins and minerals previously tolerated well no motivation / severe apathy loss of career and income/ on disability derealization/ depersonalization back and neck spasms unable to drive, shop, or eat out increased allergies to things once tolerated well ( smoke, dust, cats ) suicidal thoughts….pretty regularly and very scary nightmares jaw pain from clenching teeth ( I guess from severe stress ) agoraphobia…very heartbreaking since I used to be so busy ears ringing feeling like being hit it the back of the head with a shovel pressure in chest, like a 100 elephants are sitting on me racing pulse, even when resting increased blood pressure and cholesterol metallic taste bladder spasms loss of cognition/ mental function ( feels like I lost 50 IQ points ) difficulty concentrating and recalling facts I wrote a letter to Pfizer, detailing my story and my symptoms. They blew me off and wanted a doctors opinion of what my illness is from. No doctor will admit to Zoloft being the cause of this illness, so Pfizer pretty much told me they take no responsibility. They ruined my life, and take no responsibility. They train their drug reps to educate doctors that these drugs are harmless. They know better, but rake in too much money to do anything about it. They do not care how many lives they destroy, as long as they continue making their billions off innocent victims.”
    – – – – – –
    “My withdrawal from Seroxat/Paxil (a few years ago, now). I became very aggressive on the stuff (many arrests and court appearances), and on some days I could pop valium like smarties without it making the slightest bit of difference. When I decided it would be a clever move to stop taking it and put up with a few days of flu-like symptoms, I found out what withdrawal was really like. I slashed at my arms, I rolled around on the floor, screaming, because everything felt raw (my theory is that we ‘normally’ perceive the world through a comfortable haze of endorphins–which was stripped away) and when the police were called I freaked out completely and brandished a knife at them. My husband referred to that state as being ‘animalistic’. Needless to say, I escaped jail by a hair’s breadth. When I ended up in ER, following a dose of pepper spray in my face, I begged for Seroxat and the doc just laughed in my face and said they weren’t running a pharmacy. They did not believe there was such a thing as SSRI/SNRI withdrawal syndrome. I think they still don’t. In the cell, waiting for the court appearance, I had the worst shakes and weird feelings (derealisation, having two heads, having my head swell to the size of a water melon). The junky I shared the cell with said: “Wow, what are you on?”
    – – – – – –
    “Please consider this before commenting on antidepressants in a positive way.
    About 10 years ago, the medical school at a major university began to notice a large number of cadavers coming in (for the medical students to work on) which had indented and calcified frontal lobes in their brains. Puzzled by this, they went through the life history of each cadaver that had this anomaly, and discovered that in every case, the person had been on SSRI antidepressants. The level of brain damage indicated that each of the cadavers had been lobotomized. The people who drew the connection between the calcified and collapsed frontal lobes (the part of the brain which contains your soul) and antidepressants received offers of money to keep it secret, and when they chose to go public anyway, received anonymous death threats against their families and children if they ever went public. –I have seen many people get destroyed by antidepressants, all the while they said all was well. Invariably they go down the toilet as they eventually move toward complete and total emotional and personality flatline.”
    – – – – – –
    “I am on my 7th day of no Cymbalta after being on it for only 3 weeks. I went from 60mg to 30mg, no problem. Then 30mg to 15mg, by making my own pills from the 30mg. Brain Zaps started. Now since I am clean for 7 days the Brain Zaps are hell,[U4] I think I even blink when they hit me. Inside my head the Zaps sound like a chattering angry squirrel. The people that made this drug must have never tested it for withdrawals. I have terrible back pain, have trouble sleeping, and have even cried twice this week. I just took 50mg of benedryl and 1000mg of tylenol hoping I can sleep tonight. I also gained weight on the drug. Has anyone that dealt with the Brain Zaps stopped having them all together? They are so bad, I am afraid to drive, I now understand why some folks kill themselves coming off drugs like this one. If there is a happy ending, I would love to know about it. Almost forgot, Blood Pressure has gone thru the roof coming off this stuff.”
    – – – – – –
    “I will name the countless symptoms and probably unreversable brain damage I am living with after Effexor. There are good days in which some of the symptoms won’t arise for exception of the pain. Those are the days I can be a mother and wife but still the shadow of the energetic person I was. Back in July all the symptoms hit me all at once. Blury vision, dizzy, letargic, high pitch ringing in my ears, exhaustion, pain all over my body, joints and muscles. Muscle twitching, slurred speech, urinary incontinence at times, hair lose in patches. It is impossible for me to normally work at any type of job now. I have states where I would forget what I am doing. I have times in which I have a hard time controlling voluntary motor functions in my legs and arms (such as not being able to write, open a bottle or carry anything). Every now and then muscles will begin to twitch, then just stop, out of the blue. I became lethargic and have no energy to do anything. Not to mention times or days when I can not drive due to the chance that I would have an accident beacuse of the sudden blury vision or dizzines that make it dificult to see. Not to mention when I suddenly forget where I am going or doing.”
    – – – – – –
    “I have been on Celexa for almost three years. the results: lost a job and a marriage due to being so non complacent but gained 20 lbs. I skipped a few doses several weeks ago and decided it was time to wean myself off. I tapered down very quickly and am now dealing with the following withdrawal symptoms:
    Anxiety
    Dizziness
    Fatigue
    Headache
    Insomnia
    Diarrhea
    Nausea
    Restlessness
    Blurred vision
    Jolting electric “zaps” (at bedtime)
    Tingling sensations
    Abdominal discomfort
    Flu symptoms and general malaise
    agitation
    Vertigo
    Gait disturbances
    Sweating
    Irritability
    Aggression
    Sleep disturbance and insomnia
    Nightmares
    Vivid dreams
    Confusion
    Memory and concentration difficulties
    Crying spells
    Lethargy
    Weakness
    The aggression is the scariest part but now that I know almost everyone experiences this I feel better. From reading most of the posts it doesn’t seem to matter if you wean yourself or go cold turkey, the withdrawal symptoms appear the same.”
    – – – – – –
    I believe SSRIs “cause” neurogenesis through the brains compensatory mechanisms. By inducing a massive chemical imbalance at the synaptic level, SSRIs force the brain to respond by shutting down these connections and creating new ones (which then get shut down, and the cycle continues). Unfortunately, these new connections (axons) often resemble the type of new axonal growth (swollen/corksrew appearance) seen after recovery from a neurotoxic MDMA regimen. (editor’s note – MDMA is Ecstacy) These axons also often grow and/or project into areas where they did not before, and the significance of this is as of yet unknown.
    7. The most troubling permanent lasting adverse neurological effects you may experience after prolonged SSRI usage (and consequent STOPPING) are :
    a). Word finding troubles
    b). Absolute emotional flatness and deadness
    c). Permanently reduced sex drive
    d). An odd, pervasive social anxiety/awkwardness
    e). Trouble with coordination
    f). Bad memory
    g). Trouble retrieving words
    h). Overall paucity of thought and expression
    i). Lack of creativity and intellectual fluidity (mental fog)
    j). A lack of ability to “steer” or control the tone of your voice
    (I’ve noticed this- that I sound shaky and agitated no matter what my
    mood is, and people think I’m upset when I’m really not)
    8. After these brain damaging effects have sunken in, you may have great difficulty finding support anywhere. Talking to a p-doc may be an exercise in futility. They will want to protect their own interests and shield themselves from a possible lawsuit, hence you may be told continually to get back on meds/up your dosage. The more you protest, the less credibility you have, thus the more evidence in your p-doc’s mind that you need to go back on SSRIs.[U5]
    9. Once you realize the extent of the damage, and it sinks in beyond the denial you may initially face, it will be hard to explain to others exactly why you are not the same person you used to be. The damage is similar to a TBI (Traumatic Brain Injury) yet it might be better termed DBI (Diffuse Brain Injury).
    – – – – – –
    Cymbalta
    “Oh, how the withdrawal wrecked me. The only thing worse than taking Cymbalta was withdrawal from Cymbalta. Added to all the side effects I was already having, I very much wanted to cut myself, and got as far as sitting down with a blade, but instead I bit myself on the hand as hard as I could stand. I think I also punched myself in the thigh that same day, but it’s all sort of hazy. The first day off Cymbalta, I hallucinated, felt like my arms were really far away from the rest of my body, dissociated for most of the day, and in general, thought I was going to have to call for an ambulance. A benzo would’ve really helped, but I didn’t have a pdoc yet at the time; I had to wait three weeks and let me tell you, those were three of the most hellish weeks of my life, including feeling very much like I was having a mixed episode. Out of desperation, I took diphenhydramine because it helped the vertigo and the sleepy feeling sort of passed for “calmer.” It took at least three weeks for the withdrawal symptoms to calm down to a dull roar. When I saw my new pdoc, I was still agitated.”
    – – – – – –
    Your doctor is your worst enemy. Welbutrin is an SNRI. It blocks the metabolites in the liver that metablilze seretonin and noepinephrin. Switching to celexa, which is an SNRI is not going to help you. Doctors just have no clue as to what they are doing. You go to them with a problem, they consult ther PDR, and hand out some drugs that the pretty little pharma rep gave to them. They will give you something to destroy your brain, then give you a benzo like xanax, to combat anxiety. You cannot sleep, you are always on edge, you end up with some sort of psycological “disorder” (manufactured by the drug companies), and you are left a buned out shell of what you used to be. They tried to give my mother-in-law prozac because she was sad when her father was dying of cancer, and she was starting to go through menopause. I SCREAMED. This lady didn’t need prozac, or any other mind altering drugs. She needed to reduce her stress.
    I told her to take topical progesterone, and she turned around just fine.
    Fact: Doctors don’t know what ssri’s do to the brain
    Fact: There is no evidence of a lack of neuro transmitters.
    Fact: There is no way of measuring the level of seretonin in the brain…
    I pray for anyone in distress anywhere, and God bless and help those whose lives were destroyed by doctors who dished out meds that they know nothing about.
    ——–
    WITHDRAWAL
    did anyone else get tapered off zoloft from a doctor but still having withdrawal?
    this is how my doctor did it and I am still trying to understand why it was just down to 50mg and not less after a while: starting with my 100 mg
    week 1- 50 mg every day
    week 2 and 3 50 mg every other day
    week 4 50 mg every two days
    week 5 50 mg every three days
    week 6 off (on this week now)
    I took my last on sunday and it’s now Wednesday. last night I could not sleep, I felt very cold and I was shivering and had interrupted sleep and then got too hot all over like I was burning. I’ve had the brain zaps all along on the days I didn’t take it and some of the shivering and feeling a little dizzy too , very restless sleep on and off for these last few weeks. also some irritability, and very depressed and hopeless feelings and anger, some crying spells for no reason. I don’t want to call the doctor because obviously they don’t know what they are doing or I wouldn’t have withdrawl symptoms at all.
    – – – – – –
    My daughter began having petit mal seizures. Coincidentally, she was just recently placed on zoloft. I am sure it was only a coincidence, right? What did zoloft do to you?
    – – – – – –
    YES, ZOLOFT IS EVIL. IT RUINED MY LIFE. IT MADE ME ACT TOTALLY OUT OF CHARACTER AND I MAIMED MYSELF IN AN INDESCRIBABLE WAY.
    – – – – – –
    Zoloft destroyed my life, and my Dr. and therapist stood by and watched it all happen right before their eyes, it was like I was a project for them. I am sorry to those I affected during that time, I regret it everyday.
    ****************************************************************************
     
    Most Nations in the World Have No GMO-Free Platform To Protect Their Citizens
    Unless you live in the dozen or so nations in the world who have declared GMO (genetically modified organism) bans, then you’re likely eating GMO. Eating organic is your best chance of avoiding GM foods, but it’s almost impossible to avoid them entirely, especially if you’re living in a country that doesn’t restrict their cultivation, import or export. The United States, Canada, China, UK, Australia, Mexico, and most of South America, Asia and Africa have no formal GMO-free platforms and their use is typically unrestricted and widespread.
    Nations with no formal GMO-Free platform (in red). Nations with laws restricting GMO in most areas (in yellow), and nations who are either GMO-free or have declared national bans (green).
    Click for larger image
    The image above is a shocking reminder of how we have allowed biotech industries to take over our planet. It is my dream to one day see this image turn from the majority red to green. Countries represented in red have no enforced national laws banning GMOs, their import, export or cultivation. Most of these nations have a very large percentage of their citizens eating GM foods.
    NORTH AMERICA
    The United States is the leader in GM cultivation and now grows mostly GM varieties of corn, canola and soy. Hawaii now grows GM papayas. Approvals have also been given for GM alfalfa, zucchinis, beet sugar and tomato varieties, though not all are currently being grown. In 2010, the US planted 66.8 million hectares of soybean, maize, cotton, canola, squash, papaya, alfalfa and sugarbeet. The largest share of the GMO crops planted globally are owned by Monsanto.
    More than 30 of Monsanto’s directors, CEOs, VPs, board members, managers, scientists, attorneys and consultants also hold Federal Positions within the US government.
    Canada has widespread GM crop usage. All Canadian canola is GM, as is a large portion of the country’s soy and corn. Prince Edward Island tried to pass a ban on GMO cultivation but failed, and GM crops in the region are currently increasing.
    Despite the fact that 233 consumer and farmer groups in 26 countries have joined the “Definitive Global Rejection of GM Wheat”, Canadian MPs voted to reject stronger export rules for crops of genetically modified organisms (GMOs).[U6]
    SOUTH AMERICA
    Even though GMO continue to face strong resistance in South America, it is widespread. One third of the 134 million hectares of Genetically Modified Organisms (GMO) planted globally in 2009, were in South America. Brazil and Argentina are the main producers, with 21.4 and 21.3 million hectares respectively. Of all the countries in the world that are planting genetically modified crops, seven are in South America. They include Argentina, Bolivia, Brazil, Chile, Columbia, Paraguay and Uruguay. There are also no national restrictions in Guyana, Suriname and French Guiana to the north of the continent. Between 2008 and 2009, world production of GM crops increased eight percent, while in Brazil it rose 35 percent.[U7]
    Peru, Ecuador and Venezuela have all declared national bans on GM foods. Peru officially passed a law banning genetically modified ingredients anywhere within the country for a full decade before coming up for another review. In 2008 Ecuador declared the country GMO free and will limit its biotechnology. In 2006, Venezuela banned genetically engineered crops thanks to President Hugo Chavez Frias.[U8]
    MEXICO
    In January 2010, Slow Food Tehuacan Mixteca Popoloca convivium launched a campaign to protect traditional varieties of maize after the Mexican government gave the go ahead for the first legal plantings of GM corn following a decade-long battle. The convivium is concerned that modified genes could spread and contaminate genetically valuable native varieties and is working to educate family and farmer organizations about the richness of their country’s biodiversity, encouraging the Mexican community to be proud of their cultural heritage and to work for its revitalization. Mexico does not have any GMO-free zones.
    EUROPE
    Europe is quickly becoming the most progressive continent in the world to oppose GM foods. France, Italy, Switzerland, Hungary, Bosnia, Serbia, Croatia, Latvia and Albania have all declared many regions to be GMO-free. France made an important step in the no-GMO movement by specifically defining exactly what “GMO-free” means when it comes to food labeling[U9]. Spain and Portugal are slowing advancing but they have a long way to go before declaring most of their regions GMO-free. Britain officially supports GM crops and has trials of GMOs like potatoes planted. Austria, Greece and Poland are now completely GMO-free zones thanks to public and government support.
    AFRICA
    Egypt and Madagascar are the only two countries in Africa to ban GMO. Any agricultural imports to Egypt must have a certificate from the country of origin that the product is not genetically modified and the rule will also apply to Egyptian exports. Madagascar banned growing or importing GMO foods due to concerns over the effect on human health and environment. In Algeria both the planting and distribution of GMO foods is illegal although import laws are lax. Other countries such as Kenya, Lesotho, Ethiopia, Angola, Malawai, Mozambique and Zimbabwe have some limited restrictions in place to ban GMO imports but with many exceptions and critics claim most of the laws are not enforced.
    RUSSIA
    Russia remains GMO-free. According to the official information there is no growing of GMOs in Russia for commercial purposes. So far the Federal Environmental Assessment Commission has not adopted any commercialized GM varieties for agricultural use.[U10]
    ASIA
    India has widespread GM cotton use. The widespread planting of Monsanto’s GM cotton has led to tragedy throughout India. The Indian government even banned conventional seeds from many government seed banks in an attempt to please Monsanto (in return, the country was given International Monetary Fund loans to help its economy) and slow the nation’s poverty rates[U11]. An estimated 1,000 farmers commit suicide each month in the country as a result of the crop failure and debt caused by planting the GM seeds.[U12] Farmers were convinced to spend what was often 1,000 times the cost of conventional seed on the “magic seeds” after listening to Monsanto’s promises of increased yields and resistance to pests. Despite the promises, the crops were often destroyed by bollworms. In addition, the farmers weren’t warned that the crops would require twice as much water as conventional cotton, leading to many crops drying up and dying. The “terminator” seeds also must be purchased again every year. For farmers used to saving seed from year to year, this was often a final financial blow that led to insurmountable debt.[U13]
    With the exception of Thailand and Sri Lanka who both have GMO-free zones, all of Asia remains resistant to adopting laws to restrict imports, exports and cultivation of GMO.
    NORDIC COUNTRIES
    During the meeting of Nordic countries at Terra Madre 2010, delegates from Sapmi, Sweden, Finland, Denmark, Norway, Faroe Islands, Greenland and Iceland discussed a statement that would describe their united position on GMOs. The result was a declaration against GMOs that the convivium leaders, members and food communities could use to lobby against the introduction of these crops, presenting it to their governments and others. Iceland has declared two GMO-free regions in the country.
    AUSTRALIA and NEW ZEALAND
    All genetically modified foods intended for sale in Australia and New Zealand must undergo a safety evaluation by Food Standards Australia New Zealand, however there are no national GMO bans in either country. However there are regional bans. Tasmania’s ban on the release of GM organisms to the environment will continue until 2014. South Australia has reaffirmed their commitment to ban all commercial GM crops until 2014.
    The status of GM crops is constantly changing, both in the United States and around the world. Public outcry is rising against these largely untested foods and crops. The industry claims of “super yields” and an end to poverty and famine have proven to be dangerously inaccurate. Now, more than ever, is the time when our voices (and purchases) can make a real difference. It’s time to support labeling initiatives which may kickstart global campaigns to slowly change our red planet to green and ban GM foods once and for all.
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    Individualized Medicine: FDA Approved Ingestible Microchip Tracking Device
    Articles Health — 05 August 2012
     
     
    The Food and Drug Administration has approved an ingestible digital senor that can track physical health with the assertion that patients are not taking their medication regularly and need a tracking device inside their body to assist them in their medical care. [U14]The mainstream medical industry has a term for this new type of spying: individualized medicine.—Proteus Digital Health (PDH) released the Ingestion Event Marker (IEM) which was first approved in Europe. George Savage, co-founder and chief medical officer at PDH claims that this ushers in a new era of digital medicine that “shifts the paradigm.”–The IEM, as small as a grain of sand, can be embedded in a pill, and ingested to monitor the patient and their bodily health. The device will collect measurements such as heart rate, body position and activity.[U15] The IEM sends a signal to your smartphone; which then transmits the data to your doctor. Actual real time data about your biological make-up can be uploaded wirelessly.—Eric Topol, geneticist and cardiologist, is a professor of genomics at the globalist funded Scripps Research Institute, happily says: “The FDA validation represents a major milestone in digital medicine.—Directly digitizing pills, for the first time, in conjunction with our wireless infrastructure, may prove to be the new standard for influencing medication adherence and significantly aid chronic disease management.”—The transhumanists at 2045 Initiative support the IEM. They are a group of Russian scientists who are working toward the “realization of the possibility of a radical extension of human life by means of cybernetic technology” with the directed point of blending humanity with a “new culture”[U16] based on science.—By working with international scientists, they are exploring anthropomorphic robotics (the integration of man and machine) while modeling living systems and brain functions with artificial carriers to achieve cybernetic immortality.[U17]—The Elite are researching the possibility that become immortal may mean joining their minds with computers to be able to live forever.—The US government, always looking for new ways to manipulate, has been pouring funds into implantable microchips that could monitor soldiers and the battlefield conditions effect on their bodies.–Through brain implants , ingested in an aspirin, the electrodes “listen” to brain activity and sometimes stimulate activity to “inspire” an action or emotion. By tuning into the activity of the human brain by monitoring neurons the scientists can decipher thoughts and implant suggestions with ease.[U18]–At the Duke Neurogenetics department in Duke University Medical Center, undergraduate students are conducting experiments to gather information on people through brain scans, psychological tests and genetic markers. This study is led by Professor Ahmed Hariri, hopes to unlock the mysteries of a person’s innate propensity toward anxiety, alcoholism, and other defining psychological traits.[U19] The drug corporations are currently developing pharmacological substitutes to block and break people’s addictive propensities as aids to psychological treatments. The goal is to create a comprehensive genetic test for the mind.—As pharmaceutical corporations turn their attention toward manufacturing bio-electronics , conventional medicine is being phased out. [U20]Treatment will consist of electrical signaling, monitoring of the body by implants that can transmit massive amounts of data, both physical and neurological, but also administer drugs without the necessity of the patient being involved. Basically, you will not need to swallow a pill; the pill will be administered to you by an implanted electronic device. -Millions and millions of dollars are being spent to move our healthcare toward microchip implants that also control your brain in the name of curing neurological diseases in an endless barrage of technology that could quite simply change the way we think.—Epilepsy, diabetes, and obesity can be controlled by the globalist healthcare system with the “electronic impulses in the brain rather than pills or injections.” Electrical signals will control organ function (or failure) under the cover of less necessity for surgery or pill dependence.—Under the thumb of GlaxoSmithKline, head researcher Moncer Slaouni states the “challenge is to integrate the work – in brain-computer interfaces, materials science, nanotechnology, micro-power generation[U21] – to provide therapeutic benefit.”—In laboratory tests, rats have responded according to plan; showing that the neural microchip implant transferred information to the rat’s brain. When damaged, the microchip enabled the rat to perform functions that they could not do without the implant.—Intel has produced microchips that will collaborate with the human brain with computers and cell phones by 2020. By harnessing brainwaves a computer, keyboard, television and cell phones can be controlled and operated.—Computer giant IBM has researchers studying how the brainwaves adjust to the frequency of the electronic device within their vicinity to prefect the science of bioinformatics that will read brain activity in analyzing facial recognition, facial emotional responses and thought patterns for the “benefit” of technology.
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    In vitro effects of citrus oils against Mycobacterium tuberculosis and non-tuberculous Mycobacteria of clinical importance.
    J Environ Sci Health B. 2012;47(7):736-41
    Authors: Crandall PG, Ricke SC, O’Bryan CA, Parrish NM
    Abstract
    We evaluated the in vitro activity of citrus oils against Mycobacterium tuberculosis and other non-tuberculous Mycobacterium species. Citrus essential oils were tested against a variety of Mycobacterium species and strains using the BACTEC radiometric growth system. Cold pressed terpeneless Valencia oil (CPT) was further tested using the Wayne model of in vitro latency. Exposure of M. tuberculosis and M. bovis BCG to 0.025 % cold pressed terpeneless Valencia orange oil (CPT) resulted in a 3-log decrease in viable counts versus corresponding controls. Inhibition of various clinical isolates of the M. avium complex and M. abscessus ranged from 2.5 to 5.2-logs. Some species/strains were completely inhibited in the presence of CPT including one isolate each of the following: the M. avium complex, M. chelonae and M. avium subsp. paratuberculosis. CPT also inhibited the growth of BCG more than 99 % in an in vitro model of latency which mimics anaerobic dormancy thought to occur in vivo. The activity of CPT against drug-resistant strains of the M. avium complex and M. abscessus suggest that the mechanism of action for CPT is different than that of currently available drugs. Inhibition of latently adapted bacilli offers promise for treatment of latent infections of MTB. These results suggest that the antimycobacterial properties of CPT warrant further study to elucidate the specific mechanism of action and clarify the spectrum of activity.–PMID: 22560037 [PubMed – indexed for MEDLINE]
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    Hacking the human brain- researchers demonstrate extraction of sensitive data via brain-computer interface
    As hard as it is to believe, what many might think is the last bastion of total privacy, namely, the human mind, is quickly becoming just as vulnerable as the rest of our lives with the invention of mind-reading helmets and other ways to “hack” the mind.—Now security researchers from the University of California, Berkeley, the University of Oxford and the University of Geneva, have created a custom program to interface with brain-computer interface (BCI) devices and steal personal information from unsuspecting victims.
    The researchers targeted consumer-grade BCI devices due to the fact that they are quickly gaining popularity in a wide variety of applications including hands-free computer interfacing, video games and biometric feedback programs.—Furthermore, there are now application marketplaces – similar to the ones popularized by Apple and the Android platform – which rely on an API to collect data from the BCI device.—Unfortunately with all new technology comes new risks and until now, “The security risks involved in using consumer-grade BCI devices have never been studied and the impact of malicious software with access to the device is unexplored,” according to a press release.—The individuals involved with this project – which resulted in a research paper entitled “On the Feasibility of Side-Channel Attacks with Brain-Computer Interfaces,” include Ivan Martinovic and Tomas Ros of the Universities of Oxford and Geneva, respectively, along with Doug Davies, Mario Frank, Daniele Perito, and Dawn Song, all of the University of California, Berkeley.—The findings of these innovative researchers are nothing short of disturbing. They found “that this upcoming technology could be turned against users to reveal their private and secret information.” Indeed, they used relatively cheap BCI devices based on electroencephalography (EEG) in order to demonstrate the feasibility of surprisingly simple and effective attacks.–The information that can be gained by the attacks is incredibly sensitive, including, “bank cards, PIN numbers, area of living, the knowledge of the known persons.”–Most troubling is the fact that this represents “the first attempt to study the security implications of consumer-grade BCI devices,” which makes the success of the attacks that much more disconcerting. The researchers tested out their proprietary program on 28 different participants who, while they were obviously aware that they were cooperating in a study, were not aware that they were being “brain-hacked,” as it were.—Unfortunately, or fortunately depending on your perspective, the researchers found “that the entropy of the private information is decreased on the average by approximately 15% – 40% compared to random guessing attacks.”–Or as Sebastian Anthony put it in writing for ExtremeTech, “in general the experiments had a 10 to 40% chance of success of obtaining useful information.” The researchers leveraged a distinctive EEG signal pattern known as the P300 response. This brainwave pattern typically occurs when the subject recognizes something such as a friend’s face or a tool necessary to complete a given task.—Using the knowledge of the P300 response, the researchers created a program which utilizes a technique which those who are familiar with typical hacking might call a “brute force” method.–However, this method is only loosely comparable to the traditional brute force methods since we’re talking about using a brute force attack on the human mind.–The researchers did this by flashing pictures of maps, banks, PINs, etc. while monitoring the subject for any P300 responses.–After they had collected enough data from the subject, they were able to easily compare the captured information in order to see when a P300 response was triggered by a certain image.—
    Thus, this allowed the researchers to discover with surprising accuracy which bank the subject uses, where they live, and other information which could potentially be highly sensitive.–The key to capturing this information seems to be making the subject remain unaware of the fact that they are being attacked either through specially formulated “games” designed to steal personal information from the mind of the target or through a false sense of security engendered by social engineering techniques[U22].—Personally, I find it quite troubling that people could have their personal information stolen simply by playing what they think is a normal game controlled by a BCI device when in reality it is a carefully engineered piece of software designed to pull private data from the target’s mind. As Anthony correctly points out, “Moving forward, this brain hack can only improve in efficacy as BCIs become cheaper, more accurate, and thus more extensively used. ”However, Anthony incorrectly states, “Really, your only defense is to not think about the topic,” when in reality the P300 response can occur without consciously “thinking” about the topic.–The response can occur when a picture of a familiar face or location shows up, even if the individual isn’t thinking about the familiar person or the location. While someone could theoretically be on the defensive in an attempt to minimize their responses, the entire methodology of the hacker depends on avoiding detection to begin with. Therefore, if the target is already consciously on the defensive, the hacker has failed in their task of remaining in the shadows and carrying out the attack without the knowledge of the target.—That being said, if programs are created in a clever enough manner, I seriously doubt that most people would be able to tell that they’re being actively attacked in order to obtain their most private and sensitive information.
     
    TOP
    [U1]You would need Salt in the diet Just to detoxify the brain and the use of anti-solvents for the liver such as Arginine to remove this from the liver—garlic as well which has a form of Arginine in it—walnuts-peanuts ( mixe with vitamin C to offset any aflatoxins that may occur ) nootropics such as pyritrinol as well
    [U2]We are talking the psychiatric and psychological industry—a non medical medical industry that experiments and exploits people in the name of research and health—they victimize people with these chemicals—another weapon of MAS DESTRUCTION!!
    [U3]What else is New—they debilitate the person with chemical castration and then offer a whole new program since you no longer have a conscious and cannot feel —all you are now is a preprogrammed device waiting to be exploited—this is why you do not vaccinate and you do not play with these types of chemicals
    [U4]Brain Zaps, Brain Shivers, Brain Shocks. Head Shocks or Electrical shocks are a common side effect and withdrawal symptom from Antidepressants, but they can also occur with Benzodiazepines and Sleeping Pills. The symptoms are described as brief but repeated electric shock-like sensations in the brain and head, or originating in the brain but extending to other parts of the body. Moving one’s eyes quickly from side to side has also been shown to trigger Brain Zaps in more rapid frequency. Brain Zaps are often accompanied by disorientation, tinnitus, vertigo and lightheadedness.
    [U5]P-doc—pill doctor—or in the good ol days –the Pusher Man!
    [U6]Canada is owned by Corporates of all kinds—that is why Canada can never be free to be autonomous with it’s affairs— As Canadians we have been traded off for Corporate Rule which means a total exploitation of the country right sdown to it’s people
    [U7]Can Some One SAY a Agro COO took place
    [U8]And For this he was ostracized and made to be a Bad Guy —he did the right thing and got rid of the vipers that would have poisoned there country
    [U9]France is planting seeds and selling them as Non GMO when if fact they are Genetically modiifed
    [U10]Maybe we should be buying our food from russia rather then Ccanada or the USA or the South American Bio terrorist—what these countries do is export a form Of Bio engineered terror and this is truly a weapon of mass destruction
    [U11]A bribe here a take there and before you know it you went from poverty to slavery—and this is what Monsanto has done is enslaved the people of India with a weapon of Mass Destruction
    [U12]And this is How we deal with Poverty –and a Over Populated condition—we just allow people to commit suicide and self destruct because of a ” BRIBE” so much for Nationalism and being -Spiritually Enlightened- seems to be an oxymoron in this idea–take money to assist in poverty—cause bankruptsy of the farmers and then Death
    [U13]Again–getting support to up build the country and reduce the strain and stress of fiscal burdens and instead you increase the cost of buying seed and growing food and sabotage principles in agriculture that has sustained a nation
    [U14]You have got to be Kidding—needs assistance with there drugs—orr rather a way to monitor them and there whereabouts
    [U15]Spy monitoring chemical reaction where they can modulate the chemistry—and bring on a condition
    [U16]What Culture?? And who’s
    [U17]Humanity combining with android —makes Us what??? Connected to a AI—Alien Technolgy
    [U18]No privacy No quiet mind no Individualism—just a collective connected to a Alien Intelligence
    [U19]This is Bull Shit—this is being done to immobilize you at will there will be no free will
    [U20]Beyond addiction and straight to dependency
    [U21]The challenge is to get you to surrender your will so they can implant and connect you to the Alien Intelligence
    [U22]So if you play video games and they are connected to a CPU then you may be having your brain Hacked
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    TOP A
    HOME
     
    Show of the Month September 7 2012
     
    How Long Will Homemade Colloidal Silver
     
    Candida albicans yeast-hyphal transition and biofilm formation Its Potency
    Inhibition by Solidago virgaurea water extracts
     
    Parthenolide, a sesquiterpene lactone, expresses multiple anti-cancer and anti-inflammatory activities
     
    After-Birth Abortion- Eugenicists Say Babies are a Parasitic Burden on Society
     
    Thyme May Be Better for Acne Than Prescription Creams
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    How Long Will Homemade Colloidal Silver Last Before It Begins to Lose Its Potency
     
    How Long Will Homemade Colloidal Silver Last Before It Begins to Lose Its Potency?
    Tens of thousands of people throughout North America and around the world now make their own home-made colloidal silver using colloidal silver generators.
     
    By far the #1 question — How long will a batch of homemade colloidal silver last before it begins to lose its potency?
     
    Rule of Thumb— If you know what sign to look for, colloidal silver will tell you when it’s beginning to lose potency. –The general rule of thumb is to watch for precipitation of silver particles in your storage container. —
    “Precipitation” means the silver particles are beginning to fall out of suspension in the solution. The resulting residue will begin to visibly coat the sides or bottom of your storage container. That is the sure sign that your batch of homemade colloidal silver (or even store bought colloidal silver, for that matter) is beginning to lose its potency.—All you have to do is examine your storage container to see whether or not a light silver-gray residue is beginning to form on the sides or bottom of the container. —
    If you’re using a dark glass storage container, such as the amber glass bottles many people like to store their homemade colloidal silver in (see photo above), you may have to hold the bottle up to a bright light, or shine a flashlight through it, and carefully examine the sides and bottom. –If you see a coating or discoloration beginning to form on the glass sides or bottom, then you know your silver particles are beginning to precipitate, the batch is losing its potency, and it’s time to make a fresh batch. –Otherwise, if there is no visible residue forming in your storage container, your homemade colloidal silver is likely as fresh and potent as the day you made it.
     
    Why Do Silver Particles Fall Out of Suspension?
     
    There are a number of reasons for the precipitation of silver particles. —
    For example, if your colloidal silver generator is producing overly large silver particles, you will often see premature precipitation of the silver particles in your storage container. The more silver-gray residue you see beginning to coat the sides or bottom of your storage container, the weaker in potency your homemade colloidal silver solution is becoming.—
    Also, it’s important to note that using salt or baking soda or other additives to boost the speed of the colloidal silver-making process will add to the overall size and weight of the silver particles (due to agglomeration of the particles into larger particle clusters). This will ultimately cause your silver particles to precipitate prematurely and begin forming a residue on the sides or bottom of your storage container. Once again, this is a sure sign that your batch of homemade colloidal silver is beginning to lose its potency.
     
    What’s more, if your storage container is exposed to excessive heat or excessive cold or even excessive sunlight or other bright light for prolonged periods of time, then precipitation of the silver particles could begin taking place.
     
    The bottom line is that any time you can see that your silver particles are precipitating our of solution and coating the bottom or sides of your storage container, then it’s time to make a fresh, new batch of colloidal silver. It’s that simple.
     
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    Inhibition of Candida albicans yeast-hyphal transition and biofilm formation by Solidago virgaurea water extracts.–
    J Med Microbiol. 2012 Jul;61(Pt 7):1016-22 –Authors: Chevalier M, Medioni E, Prêcheur I
    Abstract
    Xerostomia is a decrease of saliva secretion, which can unbalance the oral microflora, mainly to the benefit of Candida albicans. The aim of the present study was to find a plant extract that could create an unfavourable environment for Candida, and would, therefore, be appropriate for use in a dry-mouth daily-care mouthwash. Water extract from the herbaceous plant Solidago virgaurea (Goldenrod)[U1] was selected due to its saponin content (plant detergents). Saponin concentrations reached 0.7 and 0.95 mg ml(-1) in S. virgaurea subsp. virgaurea and S. virgaurea subsp. alpestris extracts, respectively. C. albicans was grown in liquid medium and cells were counted by microscopic examination after 0, 4 and 24 h of incubation. Solidago extracts did not inhibit the growth of C. albicans (four strains), Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus mutans, Streptococcus salivarius or Enterococcus faecalis. When inocula were incubated with Solidago extract for 4 and 24 h, we observed a decrease in Candida yeast-hyphal transition.[U2] Candida biofilms were then prepared in microtitre plates and treated with plant extracts at 0 h, to estimate biofilm formation, or at 18 h to estimate the effect of the saponin on pre-formed biofilms. Biofilm formation and pre-formed biofilms were both strongly inhibited. In conclusion, the S. virgaurea extract was efficient against two key virulence factors of C. albicans: the yeast-hyphal transition phase and biofilm formation.-PMID: 22422572 [PubMed – indexed for MEDLINE]
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    Parthenolide, a sesquiterpene lactone, expresses multiple anti-cancer and anti-inflammatory activities.
    Inflammation. 2012 Apr;35(2):560-5–Authors: Mathema VB, Koh YS, Thakuri BC, Sillanpää M
    Abstract
    Parthenolide, a naturally occurring sesquiterpene lactone derived from feverfew (Tanacetum parthenium), exhibits exceptional anti-cancer and anti-inflammatory properties, making it a prominent candidate for further studies and drug development. In this review, we briefly investigate molecular events and cell-specific activities of this chemical in relation to cytochrome c, nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB), signal transduction and activation of transcription (STAT), reactive oxygen species (ROS), TCP, HDACs, microtubules, and inflammasomes. This paper reports that parthenolide shows strong NF-κB- and STAT-inhibition-mediated transcriptional suppression of pro-apoptotic genes. This compound acts both at the transcriptional level and by direct inhibition of associated kinases (IKK-β). Similarly, this review discusses parthenolide-induced ROS-mediated apoptosis of tumor cells via the intrinsic apoptotic signaling pathway. The unique ability of this compound to not harm normal cells but at the same time induce sensitization to extrinsic as well as intrinsic apoptosis signaling in cancer cells provides an important, novel therapeutic strategy for treatment of cancer and inflammation-related disorders.—PMID: 21603970 [PubMed – indexed for MEDLINE]
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    After-Birth Abortion- Eugenicists Say Babies are a Parasitic Burden on Society
     
    According to Alberto Giubilini and Francesca Minerva, “after-birth abortion” is proposed as a form of “contraception” that would allow babies to be killed after they are born.
    In a paper published in the Journal of Medical Ethics:
    “[W]hen circumstances occur after birth such that they would have justified abortion, what we call after-birth abortion should be permissible. [U3]… [W]e propose to call this practice ‘after-birth abortion’, rather than ‘infanticide,’ to emphasize that the moral status of the individual killed is comparable with that of a fetus … rather than to that of a child.–Therefore, we claim that killing a newborn could be ethically permissible in all the circumstances where abortion would be.[U4] Such circumstances include cases where the newborn has the potential to have an (at least) acceptable life, but the well-being of the family is at risk.”—Giubilini and Minerva believe that infants are a “threat” to parents because of their financial burden to their parents and that this justifies the murder of new-born babies.-In the Senate, Joe Pitts and Chris Smith spoke out against this ideology. Smith explains: “Giubilini and Minerva say the devaluation of new-born babies is inextricably linked to the devaluation of unborn children.”–Ann Furedi of the British Pregnancy Advisory -Board stated that it was of no consequence to define the point when a fetus is subject to legal limitation with regard to abortion rights. Giubilini and Minerva agree with this summation by stating that “merely being human is not in itself a reason for ascribing someone a right to life. Indeed, many humans are not considered subjects of a right to life,” such as “spare embryos where research on embryo stem cells is permitted” or “fetuses where abortion is permitted.”[U5]—By defining personhood as being established “some time” after birth, Giubilini and Minerva assert that a fetus has no claim to personhood, and therefore no right to life.
    They write that-“n order for a harm to occur, it is necessary that someone is in the condition of experiencing that harm. If a potential person, like a fetus and a newborn, does not become an actual person, like you and us, then there is neither an actual nor a future person who can be harmed, which means that there is no harm at all. … In these cases, since non-persons have no moral rights to life, there are no reasons for banning after-birth abortions. … [U1]—-Indeed, however weak the interests of actual people can be, they will always trump the alleged interest of potential people to become actual ones, because this latter interest amounts to zero.”
    Giubilini and Minerva support previous arguments for infanticide regardless of whether or not the baby were given a short lifespan due to a medical prognosis.-Simply by being born the baby is regarded as an “unbearable burden on someone, then people should be given the chance of not being forced to do something they cannot afford.”[U2]—Parents, relatives and even society should be enabled to force a mother to submit her child to infanticide because of the benefits that one less person would bring to our world.[U3]—Giubilini and Minerva state that infants are dependent on parents just as fetuses are parasites to the mother’s body. And since no one can ensure that this person will not die prematurely in the future, the investment of resources, time and emotional support cannot be assumed to be a right of the infant.—During pregnancy, the development of the fetus can reveal defects that can legally warrant a partial-birth abortion. Giubilini and Minerva argue that this fact can be extended to after birth because a defective baby can be an “economical, social or psychological” burden because of the energy needed to care for the child.—They say that “people should be given the chance of not being forced to do something they cannot afford.”—The prevention of right to life for infants has another supporter in a study published by the Archives of General Psychiatry (AGP) that asserted pre-mature babies are at an increased risk for bipolar disorder, depression and a wide range of psychosis that would render them a danger to themselves and others later in life[U4].—Marjorie Wallace, chief executive of a SANE, a mental health charity, stated: “We already knew that premature birth may be linked to schizophrenia, but to see evidence linking it to a range of psychiatric conditions which required hospitalization is striking.”[U5]–While Giubilini and Minerva use eugenics agendas to coerce the public into believing that society would be better off without certain “burdensome” infants, an outright attack on fertility is taking place. –[U6]Dr. Martin Matzuk , professor of molecular biology, molecular and human genetics, and pharmacology at Baylor College of Medicine (BCM), is working on a birth-control pill for men that blocks the proteins essential for sperm production – rendering men “voluntarily” infertile.[U7]–The BCM has a long history of working to expanding the eugenics agenda with the use of genetic technologies; including collaboration with the German Nazis and their march toward using genetics to create a “better human race”.—By looking for “justice as fairness” with the ethical practice of genetics and eugenics concerning applied science and social constructs.—The advantage of eugenics ideology in genetic technology is viewed as “the greatest benefit of individuals with the least advantages.” And so by subverting the fact of eugenics in genetic advances will alleviate prejudice and make sure that the eugenics agenda is devoid of negative perceptions so that the genetically disadvantaged could be touted as the beneficiaries of eugenic applications in genetic technologies.—Last month, the Bill and Melinda Gates Foundation (BMGF) hosted The London Family Planning Summit (LFPS) where the BMGF secured funding for depopulation efforts in Africa, India and the Southeast Asian region.
    Melinda Gates believes that if she can prevent 40% of people who would otherwise have been born, she could justify her family planning scheme to make women healthier who’s “families are more successful and their communities are more prosperous.”—Simply put: the BMGF has classified “unwanted” pregnancies as justification for killing people and they are focusing on eventually eliminating this number to reduce the world’s population. Africa, a big focus for the BMGF is being targeted along with Muslim nations.—In this propaganda cartoon, the depiction of brown and black women as disfigured potatoes having much more fun because they have fewer children is not only offensive, but telling of how these global Elite view the people they purport to be “saving”.—By preventing births, the film says that 600,000 people would not be born. Contraception as a first step in the global Elite’s plan to depopulation by appearing to help save lives of women could be quite effective.
     
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    Thyme May Be Better for Acne Than Prescription Creams
     
    Thyme. Herbal preparations of thyme could be more effective at treating skin acne than prescription creams, new research suggests.
    ScienceDaily (Mar. 27, 2012) — Herbal preparations of thyme could be more effective at treating skin acne than prescription creams, according to research recently presented at the Society for General Microbiology’s Spring Conference in Dublin. Further clinical testing could lead to an effective, gentler treatment for the skin condition.—Researchers from Leeds Metropolitan University tested the effect of thyme, marigold and myrrh tinctures on Propionibacterium acnes — the bacterium that causes acne by infecting skin pores and forming spots, which range from white heads through to puss-filled cysts. The group found that while all the preparations were able to kill the bacterium after five minutes exposure, thyme was the most effective of the three. What’s more, they discovered that thyme tincture had a greater antibacterial effect than standard concentrations of benzoyl peroxide — the active ingredient in most anti-acne creams or washes.–Dr Margarita Gomez-Escalada who is leading the research project explained how tinctures are made from plants and herbs. “The plant material is steeped in alcohol for days or even weeks to prepare a tincture. This process draws out the active compounds from the plant. While thyme, marigold and myrrh are common herbal alternatives to standard antibacterial skin washes, this is the first study to demonstrate the effect they have on the bacterium that causes the infection leading to acne,” she said. The researchers used a standard in vitro model that is used to test the effect of different substances applied to the skin. The effects of the tinctures were measured against an alcohol control — proving their antibacterial action was not simply due to the sterilizing effect of the alcohol they are prepared in.—-These initial findings pave the way for more research into the use of tinctures as a treatment for acne. “We now need to carry out further tests in conditions that mimic more closely the skin environment and work out at the molecular level how these tinctures are working. If thyme tincture is proven to be as clinically effective as our findings suggest, it may be a natural alternative to current treatments,” explained Dr Gomez-Escalada.—A herbal treatment for acne would be very welcome news — particularly for acne sufferers who experience skin sensitivity. “The problem with treatments containing benzoyl peroxide is the side-effects they are associated with,” said Dr Gomez-Escalada. “A burning sensation and skin irritation are not uncommon. Herbal preparations are less harsh on the skin due to their anti-inflammatory properties while our results suggest they can be just as, if not more, effective than chemical treatments.”
    Story Source-The above story is reprinted from materials provided by Society for General Microbiology.
     
     
    TOP A
    [U1]You know what is even more alarming these to asses from waste—may actually be extraterrestrial defining what makes us human and then stating that if they are gotten to before they are developed then they are nothing more then human Byproduct????
    [U2]Life is boiling down to a financial report??? This is huge eh—when couples start out a lot are not well off and start families—they would be financially strained—that’s life in the end —things progress and people evolve financially and come out ok—so this dichotomy is about again stating something and then just makig it ok!!
    [U3]Hey we are doing what China did killing off all females and there villages would force the mums to surrender to the state the fetuses—we are now —Going to be Worse
    [U4]Interesting Eh—they have the Ability of God to make that kind of prediction—and when did Psychiatry ever become a real science—even among there peers they are laughed at and are not respected or treated as a branch of health and in fact are disdained at—and then we are to believe them on this ?
    [U5]Is this presumption—a hypothetisi—
    [U6]Now if you believe in Aliens –there is a species out there that actually hate any 2 male/female relationship to occur and work and weave to destroy that connection—makes you wonder about this—
    [U7]When these doctors use this on themselves after 20 years let’s see if there balls are still intact—or if there male organ is still there—you never know with the medical if this is a form of chemical castration
    [U1]Tea—or percolated tea
    [U2]Any of the threadlike filaments forming the mycelium of a fungus.
    [U3]Why not call it what it really is—Resources—you have your child killed off like offering Human Saccarifice to the gods/ Aliens—of a millennium —when the practice of offering infants to dagon by throwing infants and babies into a fiery pit–or ripping out ther hearts and the blood being drank to fill the belly of alien/gods—the differnce today is the Genetic material will be used for some transhuman or genetic abomination —
    [U4]What a Crock of Horse SHIT!!!—you ‘re going to re define the paradigm and Just by saying it is OK that is going to make it OK—-wow that means I can say it is ok for me to have a million dollars given to me by the gov’t because as a Citizen I am entitled to this and the Gov’t is going to give this to me –because I said so!!!! Someone give this person head a shake!!!!
    [U5]Now we are Playing god –determining what is and is not life—again the arrogance is unbelievable
    [U6]You know what is even more alarming these to asses from waste—may actually be extraterrestrial defining what makes us human and then stating that if they are gotten to before they are developed then they are nothing more then human Byproduct????
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    Show of the Month September 10- 2012
     
    Cynarin-rich sunflower (Helianthus annuus) sprouts possess both antiglycative and antioxidant activities
     
    Ig Human and Soil Bacteria Swap Antibiotic-Resistance Genes
     
    Aspirin May Lower the Risk of Pancreatic Cancer
     
    Daily Aspirin Usage Linked to Lower Cancer Mortality
     
    Growing Strong Muscles Without Working Out
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    Cynarin-rich sunflower (Helianthus annuus) sprouts possess both antiglycative and antioxidant activities.
    J Agric Food Chem. 2012 Mar 28;60(12):3260-5
    Authors: Sun Z, Chen J, Ma J, Jiang Y, Wang M, Ren G, Chen F
    Abstract
    The present study examined the antiglycative and antioxidant properties of four edible sprouts popular in Chinese markets. In a protein-reducing sugar model, the sunflower sprout Helianthus annuus exhibited the strongest inhibitory effects against the formation of advanced glycation end products (AGEs).[U1] At a concentration of 1.0 mg/mL, its inhibitory rate achieved 83.29%, which is stronger than that of aminoguanidine (1 mM), a well-known synthetic antiglycative agent (with an inhibitory rate of 80.88%). The antioxidant capacity of H. annuus was also much stronger than other sprout samples in terms of free radical scavenging and reducing properties. An active ingredient contributing to the observed activities was identified as cynarin (1,5-dicaffeoylquinic acid). This is the first report of the novel function of cynarin to intervene against glycoxidation. Given the key roles of AGEs and oxidation in the pathogenesis of diabetes, the sunflower sprout H. annuus rich in cynarin may be regarded as a beneficial food choice for diabetic patients.—PMID: 22394088 [PubMed – indexed for MEDLINE]
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    Ig Human and Soil Bacteria Swap Antibiotic-Resistance Genes
     
    Escherichia coli bacteria of the strain O157:H7. Soil bacteria and bacteria that cause human diseases have recently swapped at least seven antibiotic-resistance genes.)—-ScienceDaily (Aug. 30, 2012) — Soil bacteria and bacteria that cause human diseases have recently swapped at least seven antibiotic-resistance genes, researchers at Washington University School of Medicine in St. Louis report Aug. 31 in Science.According to the scientists, more studies are needed to determine how widespread this sharing is and to what extent it makes disease-causing pathogens harder to control.—-“It is commonplace for antibiotics to make their way into the environment,” says first author Kevin Forsberg, a graduate student. “Our results suggest that this may enhance drug resistance in soil bacteria in ways that could one day be shared with bacteria that cause human disease.”—[U2]Among the questions still to be answered: Did the genes pass from soil bacteria to human pathogens or vice versa? And are the genes just the tip of a vast reservoir of shared resistance? Or did some combination of luck and a new technique for studying genes across entire bacterial communities lead the scientists to discover the shared resistance genes?–Humans only mix their genes when they produce offspring, but bacteria regularly exchange genes throughout their lifecycles. This ability is an important contributor to the rapid pace of bacterial evolution. When a bacterial strain develops a new way to beat antibiotics, it can share the strategy not only with its descendants but also with other bacteria. Earlier studies by other scientists have identified numerous resistance genes in strains of soil bacteria. However, unlike the seven genes described in this report, the earlier genes were dissimilar to their analogs in disease-causing bacteria, implying that they had crossed between the bacterial communities a long time ago.—Most of the antibiotics used to fight illness today originated from the soil. Bacteria use the antibiotics, in part, as weapons to compete with each other for resources and survival. Scientists have long acknowledged that gives environmental bacteria an evolutionary incentive to find ways to beat antibiotics.–“We wanted to try to get a broader sense of how often and extensively antibiotic-resistance genes are shared between environmental bacteria and pathogens,” says senior author Gautam Dantas, PhD, assistant professor of pathology and immunology.—The researchers isolated bacteria from soil samples taken at various U.S. locations. The bacteria’s DNA was broken into small chunks and randomly inserted into a strain of Escherichia coli that is vulnerable to antibiotics. Scientists treated the altered E. coli with multiple antibiotics.—“We knew that any E. coli that continued to grow after these treatments had picked up a gene from the soil bacteria that was helping it fight the antibiotics,” Forsberg says. Scientists took the DNA from soil bacteria out of the surviving E. coli and prepared it for high-throughput sequencing. Dantas’ laboratory has developed techniques that make it possible to simultaneously sequence and analyze thousands of chunks of DNA from many diverse microorganisms. The DNA can be selected for a single function, such as antibiotic resistance. When the scientists compared antibiotic-resistance genes found in the soil bacteria to disease-causing bacteria, they were surprised to find some genes were identical not only in the sections of the genes that code for proteins but also in nearby non-coding sections that help regulate the genes’ activities.–Since bacteria have such large population sizes and rapid reproduction times, their DNA normally accumulates mutations and other alterations much more quickly than the DNA of humans. The lack of changes in the resistance genes identified in the study suggests that the transfers of the genes must have occurred fairly recently[U3], according to Dantas.-In some soil bacteria, the genes are present in clusters that make the bacteria resistant to multiple classes of antibiotics, including forms of penicillin, sulfonamide and tetracycline.—“I suspect the soil is not a teeming reservoir of resistance genes,” Dantas says. “But if factory farms or medical clinics continue to release antibiotics into the environment, it may enrich that reservoir, potentially making resistance genes more accessible to infectious bacteria.”–Story Source-The above story is reprinted from materials provided by Washington University School of Medicine. The original article was written by Michael C. Purdy. —Journal Reference-K. J. Forsberg, A. Reyes, B. Wang, E. M. Selleck, M. O. A. Sommer, G. Dantas. The Shared Antibiotic Resistome of Soil Bacteria and Human Pathogens. Science, 2012; 337 (6098): 1107 DOI: 10.1126/science.1220761
     
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    Aspirin May Lower the Risk of Pancreatic Cancer
    ScienceDaily (Apr. 10, 2011) — The use of aspirin at least once per month is associated with a significant decrease in pancreatic cancer risk, according to results of a large case-control study presented at the AACR 102nd Annual Meeting 2011, held in Orlando, Florida, April 2-6.— For the current study, Tan and colleagues enrolled 904 patients who had documented pancreatic cancer and compared them with 1,224 healthy patients. All patients were at least 55 years old and reported their use of aspirin, NSAIDs and acetaminophen by questionnaire.–Results showed that people who took aspirin at least one day during a month had a 26 percent decreased risk of pancreatic cancer compared to those who did not take aspirin regularly. The effect was also found for those who took low-dose aspirin for heart disease prevention at 35 percent lower risk, according to Tan.—The researchers did not see a benefit from non-aspirin NSAIDs or acetaminophen. “This provides additional evidence that aspirin may have chemoprevention activity against pancreatic cancer,” said Tan. He added that more data must be gathered before we can prove a real benefit.–Story Source-The above story is reprinted from materials provided by American Association for Cancer Research.
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    Daily Aspirin Usage Linked to Lower Cancer Mortality
    ScienceDaily (Aug. 10, 2012) — A large new observational study finds more evidence of an association between daily aspirin use and modestly lower cancer mortality, but suggests any reduction may be smaller than that observed in a recent analysis. The study, appearing early online in the Journal of the National Cancer Institute (JNCI), provides additional support for a potential benefit of daily aspirin use for cancer mortality[U4], but the authors say important questions remain about the size of the potential benefit. —A recent analysis pooling results from existing randomized trials of daily aspirin for prevention of vascular events found an estimated 37% reduction in cancer mortality among those using aspirin for five years or more. But uncertainty remains about how much daily aspirin use may lower cancer mortality, as the size of this pooled analysis was limited and two very large randomized trials of aspirin taken every other day found no effect on overall cancer mortality.—For the current study, American Cancer Society researchers led by Eric J. Jacobs, Ph.D., analyzed information from 100,139 predominantly elderly participants in the Cancer Prevention Study II Nutrition Cohort who reported aspirin use on questionnaires, did not have cancer at the start of the study, and were followed for up to 11 years. They found daily aspirin use was associated with an estimated 16% lower overall risk of cancer mortality, both among people who reported taking aspirin daily for at least five years and among those who reported shorter term daily use. The lower overall cancer mortality was driven by about 40% lower mortality from cancers of the gastrointestinal tract (such as esophageal, stomach, and colorectal cancer) and about 12% lower mortality from cancers outside the gastrointestinal tract.———The reduction in cancer mortality observed in the current study is considerably smaller than the 37% reduction reported in the recent pooled analysis of randomized trials. The authors note that their study was observational, not randomized, and therefore could have underestimated or overestimated potential effects on cancer mortality if participants who took aspirin daily had different underlying risk factors for fatal cancer than those who did not. However, the study’s large size is a strength in determining how much daily aspirin use might lower cancer mortality.—“Expert committees that develop clinical guidelines will consider the totality of evidence about aspirin’s risks and benefits when guidelines for aspirin use are next updated,” said Dr. Jacobs. “Although recent evidence about aspirin use and cancer is encouraging, it is still premature to recommend people start taking aspirin specifically to prevent cancer. Even low-dose aspirin can substantially increase the risk of serious gastrointestinal bleeding. Decisions about aspirin use should be made by balancing the risks against the benefits in the context of each individual’s medical history. Any decision about daily aspirin use should be made only in consultation with a health care professional.”–Story Source-The above story is reprinted from materials provided by American Cancer Society, via EurekAlert!, a service of AAAS. -Journal Reference-Eric J. Jacobs, Christina C. Newton, Susan M. Gapstur, Michael J. Thun. Daily Aspirin Use and Cancer Mortality in a Large US Cohort. Journal of the National Cancer Institute, August 10, 2012 DOI: 10.1093/jnci/djs318
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    Growing Strong Muscles Without Working Out? ‘Hulk’ Protein, Grb10, Controls Muscle Growth
    ScienceDaily (Aug. 30, 2012) — Scientists have moved closer toward helping people grow big, strong muscles without needing to hit the weight room. Australian researchers have found that by blocking the function of a protein called Grb10 while mice were in the womb, they were considerably stronger and more muscular than their normal counterparts. This discovery appears in the September 2012 issue of The FASEB Journal. Outside of aesthetics, this study has important implications for a wide range of conditions that are worsened by, or cause muscle wasting, such as injury, muscular dystrophy, Type 2 diabetes, and problems produced by muscle inflammation.—“By identifying a novel mechanism regulating muscle development, our work has revealed potential new strategies to increase muscle mass,[U5]” said Lowenna J. Holt, Ph.D., a study author from the Diabetes and Obesity Research Program at the Garvan Institute of Medical Research in Sydney, Australia. “Ultimately, this might improve treatment of muscle wasting conditions, as well as metabolic disorders such as Type 2 diabetes.”—To make this discovery, Holt and colleagues compared two groups of mice. Once group had disruption of the Grb10 gene, and were very muscular. The other group, where the Grb10 gene was functional, had normal muscles. Researchers examined the properties of the muscles in both adult and newborn mice and discovered that the alterations caused by loss of Grb10 function had mainly occurred during prenatal development. These results provide insight into how Grb10 works, suggesting that it may be possible to alter muscle growth and facilitate healing, as the processes involved in muscle regeneration and repair are similar to those for the initial formation of muscle.[U6]–“Don’t turn in your gym membership just yet,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “If you want big muscles, the classic prescription still applies: lift heavy things, eat and sleep right, and have your hormones checked. But this study shows that when we understand the basic science of how muscle fibers grow and multiply, we will be able to lift the burden — literally — of muscle disease for many of our patients.”—Story Source-The above story is reprinted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS. –Journal Reference-L. J. Holt, N. Turner, N. Mokbel, S. Trefely, T. Kanzleiter, W. Kaplan, C. J. Ormandy, R. J. Daly, G. J. Cooney. Grb10 regulates the development of fiber number in skeletal muscle. The FASEB Journal, 2012; 26 (9): 3658 DOI: 10.1096/fj.11-199349
     
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    [U1]Extrememly Effective Anti Aging effect-it appears to block the breaking down of the cells protein/sugars–and it appears to be a food of choice for Diabetics as wll—
    [U2]This is already happening—the Gut flora is now manufacturing new strands of genetic material causing the intestinal tract and digestive system to falter and to have wide spread yeast or fungal or viral penetration where it could not otherwise be—this has been going on globally and the ailments and illnesses are a direct result of food pathogens caused byt outside chemicals–estrogens- pesticides -insecticides and fungals—this has been disrupting the flow of people staying healthy
    [U3]Now here’s a thought—what if the chemtrail fallout from the sky with the radioactive materials—toxic metals such as aluminum ( one of the worst if not the worst) barium titanium-baterial- fungal-microbial-viral saturated the soil —wna what if you added a Genetically Modified seed to this mix—what happens??? what if we added more genetic material with this what is the consideration or theory here—–it is imperative we stop the chemming of our planet and the genetically altering of the earth—these are the real weapons of mass destruction
    [U4]Early Studies shown that when aspirin was combined with arginine it reduced or cured Pancreatic cancers–and lung —and intestinal —the effect was pronounced with the combination—if you have a cnacer this is something to explore–
    [U5]GENETICS ANYONE —People that is
    [U6]Human Genetic?? Imagine while your being born—Mum has a chip in her and now is being read by a monitor and they decide to releases a pathogen—scary
     
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    Show of the Mont September 14-2012
     
    COPPER AND ZINC SALICYLATES
     
    Bacterial Cause Found for Skin Condition Rosacea
     
    Aqueous garlic extract and its phytochemical profile– special reference to antioxidant status
     
    Hexavalent chromium and its effect on health: possible protective role of garlic
     
    Scientists Pursue Connection between Infectious Disease Afflicting Cattle and Morgellons Disease Affecting Humans

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    COPPER AND ZINC SALICYLATES—-Two Excellent Inflammation Fighters
    By Walter Last
    Copper is an essential trace mineral. All tissues of the body need it for normal metabolic functions. Sometimes there is too much of the inorganic form in drinking water (acid water flowing through copper pipes). It can then gradually accumulate in the body and lead to toxicity symptoms with signs of zinc deficiency, over-stimulation, psychosis and liver damage.However, in organic  form as chelates or copper complexes it is excellent for reducing inflammations, strengthening connective tissue, restoring hair colour and the oxidative energy metabolism as well as fighting parasites and cancer and may sometimes improve brain and liver functions.—If you give animals a choice between drinking normal water and water in which a copper pipe has been immersed, they will reportedly prefer the high copper water. This helps to keep them free of parasites. Copper armbands are well known to reduce arthritis. Copper serum levels are elevated up to threefold above normal with inflammations and with many chronic and infectious diseases, apparently because the body mobilises all tissue stores of copper to fight the condition. During remissions the copper levels return back to normal.—The most effective anti-inflammatory agents are copper complexes. Commonly these are related to salicylic acid. In addition, copper ascorbate has strong anti-viral properties. Copper salicylate has a better anti-inflammatory effect than cortisone but without the side effects. In addition it has also good anti-cancer, anti-tremor and anti-convulsive properties, suitable for treatment of epilepsy and possibly Parkinson’s disease. Children with severe copper deficiency constantly have convulsive seizures. Another feature of severe copper deficiency is degeneration of the central nervous system. There are at least 6 important copper-dependent enzymes in the brain. One of these is required for the conversion of tyrosine into dopamine which is lacking in Parkinson’s disease. A copper enzyme is also needed for the synthesis of adrenalin (epinephrine).–In experiments copper salicylate prevented chemically induced skin cancers. Furthermore, a single application resulted in a 55% reduction in experimental animal tumours in 20 weeks. The main metabolic defect of cancer cells, according to Dr Johanna Budwig and other researchers, is a deficiency of the enzyme cytochrome oxidase. This causes a blockage in the cellular respiration or oxidative energy production of the affected cells. Budwig claims that plenty of linseed oil and sulphur amino acids (L-cysteine and especially L-methionine) help to correct this situation.—Cytochrome oxidase is a copper dependent enzyme and additional copper might be of further benefit. In the final stages of this oxidative energy production electrons are transferred to copper (II) and iron (III) in the cytochrome oxidase to form copper (I) and iron (II). In the last step these electrons are then transferred to oxygen, which now can attract hydrogen ions to form water. In cancer cells this transfer of electrons to oxygen is blocked and energy is being produced very inefficiently by converting glucose into lactic acid.–However, practical experience has shown that copper is more important to prevent cancer or a regrowth of tumours and possibly with dormant tumours. If growing tumours are present, then copper is needed to form new blood vessels. Taking high amounts of zinc creates a relative copper deficiency and helps to prevent the formation of new blood vessels.—Copper salicylates have a similar action as superoxide dismutase (SOD) to protect cells from free radicals. Dr John R.J. Sorenson at the University of Arkansas has done most of the research work on copper complexes. In one of his publications he states that with the exception of Wilson’s disease, there are no chronic degenerative diseases in man known to result from non-industrial exposure to copper.–Dr Werner Hangerter, head of medicine at the University of Kiel, successfully used copper salicylates for over 20 years with more than 1100 patients with rheumatoid arthritis and other inflammatory conditions. Of 620 patients with rheumatoid arthritis 65% became symptom free and another 23% improved significantly, only 12% remained unchanged. With acute rheumatic fever 100% became symptom free. Also neuromuscular problems such as sciatica, neuralgia and cervical spine-shoulder problems responded very well. Even short-term treatment of rheumatoid arthritis resulted in long-term remissions or improvements.—The therapeutic potency and safety of the copper complexes of aspirin (acetyl-salicylic acid) and salicylic acid is much better than for aspirin itself or for inorganic copper. These complexes are 5 to 8 times more effective than aspirin but less toxic. The therapeutic index (the margin between effectiveness and toxic effects) has been stated as being significantly greater than for other anti-inflammatory drugs. While aspirin causes or aggravates peptic ulcers, the copper complexes have a better ulcer-healing effect than commonly used anti-inflammatory ulcer drugs. Harmful effects of aspirin, salicylic acid and similar drugs apparently arise because they bind copper in the body and cause a localised copper deficiency in the tissues.—Unfortunately, copper salicylate or other effective copper complexes are not normally available or only in very low doses, presumably because they cannot be patented. However, they are relatively easy to make for someone who wants to experiment. Order salicylic acid through a cooperating pharmacist and dissolve 2 g or about half a teaspoonful in half a litre of hot water.–Use covered glassware and distilled or de-ionised water and several pieces of copper with a large surface area immersed in it. Keep it warm, between 60º and 90ºC or just below boiling. Add more water as required and adjust the final volume to 500 ml. At first a light yellow-greenish colour develops, but at one point the colour considerably deepens. This may happen after 15 to 20 hours of heating and you may now let it cool and fill into a glass bottle.—Near the end of the heating process and during storage black copper oxide starts forming and slowly accumulates at the bottom. This is due to copper being converted from the original one-valent copper (I) salicylate to two-valent copper (II) salicylate. With this, the salicylic acid binds only half of the dissolved copper and the rest becomes copper oxide. The effectiveness of the solution does not seem to be affected by this and the amount of copper in the complex is not related to its potency. From time to time you may decant the solution from any settled copper oxide and crystals or filter it through tissue paper.—Copper (I) salicylate is a strong antioxidant and also appears to have good anti-inflammatory qualities, but all the published papers are on copper (II) salicylate. However the only data for a Cu (I) complex that I could find (penicillamine) showed it to have even stronger anti-inflammatory activity than the corresponding Cu (II) complex. Initially copper (I) will dominate in the self-prepared copper salicylate but the more copper oxide precipitates the more will copper (II) gain the upper hand. While salicylic acid only dissolves in hot water, copper (II) salicylate is easily soluble in cold water and is very stable and generally well tolerated when taken orally.Copper salicylate is also excellent for external use as packs or rubs on sites of tumours and inflammation, also rubbing it on skin prone to skin cancer. To improve its skin absorption you may mix it with some aloe vera gel or follow the copper salicylate rub with some aloe vera.—For internal use with generalised inflammations or other indications 60 mg of copper salicylate have been used in clinical trials once or twice and up to four times daily. Try a teaspoonful (approximately 25 mg of copper salicylate) three times daily in liquids with meals, preferably under professional supervision. For short-term use you may also double this amount. When it produces the desired effect, cut back to a maintenance dose of 1 teaspoonful a
    day or interrupt the intake after 2 weeks to see what happens.—Copper (I) salicylate is a strong antioxidant and may interfere with oxygen therapy. Therefore, it is advisable to alternate periods of taking high doses of copper salicylate with periods of intensive oxygen therapy. However, external application of copper salicylate should still be fine during oxygen therapy.—Another possibility of making copper salicylate yourself is by ingesting sodium salicylate and a copper chelate together. Copper salicylate then appears to form in the stomach. In some countries sodium salicylate is available as tablets, in others it may be obtained from a friendly chemist/pharmacist as a crystallised powder. Copper chelate, commonly as amino acid chelate or gluconate, may be available from a health food shop or over the Internet. Taking a 650 mg tablet of sodium salicylate together with 5 mg of copper in chelated form has reportedly eliminated severe arthritic pain. As maintenance dose a 350 mg tablet of sodium salicylate together with 2.5 mg of copper have been taken up to three times a day. If the sodium salicylate is available as powder, you may assume that a level teaspoonful is about 4 g. By dividing this into 6 equal portions you will have about 650 mg per portion.—You also find a source of copper salicylate tablets on the Internet or you may be able to obtain copper (II) salicylate crystals from a supplier of laboratory or fine chemicals. In this case you could divide a rounded teaspoonful into 100 equal parts, each part would then be approximately 50 mg.——–For a potent anti-viral remedy you may produce copper ascorbate. This is not difficult either. The only problem is that ascorbic acid easily becomes oxidised in contact with metal. Therefore, it is best to exclude all air. Bring some distilled or de-ionised water to boiling and, as hot as possible, fill a 500 ml glass or hard plastic container nearly to the top. Immerse a piece of copper and add 4 to 5 g or about one teaspoon of ascorbic acid powder. Keep refrigerated and remove the copper after a few days. After part of it has been used minimise the air space by filling it into a smaller bottle or jar. As an infection fighter try a teaspoonful several times a day for up to 2 weeks.—Copper salicylate is a very stable complex and most of it appears to be excreted unchanged. Therefore, it may be regarded more as a remedy rather than a food supplement. Nevertheless, when taking this or other copper complexes, colloids or chelates over a longer period it is advisable to take additional zinc, about 30 mg a day, in order to avoid a zinc deficiency from developing.—Finally I want to stress that the use of copper salicylate and ascorbate, especially when you make these yourself, is strictly experimental and no one can take any responsibility for what you are doing. If in doubt, then use it only externally. Individuals who are sensitive to salicylates need to be extra careful but I believe that even then it will generally be well tolerated. Handle copper salicylate with care, it stains garments.–I believe that colloidal copper has similar beneficial properties as copper salicylate and you might alternate using both with some longer breaks in-between. You can make colloidal copper in the same way as colloidal silver, just use two strips of copper instead of silver electrodes. However, the use of colloidal copper is experimental as well and you have to find out by yourself how much to take and how beneficial it is for you.—The Schweitzer Formula—Zinc has strong anti-inflammatory and antibiotic properties as well but can become deficient with a high copper intake. Therefore, it is usually best to increase the intake of both minerals together. With a high copper intake, also a high zinc supplementation should be used. This may be best in the form of Schweitzer Formula, a complex formed by zinc (oxide or carbonate), boron (boric acid) and salicylic acid. This is an excellent antibiotic, disinfectant, fungicide, anti-inflammatory and healing remedy.—-The Schweitzer Formula was developed 1915 in Germany and sold worldwide since 1920. In addition to any kind of infection or inflammation, it has been used in cancer treatment, to improve the immune response and blood oxygenation. Applied externally it helps to heal injuries and skin diseases, including acne, scarring varicose veins and varicose ulcers.—You can easily make the Schweitzer Formula yourself. Dissolve 9.2 g of salicylic acid, 2.1 g of boric acid and 2.7 g of zinc oxide or 4 g of zinc carbonate in 2 litres of hot water. You may get these ingredients from a pharmacist or supplier of fine chemicals and have exact quantities weight out. However, it is sufficient to use approximate amounts. You may use 2 level teaspoons of salicylic acid and half a teaspoon each of boric acid and zinc oxide or one level teaspoon of zinc carbonate.—-However, in Australia boric acid has now been scheduled as a prescription poison. Apparently eating large amounts of boric acid mixed with castor sugar that the parents had used to eliminate ants poisoned some infants. If you cannot obtain boric acid from a friendly chemist, you may use borax instead. This introduces some additional sodium ions. While this is not desirable, I do not expect this to significantly reduce the healing qualities of the Schweitzer Formula. To get the same amount of boron you may use about 30% more borax than boric acid.—-Use distilled or de-ionised water and a non-metal container. Heat for about an hour and stir occasionally with a non-metal spoon until no more of the zinc oxide or zinc carbonate at the bottom of the container seems to dissolve. Then decant or filter into a glass container and store in a dark and cool place. Any surplus of zinc oxide or carbonate that remains undissolved shows that all the boric acid and salicylic acid have been used up. However, any surplus of boric acid would be beneficial and just supply additional boron.–As a biochemist I do not see a difference between using this solution directly and letting it crystallise and then dissolving the crystals. However, I have not been able to verify this in a clinical trial. If you do want to crystallise the complex, then let the water evaporate very slowly in a flat non-metal tray covered with fine gauze. As a general rule, the slower the crystallisation, the bigger the crystals. Therefore, keep the tray undisturbed in a cool place. For quick crystallisation and smaller crystals you may expose the tray to direct sunlight. For use you may then dissolve the crystals again in 2 litres of hot water.—–As with copper salicylate, there are no exact guidelines on how much to take. A tablespoonful has been taken 3 times daily with liquid or meals for extended periods. For shorter periods this dose has been doubled. It is also good to rub onto the skin, especially where there are any problems.—You may take this at the ratio of one tablespoon of Schweitzer Formula to one teaspoon of copper salicylate. For long-term use I would take one spoonful of each daily. I believe that long-term use of copper or zinc should be balanced by taking the other mineral as well, be it as salicylate complex, colloid or conventional remedy. I also believe that copper and zinc as complexes or colloids are safer and more effective than the long-term use of aspirin or other anti-inflammatory drugs.—-One tablespoonful of Schweitzer contains about 15 mg of zinc, 15 mg of boric acid or 2.5 mg of boron and 70 mg of salicylic acid. As with copper salicylate, most of these can be expected to be eliminated from the body as a complex. Therefore, Schweitzer Formula cannot be regarded as a zinc or boron supplement and these may need to be additionally supplemented in a different form. However, to assess any potential toxicity, we may assume that the complex completely disintegrates in the body. This would then supply only relatively low levels of the individual ingredients. Twice these amounts of zinc and boron are recommended as being beneficial and much higher amounts have been used in nutritional t
    herapy. Therefore, I cannot see any possible toxicity at least up to 3 tablespoons daily.—Also many commonly used foods are quite high in salicylates. Some individuals, especially hyperactive children are sensitive to salicylates and get a reaction from it. However, I believe that this is due to the chelating effect of salicylic acid, which may cause zinc and copper deficiency in the body. Therefore, in the form of zinc and copper complexes, salicylates may not normally cause a reaction in susceptible individuals.–After a period of use, it is advisable to interrupt using these remedies for a while and observe any effects., I want to stress again, that the use of these remedies over long periods or in high doses is experimental and you must be prepared to take responsibility for any side effects yourself.
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    Bacterial Cause Found for Skin Condition Rosacea
    ScienceDaily (Aug. 28, 2012) — Scientists are closer to establishing a definitive bacterial cause for the skin condition rosacea. This will allow more targeted, effective treatments to be developed for sufferers, according to a review published in the Journal of Medical Microbiology.—Rosacea is a common dermatological condition that causes reddening and inflammation of the skin mostly around the cheeks, nose and chin. In severe cases skin lesions may form and lead to disfigurement. Rosacea affects around 3% of the population — usually fair-skinned females aged 30-50 and particularly those with weak immune systems. The condition is treated with a variety of antibiotics, even though there has never been a well-established bacterial cause.–A new review carried out by the National University of Ireland concludes that rosacea may be triggered by bacteria that live within tiny mites that reside in the skin.–The mite species Demodex folliculorum is worm-like in shape and usually lives harmlessly inside the pilosebaceous unit which surrounds hair follicles of the face. They are normal inhabitants of the face and increase in number with age and skin damage — for example, following exposure to sunlight. The numbers of Demodex mites living in the skin of rosacea patients is higher than in normal individuals, which has previously suggested a possible role for the mites in initiating the condition.—More recently, the bacterium Bacillus oleronius was isolated from inside a Demodex mite and was found to produce molecules provoking an immune reaction in rosacea patients. Other studies have shown patients with varying types of rosacea react to the molecules produced by this bacterium — exposing it as a likely trigger for the condition. What’s more, this bacterium is sensitive to the antibiotics used to treat rosacea.—Dr Kevin Kavanagh who conducted the review explained, “The bacteria live in the digestive tracts of Demodex mites found on the face, in a mutually beneficial relationship. When the mites die, the bacteria are released and leak into surrounding skin tissues — triggering tissue degradation and inflammation.”—“Once the numbers of mites increase, so does the number of bacteria, making rosacea more likely to occur. Targeting these bacteria may be a useful way of treating and preventing this condition,” said Dr Kavanagh. “Alternatively we could look at controlling the population of Demodex mites in the face.. Some pharmaceutical companies are already developing therapies to do this, which represents a novel way of preventing and reversing rosacea, which can be painful and embarrassing for many people.”—-Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo. —Journal Reference-Stanisław Jarmuda, Niamh O’Reilly, Ryszard Żaba, Oliwia Jakubowicz, Andrzej Szkaradkiewicz and Kevin Kavanagh. The potential role of Demodex folliculorum mites and bacteria in the induction of rosacea. Journal of Medical Microbiology, 2012 DOI: 10.1099/jmm.0.048090-0
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    Aqueous garlic extract and its phytochemical profile– special reference to antioxidant status.
    Int J Food Sci Nutr. 2012 Jun;63(4):431-9—Authors: Rasul Suleria HA, Sadiq Butt M, Muhammad Anjum F, Saeed F, Batool R, Nisar Ahmad A
    Abstract—Garlic (Allium sativum L) has distinct nutritional profile with special reference to its bioactive components and is used in different diet-based therapies to cure various lifestyle-related disorders. For this purpose, characterization and extraction of garlic were carried out followed by antioxidant assays. Different solvents (50% aqueous ethanol, 50% aqueous methanol and water) at different time intervals (4, 5 and 6 h) at 60°C were used to optimize aqueous extraction efficiency of garlic. Among the solvents, water extract resulted in better extraction yield (31.85 ± 2.09 g/25 g) at 5 h. The antioxidant potential of all these solvents was estimated through in vitro studies. In this context, it was observed that higher amount of total phenolic contents was present in aqueous methanol 71.87 ± 1.69% at 45 min. Antiradical (1,1-diphenyl-2-picrylhydrazyl assay) and antioxidant activity showed that the maximum value was 73.80 ± 3.69 and 83.83 ± 0.16%, respectively, in methanolic extract at 45 min while glucose diffusion and ferric reducing antioxidant power were 97.00 ± 0.20 and 32.66 ± 0.72% at p < 0.05, respectively. Aqueous garlic extract was selected as the best treatment on the basis of percentage yield and safety modulation in human body absorption. Aqueous garlic extract was subjected to pH, acidity, total soluble solids (TSS) and colour. It was observed that the pH of aqueous garlic extract decreased with the passage of time while acidity increased. It was also concluded that storage affected the value of TSS and colour significantly. L* values for colour on 0 day were 34.18 ± 0.08, whereas those on 28th day were 38.84 ± 0.03. It was predicted that 28 days storage resulted in significant increase in L* value, while a* value decreased from 4.31 ± 0.01 to 0.32 ± 0.01 at the end of storage study.—PMID: 22098476 [PubMed – indexed for MEDLINE]
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    Hexavalent chromium and its effect on health- possible protective role of garlic (Allium sativum Linn).
    J Basic Clin Physiol Pharmacol. 2011;22(1-2):3-10—Authors: Das KK, Dhundasi SA, Das SN
    Abstract—Hexavalent chromium or chromium (VI) is a powerful epithelial irritant and a confirmed human carcinogen. This heavy metal is toxic to many plants, aquatic animals, and bacteria. Chromium (VI) which consists of 10%-15% total chromium usage, is principally used for metal plating (H2Cr2O7), as dyes, paint pigments, and leather tanning, etc. Industrial production of chromium (II) and (III) compounds are also available but in small amounts as compared to chromium (VI). Chromium (VI) can act as an oxidant directly on the skin surface or it can be absorbed through the skin, especially if the skin surface is damaged. The prooxidative effects of chromium (VI) inhibit antioxidant enzymes and deplete intracellular glutathione in living systems and act as hematotoxic, immunotoxic, hepatotoxic, pulmonary toxic, and nephrotoxic agents. In this review, we particularly address the hexavalent chromium-induced generation of reactive oxygen species and increased lipid peroxidation in humans and animals, and the possible role of garlic (Allium sativum Linn) as a protective antioxidant.–PMID: 22865357 [PubMed – indexed for MEDLINE]
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    http://www.thecehf.org/morgellons-disease-research-update-august-2012.html
     
    Morgellons Disease Research Update August 2012
    Research Update …
    Scientists Pursue Connection between Infectious Disease Afflicting Cattle and Morgellons Disease Affecting Humans
    Progress moves forward as more research shows Morgellons disease has a physiologic (physical not mental) basis. ——-
    The Morgellons break through started with the research publication, Filament Formation Associated with Spirochetal Infection: a comparative approach to Morgellons Disease by Marianne Middelveen, a Canadian veterinary microbiologist and Raphael Stricker, MD. The CEHF first announced this news last fall when this peer reviewed publication appeared in the November, 2011 issue of Clinical, Cosmetic and Investigational Dermatology.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257881
    Why is this important? —-In November, 2011, Middelveen and Stricker reported to have found evidence of a veterinary analog to Morgellons (MD). BDD, an infectious disease which has plagued cattle for decades, has fibers/filaments within their tissue and lesions that were recognized as a match to those found in the controversial disease known as Morgellons (MD) in humans. Studies on fibers/filaments from cattle with the bovine hoof disease and those found in MD suffers provided startling evidence challenging the dermatologists’ unfounded assumption that MD is a psychiatric disorder called “Delusions of Parasitosis”. Anyone who suffers from Morgellons knows how real these symptoms are and how disheartening it is to be told it is all in your head. Although the publication stated that the etiology (cause) of MD was not yet known, the findings by Middelveen and Stricker provided corroborative evidence to support a physiological and, perhaps, infectious etiology, lending a new direction for further research.
    Second Study Announced by the CEHF on May 16, 2012 –Morgellon Fibres
    http://www.omicsonline.org/2155-9554/2155-9554-3-140.pdf
    Indeed, their second study, Morgellons Disease: A Chemical and Light Microscopic Study, published May, 2012 in the peer reviewed publication, Journal of Clinical & Experimental Dermatology Research, continued this BDD and MD comparison in greater detail. Researchers were able to conduct a more in-depth analysis of dermatological specimens from three Morgellons patients and biopsies from cattle with proliferative late stage BDD. Examinations were conducted by light microscopy, by chemical experiments and by immunohistological testing.
    Results of the Study … These findings confirmed that filaments/fibers from both bovine and human samples were similar in formation at the cellular level and had the chemical and physical properties of keratin. The composition of MD filaments from humans was confirmed to be keratin by immunohistological staining with antibodies specific for human keratins. Fibers from three human patients were found to be biological in origin and are produced by keratinocytes in epithelial and follicular tissues. —An interesting side note is that researchers Middelveen and Stricker found filaments/fibers associated with MD beneath unbroken skin as well as in lesions, thus, demonstrating they are not self-implanted. This confirms previous research from Dr. Randy Wymore at the OSU-Center for the Investigation of Morgellons Disease.
    Why is this important? —-The original premise–that MD is physiological is holding up to the test of scientific scrutiny.
    Morgellons Study Cited by Faculty of 1000
    http://www.thecehf.org/morgellons-study-cited-by-faculty-of-1000.html
    The quality and importance of this research is highlighted in Faculty of 1000 Award.
    Faculty of 1000 (F1000) is a global community of over 10,000 experts who select, rate and evaluate the very best articles in biology and medicine. The core mission of the F1000 is to identify and evaluate the most important articles in biology and medical research publications. The organization highlights and brings awareness to significant new research. The selection of Morgellons Disease: A Chemical and Light Microscopic Study places the work in this work in the top 2% of published articles in these fields. It classifies the study as “must read” and is certainly an honor for the entire research team. More information can be accessed at the F1000 website (http://f1000.com/716597867).
    Thank You and Congratulations to Our Researchers!! —-No one can apply to be considered for this. This research was chosen and recognized on its merits and for the importance it holds worldwide. Everyone at The Charles E. Holman Foundation and from the Morgellons community wish to express our congratulations to Marianne Middelveen, Elizabeth Rasmussen, Douglas Kahn, and Raphael Stricker for this recognition. The award was indeed serendipity. We now have documented, peer reviewed evidence published, corroborating MD is not Delusions of Parasitosis.
    MD, like BBD, has a true physical cause. “ … Because BDD is a disease in which spirochetes have been identified as primary etiologic agents, and spirochetal sero-reactivity has been associated with MD, it is reasonable to assume that spirochetal infection plays an important role in MD… Further immunohistological and electron microscopy studies are needed to solve the mystery of Morgellons …” (Middelveen and Stricker). This points the way to the next step in our research. To paraphrase Paul Harvey, stay tuned in and signed up for the next edition of Keeping You in the Loop …for the “rest of the story.”
     
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    Show of the Month Sepetember 17- 2012
    Brain-Eating Amoeba-From Tap Water
     
    Coconut Oil Could Combat Tooth Decay
     
    High Doses of Vitamin D Help Tuberculosis Patients Recover More Quickly
     
    DETAILED DESCRIPTION OF SOME SPECIFIC EMBODIMENTS
     
    Cannabidiol blocks glutamate
     
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    Brain-Eating Amoeba-From Tap Water
    Now even TAP WATER isn’t safe! Brain-eating amoeba fatal in 99% of cases ‘could come from your own faucet’
    In 2011, two people in Louisiana died after using tap water for nasal irrigation
    Amoeba known as Naegleria fowleri can infect brain and enters through nasal passage
    Once infected, organism is 99% fatal
    By Beth Stebner
    PUBLISHED: 12:37 GMT, 24 August 2012 | UPDATED: 12:37 GMT, 24 August 2012  –There could be a deadly killer in your home – the kitchen tap.Last year in Louisiana, two people died from a single-celled organism that thrives in warm, freshwater after using tap water for flushing their sinuses.The amoeba, known as Naegleria fowleri, can cause primary amoebic meningoecephalitis (PAM), which is fatal in 99 per cent of cases.–Deadly infection: The amoeba, known as Naegleria fowleri, can cause primary amoebic meningoecephalitis (PAM), which is fatal in 99 per cent of cases The nose knows: In 2011, two people in Louisiana who used tap water in neti pots to flush out their sinuses caught the deadly infection Both victims, a 51-year-old woman and a 28-year-old man, had used tap water in neti pots to flush out their sinuses and died days later. They lived in separate areas of the state. Neti pots are generally safe for use for clearing out excess mucus in the nasal cavity, but when amoebas are present, the infection has a frighteningly fatal rate. According to the Centers for Disease Control, the amoeba enters the brain through the nasal passage, especially when people go swimming in warm freshwater lakes and ponds. -In a report published by Dr Jonathan Yoder, who works at the National Center for Emerging and Zoonotic Infectious Diseases, a division of the CDC, concluded that in both cases, the victims had only come in contact with the amoeba from tap water.-He and a group of researchers tested the water from both houses. Their results were published in Clinical Infectious Diseases on August 23. Dr Yoder and the other authors found the amoeba in the kitchen spigot, shower, bathtub, and bathroom sink in the woman’s home.
     
     
    Path of infection: N. fowleri can only enter the body through the nasal passage or broken skin, not through drinking water  Growth process: The single-celled amoeba is also called a brain-eating amoeba; later symptoms can include hallucinations and seizures—They found Naegleria fowleri in a tankless water heater in the home of the 28-year-old man. The authors noted that the municipal water sources were not contaminated in either case. The residents lived in different parts of the state. The CDC says that one cannot contract the organism simply through drinking water, and urges those using nasal irrigation systems to either use distilled or bottled water, or boil their tap water for at least a minute to ensure the Naegleria fowleri amoeba is killed. The centre also notes that there have been few infections in the U.S. throughout the past decades.  Preventative measures: The CDC recommends that those near warm, fresh water avoid swimming in it, or holding your nose when going underwater–From 2002 to 2011, there were 32 infections reported. Included in those statistics are the two people from Louisiana who used neti pots to flush out their noses.—Initial symptoms begin five days after infection, but could take as long as seven, and include headache, fever, nausea, and even vomiting.—In the later phases when the amoeba reaches the brain tissue, those suffering from the infection may lose balance, hallucinate, and experience seizures, and in 99 per cent of cases, die. The CDC notes that only one person out of 123 infected has survived. It reminds those who will be swimming in warm, fresh water to use nasal plugs, hold one’s nose shut, or avoid going under water altogether, though infection from N. fowleri is extremely rare
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    Coconut Oil Could Combat Tooth Decay
    ScienceDaily (Aug. 30, 2012) — Digested coconut oil is able to attack the bacteria that cause tooth decay. It is a natural antibiotic that could be incorporated into commercial dental care products, say scientists presenting their work at the Society for General Microbiology’s Autumn Conference at the University of Warwick. The team from the Athlone Institute of Technology in Ireland tested the antibacterial action of coconut oil in its natural state and coconut oil that had been treated with enzymes, in a process similar to digestion. The oils were tested against strains of Streptococcus bacteria which are common inhabitants of the mouth. They found that enzyme-modified coconut oil strongly inhibited the growth of most strains of Streptococcus bacteria including Streptococcus mutans — an acid-producing bacterium that is a major cause of tooth decay.—Many previous studies have shown that partially digested foodstuffs are active against micro-organisms. Earlier work on enzyme-modified milk showed that it was able to reduce the binding of S. mutans to tooth enamel, which prompted the group to investigate the effect of other enzyme-modified foods on bacteria.—Further work will examine how coconut oil interacts with Streptococcus bacteria at the molecular level and which other strains of harmful bacteria and yeasts it is active against. Additional testing by the group at the Athlone Institute of Technology found that enzyme-modified coconut oil was also harmful to the yeast Candida albicans that can cause thrush. The researchers suggest that enzyme-modified coconut oil has potential as a marketable antimicrobial which could be of particular interest to the oral healthcare industry. Dr Damien Brady who is leading the research said, “Dental caries is a commonly overlooked health problem affecting 60-90% of children and the majority of adults in industrialized countries. Incorporating enzyme-modified coconut oil into dental hygiene products would be an attractive alternative to chemical additives, particularly as it works at relatively low concentrations. Also, with increasing antibiotic resistance, it is important that we turn our attention to new ways to combat microbial infection.”-The work also contributes to our understanding of antibacterial activity in the human gut. “Our data suggests that products of human digestion show antimicrobial activity. This could have implications for how bacteria colonize the cells lining the digestive tract and for overall gut health,” explained Dr Brady. “Our research has shown that digested milk protein not only reduced the adherence of harmful bacteria to human intestinal cells but also prevented some of them from gaining entrance into the cell. We are currently researching coconut oil and other enzyme-modified foodstuffs to identify how they interfere with the way bacteria cause illness and disease,” he said.—Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo.
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    High Doses of Vitamin D Help Tuberculosis Patients Recover More Quickly
    ScienceDaily (Sep. 3, 2012) — For decades before antibiotics became generally available, sunshine was used to treat tuberculosis, with patients often being sent to Swiss clinics to soak up the sun’s healing rays. Now, for the first time scientists have shown how and why heliotherapy might, indeed, have made a difference.–A study led by researchers at Queen Mary, University of London, conducted in collaboration with the Medical Research Council’s National Institute for Medical Research, has shown that high doses of vitamin D, given in addition to antibiotic treatment, appear to help patients with tuberculosis (TB) recover more quickly.—The research, which will be published online this week in the Proceedings of the National Academy of Sciences of the USA (PNAS), is the first to investigate the effect of vitamin D on the immune responses of patients receiving treatment for an infectious disease. The findings indicate that high doses of the vitamin can dampen down the body’s inflammatory response to infection, enabling patients to recover faster, with less damage to their lungs.– In addition to stimulating recovery in TB patients, the authors say their results suggest that vitamin D supplementation might help patients recover better from other diseases such as pneumonia.–Dr Adrian Martineau, senior lecturer in respiratory infection and immunity at the Blizard Institute, part of Queen Mary, University of London, who led the research, said: “These findings are very significant. They indicate that vitamin D may have a role in accelerating resolution of inflammatory responses in tuberculosis patients. This is important, because sometimes these inflammatory responses can cause tissue damage leading to the development of cavities in the lung. If we can help these cavities to heal more quickly, then patients should be infectious for a shorter period of time, and they may also suffer less lung damage.”More broadly, the ability of vitamin D to dampen down inflammatory responses without compromising the actions of antibiotics raises the possibility that supplementation might also have benefits in patients receiving antimicrobial therapy for pneumonia, sepsis and other lung infections.”–Dr Martineau and his colleagues from a number of London hospitals and institutions randomised 95 TB patients receiving standard antibiotic treatment into two groups: for the first eight weeks of their treatment, 44 received additional high dose vitamin D, while 51 received a placebo. Dr Anna Coussens at the MRC’s National Institute for Medical Research measured levels of inflammatory markers in blood samples taken from these patients, and conducted statistical analyses to determine the effects that vitamin D had on the immune response.—“We found that a large number of these inflammatory markers fell further and faster in patients receiving vitamin D,” said Dr Coussens.   -The researchers also found that Mycobacterium tuberculosis, the bacterium that causes TB, was cleared from the patients’ sputum (the phlegm coughed up from deep in the lungs) faster in those who were taking vitamin D, taking an average of 23 days to become undetectable under the microscope compared to 36 days in the patients who were taking the placebo.  Dr Martineau said it was probably too early to be recommending that all TB patients should take high-dose vitamin D in addition to the standard antibiotic treatment for the disease; more research with more patients was needed before clinical recommendations could be made. “We are hoping to do more work to evaluate the effects of higher doses and different forms of vitamin D to see if they have a more dramatic effect,” he said. The study was funded by the UK’s Medical Research Council and the British Lung Foundation. In addition to Barts and the London School of Medicine and Dentistry, part of Queen Mary, University of London, the other institutions involved in the research were the MRC’s National Institute of Medical Research, Imperial College London, Homerton University NHS Foundation Trust, Newham Chest Clinic, Whipps Cross University Hospital, Northwick Park Hospital, Guy’s and St Thomas’ NHS Foundation Trust, Lewisham Hospital, and King’s College Hospital. Story Source—The above story is reprinted from materials provided by Queen Mary, University of London, via EurekAlert!, a service of AAAS.
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    Detailed Descripition of Some Specific Embodiments
    This invention provides antioxidant compounds and compositions, such as pharmaceutical compositions, that include cannabinoids that act as free radical scavengers for use in prophylaxis and treatment of disease. The invention also includes methods for using the antioxidants in prevention and treatment of pathological conditions such as ischemia (tissue hypoxia), and in subjects who have been exposed to oxidant inducing agents such as cancer chemotherapy, toxins, radiation, or other sources of oxidative stress. The compositions and methods described herein are also used for preventing oxidative damage in transplanted organs, for inhibiting reoxygenation injury following reperfusion of ischemic tissues (for example in heart disease), and for any other condition that is mediated by oxidative or free radical mechanisms of injury. In particular embodiments of the invention, the compounds and compositions are used in the treatment of ischemic cardiovascular and neurovascular conditions, and neurodegenerative diseases. However the present invention can also be used as an antioxidant treatment in non-neurological diseases.—Molecular oxygen is essential for aerobic organisms, where it participates in many biochemical reactions, including its role as the terminal electron acceptor in oxidative phosphorylation. However excessive concentrations of various forms of reactive oxygen species and other free radicals can have serious adverse biological consequences, including the peroxidation of membrane lipids, hydroxylation of nucleic acid bases, and the oxidation of sulfhydryl groups and other protein moieties. Biological antioxidants include tocopherols and tocotrieneols, carotenoids, quinones, bilirubin, ascorbic acid, uric acid, and metal binding proteins.————–
    However these endogenous antioxidant systems are often overwhelmed by pathological processes that allow permanent oxidative damage to occur to tissue.—-Free radicals are atoms, ions or molecules that contain an unpaired electron, are usually unstable, and exhibit short half-lives. Reactive oxygen species (ROS) is a collective term, designating the oxygen radicals (e.g. .O2- superoxide radical), which by sequential univalent reduction produces hydrogen peroxide (H2 O2) and hydroxyl radical (.OH). The hydroxyl radical sets off chain reactions and can interact with nucleic acids. Other ROS include nitric oxide (NO.) and peroxy nitrite (NOO.), and other peroxyl (RO2.) and alkoxyl (RO.) radicals
     
    DEFINITIONS
    “Oxidative associated diseases” refers to pathological conditions that result at least in part from the production of or exposure to free radicals, particularly oxyradicals, or reactive oxygen species. It is evident to those of skill in the art that most pathological conditions are multifactorial, and that assigning or identifying the predominant causal factors for any particular condition is frequently difficult. For these reasons, the term “free radical associated disease” encompasses pathological states that are recognized as conditions in which free radicals or ROS contribute to the pathology of the disease, or wherein administration of a free radical inhibitor (e.g. desferroxamine), scavenger (e.g. tocopherol, glutathione) or catalyst (e.g. superoxide dismutase, catalase) is shown to produce detectable benefit by decreasing symptoms, increasing survival, or providing other detectable clinical benefits in treating or preventing the pathological state.–Oxidative associated diseases include, without limitation, free radical associated diseases, such as ischemia, ischemic reperfusion injury, inflammatory diseases, systemic lupus erythematosis, myocardial ischemia or infarction, cerebrovascular accidents (such as a thromboembolic or hemorrhagic stroke) that can lead to ischemia or an infarct in the brain, operative ischemia, traumatic hemorrhage (for example a hypovolemic stroke that can lead to CNS hypoxia or anoxia), spinal cord trauma, Down’s syndrome, Crohn’s disease, autoimmune diseases (e.g. rheumatoid arthritis or diabetes), cataract formation, uveitis, emphysema, gastric ulcers, oxygen toxicity, neoplasia, undesired cellular apoptosis, radiation sickness, and others. The present invention is believed to be particularly beneficial in the treatment of oxidative associated diseases of the CNS, because of the ability of the cannabinoids to cross the blood brain barrier and exert their antioxidant effects in the brain. In particular embodiments, the pharmaceutical composition of the present invention is used for preventing, arresting, or treating neurological damage in Parkinson’s disease, Alzheimer’s disease and HIV dementia; autoimmune neurodegeneration of the type that can occur in encephalitis, and hypoxic or anoxic neuronal damage that can result from apnea, respiratory arrest or cardiac arrest, and anoxia caused by drowning, brain surgery or trauma (such as concussion or spinal cord shock).—As used herein, an “antioxidant” is a substance that, when present in a mixture containing an oxidizable substrate biological molecule, significantly delays or prevents oxidation of the substrate biological molecule. Antioxidants can act by scavenging biologically important reactive free radicals or other reactive oxygen species (.O2-, H2 O2, .OH, HOCl, ferryl, peroxyl, peroxynitrite, and alkoxyl), or by preventing their formation, or by catalytically converting the free radical or other reactive oxygen species to a less reactive species. Relative antioxidant activity can be measured by cyclic voltametry studies of the type disclosed in Example 5 (and FIG. 3), where the voltage (x-axis) is an index of relative antioxidant activity. The voltage at which the first peak occurs is an indication of the voltage at which an electron is donated, which in turn is an index of antioxidant activity.
     
    “Therapeutically effective antioxidant doses” can be determined by various methods, including generating an empirical dose-response curve, predicting potency and efficacy of a congener by using quantitative structure activity relationships (QSAR) methods or molecular modeling, and other methods used in the pharmaceutical sciences. Since oxidative damage is generally cumulative, there is no minimum threshold level (or dose) with respect to efficacy. However, minimum doses for producing a detectable therapeutic or prophylactic effect for particular disease states can be established.
    As used herein, a “cannabinoid” is a chemical compound (such as cannabinol, THC or cannabidiol) that is found in the plant species Cannabis saliva (marijuana), and metabolites and synthetic analogues thereof that may or may not have psychoactive properties. Cannabinoids therefore include (without limitation) compounds (such as THC) that have high affinity for the cannabinoid receptor (for example Ki <250 nM), and compounds that do not have significant affinity for the cannabinoid receptor (such as cannabidiol, CBD). Cannabinoids also include compounds that have a characteristic dibenzopyran ring structure (of the type seen in THC) and cannabinoids which do not possess a pyran ring (such as cannabidiol). Hence a partial list of cannabinoids includes THC, CBD, dimethyl heptylpentyl cannabidiol (DMHP-CBD), 6,12-dihydro-6-hydroxy-cannabidiol (described in U.S. Pat. No. 5,227,537, incorporated by reference); (3S,4R)-7-hydroxy-Δ6 – tetrahydrocannabinol homologs and derivatives described in U.S. Pat. No. 4,876,276, incorporated by reference; ( )-4-[4-DMH-2,6-diacetoxy-phenyl]-2-carboxy-6,6-dimethylbicyclo[3.1. 1]hept-2-en, and other 4-phenylpinene derivatives disclosed in U.S. Pat. No. 5,434,295, which is incorporated by reference; and cannabidiol (-)(CBD) analogs such as (-)CBD-monomethylether, (-)CBD dimethyl ether; (-)CBD diacetate; (-)3′-acetyl-CBD monoacetate; and . -.AF11, all of which are disclosed in Consroe et al., J. Clin. Phannacol. 21:428S-436S, 1981, which is also incorporated by reference. Many other cannabinoids are similarly disclosed in Agurell et al., Pharmacol. Rev. 38:31-43, 1986, which is also incorporated by reference.
    As referred to herein, the term “psychoactivity” means “cannabinoid receptor mediated psychoactivity.” Such effects include, euphoria, lightheadedness, reduced motor coordination, and memory impairment. Psychoactivity is not meant to include non-cannabinoid receptor mediated effects such as the anxiolytic effect of CBD.
    The “lipoxygenase enzyme activity” refers to the relative level of lipoxygenase enzyme activity for a particular lipoxgenase, such as 5-, 15- or 12-lipoxygenase, as measured in Example 8. A compound would be said to “selectively inhibit a lipoxgenase enzyme” if the concentration of inhibitor required to reduce enzyme activity by 50% was at least about 5 times less than the amount required to reduce activity of a second lipoxgenase enzyme by the same degree (under the same conditions, i.e. temperature, substrate concentration, etc.)
    The term “lower alkyl” refers to a cyclic, branched or straight chain monovalent alkyl radical of one to seven carbon atoms. This term is further exemplified by such radicals as methyl, ethyl, n-propyl, i-propyl, n-butyl, t-butyl, i-butyl (or 2-methylpropyl), cyclopropylmethyl, i-amyl, n-amyl, hexyl and heptyl. Lower alkyl groups can also be unsubstituted or substituted, where a specific example of a substituted alkyl is 1,1-dimethyl heptyl.
     
    “Hydroxyl” refers to –OH.
    “Alcohol” refers to R–OH, wherein R is alkyl, especially lower alkyl (for example in methyl, ethyl or propyl alcohol). An alcohol may be either linear or branched, such as isopropyl alcohol.
    “Carboxyl” refers to the radical –COOH, and substituted carboxyl refers to –COR where R is alkyl, lower alkyl or a carboxylic acid or ester.
     
    The term “aryl” or “Ar” refers to a monovalent unsaturated aromatic carbocyclic group having a single ring (e.g. phenyl) or multiple condensed rings (e.g. naphthyl or anthryl), which can optionally be unsubstituted or substituted with, e.g., halogen, alkyl, alkoxy, alkylthio, trifluoromethyl, acyloxy, hydroxy, mercapto, carboxy, aryloxy, aryl, arylalkyl, heteroaryl, amino, alkylamino, dialkylamino, morpholino, piperidino, pyrrolidin-1-yl, piperazin-1-yl, or other functionality.
    The term “alkoxy” refers to a substituted or unsubstituted alkoxy, where an alkoxy has the structure –O–R, where R is substituted or unsubstituted alkyl. In an unsubstituted alkoxy, the R is an unsubstituted alkyl. The term “substituted alkoxy” refers to a group having the structure –O–R, where R is alkyl which is substituted with a non-interfering substituent. The term “arylalkoxy” refers to a group having the structure –O–R–Ar, where R is alkyl and Ar is an aromatic substituent. Arylalkoxys are a subset of substituted alkoxys. Examples of useful substituted alkoxy groups are: benzyloxy, naphthyloxy, and chlorobenzyloxy.
    The term “aryloxy” refers to a group having the structure –O–Ar, where Ar is an aromatic group. A particular aryloxy group is phenoxy.
    The term “heterocycle” refers to a monovalent saturated, unsaturated, or aromatic carbocyclic group having a single ring (e.g. morpholino, pyridyl or faryl) or multiple condensed rings (e.g. indolizinyl or benzothienyl) and having at least one heteroatom, defined as N, O, P, or S, within the ring, which can optionally be unsubstituted or substituted with, e.g. halogen, alkyl, alkoxy, alkylthio, trifluoromethyl, acyloxy, hydroxy, mercapto, carboxy, aryloxy, aryl, arylakyl, heteroaryl, amino, alkylamino, dialkylamino, morpholino, piperidino, pyrrolidin-1-yl, piperazin-1-yl, or other functionality.
    “Arylalkyl” refers to the groups –R–Ar and –R–HetAr, where Ar is an aryl group. HetAr is a heteroaryl group, and R is a straight-chain or branched chain aliphatic group. Example of arylaklyl groups include benzyl and furfuryl. Arylalkyl groups can optionally be unsubstituted or substituted with, e.g., halogen, alkyl, alkoxy, alkylthio, trifluoromethyl, acyloxy, hydroxy, mercapto, carboxy, aryloxy, aryl, arylalkyl, heteroaryl, amino, alkylamino, dialkylamino, morpholino, peperidino, pyrrolidin-1-yl, piperazin-1-yl, or other functionality.
    The term “halo” or “halide” refers to fluoro, bromo, chloro and iodo substituents.
    The term “amino” refers to a chemical functionality –NR’R” where R’ and R” are independently hydrogen, alkyl, or aryl. The term “quaternary amine” refers to the positively charged group –N.sup. R’R”, where R’R” and R” are independently selected and are alkyl or aryl. A particular amino group is –NH2.
     
    Cannabidiol blocks glutamate toxicity
     
    Cannabidiol blocks glutamate toxicity with equal potency regardless of whether the insult is mediated by NMDA, AMPA or kainate receptors. Cannabidiol and THC have been shown to be comparable to the antioxidant BHT, both in their ability to prevent dihydrorhodamine oxidation and in their cyclic voltametric profiles. Several synthetic cannabinoids also exhibited profiles similar to the BHT, although anandamide, which is not structurally related to cannabinoids, did not. These findings indicate that cannabinoids act as antioxidants in a non-biological situation, which was confirmed in living cells by showing that cannabidiol attenuates hydroperoxide induced neurotoxicity. The potency of cannabidiol as an antioxidant was examined by comparing it on an equimolar basis with three other commonly used compounds.
    In the AMPA/kainate receptor dependent neurotoxicity model, cannabidiol neuroprotection was comparable to the potent antioxidant, BHT, but significantly greater than that observed with either α-tocopherol or ascorbate. This unexpected superior antioxidant activity (in the absence of BHT tumor promoting activity) shows for the first time that cannabidiol, and other cannabinoids, can be used as antioxidant drugs in the treatment (including prophylaxis) of oxidation associated diseases, and is particularly useful as a neuroprotectant. The therapeutic potential of nonpsychoactive cannabinoids is particularly promising, because of the absence of psychotoxicity, and the ability to administer higher doses than with psychotropic cannabinoids, such as THC. Previous studies have also indicated that cannabidiol is not toxic, even when chronically administered to humans or given in large acute doses (700 mg/day).
    These studies with the nonpsychotropic marijuana constituent, cannabidiol, demonstrate that protection can be achieved against both glutamate neurotoxicity and free radical induced cell death. THC, the psychoactive principle of cannabis, also blocked glutamate neurotoxicity with a potency similar to cannabidiol. In both cases, neuroprotection is unaffected by the presence of a cannabinoid receptor antagonist. These results therefore surprisingly demonstrate that cannabinoids can have useful therapeutic effects that are not mediated by cannabinoid receptors, and therefore are not necessarily accompanied by psychoactive side effects. Cannabidiol also acts as an anti-epileptic and anxiolytic, which makes it particularly useful in the treatment of neurological diseases in which neuroanatomic defects can predispose to seizures (e.g. subarachnoid hemorrhage).
    A particular advantage of the cannabinoid compounds of the present invention is that they are highly lipophilic, and have good penetration into the central nervous system. The volume of distribution of some of these compounds is at least 100 L in a 70 kg person (1.4 L/kg), more particularly at least 250 L, and most particularly 500 L or even 700 L in a 70 kg person (10 L/kg). The lipophilicity of particular compounds is also about as great as that of THC, cannabidiol or other compounds that have excellent penetration into the brain and other portions of the CNS.
    Cannabinoids that lack psychoactivity or psychotoxicity are particularly useful embodiments of the present invention, because the absence of such side effects allows very high doses of the drug to be used without encountering unpleasant side effects (such as dysphoria) or dangerous complications (such as obtundation in a patient who may already have an altered mental status). For example, therapeutic antioxidant blood levels of cannabidiol can be 5-20 mg/kg, without significant toxicity, while blood levels of psychoactive cannabinoids at this level would produce obtundation, headache, conjunctival irritation, and other problems. Particular examples of the compounds of the present invention have low affinity to the cannabinoid receptor, for example a Ki of greater than 250 nM, for example Ki≥500-1000 nM. A compound with a Ki≥1000 nM is particularly useful, which compound has essentially no psychoactivity mediated by the cannabinoid receptor
     
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    Show Of the Month  September 21-2012
     
    Precautions for Tick-Borne Disease Extend ‘Beyond Lyme’
     
    Copper Benefits
     
    Copper—and how it Protects
     
    Copper Proves Effective Against New E. Coli Strains in New Study
     
    Dry Copper Kills Bacteria On Contact
     
    Work With Germ-Killing Copper Could Save Thousands of Lives
     
    Copper Recipes
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    Precautions for Tick-Borne Disease Extend ‘Beyond Lyme’
     
    ScienceDaily (Sep. 7, 2012) — This year’s mild winter and early spring were a bonanza for tick populations in the eastern United States. Reports of tick-borne disease rose fast.—While Lyme disease is the most common tick-borne disease in the Northeast and Upper Midwest, new research results emphasize that it is not the greatest cause for concern in most Southeastern states.—The findings are published today in a paper in the journal Zoonoses and Public Health.—The majority of human-biting ticks in the North–members of the blacklegged tick species–cause Lyme disease, but these same ticks do not commonly bite humans south of mid-Virginia.–Biologist Graham Hickling of the University of Tennessee, co-author of the paper, says many patients in Southeastern states, who become sick from a tick-bite, assume they have Lyme disease, but the odds of that being the case are low.—“Ticks in the eastern U.S. collectively carry more than a dozen agents that can cause human disease,” says Hickling.—“Here in Tennessee we regularly collect lone star ticks that test positive for Ehrlichia, [a tick-borne bacterial infection]. Lone stars are an aggressive species that account for most of the human bites that we see in this region. So ehrlichiosis has to be a big concern, yet most people have never heard of it.”—In contrast, says Hickling, there have been no confirmed reports to date of the Lyme disease pathogen among the sparse populations of blacklegged ticks found in Tennessee.–“The Southeast is dominated by different tick species than the ones that attack humans in the North,” says Ellen Stromdahl, an entomologist at the U.S. Army Public Health Command and lead author of the paper.—“The lone star tick is by far the most abundant tick in the Southeast, and which species of tick bites you is critical because different ticks carry different diseases. In the Southeast you are unlikely to be bitten by the blacklegged ticks that spread Lyme disease,” Stromdahl says.–Most bites in the Southeast are from the tick species that spread spotted fever rickettsiosis and ehrlichiosis, but not Lyme disease.–A complicating factor for public health officials is that tick species are on the move, as wildlife populations, forest habitats and weather patterns change across the continent.  This spring the Tennessee Department of Health, for example, reported a 500 percent increase in tick-borne rickettsiosis.—“Identifying health risks in the face of changing climates will be critical in coming years,” says Sam Scheiner, National Science Foundation program director for the joint NSF-National Institutes of Health Ecology and Evolution of Infectious Diseases (EEID) program, which funds Hickling’s research.–At NSF, the EEID program is co-funded by the Directorates for Biological Sciences and Geosciences.–“This study will inform public health officials about what diseases are found in which areas,” says Scheiner, “so they can minimize human health problems.”–Hickling’s work is also in collaboration with scientist Jean Tsao of Michigan State University and is part of an EEID project to identify the ecological factors leading to distributions of tick species and pathogens–in particular, where the Lyme disease tick and pathogen are found.–Lyme-infected blacklegged ticks are expanding south through Virginia, and lone star ticks are moving north, the scientists have found.–The bite of the lone star tick can create a bulls-eye rash that appears like that of Lyme disease, but the rash isn’t caused by the Lyme bacteria.—The scientists say that this almost certainly leads to misdiagnosis of some patients in mid-Atlantic states, where both tick species are common.—The best way to distinguish Lyme from other tick-borne diseases is to be vigilant for tick bites, and whenever possible save any tick that manages to bite you, the biologists recommend. Store the tick in your freezer or in a vial of alcohol so it can be identified if you become ill.—In the Northeast, Lyme disease awareness campaigns have focused public attention on the nymphal blacklegged tick–which is responsible for most disease transmission and which is tinier than the adult form.–While nymphal blacklegged ticks and nymphal lone star ticks–which also bite humans–can be distinguished, the two are often confused by the public.–In one study, 13 of 20 patients reporting tick bites to physicians were given antibiotics on the assumption that they were at risk for Lyme disease, yet 53 of the 54 ticks removed from those same patients were lone star ticks, which do not spread Lyme disease.—“Where you live determines which tick species is likely to bite you,” says Tsao, “and therefore which diseases you’re most likely to contract.”–The biologists say they are happy that recent treatment recommendations have begun to emphasize the importance of considering the tick species and its infection status as part of the diagnostic process.–Their advice: Stay open-minded about which tick-borne diseases are most common in your area–and save the tick that bites you.–Story Source-The above story is reprinted from materials provided by National Science Foundation. —Journal Reference–E. Y. Stromdahl, G. J. Hickling. Beyond Lyme: Aetiology of Tick-borne Human Diseases with Emphasis on the South-Eastern United States. Zoonoses and Public Health, 2012; 59: 48 DOI: 10.1111/j.1863-2378.2012.01475.x

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    Copper Benefits—
    Aneurysm may occur as a result of Copper deficiency.  –Copper may help to prevent abnormal Blood Clotting.-Copper deficiency may cause Congestive Heart Failure. -Copper is involved in the production of Red Blood Cells (via its involvement in the production of Hemoglobin). -Copper (in correct dosages) may enhance the health of the Heart-Optimal Copper levels may help to prevent damage to the Cardiac Muscle (i.e. the Muscle of the Heart).  —Cells–Impaired Growth may occur as a result of Copper deficiency.  —Digestive System—Many Celiac Disease patients are found to be deficient in Copper (indicating that supplemental Copper may benefit Celiac Disease patients). –Infant Diarrhea may occur as a result of Copper deficiency. –Eyes/Vision—Optimal Copper levels may help to prevent Cataracts. — Increased susceptibility to Bacterial & Viral Diseases (infections) may occur as a result of Copper deficiency: references- Copper may be a useful treatment for Acquired Immune Deficiency Syndrome (AIDS) patients (Copper inhibits HIV Protease, a component of the HIV virus)–However it has not yet been proven (nor disproven) that supplemental Copper can inhibit HIV Protease in vivo (within the body) as opposed to in vitro (in the test tube).—Optimal Copper levels may enhance the body’s resistance to Candida albicans proliferation.  Copper may be essential for the proper function of the Immune System and damage to the Immune System may occur as a result of Copper deficiency—Copper deficiency may reduce the production of Antibodies. Copper may be essential for the production of Neutrophils – Neutropenia (low Neutrophils count) may occur as a result of Copper deficiency. – Copper is involved in the formation of Bones—Copper may be required for the healing of Fractures (due to Copper being an essential component of the Lysyl Oxidase enzyme that catalyzes the final step in the synthesis of Collagen which is essential for the healing of Fractures) and supplemental Copper may accelerate the healing of Fractures.  People who are deficient in Copper may be more susceptible to Fractures.Osteoporosis may occur as a result of Copper deficiency.  Copper is required for the health of Connective Tissues–Copper may stimulate the (desirable) cross-linking of Collagen fibers (by activating the Lysyl Oxidase enzyme). -Copper may stimulate the formation of Elastin in Connective Tissues. —33% of the body’s Copper concentrates in the Muscles.–        Copper may alleviate Rheumatoid Arthritis—Copper bracelets may react with the Fatty Acids in the Skin to form Copper salts which are able to be absorbed into the Skin (this has been scientifically validated).—The Copper Salicylate form of Copper (consumed orally or applied topically) may be an effective treatment for the symptoms of Rheumatoid Arthritis and claimed to be the best form of Copper for the treatment of Rheumatoid Arthritis (due to it very closely mimicking the function of Superoxide Dismutase (SOD), a natural Antioxidant enzyme).  Vitiligo may occur as a result of Copper deficiency. —
     
    Copper—and how it Protects
     
    Copper Can Help In The Battle Against Influenza A H1N1, Says Scientist
    ScienceDaily (July 24, 2009) — A leading microbiologist from the University of Southampton has told a conference that his research has found copper is effective in inhibiting the influenza A H1N1 virus.—Copper appears to have broad spectrum antiviral activity because it is also effective, not only against RNA-based influenza, but also against DNA-based adenovirus 40/41 which causes gastrointestinal infections.—Speaking at the BIT Life Sciences 2nd Annual World Summit on Antivirals in Beijing, China this week, Professor Bill Keevil, from the University’s School of Biological Sciences, added that he believed copper could be used to reduce the spread of flu in public places.—“With the ongoing threat of contamination by influenza A viruses, such as H1N1, there is a real and pressing need to utilise all appropriate and effective measures with proven antimicrobial qualities,” commented Professor Keevil. “It is recognised that many infectious diseases are spread by hand contact and studies have now repeatedly shown that the use of copper as a surface material in key public places such as hospitals and food preparation areas offers the potential to substantially restrict and reduce the spread of harmful infection”. The influenza aspect of the study, completed in 2007, involved a series of experiments testing incubation of influenza A on copper and stainless steel surfaces. Results showed that, after incubation for 1 hour on copper, 75% of the virus was eradicated, and after 6 hours, less than 500 viral particles remained active (greater than 99.99% or 10,000-fold decrease). Similar inactivation rates have now been observed for adenovirus 40/41.–Professor Keevil added: “These public health benefits, supported by extensive antimicrobial efficacy testing, are underpinned by the fact that copper, brass and bronze are capable of killing a range of harmful and potentially deadly micro-organisms.”–The study has contributed further to the understanding of copper’s antimicrobial qualities, which actively inhibit the growth of bacteria, fungi and viruses.–Story Source-The above story is reprinted from materials provided by University of Southampton, via AlphaGalileo.
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    Copper Proves Effective Against New E. Coli Strains in New Study
    ScienceDaily (June 2, 2011) — As the World Health Organisation suggests the E. coli outbreak in Germany is a strain never before seen in an outbreak — O104:H4 — laboratory science conducted at the University of Southampton indicates a role for copper in preventing the spread of such infections.—Professor Bill Keevil, Head of the Microbiology Group and Director of the Environmental Healthcare Unit at the University of Southampton, explains: “A study looking at copper’s efficacy against new strains of E. coli has just been completed. Although it did not specifically look at O104, all the strains investigated have died rapidly on copper.”—On a dry copper surface, the study shows 10 million E. coli bacteria are eliminated within 10 minutes. On a wet copper surface, one could expect a total kill within around 45 minutes. This antimicrobial property is inherent to the metal, and shared with alloys such as brass and bronze.—In the wake of this outbreak, hand washing and careful food preparation have been highlighted as key concerns, as has cross-contamination. Any raw food placed on a work surface can contaminate other food, or have bacteria transferred onto it from previous items resting there. Deployed as a touch surface in food preparation areas, copper will continuously kill any pathogens that settle on it, reducing the risk of cross-contamination, and helping to prevent the spread of infection.–Professor Keevil will be presenting his findings at the forthcoming WHO International Conference on Prevention and Infection Control in Geneva on 30 June.–Story Source-The above story is reprinted from materials provided by University of Southampton, via EurekAlert!, a service of AAAS.
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    Dry Copper Kills Bacteria On Contact
    ScienceDaily (Feb. 22, 2011) — Metallic copper surfaces kill microbes on contact, decimating their populations, according to a paper in the February 2011 issue of the journal Applied and Environmental Microbiology. They do so literally in minutes, by causing massive membrane damage after about a minute’s exposure, says the study’s corresponding author, Gregor Grass of the University of Nebraska, Lincoln. This is the first study to demonstrate this mechanism of bacteriocide.—“When microbes were exposed to copper surfaces, we observed contact killing to take place at the rate of tens to hundreds of millions of bacterial cells within minutes,” says Grass. “This means that usually no live microorganisms can be recovered from copper surfaces after exposure.”—Thus, such surfaces could provide a critical passive defense against pathogens in hospitals, where hospital-acquired infections are becoming increasingly common and costly, killing 50,000-100,000 Americans annually, and costing more than $8 billion, according to one estimate. Still, Grass cautions that “metallic copper surfaces will never be able to replace other hygiene-improving methods already in effect,” although they “will certainly decrease the costs associated with hospital-acquired infections and curb human disease as well as save lives.” However, he expects this strategy to be inexpensive, because “the effect does not wear off.”—Critically, the researchers provide strong evidence that genotoxicity through mutations and DNA lesions is not a cause of dry copper’s antimicrobial properties. This is important, because mutations can cause cancer in animals and humans, and the lack of such mutations in bacteria from copper means that copper does not endanger humans.—The relevant experiment was particularly interesting. The bacterium, Deinococcus radiodurans, is unusually resistant to radiation damage, as its DNA repair mechanisms are especially robust. The hypothesis: if metallic copper kills by causing DNA damage, D. radiodurans should be immune to copper. It is not.It is important to note that only dry copper surfaces are amazingly lethal to bacteria. The difference between dry and wet surfaces, such as copper pipes, is that only dry surfaces are inhospitable environments for bacterial growth. Bacteria can easily grow and reproduce in wet environments, and in so doing, they can develop resistance to copper. Resistance has not been observed to develop on dry copper surfaces.—-Story Source:– Journal Reference-C. E. Santo, E. W. Lam, C. G. Elowsky, D. Quaranta, D. W. Domaille, C. J. Chang, G. Grass. Bacterial Killing by Dry Metallic Copper Surfaces. Applied and Environmental Microbiology, 2010; 77 (3): 794 DOI: 10.1128/AEM.01599-10
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    Work With Germ-Killing Copper Could Save Thousands of Lives
     
    Roberto del Rio Children’s Hospital, the oldest pediatric facility in Chile, installed antimicrobial copper surfaces in its intensive care and treatment rooms to reduce the risk of infection. The installation was a first for Latin America, following a growing number of installations in Europe, Asia and North America. –ScienceDaily (Sep. 7, 2012) — When Adam Estelle graduated from the University of Arizona’s materials science and engineering program four years ago, he had no idea he would be involved in saving thousands of lives.–Like most graduates, he was just hoping to find a job — preferably in Tucson, Ariz., because he wasn’t interested in big-city life. What happened next was a job offer from the Copper Development Association in New York City.–The technology is based on copper alloys that kill bacteria, fungi and viruses. The metals can be fashioned into everything from IV poles to sinks to bed rails — just about anything that is frequently touched in hospitals.—While these surfaces might look benign, they’re covered with organisms that contribute to hospital-acquired infections, the fourth leading cause of death in the United States, killing more people than AIDS and breast cancer combined. That’s 2 million infections annually, and 100,000 deaths — one infection for every 20 people admitted to hospitals.–While disease-causing organisms can lurk on stainless steel surfaces for two weeks, according to a recent UA research study, 99.9 percent die within two hours on surfaces that contain at least 60 percent copper, Estelle says.—Estelle has been working with four other engineers at the Copper Development Association, a not-for-profit trade group, to develop a market for copper alloys in the health care industry. They also have been helping manufacturers gear up for producing copper alloy products.–Part of that effort has involved gaining EPA certification for the antimicrobial effects of copper so manufacturers can advertise the health benefits of these products. The second part, which has been Estelle’s major focus for the past two years, was to retrofit the Ronald McDonald House in Charleston, S.C., with copper alloy stair railings, door hardware, sinks, faucets, counter tops, kitchen tables, chair arms, and other surfaces that are frequently touched by patients, visitors and staff.–This has been a win-win for everyone, Estelle explained, creating a safer environment for families and children, while at the same time helping the first wave of manufacturers tool up and commercialize lines of copper products that can now be marketed to hospitals.–“One of our first commercial products is a beautiful seamless counter top and sink bowl manufactured by Elkay Commercial Products,” Estelle said. “We installed about forty of these in the Ronald McDonald House.” Elkay is among ten manufacturers now marketing antimicrobial copper alloy products to the health care industry.–Surfaces at the Ronald McDonald House were swabbed and tested for bacteria for ten weeks before the new copper alloy products were installed. “Follow-up tests on the items converted to copper showed they carried 94 percent fewer bacteria,” Estelle said. “We are now trying to recreate the Charleston project at other Ronald McDonald Houses around the world to create a safer living and working environment for the children, families and staff.”—Now, with the Ronald McDonald House pilot project completed and EPA approval secured, the next step is to convince hospitals to replace traditional surfaces that are not worn out with copper alloy ones. New policies from the Centers for Medicare and Medicaid Services that go into effect next year should help spur this changeover. Treatment for hospital-acquired infections costs between $35 billion and $45 billion each year in the U.S., and Medicare and Medicaid will no long reimburse hospitals for that treatment if the infections are judged to have been preventable and a hospital mistake.–But even without the new rules, the changeover makes economic sense, Estelle explained. Under today’s reimbursement system, individual hospitals spend $5 million on average each year to treat infections. “Even on the low end, it’s $30,000 per infection,” he said. Clinical trials at three hospitals funded by the U.S. Department of Defense have recently proved that copper surfaces can reduce infections in the intensive care unit by more than 50 percent.–Using published estimates, about 500,000 Americans will contract an infection this year in the ICU. This will cost our hospitals an additional $3.5 billion in treatment, and about 40,000 people will not survive the ordeal. The clinical trial results suggest that installing copper surfaces could cut these figures in half.—“By implementing these surfaces, hospitals can see real, continuous savings year after year,” Estelle said. “This is a passive way to prevent infection that doesn’t depend on human behavior, such as hand-washing or hydrogen peroxide vapor machines. There is no need for maintenance beyond the normal surface cleaning procedures that are already in place.”—,.”Story Source–The above story is reprinted from materials provided by University of Arizona College of Engineering, via Newswise.
     
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    Copper Recipe —
    Chlorophyll2 table spoons—vitamin C 3 grams and Zinc 30-50 mgs-manganese 8 mgs—-mix your Vitamin C and chlorophyll in a tiny glass—and consume them—cahse with water or juice or cool tea afterwards—this will Boost S O D in both the mitochandria and the cells—the combination should as well boost the immune system on several fronts and stabilizing Glutathione as well
     
    Copper Colloidal—1  -2 tablespoon 3 grams of vitamin C  and Salicyclic acid 50 mgs—and 2 oz of water –Mix well and consume this  will alleviate pain in moments and will kill of viral and bacterial pathogens
     
    You can also do this in dry form
    3 grams of Vitamin C—2 mgs of copper and 30 mgs of zinc and the salicyclic acid 50 mgs-may find relief with this for hours
     
     
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    Show Of the Month  September 24-2012
     
    How LOW Cholesterol Can Harm Your Health
    Grain-Wheat-Chronic Poison
    Nutritional Supplement Offers Promise in Treatment of Unique Form of Autism
     
    Myocardial infarction in relation to mercury and fatty acids from fish
     
    Supplement Your Stem Cells—how to look at this study
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    How LOW Cholesterol Can Harm Your Health
    You’ve heard for decades about the dangers of high cholesterol, but did you know that LOW cholesterol can lead to violence towards self and other, and has been linked to premature aging, death and other adverse health effects?–In a world gone mad with anti-cholesterol anxiety, and where gobbling down pharmaceuticals designed to poison the body into no longer synthesizing it is somehow considered sane behavior, it is refreshing to look at some of the research on the health benefits of cholesterol, or conversely, the dangers of low cholesterol.
    Benefits of Cholesterol
    Cholesterol Is Needed To Prevent Aggression
    It has been known for almost 30 years that low serum cholesterol levels are associated with habitually violent tendencies of homicidal offenders under the influence of alcohol. Since then, there are at least 8 other studies that have either confirmed or explored the cholesterol-violence link, including both violence towards self and other.  One of the possible explanations for this association was discussed in an article published in the British Journal of Psychiatry in 1993: “One of the functions of serotonin in the central nervous system is the suppression of harmful behaviour impulses…Low membrane cholesterol decreases the number of serotonin receptors. Since membrane cholesterol exchanges freely with cholesterol in the surrounding medium, a lowered serum cholesterol concentration may contribute to a decrease in brain serotonin, with poorer suppression of aggressive behaviour”.[ii] Not surprisingly, several reports have now surfaced on cholesterol-lowering statin drugs contributing to irritability and/or aggression.
    Cholesterol Is Needed To Fight Cancer
    The inverse relationship between cholesterol levels and the risk for a variety of cancers, and mortality associated with cancer, has been known about since the late 80′s.[iii] Since then, the cholesterol-cancer connection has been confirmed over and over again. It is to be expected, therefore, that statin drug use would be linked with increased cancer incidence, which indeed it is.[iv] Even when you take so-called “bad” LDL-cholesterol and administer it to a culture of highly malignant, multi-drug resistant leukemia cells, the cells lose their resistance to chemotherapy.
     
    Cholesterol Is Needed To Prevent Hemorrhagic Stroke
    There are two types of stroke:
    1) Ischemic, associated with lack of blood flow and oxygen to the brain
    2) Hemorrhagic, associated with the rupture of a blood vessel in the brain, and bleeding.
    The risk for the former, in theory, could be raised in the presence of excessive oxidized cholesterol. However, it is the risk for the second, hemorrhagic stroke, which is increased when cholesterol levels are low. Noted as far back as 1994 in the British Medical Journal, in an article titled, “Assessing possible hazards of reducing serum cholesterol,” researchers found “The only cause of death attributable to low serum cholesterol concentration was haemorrhagic stroke.”[vi]  Other studies can be viewed that confirm this association on our stroke-cholesterol link page.
    Cholesterol Is Needed for Memory
    Low HDL cholesterol has been identified as a risk factor for deficit and decline in memory in midlife. [vii] Even in Parkinson’s disease, higher total serum cholesterol concentrations are associated with slower clinical progression of the disease.[viii]Statin drugs, which inhibit the production of cholesterol, hence severely affecting the brain, are now required by the FDA to display the black box warning that they may adversely affect the memory.[ix] We have indexed over 50 studies from the National Library of Medicine’s bibliographic database, Medline, on the neurotoxicity of statin drugs, with six of these specifically addressing statin-induced memory impairment.
    Cholesterol is Needed for Longevity
    In a fascinating study published in PLoS in 2011, telomere length – the shoestring cap-like ends of the chromosomes which prevent DNA damage associated with cellular aging – was linked to higher LDL and total cholesterol levels. The longer the length of these protective caps, the higher the cholesterol.[x]  Indeed, several studies indicate that lower cholesterol is associated with increased mortality.
    Cholesterol Helps Us Fight Infection
    It has been observed that a cholesterol-rich diet improves patients with tuberculosis, leading researchers to suggest “cholesterol should be used as a complementary measure in antitubercular treatment.”[xi] Cholesterol-lowering drugs, incidentally, exhibit immunosuppressive and potent immunotoxic properties, likely in part due to their cholesterol depleting effects.
    Given that cholesterol is essential for all animal life and that each cell is capable of synthesizing it from simpler molecules, we should not be surprised by examples provided above of cholesterol’s significant health benefits.  Nor should it be surprising that cholesterol-lowering drugs have over 300 adverse health effects.  For now, suffice it to say, that conventional medical practice would do well to receive instruction from basic principles of biology, rather than simply the drug-company marketing copy it increasingly falls prey to.
    Article Sources
    M Virkkunen. Serum cholesterol levels in homicidal offenders. A low cholesterol level is connected with a habitually violent tendency under the influence of alcohol. Neuropsychobiology. 1983 ;10(2-3):65-9. PMID: 6674827
    [ii] K Hawthon, P Cowen, D Owens, A Bond, M Elliott. Low serum cholesterol and suicide. Br J Psychiatry. 1993 Jun ;162:818-25. PMID: 7980726
    [iii] P Knekt, A Reunanen, A Aromaa, M Heliövaara, T Hakulinen, M Hakama. Serum cholesterol and risk of cancer in a cohort of 39,000 men and women. J Clin Epidemiol. 1988;41(6):519-30. PMID: 3290396
    [iv] GreenMedInfo.com, Focused Articles: Cancer-Statin Drug Link.
    [v] Yu Shu, Hu Liu. Reversal of P-glycoprotein-mediated multidrug resistance by cholesterol derived from low density lipoprotein in a vinblastine-resistant human lymphoblastic leukemia cell line. Biochem Cell Biol. 2007 Oct;85(5):638-46. PMID: 17901905
    [vi] M R Law, S G Thompson, N J Wald. Assessing possible hazards of reducing serum cholesterol.BMJ. 1994 Feb 5;308(6925):373-9. PMID: 8124144
    [vii] Archana Singh-Manoux, David Gimeno, Mika Kivimaki, Eric Brunner, Michael G Marmot. Low HDL cholesterol is a risk factor for deficit and decline in memory in midlife: the Whitehall II study.Arterioscler Thromb Vasc Biol. 2008 Aug;28(8):1556-62. Epub 2008 Jun 30. PMID: 18591462
    [viii] Xuemei Huang, Peggy Auinger, Shirley Eberly, David Oakes, Michael Schwarzschild, Alberto Ascherio, Richard Mailman, Honglei Chen, . Serum Cholesterol and the Progression of Parkinson’s Disease: Results from DATATOP. PLoS One. 2011 ;6(8):e22854. Epub 2011 Aug 11. PMID:21853051
    [ix] Weeks MD, Black box warning changes for statin drugs, March 4th, 2012
    [x] Paul G Shiels, Liane M McGlynn, Alan Macintyre, Paul C D Johnson, G David Batty, Harry Burns, Jonathan Cavanagh, Kevin A Deans, Ian Ford, Alex McConnachie, Agnes McGinty, Jennifer S McLean, Keith Millar, Naveed Sattar, Carol Tannahill, Yoga N Velupillai, Chris J Packard. Accelerated Telomere Attrition Is Associated with Relative Household Income, Diet and Inflammation in the pSoBid Cohort. PLoS One. 2011 ;6(7):e22521. Epub 2011 Jul 27. PMID:21818333
    [xi] Carlos Pérez-Guzmán, Mario H Vargas, Francisco Quiñonez, Norma Bazavilvazo, Adriana Aguilar. A cholesterol-rich diet accelerates bacteriologic sterilization in pulmonary tuberculosis.Chest. 2005 Feb;127(2):643-51. PMID: 15706008
    ****************************************************************************
    Grain-Wheat-Chronic Poison
    (CBS News) Modern wheat is a “perfect, chronic poison,” according to Dr. William Davis, a cardiologist who has published a book all about the world’s most popular grain. -Davis said that the wheat we eat these days isn’t the wheat your grandma had: “It’s an 18-inch tall plant created by genetic research in the ’60s and ’70s,” he said on “CBS This Morning.” “This thing has many new features nobody told you about, such as there’s a new protein in this thing called gliadin. It’s not gluten. I’m not addressing people with gluten sensitivities and celiac disease. I’m talking about everybody else because everybody else is susceptible to the gliadin protein that is an opiate. This thing binds into the opiate receptors in your brain and in most people stimulates appetite, such that we consume 440 more calories per day, 365 days per year.”–Asked if the farming industry could change back to the grain it formerly produced, Davis said it could, but it would not be economically feasible because it yields less per acre. However, Davis said a movement has begun with people turning away from wheat – and dropping substantial weight. –“If three people lost eight pounds, big deal,” he said. “But we’re seeing hundreds of thousands of people losing 30, 80, 150 pounds. Diabetics become no longer diabetic; people with arthritis having dramatic relief. People losing leg swelling, acid reflux, irritable bowel syndrome, depression, and on and on every day.”–To avoid these wheat-oriented products, Davis suggests eating “real food,” such as avocados, olives, olive oil, meats, and vegetables. “(It’s) the stuff that is least likely to have been changed by agribusiness,” he said. “Certainly not grains. When I say grains, of course, over 90 percent of all grains we eat will be wheat, it’s not barley… or flax. It’s going to be wheat. –“It’s really a wheat issue.”–Some health resources, such as the Mayo Clinic, advocate a more balanced diet that does include wheat. But Davis said on “CTM” they’re just offering a poor alternative. –“All that literature says is to replace something bad, white enriched products with something less bad, whole grains, and there’s an apparent health benefit – ‘Let’s eat a whole bunch of less bad things.’ So I take…unfiltered cigarettes and replace with Salem filtered cigarettes, you should smoke the Salems. That’s the logic of nutrition, it’s a deeply flawed logic. What if I take it to the next level, and we say, ‘Let’s eliminate all grains,’ what happens then?—“That’s when you see, not improvements in health, that’s when you see transformations in health.”
    http://www.cbsnews.com/8301-505269_162-57505149/modern-wheat-a-perfect-chronic-poison-doctor-says/?tag=cbsnewsSectionContent.8
     
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    Nutritional Supplement Offers Promise in Treatment of Unique Form of Autism
     
    ScienceDaily (Sep. 6, 2012) — An international team of researchers, led by scientists at the University of California, San Diego and Yale University schools of medicine, have identified a form of autism with epilepsy that may potentially be treatable with a common nutritional supplement.–The findings are published in the Sept. 6, 2012 online issue of Science.–Roughly one-quarter of patients with autism also suffer from epilepsy, a brain disorder characterized by repeated seizures or convulsions over time. The causes of the epilepsy are multiple and largely unknown. Using a technique called exome sequencing, the UC San Diego and Yale scientists found that a gene mutation present in some patients with autism speeds up metabolism of certain amino acids. These patients also suffer from epileptic seizures. The discovery may help physicians diagnose this particular form of autism earlier and treat sooner.–The researchers focused on a specific type of amino acid known as branched chain amino acids or BCAAs. BCAAs are not produced naturally in the human body and must be acquired through diet. During periods of starvation, humans have evolved a means to turn off the metabolism of these amino acids. It is this ability to shut down that metabolic activity that researchers have found to be defective in some autism patients.—“It was very surprising to find mutations in a potentially treatable metabolic pathway specific for autism,” said senior author Joseph G. Gleeson, MD, professor in the UCSD Department of Neurosciences and Howard Hughes Medical Institute investigator. “What was most exciting was that the potential treatment is obvious and simple: Just give affected patients the naturally occurring amino acids their bodies lack.”—Gleeson and colleagues used the emerging technology of exome sequencing to study two closely related families that have children with autism spectrum disorder. These children also had a history of seizures or abnormal electrical brain wave activity, as well as a mutation in the gene that regulates BCAAs. In exome sequencing, researchers analyze all of the elements in the genome involved in making proteins.—In addition, the scientists examined cultured neural stem cells from these patients and found they behaved normally in the presence of BCAAs, suggesting the condition might be treatable with nutritional supplementation. They also studied a line of mice engineered with a mutation in the same gene, which showed the condition was both inducible by lowering the dietary intake of the BCAAs and reversible by raising the dietary intake. Mice treated with BCAA supplementation displayed improved neurobehavioral symptoms, reinforcing the idea that the approach could work in humans as well.–“Studying the animals was key to our discovery,” said first author Gaia Novarino, PhD, a staff scientist in Gleeson’s lab. “We found that the mice displayed a condition very similar to our patients, and also had spontaneous epileptic seizures, just like our patients. Once we found that we could treat the condition in mice, the pressing question was whether we could effectively treat our patients.”—Using a nutritional supplement purchased at a health food store at a specific dose, the scientists reported that they could correct BCAA levels in the study patients with no ill effect. The next step, said Gleeson, is to determine if the supplement helps reduce the symptoms of epilepsy and/or autism in humans.—“We think this work will establish a basis for future screening of all patients with autism and/or epilepsy for this or related genetic mutations, which could be an early predictor of the disease,” he said. “What we don’t know is how many patients with autism and/or epilepsy have mutations in this gene and could benefit from treatment, but we think it is an extremely rare condition.”
    Co-authors are Paul El-Fishawy, Child Study Center, Yale University School of Medicine; Hulya Kayserili, Medical Genetics Department, Istanbul University, Turkey; Nagwa A. Meguid, Rehab O. Khalil, Adel F. Hashish and Hebatalla S. Hashem, Department of Research on Children with Special Needs, National Research Centre, Cairo, Egypt; Eric M. Scott, Jana Schroth, Jennifer L. Silhavy, Neurogenetics Laboratory, Howard Hughes Medical Institute, Department of Neurosciences, UC San Diego; Majdi Kara, Pediatric Department, Tripoli Children’s Hospital, Libya; Tawfeq Ben-Omran, Clinical and Metabolic Genetics Division, Department of Pediatrics, Hamad Medical Corporation, Doha, Qatar; A. Gulhan Ercan-Sencicek, Stephan J. Sanders and Matthew W. State, Program on Neurogenetics, Child Study Center, Department of Psychiatry and Department of Genetics, Yale University School of Medicine; Abha R. Gupta, Child Study Center, Department of Pediatrics, Yale University School of Medicine; Dietrich Matern, Biochemical Genetics Laboratory, Department of Laboratory Medicine and Pathology, Mayo Clinic; Stacy Gabriel, Broad Institute of Harvard and Massachusetts Institute of Technology; Larry Sweetman, Institute of Metabolic Disease, Baylor Research Institute; Yasmeen Rahimi and Robert A. Harris, Roudebush VA Medical Center and Department of Biochemistry and Molecular Biology, Indiana University School of Medicine.–Funding for this research came, in part, from the National Institutes of Health (grants P1HD070494, R01NS048453, P30NS047101, RC2MH089956, K08MH087639, T32MH018268, U54HG003067), the Center for Inherited Disease Research, the Simons Foundation Research Initiative, Veterans Administration Merit Award, the German Research Foundation, the American Academy of Child and Adolescent Psychiatry Pilot Research Award/Elaine Schlosser Lewis Fund and the American Psychiatric Association/Lilly Research Fellowship.—Story Source-The above story is reprinted from materials provided by University of California, San Diego, via Newswise. –Journal Reference-Gaia Novarino, Paul El-Fishawy, Hulya Kayserili, Nagwa A. Meguid, Eric M. Scott, Jana Schroth, Jennifer L. Silhavy, Majdi Kara, Rehab O. Khalil, Tawfeg Ben-Omran, A. Gulhan Ercan-Sencicek, Adel F. Hashish, Stephan J. Sanders, Abha R. Gupta, Hebatalla S. Hashem, Dietrich Matern, Stacey Gabriel, Larry Sweetman, Yasmeen Rahimi, Robert A. Harris, Matthew W. State, and Joseph G. Gleeson. Mutations in BCKD-kinase Lead to a Potentially Treatable Form of Autism with Epilepsy. Science, 2012; DOI: 10.1126/science.1224631
     
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    Myocardial infarction in relation to mercury and fatty acids from fish: a risk-benefit analysis based on pooled Finnish and Swedish data in men1,2,3,4
    Maria Wennberg,
    Ulf Strömberg,
    Ingvar A Bergdahl,
    Jan-Håkan Jansson,
    Jussi Kauhanen,
    Margareta Norberg,
    Jukka T Salonen,
    Staffan Skerfving,
    Tomi-Pekka Tuomainen,
    Bengt Vessby, and
    Jyrki K Virtanen
    + Author Affiliations
    1From the Departments of Public Health and Clinical Medicine, Occupational and Environmental Medicine (MW and IAB), Medicine (J-HJ), and Epidemiology and Global Health (MN), Umeå University, Umeå, Sweden; the Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden (US and SS); the Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland (JK, T-PT, and JKV); Metabolic Analytical Services Oy, Helsinki, Finland (JTS); and the Department of Public Health and Caring Science, Uppsala University, Uppsala, Sweden (BV).
    + Author Notes
    ↵2 This article reflects the views of the authors only; the European Union is not liable for any use that may be made of the information. Funding sources had no role in the study design; the collection, analysis, or interpretation of data; the writing of the report; or the decision to submit the manuscript for publication.
    ↵3 Supported by the European Union [Sixth Framework Programme: PHIME (Public Health Impact of long-term, low-level Mixed Element Exposure in susceptible population strata); grant FOOD-CT-2006-016253] and the Swedish Research Council Formas. Additional support was provided by the Academy of Finland (grant 121206; to JKV), the Foundation of Medical Research in Skellefteå, and the Research Unit, Department of Medicine, Skellefteå Hospital.
    ↵4 Address reprint requests and correspondence to M Wennberg, Occupational and Environmental Medicine, Umeå University, 901 87 Umeå, Sweden. E-mail: [email protected]
    Abstract
    Background: Exposure to methylmercury from fish has been associated with increased risk of myocardial infarction (MI) in some studies. At the same time, marine n−3 (omega-3) PUFAs are an inherent constituent of fish and are regarded as beneficial. To our knowledge, no risk-benefit model on the basis of data on methylmercury, PUFA, and MI risk has yet been presented.
    Objective: The objective of this study was to describe how exposure to both marine n−3 PUFAs and methylmercury relates to MI risk by using data from Finland and Sweden.
    Design: We used matched case-control sets from Sweden and Finland that were nested in population-based, prospective cohort studies. We included 361 men with MI from Sweden and 211 men with MI from Finland. MI risk was estimated in a logistic regression model with the amount of mercury in hair (hair-Hg) and concentrations of n−3 PUFAs (EPA and DHA) in serum (S-PUFA) as independent variables.
    Results: The median hair-Hg was 0.57 μg/g in Swedish and 1.32 μg/g in Finnish control subjects, whereas the percentage of S-PUFA was 4.21% and 3.83%, respectively. In combined analysis, hair-Hg was associated with higher (P = 0.005) and S-PUFA with lower (P = 0.011) MI risk. Our model indicated that even a small change in fish consumption (ie, by increasing S-PUFA by 1%) would prevent 7% of MIs, despite a small increase in mercury exposure. However, at a high hair-Hg, the modeled beneficial effect of PUFA on MI risk was counteracted by methylmercury.
    Conclusions: Exposure to methylmercury was associated with increased risk of MI, and higher S-PUFA concentrations were associated with decreased risk of MI. Thus, MI risk may be reduced by the consumption of fish high in PUFAs and low in methylmercury.
    **********************************************************************
    Supplement Your Stem Cells—how to look at this study
    ScienceDaily (Apr. 7, 2010) — A nutritional supplement could stimulate the production of stem cells integral for repairing the body. Research published in BioMed Central’s open access Journal of Translational Medicine suggests that a commercially-available supplement can increase the blood circulation of hematopoietic stem cells, which can give rise to all blood cells, and endothelial progenitor cells, which repair damage to blood vessels.—Thomas E. Ichim from Medistem Incorporated, USA worked with a team of 13 researchers from industry and academia to further investigate whether this supplement, containing a cocktail of green tea, astralagus, goji berry extracts, ‘good’ bacteria Lactobacillus fermentum, antioxidant ellagic acid, immune enhancer beta 1,3 glucan and vitamin D3, was able to increase the number of stem cells circulating in the blood. They recruited 18 healthy adults aged between 20 and 72 who stopped any other dietary supplements 4-5 days before starting a two-week course of this supplement, taking it twice daily. The researchers took blood from the participants before they started the course and on days 1, 2, 7 and 14 to test for signs of stem cell activity by looking for cells expressing the genetic stem cell markers CD133, CD34 and KDR. They then confirmed whether taking the supplement changed the overall levels of hematopoietic stem cells and endothelial progenitor cells in the blood by using HALO (Hematopoietic Assay via Luminescent Output) and colony forming assays respectively.—Hematopoietic stem cells and endothelial progenitor cells increased after taking the nutritional supplement, suggesting that the supplement may be a useful stimulator for both types of stem cells. In this study, the levels of these stem cells peaked at 2-7 days and started to drop at 14 days, suggesting that this supplement could be used for continuous treatment for conditions associated with decreases in these stem cells such as Alzheimer’s Disease. Other therapeutic treatments used to recruit hematopoietic stem cells are not viable as long-term solutions due to costs and increased health risks caused by the extremely high levels of stem cells that these treatments maintain in the blood.—“To our knowledge, this is the first study demonstrating profound mobilization effect with possible clinical significance by a food supplement-based approach,” say the authors, adding, “Indeed it may be possible that our supplement could be beneficial in conditions associated with reduced progenitor cells such as diabetes or in smokers which possess lower baseline values as compared to controls.” Although they are quick to add, “However, given commercial pressures associated with this largely unregulated field, we propose detailed scientific investigations must be made before disease-associated claims are made by the scientific community.”–Story Source-The above story is reprinted from materials provided by BioMed Central, via EurekAlert!, a service of AAAS. –Journal Reference-Nina A Mikirova, James A Jackson, Ron Hunninghake, Julian Kenyon, Kyle WH Chan, Cathy A Swindlehurst, Boris Minev, Amit N Patel, Michael P Murphy, Leonard Smith, Famela Ramos, Doru T Alexandrescu, Thomas E Ichim and Neil H Riordan. Nutraceutical augmentation of circulating endothelial progenitor cells and hematopoietic stem cells in human subjects. Journal of Translational Medicine, (in press) [link]
     
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    Show of the Month September 28 2012
    Omega-3 Fish Oil Supplements May Not Offer Heart Benefits After All
    Grape seed extract enhances neurogenesis in the hippocampal dentate gyrus in C57BL/6 mice
    Grain-Wheat-Chronic Poison
    18 Causes of Mineral Depletion
    US and China Caught Secretly Testing GMO Rice on Children
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    Omega-3 Fish Oil Supplements May Not Offer Heart Benefits After All
    12 Sep 2012
    A review of 20 studies covering nearly 70,000 participants finds no statistically significant evidence that supplementation with omega-3 polyunsaturated fatty acids (PUFAs), commonly referred to as fish oil supplements, is linked to a lower risk of heart attack, stroke, or premature death.–However, in their attempt to clarify the recent controversy surrounding the use of omega-3 supplements, the authors do not rule out the possibility that certain groups may benefit, and call for future studies to look more closely at this.–Evangelos Rizos, of the University Hospital of Ioannina, Ioannina, Greece, and colleagues write about their findings in the 12 September issue of JAMA.—Omega-3 PUFAs are considered essential for healthy development of the heart and other parts of the body, and food sources rich in these include nuts and seeds, and oily fish such as salmon, mackerel, herring and sardines. As supplements they are typically given in the form of fish oil.—Although it is not clear how they help the heart and circulation, there are suggestions omega-3 PUFAs lower triglyceride levels, prevent serious arrythmias, reduce the clumping of platelets, and lower blood pressure.
    However, the authors write that-“Considerable controversy exists regarding the association of omega-3 polyunsaturated fatty acids (PUFAs) and major cardiovascular end points.”—For years, omega 3 fish oils have been recommended by health organisations to help reduce heart disease. However, a review of recent studies has questioned this. —Although some randomized studies suggest omega-3 PUFAs prevent heart disease, others refute this, they explain, noting also that many medical and health societies support their use for patients after heart attack (MI, myocardial infarction), either as supplements or through dietary advice.–Regulatory authorities also appear to have different views. The US Food and Drug Administration (FDA) has approved the use of omega-3 PUFAs only for lowering triglycerides in patients with overt hypertriglyceridemia, while some, but not all, European regulators have approved them for reducing cardiovascular risk.—“The controversy stemming from the varying labeling indications causes confusion in everyday clinical practice about whether to use these agents for cardiovascular protection,” write Rizos and colleagues.–Thus, in an attempt to clarify the situation, they carried out a large-scale statistical review of the available evidence from randomized controlled studies, looking at the link between omega-3 PUFAs and major cardiovascular outcomes such as stroke and heart attacks, and also premature death.—From a search of the well-known databases, they found 3,635 studies, from which 20 matched their criteria. These provided data for a pooled analysis on 68,680 randomized patients, and events that included 7,044 deaths, 3,993 cardiac deaths, 1,150 sudden deaths, 1,837 heart attacks, and 1,490 strokes.—Taking all the included supplement studies together, the researchers found no significant association between use of omega-3 PUFAs and all-cause mortality, cardiac death, sudden death, heart attack (MI), and stroke.———They conclude-“… omega-3 PUFAs are not statistically significantly associated with major cardiovascular outcomes across various patient populations.”–They suggest their findings “do not justify the use of omega-3 as a structured intervention in everyday clinical practice or guidelines supporting dietary omega-3 PUFA administration.”—However, they also note that as scientists continue to do more randomized studies in this field, it would be useful to do some that look more closely at how these supplements might benefit individual risk groups, and use more refined measures such as dose, adherence and baseline intake.—In other words, while looking at all the evidence as a whole does not appear to support the idea that omega-3 PUFA supplements benefit the heart, this broad-brush picture could be missing details: there may be certain groups that do benefit, and this may also depend on factors such as the supplement dose and how long they take it for.
    Other studies on fish oils—Some other recent individual studies, published in Medical News Today, have also concluded that fish oils do not appear to provide some of the benefits people had previously taken for granted. Researchers from the London School of Hygiene & Tropical Medicine found that taking omega-3 fish oil supplements appears not to protect older people from cognitive decline.
    In contrast, a study published on September 10th found that DHA intake may help improve reading and behavior in healthy but underperforming children. DHA is an omega-3 fatty acid. You can look up other studies related to omega-3 fish oils in our archive.
    Written by Catharine Paddock PhD
    References-“Association Between Omega-3 Fatty Acid Supplementation and Risk of Major Cardiovascular Disease Events: A Systematic Review and Meta- analysis”; Evangelos C. Rizos, Evangelia E. Ntzani, Eftychia Bika, Michael S. Kostapanos, Moses S. Elisaf; JAMA, published online 12 September 2012; dDOI:10.1001/2012.jama.11374; Link to Abstract. Additional source: American Medical Association press release.
     
    Please use one of the following formats to cite this article in your essay, paper or report:
    MLA
    Catharine Paddock PhD. “Omega-3 Fish Oil Supplements May Not Offer Heart Benefits After All.” Medical News Today. MediLexicon, Intl., 12 Sep. 2012. Web.
    13 Sep. 2012. <http://www.medicalnewstoday.com/articles/250142.php&gt;
    APA
    Catharine Paddock PhD. (2012, September 12). “Omega-3 Fish Oil Supplements May Not Offer Heart Benefits After All.” Medical News Today. Retrieved from
    http://www.medicalnewstoday.com/articles/250142.php.
     
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    Grape seed extract enhances neurogenesis in the hippocampal dentate gyrus in C57BL/6 mice.
    Phytother Res. 2011 May;25(5):668-74–Authors: Yoo DY, Kim W, Yoo KY, Lee CH, Choi JH, Yoon YS, Kim DW, Won MH, Hwang IK
    Abstract
    The effects of grape seed extract (GSE), a major source of phenolic compounds, were examined on cell proliferation, neuroblast differentiation and integration into granule cells in the hippocampal dentate gyrus (DG) of middle-aged (12 month-old) mice using Ki67, doublecortin (DCX) immunohistochemistry and 5′-bromo-2-deoxyguanosine (BrdU)/calbindin D-28k (CB) double immunofluorescence study, respectively. GSE (25, 50 and 100 mg/kg) was administered orally for 28 days, and the animals were treated with 50 mg/kg BrdU intraperitoneally on the day of first GSE treatment. In the vehicle-treated group, Ki67 and DCX immunoreactivity was detected in the subgranular zone of the DG (SZDG). GSE treatment dose-dependently increased the number of Ki67 and DCX immunoreactive cells, particularly the number of DCX immunoreactive neuroblasts with well-developed (tertiary) dendrites. GSE also dose-dependently increased DCX protein levels. In addition, GSE treatment increased significantly the number of BrdU/CB double labeled granule cells. These results suggest that GSE significantly increases cell proliferation, neuroblast differentiation and integration into granule cells in the DG, and the consumption of GSE enhances the plasticity of hippocampus in middle-aged mice.—PMID: 21043032 [PubMed – indexed for MEDLINE]
    ****************************************************************************
    Grain- Wheat Chronic Poison
    (CBS News) Modern wheat is a “perfect, chronic poison,” according to Dr. William Davis, a cardiologist who has published a book all about the world’s most popular grain. -Davis said that the wheat we eat these days isn’t the wheat your grandma had: “It’s an 18-inch tall plant created by genetic research in the ’60s and ’70s,” he said on “CBS This Morning.” “This thing has many new features nobody told you about, such as there’s a new protein in this thing called gliadin. It’s not gluten. I’m not addressing people with gluten sensitivities and celiac disease. I’m talking about everybody else because everybody else is susceptible to the gliadin protein that is an opiate. This thing binds into the opiate receptors in your brain and in most people stimulates appetite, such that we consume 440 more calories per day, 365 days per year.”–Asked if the farming industry could change back to the grain it formerly produced, Davis said it could, but it would not be economically feasible because it yields less per acre. However, Davis said a movement has begun with people turning away from wheat – and dropping substantial weight. –“If three people lost eight pounds, big deal,” he said. “But we’re seeing hundreds of thousands of people losing 30, 80, 150 pounds. Diabetics become no longer diabetic; people with arthritis having dramatic relief. People losing leg swelling, acid reflux, irritable bowel syndrome, depression, and on and on every day.”–To avoid these wheat-oriented products, Davis suggests eating “real food,” such as avocados, olives, olive oil, meats, and vegetables. “(It’s) the stuff that is least likely to have been changed by agribusiness,” he said. “Certainly not grains. When I say grains, of course, over 90 percent of all grains we eat will be wheat, it’s not barley… or flax. It’s going to be wheat. –“It’s really a wheat issue.”–Some health resources, such as the Mayo Clinic, advocate a more balanced diet that does include wheat. But Davis said on “CTM” they’re just offering a poor alternative. –“All that literature says is to replace something bad, white enriched products with something less bad, whole grains, and there’s an apparent health benefit – ‘Let’s eat a whole bunch of less bad things.’ So I take…unfiltered cigarettes and replace with Salem filtered cigarettes, you should smoke the Salems. That’s the logic of nutrition, it’s a deeply flawed logic. What if I take it to the next level, and we say, ‘Let’s eliminate all grains,’ what happens then?—“That’s when you see, not improvements in health, that’s when you see transformations in health.”
    http://www.cbsnews.com/8301-505269_162-57505149/modern-wheat-a-perfect-chronic-poison-doctor-says/?tag=cbsnewsSectionContent.8
     
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    18 Causes of Mineral Depletion
    Soil Depletion
    Antacids & Acid blockers
    Low Stomach Acid/Hypochlorhydria
    Cortisone
    Pharmaceutical Drugs
    Birth Control Pills
    Coffee
    Alcohol
    Soda consumption
    Sugar
    Excess Insulin
    Excess Estrogen
    Hyperthyroidism
    The Standard American Diet (S.A.D diet
    Excess Grains
    Dietary Insufficiency
    Heavy Metal Toxicity
    – Mercury – Aluminum – Lead
    Radiation
    ***************************************************************************************
    US and China Caught Secretly Testing GMO Rice on Children
     
    Instead of putting genetically modified foods through proper trials as consumers have been demanding for years, it appears the United States Department of Agriculture in alliance with the Chinese government have instead chosen to secretly test their latest GMO rice on young Chinese children. What’s particularly interesting is the fact that the agencies decided they even needed to test the rice, after claiming that GMO rice and all other GM creations are virtually identical to natural foods.–
    Currently under investigation by Chinese health officials, the research project was cracked wide open after Greenpeace reportedly corresponded with the Chinese Centre for Disease Control and Prevention to expose the ongoing research. Currently, Greenpeace is calling for a stop to the trials which are reportedly continuing in the field. Citing health and environmental risks, Greenpeace says that the studies are taking place on roughly 24 children aged between six and eight years old. It has also been said that the parents likely were completely unaware or misinformed.—The USDA seeks to examine the effects of the GMO rice on the young children, also known as genetically modified ‘golden rice’.—Shortly after the news came out, China’s version of Twitter exploded with outrage as Chinese government organizations went into overdrive to downplay the studies. A Tufts University PR spokesperson, the very university developing the rice, claimed to no knowledge of the event and decried it as inhumane and unethical. PR rep Andrea Grossman stated that the GMO rice creators had always placed the ‘highest importance’ on human health—We have always placed the highest importance on human health, and we take all necessary steps to ensure the safety of human research subjects.—One Chinese author indicated in the secret GMO rice trials, Shi-an Yin, was suspended from his work. The second claimed to have no idea the study was going on and was therefore not arrested or even suspended.—For the USDA to be secretly testing genetically modified foods on young children while disregarding all calls for real analysis in the United States shows just how the agency is trying to hide. After all, why would you not perform trials out in the open if the results were so favorable? Likely because their previous secret tests were not favorable, and the agency is determining just how detrimental new GMO rice really is.

    #2644
    AvatarEK
    Keymaster

    The U.S. Drug Enforcement Administration classifies ADHD drugs as Scheudle ll,
    in the same class of highly addictive drugs as morphine, opium and cocaine.
    Common brand name stimulants, also known as ADHD drugs, include Ritalin, Concerta, Adderall, Metadate, Vyvanse, Provigil.
    A) Drug Agency Regulatory Warnings on Stimulants/ADHD drugs – There have 31 drug regulatory agency warnings from eight countries including warnings of stimulant induced heart problems, suicide, violence, depression, mania, psychosis, hallucinations and death. See Tab A
    B) Drug Studies on Stimulants – There have been 119 studies in twelve countries on stimulant induced side effects including birth defects, heart problems, depression, suicidal ideation, violence, hallucinations, mania, psychosis, homicidal ideation and death. See Tab B
    C) Adverse Reaction Reports filed with the US FDA — There have been 14,158 adverse reactions reported to the US FDA in connection with stimulants. See Tab C
    Tab A) Stimulant Drug Warnings:
    There have been 31 warnings from eight countries (United States, United Kingdom, Canada, Japan, Australia, New Zealand, France and Singapore) warning that stimulants cause harmful side effects, which include:
    12 warnings on stimulants causing heart problems
    8 warnings on stimulants causing mania/psychosis
    8 warnings on stimulants causing death
    3 warnings on stimulants causing hallucinations
    2 warnings on stimulants causing depression
    2 warnings on stimulants causing violence, hostility or aggression
    2 warnings on stimulants causing seizures
    1 warning on stimulants causing suicide risk/attempts
    1 warning on stimulants causing anxiety
    Back to Top
    Tab B) Stimulant Drug Studies:
    There are 20 studies from four countries (United States, Australia, Denmark and Italy) showing that stimulants cause harmful side effects, including:
    5 studies on stimulants causing medication abuse
    3 studies on stimulants causing heart problems
    2 studies on stimulants causing death
    1 study on stimulants causing suicide risk/attempts
    1 study on stimulants causing birth defects
    1 study on stimulants causing violence
    1 study on stimulants causing homicidal ideation
    1 study on stimulants causing depression
    1 study on stimulants causing mania, psychosis and hallucinations
    Back to Top
    Tab C – Stimulant Drug Side Effects Reported to the FDA:
    The Adverse Drug Reactions that have been reported to the FDA’s Adverse Event Reporting System (MedWatch), between 2004 and 2011 include:
    871 cases of stimulants causing reactions related to suicide (completed suicides, suicide attempts, suicidal ideation and suicidal behavior)
    636 cases of stimulants causing aggression
    593 cases of stimulants causing hallucinations
    499 cases of stimulants causing anxiety
    495 cases of stimulants causing abnormal behavior
    464 cases of stimulants causing depression
    220 cases of stimulants causing death/sudden death
    147 cases of stimulants causing mania
    52 cases of stimulants causing homicidal ideation
    44 cases of stimulants causing diabetes
    30 cases of stimulants causing hostility
    25 cases of stimulants causing coma
    23 cases of stimulants causing physical Assault
    21 cases of stimulants causing birth defects
    13 cases of stimulants causing violence-related symptoms
    12 cases of stimulants causing psychosis
    11 cases of stimulants causing homicide
    9 cases of stimulants causing sexual dysfunction
    1 case of stimulants causing stillbirth
    Search CCHR’s Psychiatric Drug Side Effects database for more information
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    Modulation of apoptosis in human hepatocellular carcinoma (HepG2 cells) by a standardized herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizomes with anti- hepatocarcinogenic effects.
    BMC Complement Altern Med. 2012;12:25
    Authors: Samarakoon SR, Thabrew I, Galhena PB, Tennekoon KH
    Abstract
    BACKGROUND: A standardized poly-herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizome[U1]s used traditionally in Sri Lanka for cancer therapy has been demonstrated previously, to have anti-hepatocarcinogenic potential. Cytotoxicity, antioxidant activity, anti-inflammatory activity, and up regulation of p53 and p21 activities are considered to be some of the possible mechanisms through which the above decoction may mediate its anti-hepatocarcinogenic action. The main aim of the present study was to determine whether apoptosis is also a major mechanism by which the decoction mediates its anti-hepatocarcinogenic action.
    METHODS: Evaluation of apoptosis in HepG2 cells was carried out by (a) microscopic observations of cell morphology, (b) DNA fragmentation analysis, (c) activities of caspase 3 and 9, as well as by (d) analysis of the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins associated with cell death.
    RESULTS: The results demonstrated that in HepG2 cells, the decoction can induce (a) DNA fragmentation and (b) characteristic morphological changes associated with apoptosis (nuclear condensation, membrane blebbing, nuclear fragmentation and apoptotic bodies). The decoction could also, in a time and dose dependent manner, up regulate the expression of the pro-apoptotic gene Bax and down regulate expression of anti-apoptotic Bcl-2 gene (as evident from RT-PCR analysis, immunohistochemistry and western blotting). Further, the decoction significantly (p < .001) enhanced the activities of caspase-3 and caspase-9 in a time and dose dependent manner.—CONCLUSIONS: Overall findings provide confirmatory evidence to demonstrate that the decoction may mediate its reported anti-hepatocarcinogenic effect, at least in part, through modulation of apoptosis.—PMID: 22458551 [PubMed – indexed for MEDLINE]
    Recipe for making this decoction of Black seed and Smilax ( sarsaparilla)—take equal parts of each herb and boil them down to at least half of the volume of water you put in— I.E 2 pint down to 1 pint or less ( 500mls for the metric to 250 mls)—and then use small amounts 1-2 oz increments 4-5 times daily
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    Sesame and Rice Bran Oil Lowers Blood Pressure, Improves Cholesterol
    ScienceDaily (Sep. 18, 2012) — People who cooked with a blend of sesame and rice bran oils saw a significant drop in blood pressure and improved cholesterol levels, according to new research presented at the American Heart Association’s High Blood Pressure Research 2012 Scientific Sessions.—The researchers found cooking with a combination of these oils in a variety of ways worked nearly as well as a commonly prescribed high blood pressure medication, and that the use of the oil blend with medication yielded even more impressive results.—“Rice bran oil, like sesame oil, is low in saturated fat and appears to improve a patient’s cholesterol profile,” said Devarajan Sankar, M.D, Ph.D., a research scientist in the Department of Cardiovascular Disease at Fukuoka University Chikushi Hospital in Chikushino, Japan. “Additionally, it may reduce heart disease risk in other ways, including being a substitute for less healthy oils and fats in the diet[U2] .”–The 60-day study in New Delhi, India, divided 300 people with mild to moderately high blood pressure into three groups. One group was treated with a commonly used blood pressure lowering medication called a calcium-channel blocker (nifedipine). The second group was given the oil blend and told to use about an ounce each day in their meals.—The final group received the calcium channel blocker and the oil blend.—-All three groups, with approximately an equal number of men and women, average age of 57, saw drops in their systolic blood pressure. Systolic blood pressure is the top number in a blood pressure reading and measures the force of blood against your artery walls when the heart is pumping.—Systolic blood pressure dropped an average of 14 points for those using only the oil blend and 16 points for those taking medication. Those using both saw a 36-point drop.—Diastolic blood pressure also dropped significantly: 11 points for those eating the oil, 12 for those on medication and 24 for those using both. Diastolic blood pressure is the bottom number in a blood pressure reading that measures the force of blood against your artery walls when your heart is at rest between beats.—As for cholesterol, those using the oils saw a 26 percent drop in their LDL (“bad” cholesterol) and a 9.5 percent increase in the HDL (“good” cholesterol[U3] ), while no changes in cholesterol were observed for the patients who used only the calcium-channel blocker. Those who took the calcium channel blocker and the oils had a 27 percent drop in LDL levels and a 10.9 percent increase in the HDL[U4] . Healthier fatty acids and antioxidants, such as sesamin, sesamol, sesamolin and oryzanol, in the oil blends may be responsible for the results, Sankar said. These antioxidants, mono and poly unsaturated oils are compounds found in plants and have been linked with lower blood pressure and total cholesterol in earlier studies.–Additional studies are needed to determine if the oil blend is as beneficial as it seems. The combination was made specifically for this study, and there are no plans to market it commercially, Sankar said. Blending these oils yourself would not necessarily produce these effects.–Co-authors are.Ravinder Singh, M.B.B.S., and Biprabuddha Chatterjee, M.Sc.-Story Source-The above story is reprinted from materials provided by American Heart Association.
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    Chlorophyll revisited~~ anti-inflammatory activities of chlorophyll a and inhibition of expression of TNF-α gene by the same.
    Inflammation. 2012 Jun;35(3):959-66
    Authors: Subramoniam A, Asha VV, Nair SA, Sasidharan SP, Sureshkumar PK, Rajendran KN, Karunagaran D, Ramalingam K
    Abstract–In view of the folklore use of green leaves to treat inflammation, the anti-inflammatory property of chlorophylls and their degradation products were studied. Chlorophyll a and pheophytin a (magnesium-free chlorophyll a) from fresh leaves showed potent anti-inflammatory activity against carrageenan-induced paw edema in mice and formalin-induced paw edema in rats.[U5] Chlorophyll a inhibited bacterial lipopolysaccharide-induced TNF-α (a pro-inflammatory cytokine) gene expression in HEK293 cells, but it did not influence the expression of inducible nitric acid synthase and cyclooxygenase-2 genes. Chlorophyll b only marginally inhibited both inflammation and TNF-α gene expression. But both chlorophyll a and chlorophyll b showed the same level of marginal inhibition on 12-O-tetradecanoyl-phorbol-13-acetate-induced NF-κB activation. Chlorophylls and pheophytins showed in vitro anti-oxidant activity. The study shows that chlorophyll a and its degradation products are valuable and abundantly available anti-inflammatory agents and promising for the development of phytomedicine or conventional medicine to treat inflammation and related diseases.—PMID: 22038065 [PubMed – indexed for MEDLINE]
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    Chlorophyll is a chemoprotein commonly known for its contribution to the green pigmentation in plants, and is related to protoheme, the red pigment of blood. It can be obtained from green leafy vegetables (broccoli, Brussel sprouts, cabbage, lettuce, and spinach), algae (Chlorella and Spirulina), wheat grass, and numerous herbs (alfalfa, damiana, nettle, and parsley).–Chlorophyll has been used traditionally to improve bad breath and other forms of body odor including odors of the urine, feces, and infected wounds. More recently chlorophyll has been used to aid in the removal of various toxins via the liver and remains a key compound for improving the function of essential detoxification pathways. Supportive evidence suggests it may be used as an anti-inflammatory agent for conditions, such as pancreatitis as well as exhibiting potent antioxidant and chemoprotective activities. Scientific research has demonstrated it may be an effective therapeutic agent in the treatment of herpes simplex, benign breast disease, chemoprevention, tuberculosis, and rheumatoid arthritis. Type 2 diabetes and obesity are also being explored as areas where chlorophyll can also be used.
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    Bacterial Cause Found for Skin Condition Rosacea
    ScienceDaily (Aug. 28, 2012) — Scientists are closer to establishing a definitive bacterial cause for the skin condition rosacea. This will allow more targeted, effective treatments to be developed for sufferers, according to a review published in the Journal of Medical Microbiology.—Rosacea is a common dermatological condition that causes reddening and inflammation of the skin mostly around the cheeks, nose and chin. In severe cases skin lesions may form and lead to disfigurement[U6]. Rosacea affects around 3% of the population — usually fair-skinned females aged 30-50 and particularly those with weak immune systems. The condition is treated with a variety of antibiotics, even though there has never been a well-established bacterial cause.[U7]–A new review carried out by the National University of Ireland concludes that rosacea may be triggered by bacteria that live within tiny mites that reside in the skin.–The mite species Demodex folliculorum is worm-like in shape and usually lives harmlessly inside the pilosebaceous unit which surrounds hair follicles of the face. They are normal inhabitants of the face and increase in number with age and skin damage — for example, following exposure to sunlight. The numbers of Demodex mites living in the skin of rosacea patients is higher than in normal individuals[U8], which has previously suggested a possible role for the mites in initiating the condition.—More recently, the bacterium Bacillus oleronius was isolated from inside a Demodex mite[U9] and was found to produce molecules provoking an immune reaction in rosacea patients. Other studies have shown patients with varying types of rosacea react to the molecules produced by this bacterium — exposing it as a likely trigger for the condition. [U10]What’s more, this bacterium is sensitive to the antibiotics used to treat rosacea.—Dr Kevin Kavanagh who conducted the review explained, “The bacteria live in the digestive tracts of Demodex mites found on the face, in a mutually beneficial relationship. When the mites die, the bacteria are released and leak into surrounding skin tissues — triggering tissue degradation and inflammation.”[U11]—“Once the numbers of mites increase, so does the number of bacteria, making rosacea more likely to occur. Targeting these bacteria may be a useful way of treating and preventing this condition,” said Dr Kavanagh. “Alternatively we could look at controlling the population of Demodex mites in the face.. Some pharmaceutical companies are already developing therapies to do this, which represents a novel way of preventing and reversing rosacea, which can be painful and embarrassing for many people.”—-Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo. —Journal Reference-Stanisław Jarmuda, Niamh O’Reilly, Ryszard Żaba, Oliwia Jakubowicz, Andrzej Szkaradkiewicz and Kevin Kavanagh. The potential role of Demodex folliculorum mites and bacteria in the induction of rosacea. Journal of Medical Microbiology, 2012 DOI: 10.1099/jmm.0.048090-0
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    Show Of the Month October 5 2012
    Diet promotes sleep duration and quality
    Short Sleep Duration and Weight Gain– A Systematic Review
    Cell tower regulations frustrate homeowners Towers under 15 metres tall avoid municipal scrutiny
    Red wine and components flavonoids inhibit UGT2B17 in vitro
    Rhodiola Protects HPG Axis during Exercise or Physical Work
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    Diet promotes sleep duration and quality.
    Nutr Res. 2012 May;32(5):309-19–Authors: Peuhkuri K, Sihvola N, Korpela R
    Abstract–Sleep, much like eating, is an essential part of life. The mechanisms of sleep are only partially clear and are the subject of intense research. There is increasing evidence showing that sleep has an influence on dietary choices. Both cross-sectional and epidemiologic studies have demonstrated that those who sleep less are more likely to consume energy-rich foods (such as fats or refined carbohydrates), to consume fewer portions of vegetables, and to have more irregular meal patterns. In this narrative review, we pose the opposite question: can ingested food affect sleep? The purpose of this review is to discuss the evidence linking diet and sleep and to determine whether what we eat and what kind of nutrients we obtain from the food consumed before bedtime matter. In addition, scientific evidence behind traditional sleep-promoting foods such as milk and some herbal products is briefly described. These are reviewed using data from clinical trials, mostly in healthy subjects. In addition, we discuss the possible mechanisms behind these observations. Lastly, we summarize our findings that emerging evidence confirms a link between diet and sleep. Overall, foods impacting the availability of tryptophan, as well as the synthesis of serotonin and melatonin, may be the most helpful in promoting sleep. Although there are clear physiological connections behind these effects, the clinical relevance needs to be studied further.—PMID: 22652369 [PubMed – indexed for MEDLINE]
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    Short Sleep Duration and Weight Gain– A Systematic Review
    Sanjay R. Patel1 and Frank B. Hu2,3,4
    1Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, University Hospitals Case Medical Center and Case Western Reserve University, Cleveland, Ohio, USA
    2Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts, USA
    3Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
    4Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
    Correspondence: Sanjay R. Patel ([email protected])
    Received 18 April 2007; Accepted 19 July 2007; Published online 17 January 2008.
    The recent obesity epidemic has been accompanied by a parallel growth in chronic sleep deprivation. Physiologic studies suggest sleep deprivation may influence weight through effects on appetite, physical activity, and/or thermoregulation. This work reviews the literature regarding short sleep duration as an independent risk factor for obesity and weight gain.
    Methods and Procedures—A literature search was conducted for all articles published between 1966 and January 2007 using the search “sleep” and (“duration” or “hour” or “hours”) and (“obesity” or “weight”) in the MEDLINE database. Additional references were identified by reviewing bibliographies and contacting experts in the field. Studies reporting the association between sleep duration and at least one measure of weight were included.
    Results—Thirty-six publications (31 cross-sectional, 5 prospective, and 0 experimental) were identified. Findings in both cross-sectional and cohort studies of children suggested short sleep duration is strongly and consistently associated with concurrent and future obesity. Results from adult cross-sectional analyses were more mixed with 17 of 23 studies supporting an independent association between short sleep duration and increased weight. In contrast, all three longitudinal studies in adults found a positive association between short sleep duration and future weight. This relationship appeared to wane with age.
    Discussion–Short sleep duration appears independently associated with weight gain, particularly in younger age groups. However, major study design limitations preclude definitive conclusions. Further research with objective measures of sleep duration, repeated assessments of both sleep and weight, and experimental study designs that manipulate sleep are needed to better define the causal relationship of sleep deprivation on obesity.
    Introduction—Over the past several decades, the prevalence of obesity has grown to epidemic proportions. Concurrent with this rise in weight there has been a similar epidemic of chronic sleep deprivation. According to annual surveys done by the National Sleep Foundation, by 1998 only 35% of American adults were obtaining 8 h of sleep and that number had fallen to 26% by 2005 (ref. 1[U12] ).—–Evidence has grown over the past decade supporting a role for short sleep duration as a novel risk factor for weight gain and obesity. A number of causal pathways linking reduced sleep with obesity have been posited based on experimental studies of sleep deprivation. Chronic partial sleep deprivation causes feelings of fatigue which may lead to reduced physical activity (2,3). Sleep deprivation may also have neurohormonal effects that increase caloric intake (4). Because of the rapidly accelerating prevalence of sleep deprivation, any causal association between short sleep durations and obesity would have substantial importance from a public health standpoint. We performed a systematic review of the literature to assess the present evidence suggesting that sleep deprivation may represent a novel risk factor for weight gain and obesity.
    Methods and Procedures—-Relevant original articles were identified by searching the MEDLINE database (National Library of Medicine, Bethesda, MD) of articles published between 1966 and August 2006 examining the relationship between sleep duration and weight gain, obesity, or both. The primary search was performed using the keywords “sleep” and (“duration” or “hour” or “hours”) and (“obesity” or “weight”). A subsequent search was also performed using medical subheading terms. The searches were repeated in January 2007 to identify any new publications. Bibliographies of retrieved articles were reviewed, and experts in the field were contacted to further identify relevant works. Articles were restricted to studies conducted in humans presenting original research. Where data from the same cohort were presented in more than one article, only the report that most directly analyzed the sleep–weight association was included. All abstracts obtained from this search were screened. Relevant articles were obtained and evaluated for presentation of data regarding the association between sleep duration and at least one measure of weight (e.g., BMI, BMI z-score, and weight) either cross-sectionally or longitudinally. A meta-analysis was attempted, but the degree of heterogeneity among study designs, particularly with respect to the measure of association and the definition of short sleep duration, was prohibitive, and therefore a more qualitative assessment is presented. Greater weight is given to large studies, prospective cohort studies, and studies which objectively assessed sleep durations. Because of differences in the sleep requirements of children and adults, these groups are considered separately. Where results were presented graphically, authors were contacted to obtain the numeric data (3,5,6).
    Results—The keyword search initially identified a total of 1,013 citations. After screening through abstracts for relevance, 36 articles of potential relevance were identified. The medical subheading search identified an additional five articles. Fifteen articles were excluded because, though both sleep duration and weight data were collected, the association between these two factors was not assessed. Another five articles were excluded for presentation of data overlapping with another report, leaving 21 articles. Ten investigations were added after the original extraction from review of references and expert contact. The updated search in January 2007 identified 44 additional citations, of which 5 were relevant for this synthesis. Thus 36 studies were included in this analysis. Of these, 31 are cross-sectional studies, 2 are prospective cohort studies, and 3 report both cross-sectional and prospective findings. No experimental studies with weight as an outcome were identified. There are 13 studies examining the association between sleep duration and weight in pediatric populations and 23 studies of adults.
    Cross-sectional studies in children—Eleven studies were identified which assessed the cross-sectional association between sleep duration and weight in children (Table 1). All 11 works reported a positive association between short sleep duration and increased obesity. For the most part, obesity was defined by age-adjusted thresholds of BMI, which was directly measured, while sleep duration was typically obtained from questionnaires completed by parents. Because sleep requirements change through childhood, definitions of short sleep duration varied greatly based on the age of the cohort being studied.–The largest pediatric cohort to date is a Japanese birth cohort of 8,274 children assessed between the ages of 6 and 7 (ref. 7). Compared to children with a sleep duration of greater than or equal to10 h, the odds ratios (ORs) for obesity were 1.49, 1.89, and 2.89 for sleep durations of 9–10, 8–9, or <8 h, respectively. A study of 4,511 Portuguese school children aged 7–9 reported similar findings (8). Compared to a sleep duration of greater than or equal to11 h, the ORs for obesity were 2.27 and 2.56 for sleep durations of 9–10 and 8 h, respectively.—-Two studies have analyzed data from children undergoing health screens at school enrollment. A study of 6,645 German children aged 5–6 years found the ORs for obesity were 1.18 and 2.22 for sleep durations of 10.5–11.0 and <10.5 h, respectively, compared to greater than or equal to11.5 h (9). A similar study of 1,031 French 5-year-olds found the OR for obesity was 1.4 for a sleep duration <11 h (10).—Three smaller studies have examined a broader range of grade school children. A study of 422 Canadian children ages 5–10 found that compared to a sleep duration of greater than or equal to12 h, the ORs for obesity were 1.42 and 3.45 for sleep durations of 10.5–11.5 and less than or equal to10 h (11). Two small case–control studies of children aged 6–10 years, one from Brazil and one from Tunisia, reported similar findings. Giugliano and Carneiro reported obese children had 31 min shorter sleep duration than normal weight children but no significant difference was found between overweight and normal weight children (12). Ben Slama et al. found 58% of obese children had a sleep duration <8 h compared to only 11% of nonobese children (13).
    Four studies have examined the relationship between sleep duration and weight in adolescents. Two of these studies, though small, were notable for using objective measures of sleep habits. Measuring sleep duration with wrist actigraphy over a 24-h period in 383 children aged 11–16, Gupta et al. reported one of the strongest associations between short sleep duration and obesity, with the odds of obesity increasing five-fold for every hour reduction in sleep duration (14). Benefice et al., using an accelerometer worn near the hip to assess sleep over 3–4 days in 40 Senegalese girls aged 13–14 years, observed that sleep duration was reduced by 6.85 min for every 1 kg/m2 increase in BMI (15). This work was notable for demonstrating a sleep–weight relationship in a nonobese population—mean BMI was only 16.9 kg/m2. The other adolescent reports included one of 4,486 American teens (mean age 16.6 years), which found short self-reported sleep duration predicted both higher BMI z-score and overweight among boys. However, no relationship was found in girls (16). A study of 656 Taiwanese teenagers (mean age 15.0 years) found that the frequency of obtaining a sleep duration of at least 6–8 h was inversely correlated with obesity risk (17).
    The consistent findings from studies spanning five continents suggest that the reported associations are independent of ethnicity, though no formal assessment of effect modification by race has been reported. Several studies suggest boys may be more susceptible to sleep loss than girls. Sekine et al. found the OR for obesity associated with a sleep duration <8 h compared to >10 h was 5.5 in boys and 2.1 in girls (7). Similarly, Chaput et al. found that the OR for obesity associated with a sleep duration of less than or equal to10 h as opposed to greater than or equal to12 h was 5.7 in boys and 3.2 in girls (11). Knutson found the risk of being overweight increased 10% for each hour reduction in sleep duration among boys, while no significant effect was found among girls (16). A few studies have attempted to identify the causal pathway linking sleep duration to obesity. Von Kries et al. found no relationship between sleep habits and caloric intake obtained from a food frequency questionnaire (9). Gupta et al., using actigraphy, and Benefice et al., using accelerometry to estimate activity levels, each found no relationship between sleep duration and physical activity (14,15).
    Cross-sectional Studies in adults—Nineteen studies have focused on the cross-sectional relationship between sleep duration and weight in adults. The findings have been less consistent than the pediatric literature. Eleven studies reported a clear association between short sleep duration and increased weight, and two studies reported mixed findings with an association found in one gender but not in the other. Five studies reported no association between short sleep duration and increased weight, while one found short sleep duration was associated with reduced weight. In addition, six studies have found evidence that long sleep durations are also associated with increased weight resulting in a U-shaped curve between sleep duration and weight. In general, obesity has been defined as a BMI greater than or equal to30 kg/m2 based on either measured or self-reported height and weight. Habitual sleep duration has been typically obtained through questionnaire.—-The largest studies reporting on the association between sleep duration and weight were designed as prospective cohort studies to examine the effects of a wide range of behaviors on health outcomes and were not specifically designed to study sleep duration (5,18,19,20). Furthermore, data on the cross-sectional association between sleep duration and weight in these cohorts were presented as part of analyses designed to assess sleep duration as a predictor of mortality and so focused on the potential of weight to confound the sleep–mortality association. As a result, only the marginal associations between sleep duration and BMI were computed. The largest of these studies was a survey by the American Cancer Society of over 1.1 million individuals (5). This study found a U-shaped association between sleep duration and BMI among women with the minimum at 7 h and a monotonic trend in men such that longer sleep durations were associated with a lower BMI. Comparing a sleep duration of 4–7 h, women had a 1.39 kg/m2 greater BMI and men had a 0.57 kg/m2 greater BMI. The next largest study was a Japanese cohort of over 100,000 individuals (19). This is the only study to find short sleep durations associated with reduced weight. Mean BMI in those with sleep durations less than or equal to4, 5, 6, and 7 h were 22.2, 22.6, 22.9 and 22.7 kg/m2 for men and 22.6, 22.9, 22.9, and 22.9 kg/m2 for women. A second Japanese cohort of over 10,000 individuals found no association between sleep duration and weight (20). On the other hand, a Scottish study of 6,797 individuals found mean BMI was 0.3 kg/m2 greater among men with a sleep duration <7 h compared to 7–8 h (18). Two other studies considered weight as a secondary outcome. The Sleep Heart Health Study, in studying the association of sleep duration with hypertension, found a U-shaped association between sleep duration and weight with BMI 0.7 and 0.4 kg/m2 greater in those with sleep durations <6 and 6–7 h compared to 7–8 h (21). A Swedish study of sleep duration and diabetes found sleep duration was inversely correlated with both BMI (r = -0.06) and waist-to-hip ratio (r = -0.08) (ref. 22).
    Two studies using population-based sampling techniques have directly assessed the relationship between short sleep duration and obesity in middle-aged populations. The larger studied 3,158 adults and found an inverse association between sleep duration and obesity with a minimum risk associated with a sleep duration of 8–9 h (23). Compared to this group, the ORs for obesity were 1.85, 1.49, 1.24, and 1.09 for sleep durations less than or equal to5, 5–6, 6–7, and 7–8 h. A second study of 1,772 Spanish subjects found a similar association with the odds of obesity 39% greater in those with a sleep duration of less than or equal to6 h compared to a sleep duration of 7 h.
    Several studies have examined the sleep–weight association in working populations. A survey of 4,878 Brazilian truck drivers found a sleep duration <8 h per day was associated with a 24% greater odds of obesity (24). Similarly, a survey of 4,793 Hong Kong union members found an inverse correlation between sleep duration and BMI (r = -0.037, P = 0.02) (ref. 25). This relationship was almost exclusively observed in men. In contrast, a French study of 3,127 workers found that while no association between sleep duration and weight was found in men, among women, those with a sleep duration of less than or equal to6 h had a 0.63 kg/m2 greater mean BMI than those with longer sleep durations (26). In a study of 1,024 government workers in Wisconsin, a U-shaped association was found using sleep duration based on sleep diaries (27). In multivariate modeling, the minimum BMI corresponded to a sleep duration of 7.7 h. A cross-sectional study of 990 employed adults in Iowa found that BMI was 0.42 kg/m2 greater for each hour reduction in sleep duration (28).
    Analysis of a Canadian family-based cohort supports the presence of a U-shaped relationship between sleep duration and obesity (29). The ORs for obesity were 1.63 and 1.51 in women with sleep durations of 5–6 and 9–10 h compared to 7–8 h. The corresponding values in men were 1.72 and 1.18. Similar associations were found between sleep duration and waist-to-hip ratio, body fat mass, and skinfold thicknesses.
    Two reports have specifically examined the association between sleep duration and weight in geriatric cohorts. Both were designed to define normative sleep habits in the elderly and considered weight as a predictor of sleep duration. The first study recruited 8,091 individuals over the age of 55 from seven European nations (30). Obesity did not predict being in the lowest 5th percentile of sleep durations. A study of 1,026 French subjects over 60 found those with a BMI >27 kg/m2 were 3.6 times more likely to report nocturnal sleep duration in the lowest 5th percentile than those with BMI of 20–25 kg/m2 (31). However, the obese were also more likely to report daytime naps so that no association existed between total sleep duration and obesity.–Only one study of adults has examined the sleep–weight relationship using an objective measure of sleep duration. Lauderdale et al. investigated predictors of sleep duration in 669 individuals and used 72-h actigraphy to assess average sleep duration (32). In multivariate analysis, the study found a weak inverse correlation between sleep duration and BMI that was not statistically significant.—Two studies have examined the association between sleep habits and weight in clinic populations. Among 924 Americans attending a primary care clinic, sleep duration was longest in those with BMI <25 kg/m2 (33). In a study of 453 Japanese clinic patients, the odds of obesity was nearly double in those with a sleep duration <6 h (34).—Overall, the cross-sectional data in adults suggest short sleepers are heavier though the findings are much less consistent than the pediatric data. Several reports have noted a U-shaped association between sleep duration and weight in adults with the lowest BMI associated with a sleep duration of 7–8 h (5,21,27,29). If this relationship is truly U-shaped, studies that force a linear relationship in modeling the sleep–weight association would underestimate the true effect of short sleep duration and might explain the negative findings in some studies. Ethnic differences in susceptibility to sleep deprivation may also explain the disparate findings, as two of the three Japanese studies were negative. Although no study has directly examined differential susceptibility by ethnicity, several studies have noted that both obesity and sleep deprivation are more common among African Americans than whites (23,32). Findings on differences in gender susceptibility have been mixed. While several studies suggested a greater vulnerability in women (5,26,29,33), at least two reports found an association between short sleep duration and obesity existed only in men (18,25).—In terms of understanding the mechanism of any sleep–weight association, four of the studies finding an association between short sleep duration and obesity found this association could not be explained by differences in physical activity (18,26,29,35). In addition, one of the negative studies also found no relationship between sleep duration and physical activity (32). None of the studies assessed caloric intake. However, two studies examined biomarkers that may be relevant to appetite. Short sleep durations were associated with suppressed leptin levels in both the Quebec Family Study and the Wisconsin Sleep Cohort Study after adjusting for obesity (27,29). Short sleep durations were also associated with elevated ghrelin levels in the Wisconsin cohort (27).
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    Cell tower regulations frustrate homeowners Towers under 15 metres tall avoid municipal scrutiny
    Cellular towers sprouting around Canadian churches
    Cell tower in church parking lot draws ire of neighbours
    Health Canada: Safety of cellphones and cellphone towers
    Do you live near an unexpected cellphone tower?
    Suburban cell tower woes4:30
    Homeowners across Canada are discovering cellphone towers popping up in residential neighbourhoods that slip just under height regulations that would require the company to notify those living nearby. Oakville[U13] , Ont., resident Lisa Guglietti was in the midst of building her dream home when the mother of three noticed eight cellular network antennas strapped to the chimney of a Bell Canada building, a short distance from her son’s bedroom. “We were surprised that we weren’t notified,” she said. “We asked some of the neighbours. None of the neighbours had any clue that these cellular antenna had been put up.” Under federal regulations, cellphone companies must notify the municipality for towers at least 15 metres high, but many new installations are coming up short of the limit, at just 14.9 metres. Homeowners say the rule undermines their ability to weigh in on installations in the community. Though the antennas are an eyesore, Guglietti’s primary concern is possible health effects. Experts disagree on the impact caused by cell towers. The International Agency for Research on Cancer classifies radiofrequency electromagnetic fields, which are emitted by wireless phones and cell towers, as a possible human carcinogen. Health Canada states that radiofrequency fields given off by cellphone towers are safe as long as the facility adheres to federal regulatory requirements limiting human exposure. In an email to CBC News, a Bell spokesperson wrote that all its sites, including the Oakville, Ont., one near Guglietti’s house, “meet or exceed all federal safety and other operating requirements.”
    City councillor struggles with issue—In June, construction began on a 14.9-metre cellphone tower in a Barrie, Ont. neighbourhood that triggered a backlash over potential health concerns for those living across the street and students walking to nearby schools. “Telecommunications companies are able to come in and put these things basically wherever they want: as close to any residents, as close to any schools, and as close to any community centre they want,” Barrie, Ont. city councillor John Brassard told CBC News. “Why not make it 14.99 metres?” he asked. Since the incident, the Barrie city councillor has begun working to change federal regulations to give Canadians a voice over the placement of cell towers in their neighbourhoods. “Authority and a large part of that decision making should be made by the municipality and in consultation with Industry Canada. Not just Industry Canada alone.”
    Government, company response—CBC News requested government data on the number of towers under 15 metres erected across Canada, but Industry Canada said the department doesn’t keep a database of that information[U14] . In the last year, Ottawa has collected about $582 million in revenue from telecommunications companies rolling out their networks of cell towers[U15] . Industry Canada told CBC News that companies are required to consult with the municipality and public before installing antenna towers, unless the towers fall within a certain height. “Certain installations, including towers less than 15 metres, generally have minimal local impact and so may be excluded from municipal consultation,” an Industry Canada spokesperson said in a written statement to CBC News. After discovering the cell antennas on the large brick building next door to her new house, Guglietti contacted the federal agency. An Industry Canada official responded in an email to Guglietti on June 8, 2012 that “given that the installation at the Bell central office building on Balsam Street complies with all procedural and technical requirements, Industry Canada is not in a position to order Bell to relocate the facility.” Cell tower antennas were strapped to a chimney that was 13 metres away from the bedroom of Lisa Guglietti’s son[U16] . (Angela Gilbert/CBC) Guglietti also contacted Bell Canada, which owns the building next door, and says she was initially told it would try to find an alternative location. However, the eight cell antennas remain attached to the chimney next door.
    ‘Don’t want to be a guinea pig’ –The scientific uncertainty over the health impact of cellphone towers doesn’t sit well with Guglietti. “I’m supposed to be OK with that?” asked Guglietti. “I’m supposed to have my son exposed to these frequencies day in and day out and I have to wait. Maybe in 10 years from now I’m going to find out, ‘Oh yeah there is, there can be health hazards in living so close to a cell tower.’ ” “I don’t want to be a guinea pig,” said Guglietti. A Bell spokesperson said in an email to CBC News that cellphone towers are being installed to meet customer demand[U17] . Guglietti said she’s certain other homeowners are dealing with similar concerns. If you have any information on this story, or other cellphone tower stories, please contact us at [email protected]. “I need to protect myself and I need to protect my family. I’m a mother and I’m sure anyone would do the same thing in our situation.” If you have any information on this story, or other cellphone tower stories, please contact us at [email protected].
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    Red wine and components flavonoids inhibit UGT2B17 in vitro.
    Jenkinson C, Petroczi A, Naughton DP.
    Abstract
    BACKGROUND: -The metabolism and excretion of the anabolic steroid testosterone occurs by glucuronidation to the conjugate testosterone glucuronide which is then excreted in urine. Alterations in UGT glucuronidation enzyme activity could alter the rate of testosterone excretion and thus its bioavailability. The aim of this study is to investigate if red wine, a common dietary substance, has an inhibitory effect on UGT2B17.
    METHODS-Testosterone glucuronidation was assayed using human UGT2B17 supersomes with quantification of unglucuronidated testosterone over time using HPLC with DAD detection. The selected red wine was analysed using HPLC and the inhibitory effects of the wine and phenolic components were tested independently in a screening assay. Further analyses were conducted for the strongest inhibitors at physiologically relevant concentrations. Control experiments were conducted to determine the effects of the ethanol on UGT2B17.
    RESULTS-Over the concentration range of 2 to 8% the red wine sample inhibited the glucuronidation of testosterone by up to 70% over 2 hours[U18] . The ethanol content had no significant effect. Three red wine phenolics, identified by HLPC analyses, also inhibited the enzyme by varying amounts in the order of quercetin (72%), caffeic acid (22%) and gallic acid (9%); using a ratio of phenolic: testosterone of 1:2.5. In contrast p-coumaric acid and chlorogenic acid had no effect on the UGT2B17. The most active phenolic was selected for a detailed study at physiologically relevant concentrations, and quercetin maintained inhibitory activity of 20% at 2 M despite a ten-fold excess of testosterone.
    CONCLUSION-This study reports that in an in vitro supersome-based assay, the key steroid-metabolising enzyme UGT2B17 is inhibited by a number of phenolic dietary substances and therefore may reduce the rate of testosterone glucuronidation in vivo. These results highlight the potential interactions of a number of common dietary compounds on testosterone metabolism. Considering the variety of foodstuffs that contain flavonoids, it is feasible that diet can elevate levels of circulating testosterone through reduction in urinary excretion. These results warrant further investigation and extension to a human trial to delineate the health implications.
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    Rhodiola Protects HPG Axis during Exercise or Physical Work
    [Salidroside protects the hypothalamic-pituitary-gonad axis of male rats undergoing negative psychological stress in experimental navigation and intensive exercise].
    [Article in Chinese]
    Wang Q, Wang J, Sun LJ, Hu LP, Li J, Shao JQ, Lu B, Wang YT, Wu B, Wang GH.
    Source-Department of Endocrinology, Nanjing University School of Medicine/Nanjing General Hospital of Nanjing Military Region, Nanjing, 210002 Jiangsu, China.
    OBJECTIVE-To study the effects of salidroside on the function and ultramicro-pathological change of the hypothalamic-pituitary-gonadal (HPG) axis of male rats in experimental navigation and intensive exercise.
    METHODS-Six-week SD rats were randomized into 3 groups: non-stress control (NC, n = 10), training control (TC, n = 12) and salidroside treatment (ST, n = 12) group. Blood samples were collected from the NC rats that did not receive any stimulus after a 7-day intragastric administration of saline. The TC rats underwent a 10-day running training with increasing load on the treadmill followed by a 7-day intragastric administration of saline. The ST rats were subjected to the same process of running training as the TC group and received intragastric administration of salidroside. Then blood samples were immediately obtained and the levels of testosterone (T), corticosterone (CORT), adrenocorticotropic hormone (ACTH), luteinizing hormone (LH) and gonadotropin-releasing hormone (GnRH) measured by radioimmunoassay. The testis histopathology was observed by HE staining, and the ultrastructural changes of the pituitaries and testes investigated by electron microscopy.
    RESULTS-The serum T level was significantly lower in the TC than in the NC group, but showed no significant difference between the ST and NC groups. HE staining revealed no significant difference in testis histopathology among the 3 groups. Ultramicro-pathology showed that the secretory granules of the pituitary cells were significantly reduced in the TC rats compared with the NC ones; the number of the granules significantly increased in the ST group compared with the TC rats; and mitochondrial swelling, increase of electron density and decrease/disappearance of mitochondrial cristae were observed in the Leydig cells of the TC rats. But no significant differences were found in the testicular cells between the ST and NC groups.
    CONCLUSION-Negative psychological stress and intensive exercise can significantly suppress the function of the HPG axis in rats. Salidroside therapy has protective effect on the HPG axis.
    TOPA

    #2645
    AvatarEK
    Keymaster

    Black Seed Plus Sarsparilla-Liver Protection
    Modulation of apoptosis in human hepatocellular carcinoma (HepG2 cells) by a standardized herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizomes with anti- hepatocarcinogenic effects.
    BMC Complement Altern Med. 2012;12:25
    Authors: Samarakoon SR, Thabrew I, Galhena PB, Tennekoon KH
    Abstract
    BACKGROUND: A standardized poly-herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizome[U19]s used traditionally in Sri Lanka for cancer therapy has been demonstrated previously, to have anti-hepatocarcinogenic potential. Cytotoxicity, antioxidant activity, anti-inflammatory activity, and up regulation of p53 and p21 activities are considered to be some of the possible mechanisms through which the above decoction may mediate its anti-hepatocarcinogenic action. The main aim of the present study was to determine whether apoptosis is also a major mechanism by which the decoction mediates its anti-hepatocarcinogenic action.
    METHODS: Evaluation of apoptosis in HepG2 cells was carried out by (a) microscopic observations of cell morphology, (b) DNA fragmentation analysis, (c) activities of caspase 3 and 9, as well as by (d) analysis of the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins associated with cell death.
    RESULTS: The results demonstrated that in HepG2 cells, the decoction can induce (a) DNA fragmentation and (b) characteristic morphological changes associated with apoptosis (nuclear condensation, membrane blebbing, nuclear fragmentation and apoptotic bodies). The decoction could also, in a time and dose dependent manner, up regulate the expression of the pro-apoptotic gene Bax and down regulate expression of anti-apoptotic Bcl-2 gene (as evident from RT-PCR analysis, immunohistochemistry and western blotting). Further, the decoction significantly (p < .001) enhanced the activities of caspase-3 and caspase-9 in a time and dose dependent manner.—CONCLUSIONS: Overall findings provide confirmatory evidence to demonstrate that the decoction may mediate its reported anti-hepatocarcinogenic effect, at least in part, through modulation of apoptosis.—PMID: 22458551 [PubMed – indexed for MEDLINE]
    Recipe for making this decoction of Black seed and Smilax ( sarsaparilla)—take equal parts of each herb and boil them down to at least half of the volume of water you put in— I.E 2 pint down to 1 pint or less ( 500mls for the metric to 250 mls)—and then use small amounts 1-2 oz increments 4-5 times daily
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    Symptoms of chemtrail spraying
    by OkanaganChemtrails @ 20.08.10 – 19:05:47
    We’ve covered this before on this blog but I believe that one way to put an end to this is to educate people how they are being poisoned. Who in their right mind wouldn’t want spraying to cease once they realize their health is being compromised? So here’s a new article and a few links to refresh everyone.
    Chemtrails – Health Effects on the General Population
    by Claude-Michel Prévost
    Over the past ten years, through research and the personal accounts of many individuals, it has become readily apparent that the aluminum and barium salt mixtures, polymer fibers, toxic chemicals and biologicals sprayed in the atmosphere are the irritants that are either directly or indirectly responsible for health problems on the rise in the United States and elsewhere.
    These toxic particulates are rapidly absorbed from the respiratory system and / or the gastrointestinal tract and are deposited in the lungs, muscles, and bone.
    This illegal aerial spraying is producing atmospheric and ground conditions detrimental to human and animal health but favorable to the growth of harmful molds / fungus.
    This overview is a partial list of health problems reported by private citizens to Chemtrail researchers.
    1.Nose and lung bleeds (the latter including several reports from nursing homes of elderly dying from lung bleed outs, we believe being directly attributable to atmospheric aerosols);
    2.Asthma and allergies;
    3.Allergic bronchopulmonary aspergillosis (ABPA) (fungus on the lungs in both infants and adults),
    4.Flu, Bronchitis and Pneumonia (in epidemic proportions, with doctors commenting to their patients on the many weeks it sometimes takes to improve and the lack of effective antibiotics to treat, including reports of pets having the flu, whole families being decimated), meningitis (inflammation / infection of the brain);
    5.Upper respiratory symptoms (wheezing, dry cough), including Pulmonary Distress Syndrome (PDS) (in newborns, infants and adults alike), Sudden Infant Death (SIDS), and increased nationwide reports of the sudden death of athletes (reported in the news media as having possibly been attributable directly to air particulates / pollution);
    6.Deaths from black mold; black or red mold on food crops (farmers reporting pH changes of soil and water), in buildings and ventilation systems (including school buildings);
    7.Arthritis-like symptoms and muscular pain (young and old alike, sometimes crippling, and in pets);
    8.Gastrointestinal distress (young and old alike, and in pets);
    9.Bladder and yeast infections (includes bed wetting, not just in infants but adults);
    10.Extreme fatigue (young and old alike);
    11.Ringing of the ears, dizziness (increasingly reported immediately preceding or after a storm or weather system);
    12.Eye problems – pink eye, blurred and deteriorating vision / nervous tics after exposure to the air outdoors;
    13.Dry / cracking skin and lips, rashes, sores and fungal infections, aging of the skin;
    14.Mental confusion / slow thinking and / or the feeling of mentally “being in a fog” (young and old alike, increasingly reported after actually being in heavy mists and fog banks);
    15.Autoimmune disorders (Lupus, Crohn’s, Addison’s Disease, Rheumatoid Arthritis, etc.)
    Note: Some of the above symptoms / illnesses can be related to other physical / environmental factors such as dehydration.)
    Aluminum
    by Remarkable-recovery.com
    Aluminum Symptoms
    Excessive amounts of aluminum can result in symptoms of poisoning. The symptoms include constipation, colic, loss of appetite, nausea, skin ailments, twitching of leg muscles, excessive perspiration, and loss of energy. People with aluminum poisoning should discontinue the use of aluminum cookware and the drinking of tap water. Small quantities of soluble salts of aluminum present in the blood causes slow form of poisoning characterized by motor paralysis and areas of local numbness, with fatty degeneration of kidney and liver. There are also anatomical changes in the nerve centres and symptoms of gastro intestinal inflammation.
    In the last few years there has been much publicity about aluminum, as well as a tentative connection of aluminum to Alzheimer Disease. According to Dr. Terry L. Franks the clinical picture is clear that Alzheimers is concurrently involved with aluminum toxicity and he also believe it is the major contributing factor to Alzheimers. It will progressively worsen in North America in the coming year because of the pervasive use of aluminum. Aluminum has the tendency to freeze up or irritate nerve endings, producing spasm and contracture. When someone is going through aluminum detoxification can actually look like an advanced case of Alzheimers Disease.
    Sources
    Cooking utensils, antacids, baking powders, antiperspirants, some soft water, aluminum foils, concrete and process foods contain aluminum (table salt, cheese slices individually wrapped), bleached flour, fluoridated water increases leaching of aluminum.
    How Aluminum Affects Health
    Nervous system
    In animal studies, aluminum blocks the action potential or electrical discharge of nerve cells, reducing nervous system activity. Aluminum also inhibits important enzymes in the brain (Na-K-ATPase and hexokinase). Aluminum may also inhibit uptake of important chemicals by nerve cells (dopamine, norepinephrine, and 5-hydroxytryptamine).
    Behavioural Effects
    Dementia resulting from kidney dialysis related to aluminum toxicity causes memory loss, loss of coordination, confusion and disorientation.
    Symptoms of Aluminum Toxicity
    Early symptoms of aluminum toxicity include: flatulence, headaches, colic, dryness of skin and mucous membranes, tendency for colds, burning pain in the head relieved by food, heartburn and an aversion to meat.
    Later symptoms include paralytic muscular conditions, loss of memory and mental confusion. Other symtpoms may include:
    Alzheimer’s disease, amyotrophic lateral sclerosis, anaemia, haemolysis, leukocytosis, porphyra, colitis, dental cavities, dementia dialactica, hypo-parathyroidism, kidney dysfunction, neuromuscular disorder, osteomalacia, Parkinson’s disease, ulcers.
    Digestive system
    Aluminum reduces intestinal activity, and by doing so can cause colic.
    Treatmnet of Toxicity
    Decreasing contact with and use of aluminum-containing substances will reduce intake and allow more aluminum to leave the body. Oral chelating agents will also help clear aluminum more rapidly. Calcium disodium edetate (EDTA) binds and clears aluminum from the body; this substance is fairly nontoxic and used as the agent for “chelation therapy,: an intravenous treatment used to pull metals such as lead from the body, and more recently used in the treatment of atherosclerosis and cardiovascular diseases.
    Deferoxamine, an iron chelator, also binds aluminum. In a study with Alzheimer’s patients, nearly 40 percent of the patients showed an improvement in symptoms with deferoxamine treatment. There is some evidence that intravenous chelation with EDTA helps Alzheimer’s patients. More research is needed to evaluate aluminum’s involvement with this disease. Recovery is excellent for removing heavy metals.
    Vitamin C
    Has been found to bind aluminum. The average dose, if the patient is relatively comfortable, is about six grams a day. Up to twelve grams is not excessive. The average time on an aluminum detoxification is three to four weeks.
    Prevention
    The best way to prevent aluminum buildup is to avoid the sources of aluminum. Eliminating foods that have aluminum additives is probably healthier overall. Not using common table salt is a positive health step as well. Some tap waters contain aluminum, this can be checked. Avoiding aluminum cookware and replacing it with stainless steel, ceramic, or glass is a good idea. Blocking skin and sweat pores with aluminum anti-perspirants.
    Barium
    by Testcountry.org
    The possibility of barium poisoning is a reality among people working in and living near heavy industrial sites such as chemical plants, factories that produce rubber products and other such places. That is because barium is one of the components used in manufacturing the products created in these plants.
    However, because many of these products end up in ordinary households, it is also possible for a person who does not work in or live near an industrial plant to experience barium poisoning. Rat poison, for instance, contains barium compounds. Some fluorescent bulbs have coatings made from barium oxide. Fish caught in waters near industrial sites may have absorbed barium from the water.
    Given the considerable probability of a person becoming afflicted with barium poisoning, how would you know for sure if you or someone living with you ingested barium at toxic levels? If you find yourself or someone living in your household with symptoms of barium poisoning, then you should act immediately.
    What Is Barium?
    In order to understand how serious barium poisoning is, we need first to understand what barium is in the first place. Barium is a heavy metal that naturally occurs in the environment. It is silvery white in appearance.
    Barium is valuable in many industries that make use of heavy metal because it can remove traces of oxygen in some chemical compounds. It also increases the luster of glass. However, barium is explosive and can react violently when mixed with water. Also, it cannot be digested by the body; barium can be poisonous if the amount the body contains exceeds tolerable levels.
    Symptoms of Barium Poisoning to Look For
    When barium accumulates in the body, it usually affects the functions of the nervous system. Barium poisoning displays symptoms that are similar to flu, which is why it is not strange to find the condition misdiagnosed as flu. Common symptoms of barium poisoning include:
    1. Muscle weakness and tremors
    2. Difficulty in breathing
    3. Stomach irritations accompanied by diarrhea
    4. Anxiety
    5. Cardiac irregularities such as abnormally high blood pressure and rapid heartbeat
    6. Paralysis
    What to Do in Case of Barium Poisoning
    In case someone in your household has just ingested something that contains barium, the first thing you need to do is to induce him or her to vomit. This will get some of the barium out of the victim’s system. You can also mix a tablespoon of Epsom salts (sodium sulfate or magnesium sulfate) with a glass of water and get the victim to drink it. Afterwards, you should bring the victim to the emergency room of the nearest hospital to make sure that he or she does not succumb to barium poisoning.
    You can also prevent barium poisoning from happening in your home. For one, you should keep your rat poison or any other chemical substances in your house that contains barium out of reach of children. Make sure that you have labeled their containers properly.
    You should also avoid eating fish that was caught near industrial sites and ascertain that the fish and seafood you eat does not contain barium or any other heavy metal. This will prevent you from accumulating barium in your system and suffer from barium poisoning later on.
    TOP B
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    [U1]East indian Sarsparilla-chinese Sarsparilla and Black seed-decoction would be a tea boiled down to a complete extract
    [U2]The less healthy oils would be soy and vegetable and canola oils or anything hydrogenated—these are toxic and become more so when heated and literally cause Genetic damage to the body
    [U3]This is outdated there is no such thing as good or bad cholesterol in fact this study shows that using these oils you’re better at regulating any blood pressure issues
    [U4]So for thos of you consuming a high carb starch type diet with sugar you are going to benefit the most from this
    [U5]Possible diuretic
    [U6]This is usually caused by pollutant fall outs that stimulate bacterial or fungal growth due to lack of oxygen anddd the consumption of foods with Disodium guaynalte and Disodium Inosinate—other places call this ribo rash as well
    [U7]Chemtrails have been being dumped on us with bacterial and microbial ,fungal and virals of all kinds they are a genetic anomaly which can impact the system with skin lesions as well
    [U8]Now if this is the case then you would have to consider what is activating them —what is stimulating there growth-is it something from the air—is there pollutants specific causing this—remember 50 years ago this was not a common issue —not until the atmospheres was completely polluted and now being chemtrailed
    [U9]Inside—was it put there genetically in a lab—was it put there due to the genetics of our foods causing there DNA to alter and become a infection carrying mite?? Something to ponder
    [U10]Planned attack?—“trigger”
    [U11]A Trojan Horse—something like a virus on a cpu looks like one thing then releases something unwanted
    [U12]Wonder if the increasing of HAARP and Chemtails have anything to do with this—or possibly a invading of our Planetary Space things doing things to take away our access to the planet —
    [U13]THIS IS WHY SO many people are not sleeping any more between the hours of 2-4 am the critical time of sleep and regeneration—this is in part one of the reason we are having a Obesity issue going on globally and the fact that the consumption or gmo’s causing GE diseases
    [U14]Very in efficient for a major Company of global Standing eh!!
    [U15]Now is this not Hilarious—they know how to collect exactly X amount of dollars but cannot determine the number of cell towers because they do not keep an inventory soooo how do they determine the tax?? makes me want to hmmm
    [U16]40 feet away
    [U17]The question I ask with these kind of statements—what customer—who demanded it—it would appear there is a higher position clientele that seem to be able so supercede the will of the people—makes you ponder the thought of who would want to violate human rights and place a dangerous bit of technology in a residential area
    [U18]Could improve the exercising-working or sex at home—both men and women have testosterone—males are 97% woman 3% it is ean essential hormone for Males in regard to brain –heart and muscle function and the reproductive system
    [U19]East indian Sarsparilla-chinese Sarsparilla and Black seed-decoction would be a tea boiled down to a complete extract
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    TOP C
    HOME
    Show of the Month October 12 2012
    How to Self-Test for an Iodine Deficiency
    List of factors that impairs thyroid function
    Adrenal Support
    Exploring many uses for topical iodine solution
    Inactivation of human viruses by povidone-iodine in comparison with other antiseptics
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    How to Self-Test for an Iodine Deficiency
    1. Dip a cotton ball into USP Tincture of Iodine.
    2. Paint a 2 inch circle of iodine on your soft skin, like the inner part of your thigh or upper arm.
    3. Wait. — If the yellowish stain disappears in less than an 4 hours; it means your body is lacking crucial iodine and has soaked it up. If the stain remains for more than 4-8 hours, you iodine levels are fine.
    ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
    Why check your iodine levels?—Low iodine levels can zap your energy and make you feel tired, edgy and worn out. Low iodine levels can even prevent you from getting a good night’s sleep. Before you go to your doctor with complaints of tossing and turning all night, aches and pains, and just feeling “blah,” you may want to perform this self-test.—Because the symptoms of an iodine deficiency are classically identical to so many other illnesses (like depression, stress, chronic fatigue, or fibromyalgia,) many doctors either misdiagnose it or miss it completely and tell you there is nothing wrong.
     
    Why are iodine levels so important?–Low levels of iodine mean your thyroid may not be functioning properly. The thyroid needs iodine to function as it helps balance hormones, regulate heartbeats, stabilize cholesterol, maintain weight control, encourage muscle growth, keep menstrual cycles regular, provide energy, and even helps you keep a positive mental attitude.—-Women are naturally prone to iodine deficiencies. That’s because the thyroid gland in women is twice as large as in men — so under normal circumstances, women need more iodine. However, when women are under stress, the need for iodine can double or triple. Yet the foods we eat contain less and less dietary iodine. For example, back in 1940, the typical American diet contained about 800 micrograms of iodine. By 1995, that amount plunged to just 135 micrograms. That’s an 83% decline.—-Two thirds of the body’s iodine is found in the thyroid gland. One of the best ways to boost your iodine levels is to add seaweed -sea vegetables to your diet. Just one teaspoon of sea vegetables a day can help you regain normal iodine levels. Incorporating seafood and fish into your diet can also help[U1] . Other foods that contain iodine are eggs and dairy products, including milk, cheese and yogurt, onions, radishes[U2] , and watercress. Some foods, called goitrogens, should be omitted for awhile as they hinder iodine utilization. These included kale, cabbage, peanuts, soy flour, Brussels sprouts, cauliflower, broccoli, kohlrabi and turnips.—[U3] To reactivate the thyroid gland, tyrosine, iodine, zinc, copper and selenium are needed so make sure that foods containing these nutrients are included in your diet. However, if you have the immune system deficiency called Hashimoto’s Thyroiditis, you should not supplement your diet with iodine as it may aggravate the condition.
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    List of factors that impairs thyroid function.
      1. Aging linked to a gradual decline of both thyroid and adrenal hormones.
     2. Alpha Lipoic Acid (does not affect everyone)
     3. Alcohol
     4. Chronic illness
     5. Cigarette smoking
     6. Diet factors. Soy products and cruciferous vegetables ­ dose dependent (avoid large quantities). Studies in animals show soy impairs T4 to T3 conversion.
     7. Drugs (Birth control pills, Lithium, Estrogens, Propranolol, Beta blockers, Dexamethasone, Methimazole and Propylthiouracil)
     8. External radiation[U4]
     9. Growth hormone deficiency
     10. Heavy metal toxicity including mercury and lead, pesticides, sodium chloride as well as sodium fluoride in city water.
     11. Hemochromatosis
     12. High Stress
     13. Low adrenal states
     14. Malnutrition (mineral deficiencies) consumption of trans fats and hydrogenated fats and a lack of good fats ­ monounsaturated ­ avocados, olive oil, palm, omega 3.
     15. Mineral and vitamin deficiencies (selenium, Vitamin A, B6 and B12)
     16. Postoperative state
     17. Physical trauma.
    Besides the above list research views that in a state of hypothyroidism, hydrocortisone production and metabolism is usually low. Hypothyroidism can be established by chronic low basal body temperature as measured by the Barnes method upon rising. Thus a direct link has been established between subnormal thyroid and inadequate adrenal production of hormones.
    Toxemia or the buildup of toxins in the body and an impairment of the detoxification pathways can be a major cause of impaired thyroid function. Link by link, the health of one organ affects the health of another. The liver, the organ through which most detoxification occurs, has the greatest burden of all.
    Today, I reasonably estimate that due to toxins in the diet, air pollution and contaminants in the water we drink and electromagnetic pollution, that the combined effect contributes to overworked adrenal and subnormal thyroid activity in at least a third or more of the population in the United States.
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    Adrenal Support
    Degeneration of the Adrenal Glands may occur as a symptom of Choline deficiency. [more info]
    Vitamin A concentrates in the Adrenal Glands and may improve the function of the Adrenal Glands. references
    Vitamin B5 may activate the Adrenal Glands and may “revive” exhausted Adrenal Glands.
    Vitamin C is essential for the function of the Adrenal Glands – the Adrenal Glands (especially the Adrenal Medulla) contain approximately 30 mg of Vitamin C – the second highest concentration of Vitamin C of any component of the body.
    Vitamin E concentrates in the Adrenal Glands (within the Adrenal Cortex). The Adrenal Glands contain 132 mcg of Vitamin E per gram).
    Adrenal Extract may improve the function of the Adrenal Glands in persons with impaired Adrenal Gland function.
    Tyrosine may relieve excessive stress on the Adrenal Glands
    Pregnenolone production (from Cholesterol) occurs primarily in the Adrenal Glands (but is also produced in smaller quantities in other areas of the body, including the Liver, Brain, Skin and Retina of the Eye).
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    Could painting a circle of iodine solution on the skin daily help get rid of the candida albicans, parasites, HHV-6, herpes, hepatitis and multiple other bacterial, fungal, parasitic and viral infections including HIV?
    Exploring many uses for topical iodine solution
     Iodine for HIV – to directly kill the virus
     Iodine to treat opportunistic infections in AIDS
     Iodine for chronic Candidiasis, EBV and CMV
     Iodine for viral hepatitis A, B, C and D
     Iodine for HHV-6 infection
     Iodine for parasites
     Iodine for herpes
     Iodine for strep and staff infections
     Iodine for sore joints and arthritis
     Iodine for rheumatism
     Iodine for the flu
     Iodine for a sore throat
     Iodine for almost any bacterial, fungal, parasitic or viral infection that exists.
     Iodine to increase the thyroid’s production of thyroxin
     Iodine to help restore normal body temperature
     Iodine to prevent and treat metabolic syndrome (obesity, diabetes and heart disease)
     Iodine is cheap, plentiful and safe to use.
    Here is how to do iodine testing and use
    1. Dip a cotton ball into USP Tincture of Iodine –Lugols will do as well
    2. Paint a 2 inch circle of iodine on your soft skin, like the inner part of your thigh or upper arm.
    3. Wait. — If the yellowish stain disappears in less than an hour; it means your body is lacking crucial iodine and has soaked it up. If the stain remains for more than 4-8 hours, your iodine levels are fine.
    Why check your iodine levels? —Low iodine levels can zap your energy and make you feel tired, edgy and worn out. Low iodine levels can even prevent you from getting a good night’s sleep. Before you go to your doctor with complaints of tossing and turning all night, aches and pains, and just feeling “blah,” you may want to perform this self-test.
    Because the symptoms of an iodine deficiency are classically identical to so many other illnesses (like depression, stress, chronic fatigue, or fibromyalgia,) many doctors either misdiagnose it or miss it completely and tell you there is nothing wrong. —About 60% of all iodine in the human body is stored in the thyroid gland at the base of the neck. A Goiter, an enlargement of the thyroid gland, can occur when iodine deficiency is prolonged over a period of time. Iodine is the most important mineral used by the thyroid gland to produce thyroxin, a hormone that regulates the metabolic rate of energy production in the cells. —Iodine deficiency and a resulting insufficient production of thyroxin is linked to a wide range of illness form chronic infection of all types including candidiasis, herpes, bacterial, fungal and viral infections. —Table salt is iodized and is a source of iodine[U5] . However, excess sodium intake from salt consumption is a toxin and impairs the production of energy in the cells. Excess sodium intake is linked to metabolic syndrome including obesity, high blood pressure, heart disease and cancer. [U6] The best sources of iodine are from sea vegetables and seafood including ocean fish[U7] . Unfortunately, most people do not consume iodine rich foods on a daily basis. Low body temperature and long term chronic infections may be directly linked to a deficiency of iodine and an impaired thyroid function.
    How much iodine to consume —-Why are iodine levels so important? Low levels of iodine mean your thyroid isn’t functioning properly. The thyroid helps balance hormones, regulate heartbeats, stabilize cholesterol, maintain weight control, encourage muscle growth, keep menstrual cycles regular, provide energy, and even helps you keep a positive mental attitude. —Women are naturally prone to iodine deficiencies. That’s because the thyroid gland in women is twice as large as in men — so under normal circumstances, women need more iodine. However, when women are under stress, the need for iodine can double or triple. Yet the foods we eat contain less and less dietary iodine. For example, back in 1940, the typical American diet contained about 800 micrograms of iodine. By 1995, that amount plunged to just 135 micrograms. That’s an 83% decline. —-Two thirds of the body’s iodine is found in the thyroid gland. One of the best ways to boost your iodine levels is to add seaweed sea vegetables to your diet. Just one teaspoon of sea vegetables a day can help you regain normal iodine levels[U8] . Incorporating seafood and fish into your diet can also help. Other foods that contain iodine are eggs and dairy products, including milk, cheese and yogurt, onions, and watercress. Some[U9] foods, called goitrogens, should be omitted for awhile as they hinder iodine utilization. These included kale, cabbage, peanuts, radishes, soy flour, Brussels sprouts, cauliflower, broccoli, kohlrabi and turnips. —-To reactivate the thyroid gland, tyrosine, iodine, zinc, copper and selenium are[U10] needed so make sure that foods containing these nutrients are included in your diet. —Editor’s note: The RDA of iodine is 150 mcg. That is just too little, in my opinion. Ideally, the average daily intake of iodine should be closer to 1000 mcg daily and higher than that for stress conditions that rapidly deplete iodine levels[U11] . Persons with systemic infections will need higher amount of iodine as this trace mineral will be rapidly bound to the infectious agents (bacterial, fungal or viral) in the process of destroying them thus leaving less iodine for the thyroid to pick up. While most people have an under active thyroid, a few people have an overactive thyroid but there is no research linking this to excess iodine intake.
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    Inactivation of human viruses by povidone-iodine in comparison with other antiseptics.
    Kawana R, Kitamura T, Nakagomi O, Matsumoto I, Arita M, Yoshihara N, Yanagi K, Yamada A, Morita O, Yoshida Y, Furuya Y, Chiba S.
    Dermatology . 1997;195 Suppl 2:29-35.
    Morioka Yuuai General Hospital, Japan.
    Inactivation of a range of viruses, such as adeno, mumps, rota-, polio- (types 1 and 3), coxsackie-, rhino-, herpes simplex, rubella, measles, influenza and human immunodeficiency viruses, by povidone-iodine (PVP-I) and other commercially available antiseptics in Japan was studied in accordance with the standardized protocol in vitro. In these experiments, antiseptics such as PVP-I solution, PVP-I gargle, PVP-I cream, chlorhexidine gluconate, alkyldiaminoethyl-glycine hydrochloride, benzalkonium chloride (BAC) and benzethonium chloride (BEC) were used. —-PVP-I was effective against all the virus species tested. PVP-I drug products, which were examined in these experiments, inactivated all the viruses within a short period of time. Rubella, measles, mumps viruses and HIV were sensitive to all of the antiseptics, and rotavirus was inactivated by BAC and BEC, while adeno-, polio- and rhinoviruses did not respond to the other antiseptics. PVP-I had a wider virucidal spectrum, covering both enveloped and nonenveloped viruses, than the other commercially available antiseptics.
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    Script of the Show October 15-2012
    Inactivation of human immunodeficiency virus by Betadine products & chlorhexidine.
    The action of three antiseptics/disinfectants against enveloped and non-enveloped viruses
    HOW SMART METERS MAY CAUSE AUTISM AND CANCER
    Aloe + Bioflavonoid ( Pectin )
    PARSLEY, THE NEW PREDNISONE— Parsley- Antiinflammatory
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    Inactivation of human immunodeficiency virus by Betadine products & chlorhexidine.
    Harbison MA, Hammer SM.
    J Acquir Immune Defic Syndr . 1989;2(1):16-20.
    Infectious Disease Section, New England Deaconess Hospital, Boston, Massachusetts.
    Eleven povidone-iodine-containing products (Betadine) and chlorhexidine gluconate solution were tested for their ability to inactivate human immunodeficiency virus (HIV) in a cell culture system. All Betadine products completely inactivated the virus at povidone-iodine concentrations of greater than or equal to 0.5% (10- to 20-fold dilutions of stock) except for Betadine Lubricating Antiseptic Gel, which required 2.5% for efficacy (1:2 dilution).
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    The action of three antiseptics/disinfectants against enveloped and non-enveloped viruses.
    Wood A, Payne D.
    J Hosp Infect . 1998 Apr;38(4):283-95.
    Results indicate that all products were effective in inactivating the enveloped viruses herpes simplex virus type 1 and human immunodeficiency virus type 1, whilst being ineffective in inactivating human coronavirusŠ..Four antiseptic/disinfectant solutions with chloroxylenol, benzalkonium chloride, cetrimide/chlorhexidine and povidone-iodine were also assessed for antiviral effect against human immunodeficiency virus in the presence of whole human blood. All four solutions proved to be effective within 1 min despite the cytotoxic nature of the compounds to the detection system. —Note from Mark Konlee: A few years ago I talked with 2 persons from different parts of the country who have been on an unusual diet for several years with striking similarities and results. They ate no meat and ate seafood, fish and or sea vegetables daily for several years. They were also both HIV positive and non-progressors and neither person had used prescribed antiviral drugs for HIV. Could the iodine and other trace minerals in the seafood they consumed have had something to do with their status as non-progressors? Could eating sea vegetables and ocean fish daily help stop HIV
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    HOW SMART METERS MAY CAUSE AUTISM AND CANCER
    Andrew Goldsworthy July 2011
    Abstract
    There is increasing evidence that wireless transmissions have biological effects, some of which are harmful, at levels that may be orders of magnitude below present safety guidelines. These guidelines were drawn up on the assumption that the radiation could only damage living tissues if it generated significant heat. It has since been shown that radiation at much lower levels has direct electrical effects. These are mainly on electrically charged cell membranes, where the low frequency pulses from the modulated microwaves make them vibrate and leak. This can give rise to many “modern illnesses” ranging from electromagnetic hypersensitivity to cancer and disorders of the immune system. The most dramatic increase in the incidence of autism due to damage to the developing brains of the fetus and young children. Modulated microwaves, such as those from cell phones, portable phones, WiFi, baby monitors and wireless smart meters are sources of potentially damaging radiation. The strength of the radiation appears to be less important than the duration and pattern of the exposure, with intermittent and repeated exposure being the most damaging. The strong regular transmissions from wireless smart meters are particularly harmful and more likely to lead to DNA damage, cancer and autism.
    Sub-thermal effects of electromagnetic radiation.
    There are thousands of scientific papers showing biological effects of non-ionizing electromagnetic radiation occurring well below the levels at which them can generate significant heat. Many of these have been reviewed at by expert scientist at http://www.bioinitiative.org and http://www.neilcherry.com/documents.php . They include harmful effects such as damage to DNA in living cells that can lead to cancer, loss of fertility, brain damage due to the disruption of the blood-brain barrier and neuronal hyperactivity leading to autism in children. Many of these effects can be attributed to the loss of structurally important calcium from cell membranes, which makes them leak. This can disrupt normal metabolism and also release DNase (which destroys DNA) from the internal structures (lysosomes) that normally recycle waste into the rest of the cell http://www.hese-project.org/hese-uk/en/papers/cell_phone_and_cell.pdf .
    Prolonged and intermittent radiation causes more damage
    The duration of the radiation seems to be more important than its strength, with the effects being cumulative as more and more cells are damaged. Interestingly, DNA damage from cell phone radiation is greater when the exposure is intermittent (5 minutes on, 10 minutes off) than when continuous (Diem et al 2005). This may be because the cells are constantly adapting and using energy to defend themselves; they drop their guard during the off period and are caught unawares when it goes on again. This constant switching uses more energy, which eventually leaves the cells less able to counteract the effects of the radiation.
    Diem et al. (2005) also found that the effect on DNA damage was still greater if the microwaves were pulsed or modulated to carry information (modulation involves sudden stops and starts of the signal, which are even more damaging).
    Smart meters, which operate 24/7 and radiate modulated microwaves intermittently, can therefore be expected to be particularly harmful to DNA.
    Microwave radiation causes cancer
    There is already evidence that heavy cell phone users are more prone to brain cancers. This has resulted in cell phones now being rated by the World Health Organisation as class 2B carcinogens. This rating may later be increased, since brain tumours normally take decades to develop and few people have been regularly using a cell phone for more than a single decade. Particularly worrying is the finding by Hardell and Carlberg (2009 ) that young people were about 5-times more likely to get brain cancer both from cordless and cell phones if they began using them before the age of 20. The regular transmissions from wireless smart meters can be expected to have much the same effect, with younger people being more at risk. This is possibly because their brain structure is still growing and developing and therefore more susceptible to damage leading to cancer.
    The effect of microwaves on autism is far worse
    The greatest damage from microwaves is when the brain is first developing in the foetus and the very young child, when it can lead to autism. Dr Dietrich Klinghardt has recently shown the relationship between microwaves and autism; a summary of his work can be found at http://electromagnetichealth.org/media-stories/#Autism .
    What is autism?
    Autism is in fact a group of life-long disorders (autistic spectrum disorders or ASD) caused by brain malfunctions and is associated with subtle changes in brain anatomy (see Amaral et al. 2008 for a review). The core symptoms are an inability to communicate adequately with others and include abnormal social behaviour, poor verbal and non-verbal communication, unusual and restricted interests, and persistent repetitive behaviour. There are also non-core symptoms, such as an increased risk of epileptic seizures, anxiety and mood disorders. ASD has a strong genetic component, occurs predominantly in males and tends to run in families.
    Genetic ASD may be caused by calcium entering neurons
    It has been hypothesised that some genetic forms of ASD can be accounted for by known mutations in the genes for ion channels that result in an increased background concentration of calcium in neurons. This would be expected to lead to neuronal hyperactivity, the formation of sometimes unnecessary and inappropriate synapses, which in turn can lead to ASD (Krey and Dolmetsch 2007).
    Electromagnetic fields let calcium into neurons too
    There has been a 60-fold increase in ASD in recent years, which cannot be accounted for by improvements in diagnostic methods and can only be explained by changes in the environment. This increase corresponds in time to the proliferation of mobile telecommunications, WiFi, and microwave ovens as well as extremely low frequency fields (ELF) from mains wiring and domestic appliances. We can now explain this in terms of electromagnetically-induced membrane leakage leading to brain hyperactivity and abnormal brain development.
    Non-ionising radiation makes cell membranes leak
    The first effect of non-ionising electromagnetic radiation is to generate small alternating voltages across the cell membranes, which destabilize them and make them leak. This can have all sorts of consequences as unwanted substances diffuse into and out of cells unhindered, and materials in different parts of the cell that are normally kept separate, become mixed.
    Why weak fields are more damaging than strong ones
    We have known since the work of Suzanne Bawin and her co-workers (Bawin et al. 1975) that modulated radio-frequency electromagnetic radiation that is far too weak to cause significant heating can nevertheless remove calcium ions (positively charged calcium atoms) from cell membranes in the brain. Later, Carl Blackman showed that this also occurs with extremely low frequency electromagnetic radiation (ELF) but only within one or more “amplitude windows”, above and below which there is little or no effect (Blackman et al. 1982; Blackman 1990). A proposed molecular mechanism for this can be found in Goldsworthy (2010). In particular, it explains why weak electromagnetic fields can have a greater effect than strong ones and why prolonged exposure to weak fields (where cells are maintained in the unstable condition for longer) is potentially more damaging than relatively brief exposure to much stronger ones.
    How calcium ions stabilize cell membranes
    This loss of calcium is important because calcium ions bind to and stabilize the negatively charged membranes of living cells. They sit between the negatively charged components of the cell membrane and bind them together rather like mortar binds together the bricks in a wall. Loss of just some of these calcium ions destabilize the membrane and make it more inclined to leak, which can have serious metabolic consequences. Among these are the effects of membrane leakage on the neurons of the brain.
    How membrane leakage affects neurons
    Neurons transmit information between one another in the form of chemical neurotransmitters that pass across the synapses where they make contact. However, the release of these is normally triggered by a brief pulse of calcium entering the cell. If the membrane is leaky due to electromagnetic exposure, it will already have a high internal calcium concentration as calcium leaks in from the much higher concentration outside. The effect of this is to put the cells into hair-trigger mode so that they are more likely to release neurotransmitters and the brain as a whole may become hyperactive (Beason and Semm 2002; Krey and Dolmetsch 2007, Volkow et al. 2011). This may not be a good thing since the brain may become overloaded leading to a loss of concentration and what we now call attention deficit hyperactive disorder (ADHD).
    How does this impact on autism?
    Before and just after its birth, a child’s brain is essentially a blank canvas, and it goes through an intense period of learning to become aware of the significance of all of its new sensory inputs, e.g. to recognise its mother’s face, her expressions and eventually other people and their relationship to him/her (Hawley & Gunner 2000). During this process, the neurons in the brain make countless new connections, the patterns of which store what the child has learnt. However, after a matter of months, connections that are rarely used are pruned automatically (Huttenlocher & Dabholkar 1997) so that those that remain are hard-wired into the child’s psyche. The production of too many and often spurious signals due to electromagnetic exposure during this period will generate frequent random connections, which will also not be pruned, even though they may not make sense. It may be significant that autistic children tend to have slightly larger heads, possibly to accommodate unpruned neurons (Hill & Frith 2003).
    Because the pruning process in electromagnetically-exposed children may be more random, it could leave the child with a defective hard-wired mind-set for social interactions, which may then contribute to the various autistic spectrum disorders. These children are not necessarily unintelligent; they may even have more brain cells than the rest of us and some may actually be savants. They may just be held back from having a normal life by a deficiency in the dedicated hard-wired neural networks needed for efficient communication.
    Autism and the economy
    The incidence of autism has increased 60-fold, in parallel with the increase in electromagnetic pollution over the last thirty years. The chance of having an autistic child may now be as high as one in fifty. Apart from the personal tragedies for the affected children and their families, autism is of enormous economic importance. In the UK alone, the annual cost to the Nation in care and lost production exceeds the annual tax revenue from the entire mobile phone industry, which is about 20billion UK pounds. http://www2.lse.ac.uk/newsAndMedia/news/archives/2009/05/MartinKnappAutism.aspx In theory the Government could close down the entire mobile phone industry and actually show a profit!
    There are ways in which the modulation of the signal can be changed to avoid this, but in the meantime, the compulsory introduction of smart meters can only contribute further to autism on a grand scale. This will be a further burden on the economy and increase the National deficit. This will far outweigh any possible advantages from the use of these meters.
    There is also a risk of legal complications for the utility companies. If it can be shown that that the consumer has taken reasonable precautions to minimise their microwave exposure by eliminating WiFi, cordless phones and wireless baby monitors from their house, the utility company could be held legally responsible for any autistic children that they may have.
    In the UK, the lifetime cost of caring for an autistic child is in the region of one million pounds. It would be reasonable to claim compensation for this amount. In the United States, it may also be possible to claim punitive damages if it can be shown that the utility company knew of this risk when they installed or refused to remove a smart meter when requested.
    Dr Andrew Goldsworthy
    Lecturer in Biology (retired)
    Imperial College London
    References
    Amaral DG, Schumann CM, Nordahl CW (2008), Neuroanatomy of Autism, Trends in Neurosciences 31: 137-145
    Bawin SM, Kaczmarek KL, Adey WR (1975), Effects of modulated VHF fields on the central nervous system. Ann NY Acad Sci 247: 74-81
    Beason RC, Semm P (2002), Responses of neurons to an amplitude modulated microwave stimulus. Neuroscience Letters 333: 175-178
    Blackman CF (1990), ELF effects on calcium homeostasis. In: Wilson BW, Stevens RG, Anderson LE (eds) Extremely Low Frequency Electromagnetic Fields: the Question of Cancer. Battelle Press, Columbus, Ohio, pp 189-208
    Blackman CF, Benane SG, Kinney LS, House DE, Joines WT (1982), Effects of ELF fields on calcium-ion efflux from brain tissue in vitro. Radiation Research 92: 510-520
    Diem E, Schwarz C, Adlkofer F, Jahn O, Rudiger H (2005). Non-thermal DNA breakage by mobile-phone radiation (1800 MHz) in human fibroblasts and in transformed GFSH-R17 rat granulosa cells in vitro. Mutation Research 583: 178-183
    Goldsworthy A (2010) , Witness Statement, http://mcs-america.org/june2010pg910111213141516.pdf
    Hardell L, Carlberg M (2009), Mobile phones, cordless phones and the risk for brain tumours. Int J Oncology 35: 5-17 DOI: 10.3892/ijo_00000307
    Hawley T, Gunner M (2000), How early experiences affect brain development. http://tinyurl.com/5u23ae
    Hill EL, Frith U (2003), Understanding autism: insights from mind and brain. Phil Trans R Soc Lond B 358 281-289
    Huttenlocher PR, Dabholkar AS (1997) Regional differences in synaptogenesis in human cerebral cortex. J Comparative Neurology 387 167-178
    Krey JF, Dolmetsch RE (2007) Molecular mechanisms of autism: a possible role for Ca2+ signaling. Current Opinion in Neurobiology. 17: 112-119
    Volkow ND, Tomasi D, Wang G, Vaska P, Fowler JS, Telang F, Alexoff D, Logan J, Wong C (2011), Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism. JAMA. 305 (8):808-813. doi: 10.1001/jama.2011.186
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    Aloe + Bioflavonoid ( Pectin )
    Aloe vera in dermatology- a brief review.
    Feily A, Namazi MR.
    Source–Department of Dermatology, Jondishapur University of Medical Sciences, Ahvaz, Iran. [email protected]
    Abstract—Aloe vera Linne or aloe barbadensis Miller is a succulent from the Aloe family (400 different species), a tropical plant which is easily grown in hot and dry climates and widely distributed in Asia, Africa and other tropical areas. The use of aloe vera is being promoted for a large variety of conditions. The aim of this systematic review was to summarize all dermatology-oriented in vitro and in vivo experiments and clinical trials on aloe vera preparations. Extensive literature search were carried out to identify all in vitro and in vivo studies as well as clinical trials on the subject. Data were extracted from these in a predefined standardized manner. Forty studies were located. The results suggest that oral administration of aloe vera in mice is effective on wound healing, can decrease the number and size of papillomas and reduce the incidence of tumors and leishmania parasitemia by >90% in the liver, spleen, and bone marrow. Topical application of aloe vera is not an effective prevention for radiation-induced injuries and has no sunburn or suntan protection. It can be effective for genital herpes, psoriasis, human papilloma virus, seborrheic dermatitis, aphthous stomatitis, xerosis, lichen planus, frostbite, burn, wound healing and inflammation. It can also be used as a biological vehicle and an anti-microbial and antifungal agent and also as a candidate for photodynamic therapy of some kinds of cancer. Even though there are some promising results with the use of aloe vera for diverse dermatologic conditions, clinical effectiveness of oral and topical aloe vera is not sufficiently and meticulously explored as yet.
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    PARSLEY, THE NEW PREDNISONE?
    Parsley has been used for years as a folk remedy for water retention, coughs, allergy, autoimmune, and chronic inflammatory disorders. Although it is one of the most potent disease-fighting plants little is known about how parsley works its magic….that is, until now. Recently, scientists set out to examine just one of the many wonders of parsley, its immune effects, in rigorous scientific detail. They looked at how parsley oil interacts with T-cells and B-cells (both types of white blood cells) and macrophages (cells that engulf and eliminate other cells). Conclusion: parsley oil acted in a similar way to drugs that suppress the immune system, like prednisone, but without the harmful side effects. As if that weren’t enough, other studies have shown that parsley has antitumor, antibacterial, and antioxidant properties.
    Karimi MH et al. “Parsley and immunomodulation.” Expert Rev Clin Immunol. 2012 May;8(4):295-7. http://www.expert-reviews.com/doi/pdf/10.1586/eci.12.12
    It is believed that parsley is one of the world’s seven most potent disease-fighting spices [8]. Although parsley has been used to treat allergy, autoimmune and chronic inflammatory disorders, the mechanism underlying its beneficial effects in these immune-mediated diseases have been rarely investigated. Of the various therapeutically beneficial aspects of parsley, we decided to examine the immunomodulatory effects of this plant.
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    Parsley- Antiinflammatory
    Throughout history, herbs have been utilized as an important constituent of foods, industry and folk medicine. One of the widely used vegetal species in various nations’ medicine is parsley (Petroselinum crispum), which has remedial effects as a powerful diuretic agent [1,2], an abortifacient [3–5] and an expectorant [6,7]. Parsley is a native herb of the central Mediterranean region (southern Italy, Algeria and Tunisia), which is in the Apiaceae family, and is a species of Petroselinum [8]. It is believed that parsley is one of the world’s seven most potent disease-fighting spices [8]. Although parsley has been used to treat allergy, autoimmune and chronic inflammatory disorders, the mechanism underlying its beneficial effects in these immune-mediated diseases have been rarely investigated. Of the various therapeutically beneficial aspects of parsley, we decided to examine the immunomodulatory effects of this plant. In our study, the effects of parsley essential oil on phytohemagglutinin (PHA)-stimulated splenocytes (T cells) and lipopolysaccharide (LPS)-stimulated B cells, as the main effector cells in adaptive immune system, was examined. In addition, the suppressive activity of different concentrations (0.01–100 μg/ml) of parsley essential oil on macrophages and LPS-stimulated macrophages for evaluation of nitric oxide (NO) was studied [9]. The methyl tetrazolium method was performed to survey the proliferation of mitogen-stimulated splenocytes as well as the viability of pretreated macrophages [9]. NO production of both macrophage groups was determined in the Griess reaction [9]. Parsley essential oil suppressed the proliferation of PHA-stimulated splenocytes at all applied concentrations. Similarly, it had a suppressive effect on the unstimulated and LPS-stimulated splenocytes, but only at high concentrations (10 and 100 μg/ml). NO production by unstimulated and stimulated macrophages was reduced by parsley essential oil; although, in all concentrations, unstimulated ones produced lower amounts of NO compared to the control group. These results can propose the suppressive effect of parsley essential oil on macrophages, as the major cells involved in the innate immune system [9].–The use of immunosuppressive drugs to control unwanted immune responses such as allergies, autoimmune disease and transplant rejection has grown over the past few years. The disadvantages and side effects of any immunosuppressive treatment are a significant and growing anxiety [10]. Some serious side effects including nephrotoxicity, hepatotoxicity, induction of diabetes, hypertension and neurotoxicity have been stated for various immunosuppressive drugs [10,11]. Thus, healthier and lower risk therapeutics are required. In this regard, more attention has been recently made on natural products. For example, the immunosuppressive activity of various herbal plants and ingredients including Achillea talagonica, [12] Plantago ovata [13], Boerhaavia diffusa [14], Stachys obtsicrena [15], Pollen Typhae [10] and Silymarin [16] has been explored. Parsley has also been shown to possess other biological activities than these described here. Several studies have suggested anticancer potential of parsley. By means of ascorbic acid‑induced lipid peroxidation, the antilipoperoxidant activity of parsley extracts has been shown [10,17,18]. The antioxidant activity of parsley essential oil has been confirmed in other investigations. Wong et al. indicated that the phenolic compounds of parsley were responsible for its antibacterial and antioxidant activity [19]. Zhang and his coworkers demonstrated the antioxidant activity of this herb in terms of b-carotene bleaching capacity and free radical scavenging activity [7]. This concept was then supported by further studies [20]. Parsley possesses several flavonoids such as apiin and luteolin, and its essential oil contains apiol and myristicin. These components are believed to be responsible for the therapeutic effects of parsley [17,21]. Kandaswami et al. indicated the direct and indirect effects of flavonoids on tumor cells. Their studies showed that the hydroxylation pattern of the B-ring of the flavons and flavonols, such as luteolin and quercetin, seemed to affect their angionesis and anticancer activity, especially the inhibition of protein kinase activity and antiproliferation [22]. Robak and his coworkers believe that flavonoids are the superoxide anion scavengers of the media and this effect can also lead to their anti-inflammatory effects [23]. Daly et al. observed bioactive phytochemicals, including carotenoids, in parsley [6]. Carotenoids were shown to be associated with a low risk of several human chronic disorders including age-related macular degeneration and certain cancers. Matching the wide use of this vegetal species as a diuretic in folk medicine, natriuretic and hypotensive effects of parsley were demonstrated in studies by Kreydiyyeh and Usta, and de Campos et al. [1,2]. Further studies indicated more biological effects of parsley plants, such as provitamine A activity, and influencing the cell signaling pathways [22,23]. In summary, parsley is a plant with various biological activities. With respect to its immunomodulatory effects, we found that its inhibitory effect on PHA-stimulated splenocytes might be due to the production of cytokines such as IFN-g and IL-2, which are vital for T-cell proliferation or it may influence the signaling pathways. Our results indicated that parsley essential oil can modulate the activity of macrophages without exerting cytotoxic effect. The immunomodulatory effect of parsley essential oil and its modulatory effects on NO production and function of macrophages may identify it as a useful natural candidate to treat some autoimmune and allergic diseases; however, its further application needs more investigation.
    References
    1 Kreydiyyeh SI, Usta J. Diuretic effect and mechanism of action of parsley. J. Ethnopharmacol. 79, 353–357 (2002).
    2 de Campos KE, Balbi APC, De Freitas Alves MJQ. Diuretic and hypotensive activity of aqueous extract of parsley seeds (Petroselinum sativum Hoffm.) in rats. Braz. J. Pharmacog. 19(1A), 41–45 (2009).
    3 Tyler VE. The Honest Herbalist (3rd Edition). Pharmaceutical Products Press, London, UK, 235–236 (1993).
    4 Anderson LA, Newall CA, Phillipson JDA. Guide for Health-care Professionals. The Pharmaceutical Press, London, UK, 203–204 (1996).
    5 Robbers JE, Tyler VE. Tyler’s Herbs of Choice. The Therapeutic Use of Phytochemicals. Haworth Herbal Press, NY, USA, 92 (1999).
    6 Daly T, Jiwan MA, O’Brein M, Aherne SA. Carotenoid content of commonly consumed herbs and assessment of their bioaccessibility using an in vitro digestion model. Plant. Foods Hum. Nutrit. 65(2), 164–169 (2010).
    7 Zhang H, Chen F, Wang X, Yao HY. Evaluation of antioxidant activity of parsley (Petroselinum crispum) essential oil and identification of its antioxidant constituents. Food Res. Int. 39(8), 833–839 (2006).
    8 Lopez MG, Sanchez-Mendoza IR, Ochoa-Alejo N. Compartive study of volatile components and fatty acids of plants and in-vitro cultures of parsley (Petroselinum crispum [Mill] nym ex hill). J. Agric. Food Chem. 47, 3292–3296 (1999).
    9 Yousofi A, Daneshmandi S, Soleimani N, Bagheri K, Karimi MH. Immunomodulatory effect of Parsley (Petroselinum crispum) essential oil on immune cells: mitogen-activated splenocytes and peritoneal macrophages. Immunopharmacol. Immunotoxicol. 34(2), 303–308 (2012).
    10 Vial T, Descotes J. Immunosuppressive drugs and cancer. Toxicology 185(3), 229–240 (2003).
    11 Qin F, Sun HX. Immunosuppressive activity of pollen typhae ethanol extract on the immune responses in mice. J. Ethnopharmacol. 102, 424–429 (2005).
    12 Rezaeipoor R, Saeidnia S, Kamalinejad M. Immunosuppressive activity of Achillea talagonica on humoral immune responses in experimental animals. J. Ethnopharmacol. 65, 273–276 (1999).
    13 Rezaeipoor R, Saeidnia S, Kamalinejad M. The effect of Plantago ovata on humoral immune responses in experimental animals. J. Ethnopharmacol. 72, 283–286 (2000).
    14 Mehrotra S, Mishra KP, Maurya R, Srimal RC, Singh VK. Immunomodulation by ethanolic extract of Boerhaavia diffusa roots. Int. Immunopharmacol. 2, 987–996 (2002).
    15 Amirghofran Z, Bahmani M, Azadmehr A, Javidnia K. Immunomodulatory and apoptotic effects of Stachys obtusicrena on proliferative lymphocytes. Med. Sci. Monit. 13(6), BR145–BR150 (2007).
    16 Gharagozloo M, Velardi E, Bruscoli S et al. Silymarin suppress CD4+ T cell activation and proliferation: effects on NF-kB activity and IL-2 production. Pharmacol. Res. 61(5), 405–409 (2010).
    17 Mimica-Dukić N, Popović M. Apiaceae species. A promising sources of pharmacologically active compounds I: Petrosellinum crispum, Apium greveolens and Pastinaca sativa. In: Recent Progress in Medicinal Plants. Govil JN, Singh VK (Eds). Studium Press LLC, TX, USA (2007).
    18 Fejes S, Blázovics A, Lemberkovics E, Petri G, Szöke E, Kéry A. Free radical scavenging and membrane protective effects of methanol extracts from Anthriscus cerefolium L. (Hoffm.) and Petroselinum crispum (Mill.) Nym. ex A. W. Hill. Phytother. Res. 14(5), 362–365 (2000).
    19 Wong PYY, Kitts DD. Studies on the dual antioxidant and anti bacterial properties of parsley (Petroselinum crispum) and cilantro (Coriandrum sativum) extracts. Food Chem. 97, 505–515 (2006).
    20 Kolarovic J, Popovic M, Zlinská J, Trivic S, Vojnovic M. Antioxidant activities of celery and parsley juices in rats treated with doxorubicin. Molecules 15, 6193–6204 (2010).
    21 Lombaert GA, Siemens KH, Pellaers P, Mankotia M, Ng W. Furanocoumarins in celery and parsnips: method and multiyear Canadian survey. J. AOAC Int. 84, 1135–1143 (2001).
    22 Kandaswami C, Lee LT, Lee PP et al. The antitumor activities of flavonoids. In Vivo 19(5), 895–909 (2005).
    23 Robak J, Rys Z, Gryglewski J. Flavonoids are scavengers of super oxide anions. Biochem. Pharm. 37, 837–841 (1998)
     
    TOP D
    [U1]Again this information is somewhat outdated—since mercury is in most fish consumed today it is arguably that the mercury can further diminish your low iodine levels—so again an alternative maybe eating grass fed beef which will have iodine in them based on the feed and without the mercury or seek other sources of aquatic life that may feed on seaweed to obtain the iodine
    [U2]Radishes can be goiterogenic so again if you do consume them not often and should be utilizing seaweed or watercress with it
    [U3]These are the goiterogenic goods
    [U4]Smart Meter-Cell Phone—HAARP -Microwaves
    [U5]A bad source—you would need to take 650grams -1 lb 7oz-to get the equivalent 1 drop of lugols
    [U6]The key word is EXCESS!!
    [U7]AGAIN this is only if the pollution is low and fish all has some form of arsenic and mercury so if you eat fish make sure that it is marinated properly with anti mercury substances—so that when being consumed the toxins are neutralized
    [U8]Now this is where it gets tricky—it does not say how long it will take—but it gives the feeling or perspective that it will be quick—this IS NOT SO—it will be contingent on health—how much you are lacking—and what other complimentary minerals or aminos you may be missing as well
    [U9]Other then Watercress the rest of the foods mentioned will be determined in there geographical areas which will determine how much is in the soil And how much is absorbed if any—the iodine that is
    [U10]ACTIVATE the Thyroid
    [U11]Even this is to low way to low-1000mcgs = 1mg the suggested daily dose is 13 mgs to sustain adequate levels—and use more depending on life style and exposure to environments
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    TOP E
    HOME
    Show of the Month October 19-2012
    Coffee Drinkers Have Lower Risk of Death- Study Suggests
    Potato Storage- Essential Oils as Antigerminants
    Top 10 Foods Highest in Potassium
    EFSA publishes initial review on GM maize and herbicide study
    Claims on many supplements don’t comply with law, report says
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    Coffee Drinkers Have Lower Risk of Death- Study Suggests
    A new study found that older adults who drank coffee — caffeinated or decaffeinated — had a lower risk of death overall than others who did not drink coffee.
    ScienceDaily (May 19, 2012) — Older adults who drank coffee — caffeinated or decaffeinated — had a lower risk of death overall than others who did not drink coffee, according a study by researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, and AARP.—Coffee drinkers were less likely to die from heart disease, respiratory disease, stroke, injuries and accidents, diabetes, and infections, although the association was not seen for cancer. These results from a large study of older adults were observed after adjustment for the effects of other risk factors on mortality, such as smoking and alcohol consumption. Researchers caution, however, that they can’t be sure whether these associations mean that drinking coffee actually makes people live longer. The results of the study were published in the May 17, 2012 edition of the New England Journal of Medicine.—Neal Freedman, Ph.D., Division of Cancer Epidemiology and Genetics, NCI, and his colleagues examined the association between coffee drinking and risk of death in 400,000 U.S. men and women ages 50 to 71 who participated in the NIH-AARP Diet and Health Study. Information about coffee intake was collected once by questionnaire at study entry in 1995-1996. The participants were followed until the date they died or Dec. 31, 2008, whichever came first.—The researchers found that the association between coffee and reduction in risk of death increased with the amount of coffee consumed. Relative to men and women who did not drink coffee, those who consumed three or more cups of coffee per day had approximately a 10 percent lower risk of death. Coffee drinking was not associated with cancer mortality among women, but there was a slight and only marginally statistically significant association of heavier coffee intake with increased risk of cancer death among men.–“Coffee is one of the most widely consumed beverages in America, but the association between coffee consumption and risk of death has been unclear. We found coffee consumption to be associated with lower risk of death overall, and of death from a number of different causes,” said Freedman. “Although we cannot infer a causal relationship between coffee drinking and lower risk of death, we believe these results do provide some reassurance that coffee drinking does not adversely affect health.”—The investigators caution that coffee intake was assessed by self-report at a single time point and therefore might not reflect long-term patterns of intake. Also, information was not available on how the coffee was prepared (espresso, boiled, filtered, etc.); the researchers consider it possible that preparation methods may affect the levels of any protective components in coffee.—“The mechanism by which coffee protects against risk of death — if indeed the finding reflects a causal relationship — is not clear, because coffee contains more than 1,000 compounds that might potentially affect health,” said Freedman. “The most studied compound is caffeine, although our findings were similar in those who reported the majority of their coffee intake to be caffeinated or decaffeinated.”—Story Source-The above story is reprinted from materials provided by National Institutes of Health. –Journal Reference-Neal D. Freedman, Yikyung Park, Christian C. Abnet, Albert R. Hollenbeck, Rashmi Sinha. Association of Coffee Drinking with Total and Cause-Specific Mortality. New England Journal of Medicine, 2012; 366 (20): 1891 DOI: 10.1056/NEJMoa1112010
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    Potato Storage- Essential Oils as Antigerminants
    ScienceDaily (Oct. 5, 2012) — One of the critical moments in the final quality of the potato occurs during its storage, as there exists the risk of sprouting or rotting due to pathogenic agents such as bacteria and fungi. In order to avoid this, agricultural engineer David Gómez Castillo carried out research for his PhD on the possibility of substituting the current use of chemical products by treating the tuber with essential oils of mint, caraway, coriander, eucalyptus and clove, “which have proved to be great potential inhibitors in the main problems detected.”—The chemical product Clorprofam (CIPC) is the most commonly used as a sprout suppressant on stored potatoes. Nevertheless, possible reductions in permitted dosages, market and consumer pressures seeking healthier and, moreover, more environmentally-friendly products, have made it necessary to find alternatives to these synthetic products, with the market, culinary and technological quality of the potato remaining unaltered.—This is the context of the research by David Gómez Castillo, who has evaluated alternative treatment using essential oils of mint, caraway, coriander, eucalyptus and clove. In concrete, he studied the effect of applying these oils with table-stock varieties of the potato (Agata and Monalisa) and industrial ones (Agria and Kennebec), and compared the results thereof with those that had been treated chemically.
    A good alternative—The research analysed two parameters: the commercial quality (germination, texture and colour of the tuber) and the culinary and technological quality (colour and texture of slices of the potato, dry material, total soluble solids, reductor sugars and sensorial analysis). Evaluations at 10, 25, 40, 55 and 70 days in storage were also undertaken, the antimicrobial effect of essential oils being assessed for the principal phytopathogens (fungi and bacteria).—According to Mr Gómez, “we found a high antigerminant capacity with treatment using the essential oil of coriander for industrial crops, and with the essential oil of mint for both industrial and table-stock crops. These showed great inhibitory potential on the principal phytopathogenic problems studied and all this makes a good alternative to CPIC use for storage of potatoes.”—It was also shown that the essential oil of eucalyptus, for its high antigerminant capacity with table-stock potatoes, “could be another alternative for reducing post-harvest losses due to phytopathogenic problems, obtaining even better results if the treatment is accompanied by the essential oil of clove.”–In the opinion of this researcher, the use of treatment with essential oils in the storage of potatoes “can provide added value in the application of antigerminant treatment, due to its efficacy in controlling the progress of important phytopathogens.”—Story Source-The above story is reprinted from materials provided by Basque Research.
    Recipe for AntiPhytopathegenic for Potato’s—take either a combination of peppermint and coriander add 2 drops each to either a Sprayer with water—make sure the Essential oils are dispersed well in the water—blend in a blender for about 2 minutes to mix—once done then spray the potatoes being stored—or take a vaporiser and add the oils into the vaporiser and allow it to mist the air as well—this will cause the components to be air borne and will reduce the break down—-this same principle can be done with other things as well or even utilize this principle to do a room or household to eliminate pathogens that might be airborne—keep the potatoes in a cool place for storage as well will reduce spoilage
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    Top 10 Foods Highest in Potassium
    Potassium is an essential nutrient used to maintain fluid and electrolyte balance in the body. A deficiency in potassium causes fatigue, irritability, and hypertension (increased blood pressure). Overdose of potassium from natural sources is nearly impossible, however, it is possible to consume too much potassium via potassium salts which can lead to nausea, vomiting, and even heart attack. Potassium from natural food sources, like the ones listed below, are considered safe and healthy. The current percent daily value for potassium is a whopping 3.5 grams, below is a list of high potassium foods. For more foods high in potassium please see the lists of potassium rich foods, fruits high in potassium, and vegetables high in potassium.
    #1: Dried Herbs
    Long used for medicinal purposes, herbs are packed with nutrients and potassium is no exception. Dried Chervil contains the most potassium with 4.7g (135% DV) per 100g serving, or 95mg (3% DV) per tablespoon. It is followed by Dried Coriander (3% DV) per tblsp, Dried Parsley (2% DV), Dried Basil, Dried Dill, Dried Tarragon, Ground Turmeric, Saffron, and finally Dried Oregano with 50mg (1% DV).
    Click to see complete nutrition facts
    #2: Avocados
    Avocados are great when made into guacamole or in a salad. 100 grams will provide 485mg of potassium or 14% of the DV. That is 1.1g (32% DV) in one cup pureed, and 975mg (28% DV) in a single avocado (201 grams).
    Click to see complete nutrition facts || More Fruits High in Potassium
    #3: Paprika and Red Chili Powder
    Either paprika or red chili powder add a nice kick to any dish, and with all the potassium they provide you have good reason to start adding them. Paprika provides the most potassium with 2.3g (67% DV) per 100 gram serving, or 164mg (5% DV) per tablespoon. Chili powder will provide 1.9g (55% DV) per 100 gram serving or 153mg (4% DV) per tablespoon. Click to see complete nutrition facts
    #4: Cocoa Powder and Chocolate
    Dark chocolate is an excellent source of iron and zinc in addition to potassium. Pure cocoa powder without any fat, milk, or sugar, provides the most potassium with 1.5 grams (44% DV) in a 100g serving, or 1.3g (37% DV) per cup, and 76mg (2% DV) per tablespoon. Unsweetened baking chocolate provides 830mg (24% DV) per 100 gram serving or 241mg (7% DV) per square. Most sweetened milk chocolates will provide around 272mg (11% DV) per 100 gram serving, and 164mg (5% DV) per bar (1.5oz). Click to see complete nutrition facts
    #5: Dried Apricots, Prunes, Zante Currants, and Raisins
    Most common as a snack, dried apricots and prunes can also be chopped and served in a salad. A good source of fiber and many other vitamins, apricots provide 1.9g (53%DV) of potassium per 100g serving (about 20 dried apricots). Prunes provide 1g (30% DV) per 100g serving, or 1.4g (40% DV) per cup. Zante currants are really a type of grape and taste very similar to raisins. Zante currants provide 892mg (25% DV) of potassium per 100g serving, or 1.3g (37% DV) per cup. Raisins provide almost the same amount with 825mg (24% DV) per 100 gram serving, or 1.2g (24% DV) per cup. Click to see complete nutrition facts
    #6: Pistachios and Other Nuts
    Pistachios are a delicious snack, and a great addition to salads. 100 grams (~3/4cup) will provide 1g (30% DV) of potassium. Other nuts high in potassium include Beechnuts (29% DV per 100g), Ginko nuts (29% DV), Chestnuts (28% DV), Almonds (21% DV), Hazelnuts (19% DV), Cashews (18% DV), Pine nuts (17% DV), Coconuts (16% DV), and Walnuts (15% DV).
    Click to see complete nutrition facts
    #7: Seeds (Pumpkin, Squash, Sunflower, and Flax)
    A popular food in the Middle East and East Asia pumpkin and squash seeds contain about 919mg (26% DV) of potassium per 100g serving, 588mg (17% DV) per cup. If you can’t find these in your local supermarket you will surely find them in Middle Eastern or East Asian specialty stores. Alternatively, you can also save any pumpkin and squash seeds you have and roast them in your oven. The seeds are typically eaten by cracking the outer shell and eating the seed inside. Sunflower seeds are also a good source of potassium, providing 850mg (24% DV) per 100 gram serving, or 1.1g (31% DV) per cup. Flax seeds provide 813mg (23% DV) of potassium per 100 gram serving, or 1.4g (39% DV) per cup, and 81mg (2% DV) per tablespoon.
    Click to see complete nutrition facts. Buy Pumpkin Seeds from Amazon.com
    #8: Fish (Pompano, Salmon, Halibut, Tuna)
    Fish has many health benefits and is a great source of potassium. Pompano provides the most with 636mg (18% DV) per 100 gram serving, or 540mg (15% DV) per fillet (3 ounces, 85 grams). It is followed by Salmon which provides 534mg (15% DV) per 3 ounce serving, Halibut, Yellow Fin Tuna, Lingcod, Mackerel, Anchovies, Herring, Cod, Snapper, Rockfish, Tilefish, Grouper, and finally Trout with 394mg (11% DV) in a 3 ounce serinvg. Cooking fish with dry heat is the best way to preseve the potassium content. Click to see complete nutrition facts
    #9: Beans
    White beans provide the most potassium with 561mg (16% DV) per 100 gram serving, 1g (29% DV) per cup cooked. White beans are followed by Adzuki Beans, Soy Beans, Lima Beans, Pinto Beans, Kidney Beans, Great Northern Beans, Navy Beans, Pigeon Peas, Cranberry (Roman) Beans, French Beans, Lentils, Split Peas, Black Beans, Hyancinth, and finally Yardlong Beans with 539mg (15% DV) per cup cooked.
    Click to see complete nutrition facts
    #10: Dates (Medjool)
    Dates are great as a snack, as an addition to fruits salads, or even savory stews. Medjool dates provide 696mg (20% DV) per 100 gram serving, or 167mg (5% DV) in a single date.
    Click to see complete nutrition facts
    Read more at http://www.healthaliciousness.com/articles/food-sources-of-potassium.php#cTUeesXT5EcLhruM.99
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    EFSA publishes initial review on GM maize and herbicide study
    The European Food Safety Authority has concluded that a recent paper raising concerns about the potential toxicity of genetically modified (GM) maize NK603 and of a herbicide containing glyphosate is of insufficient scientific quality to be considered as valid for risk assessment.—EFSA’s initial review found that the design, reporting and analysis of the study, as outlined in the paper, are inadequate. To enable the fullest understanding of the study the Authority has invited authors Séralini et al to share key additional information.–Such shortcomings mean that EFSA is presently unable to regard the authors’ conclusions as scientifically sound. The numerous issues relating to the design and methodology of the study as described in the paper mean that no conclusions can be made about the occurrence of tumours in the rats tested.—Therefore, based on the information published by the authors, EFSA does not see a need to re-examine its previous safety evaluation of maize NK603 nor to consider these findings in the ongoing assessment of glyphosate.—EFSA assessed the paper against recognised good scientific practices, such as internationally agreed study and reporting guidelines.—-Per Bergman, who led EFSA’s work, said: “Some may be surprised that EFSA’s statement focuses on the methodology of this study rather than its outcomes; however, this goes to the very heart of the matter. When conducting a study it is crucial to ensure a proper framework is in place. Having clear objectives and the correct design and methodology create a solid base from which accurate data and valid conclusions can follow. Without these elements a study is unlikely to be reliable and valid.”—The Director of Scientific Evaluation of Regulated Products added that the consideration of possible long-term effects of GMOs has been, and will continue to be, a key focus of EFSA’s work to protect animals, humans and the environment.—-EFSA’s preliminary review issued today is the first step in a two-stage process. A second analysis will be delivered by the end of October 2012. This will take into account any additional information from the study authors, who will be given an opportunity to supply study documentation and procedures to the Authority to ensure the broadest possible understanding of their work. It will also include an overview of Member State assessments of the paper and an analysis from the German authorities responsible for the assessment of glyphosate.
    Main findings of Initial Review—The task force, whose members were drawn from the Authority’s GMO, pesticide and scientific assessment units, has outlined a list of issues about the paper that would need to be resolved before it could be viewed as well-conducted and properly-reported study.
    The strain of rat used in the two-year study is prone to developing tumours during their life expectancy of approximately two years. This means the observed frequency of tumours is influenced by the natural incidence of tumours typical of this strain, regardless of any treatment. This is neither taken into account nor discussed by the authors.
    The authors split the rats into 10 treatment sets but established only one control group. This meant there was no appropriate control for four sets – some 40% of the animals – all of whom were fed GM maize treated or not treated with a herbicide containing glyphosate.
    The paper has not complied with internationally-recognised standard methods – known as protocols – for setting up and carrying out experiments. Many of these procedures are developed by the OECD (Organisation for Economic Cooperation and Development).
    For a study of this type, the relevant OECD guideline specifies the need for a minimum of 50 rats per treatment group. Séralini et al used only 10 rodents per treatment set. The low number of animals used is insufficient to distinguish between the incidence of tumours due to chance rather than specific treatment effects.
    The authors have not stated any objectives, which are the questions a study is designed to answer. Research objectives define crucial factors such as the study design, correct sample size, and the statistical methods used to analyse data – all of which have a direct impact on the reliability of findings.
    No information is given about the composition of the food given to the rats, how it was stored or details of harmful substances – such as mycotoxins – that it might have contained.
    It is not possible to properly evaluate the exposure of the rats to the herbicide as intake is not clearly reported. The authors report only the application rate of the herbicide used to spray the plants and the concentration added to the rats’ drinking water but report no details about the volume of the feed or water consumed.
    The paper does not employ a commonly-used statistical analysis method nor does it state if the method was specified prior to starting the study. The validity of the method used is queried and there are questions over the reporting of tumour incidence. Important data, such as a summary of drop outs and an estimation of unbiased treatment effects have not been included in the paper.
    Many endpoints – what is measured in the study – have not been reported in the paper. This includes relevant information on lesions, other than tumours, that were observed. EFSA has called on the authors to report all endpoints in the name of openness and transparency.
    Review of the Séralini et al. (2012) publication on a 2-year rodent feeding study with glyphosate formulations and GM maize NK603
    Letter to Prof. Séralini regarding EFSA’s Review of the Séralini et al. (2012) publication on a 2-year rodent feeding trial with Glyphosate Formulations and GM maize NK603 as published online on 19 September 2012 in Food and Chemical Toxicology, 4 October 2012
    Notes to editors:
    EFSA set up a multi-disciplinary task force in response to an urgent request from the European Commission to evaluate a paper by Séralini et al to assess whether its findings could lead the Authority to reconsider its previous opinion on maize NK603. The two-year study, published in the journal Food and Chemical Toxicology on 19 September 2012, has suggested that consumption of the GM maize and a herbicide containing glyphosate at levels below officially-safe limits are linked to a reported increase in incidence of tumours in rats.
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    Claims on many supplements don’t comply with law, report says
    The structure function claims on many dietary supplement products do not comply with federal law,
    a government report released on Wednesday The[U1] report recommends greater regulatory
    powers for FDA to bring products into compliance[U2] .—Industry sources reacted negatively to the assertion
    that FDA needs new statutory powers, but were more accommodating on the report’s suggestions on how
    the claims notification process should be tightened up[U3] . The report, conducted by the Office of Inspector
    General of the United States Department of Health and Human Services, looked at the claims on 127 dietary s
    upplements in the weight loss and immune support The report looked at the label language and what kind
    of evidence was cited to back up the claims, to judge compliance with FDA-mandated notifications and disclaimers
    and to see how many claims trended over into prohibited disease claim territory. The report said that the
    popularity of structure function claims is on the rise, and maintains that problems with the use
    of these claims is on the rise, too. Report cites thin supporting evidence The report’s broad conclusions
    were these: Many claims were not backed by evidence from human studies[U4] . Of the human studies
    supplied by manufacturers in response to HHS requests, few appeared to satisfy FDA recommendations
    in every respect in terms of study design and relevance to the meaning of the claim[U5] . It also found
    that 20% of the supplements in the sample were making prohibited disease claims and that 7% lacked
    the disclaimer that is supposed to accompany every structure function claim. The report went on to
    recommend that FDA should seek additional statutory authority to regulate label claims to make sure
    that suitable evidence exists to back up the claim, to make sure that proper label notifications are
    in place and to make sure companies are not making illegal disease claims In[U6] addition, it said FDA
    needs to clean up its tracking of who is making what claims, and who has complied with the requirement of a 30-day
    prior notification of the use of a claim on a product. Immediate reaction Report overreaches Reaction from trade
    groups and industry observers was swift and decisive. The Office of Inspector General reviewed just 127 supplements
    out of an estimated 29,000 products on the market. This small sample of supplements shouldn’t smear the entire industry,
    said John Shaw, executive director and CEO of the Natural Products Foundation. The president and CEO of the
    organization, said, What’s most disappointing is that this was not a random sampling [of the industry].The vast majority
    of the industry, including our members, is doing the right thing. These reports give good companies a black eye,
    he said.The small sample size and big conclusions also was an issue for Marc Ullman, who has worked with the
    http://www.naturalproductsfoundation.org/index.php?src=gendocsref=truth_in_advertisingcategory=FoundationPrograms
    ” Natural Products Foundation’s Truth in Advertising industry self-regulation effort. They are recommended sweeping
    changes to the law, the imposition of vast new regulatory burdens on FDA based on the fact that (a small number)
    of dietary supplements didn’t pass substantiation. To me it seems quite a reach, Ullman, an attorney with the New
    York-based firm Ullman, Shapiro Ullman, told a reporter. I cannot fathom the kind of broad generalizations they
    made based on this kind of sample size. Nuanced response to report’s recommendations Regarding the recommendations,
    Mister said CRN was very supportive of FDA to do more, especially when it came keeping better
    track of health claim notifications, which companies are supposed to send in 30 days prior to a
    product hitting the But the first recommendation, calling for FDA to ‘statutory authority to review
    substantiation for structure/function claims to determine whether they are truthful and not
    misleading[U7] ,’ is a non-starter, he said.This sounds like pre-market approval to us, Mister said. I do hope that
    FDA sees that some of this is targeted towards them, he added. The agency needs to manage the information they
    already have. Structure/function claims and registrations need to be catalogued to be accessible.The methodology
    of the report divided up the supplements more or less equally between the weight loss and immune sectors, and
    also about equally between supplements purchased in retail outlets on the Internet. This last detail interested Tony
    Young, legal counsel for the American Herbal Products Association, especially in relation to the finding that 20% of
    products were making disease claims. An interesting question would be whether those were products purchased off the
    Internet or in retail stores. We expect that there is a higher standard out there to get products on retail shelves and
    that most of the major retailers don’t carry products that make that kind of claim, he said. No public health risk At
    the end of the day, Young said, there is no imminent public health risk in the report’s findings. Whether FDA should
    expend substantial resources doing the kinds of things that were suggested is a decision that FDA would have to make
    with regard to all of the other public health priorities,” he said.The report might go overboard in its enforcement
    recommendations, Ullman said, but that doesn’t obviate legitimate questions about how some companies market their
    products As an industry we need to recognize—and we do recognize—that there is a problem, he said, going on to cite NPF’s
    Truth in Advertising effort and CRN’s cooperation with the “http://www.bbb.org/us/national-advertising-division/&#8221;
    National Advertising Division as appropriate ways to self-police label claims.Everybody in our industry argues that there
    should be more enforcement with respect to unlawful disease claims so there is pretty much unanimity on that,
    Young said[U8] .
    TOP E
    [U1] A new attack on supplements
    [U2]Drug Companies want to debilitate the industry further for easier acquisition of that health food industry market—where the owners will surrender there companies and sell out
    [U3]This is the HFI-health food industry caving in and surrendering—the industry should be looking after itself without gov’t interference—
    [U4]This is the EFSA—european food and safe authority nonsence—this is the FDA compliance with the EFSA
    [U5]Again EFSA
    [U6]Gov’t interference—again to debilitate the industry to a point where they either bail out or surrender—the health food industry as well a the consumers need to collaborate and get rid of the common enemy Gov’t
    [U7]Is this not the dumbest thing you ever heard? The wolf guarding the hen house—the industry is going to ask the gov’t to monitor the competition??? What a deception here
    [U8]This is really disappointing—the big players what the FDA to do there dirty work for them so they can eliminate all competition and have it all under 1 umbrella this is what is really going on a destruction of a free enterprise effect and everyone has to comply and the independent is going to either be absorbed or eliminated from the market
     
    [U1]Smart Meter-Cell Phone—HAARP -Microwaves
    [U2] A new attack on supplements
    [U3]Drug Companies want to debilitate the industry further for easier acquisition of that health food industry market—where the owners will surrender there companies and sell out
    [U4]This is the HFI-health food industry caving in and surrendering—the industry should be looking after itself without gov’t interference—
    [U5]This is the EFSA—european food and safe authority nonsence—this is the FDA compliance with the EFSA
    [U6]Again EFSA
    [U7]Gov’t interference—again to debilitate the industry to a point where they either bail out or surrender—the health food industry as well a the consumers need to collaborate and get rid of the common enemy Gov’t
    [U8]Is this not the dumbest thing you ever heard? The wolf guarding the hen house—the industry is going to ask the gov’t to monitor the competition??? What a deception here
    [U9]This is really disappointing—the big players what the FDA to do there dirty work for them so they can eliminate all competition and have it all under 1 umbrella this is what is really going on a destruction of a free enterprise effect and everyone has to comply and the independent is going to either be absorbed or eliminated from the market
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    TOP F
    HOME
     
    Show of the Month October 22-2012
    Antioxidant May Prevent, Even Cure, Cataracts and Other Degenerative Eye Disorders
    Caffeine May Block Inflammation Linked to Mild Cognitive Impairment
    Cannabis Extract Eases Muscle Stiffness Typical of Multiple Sclerosis
    Cannabis as Painkiller
    Mushroom Compound Suppresses Prostate Tumors
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    Antioxidant May Prevent, Even Cure, Cataracts and Other Degenerative Eye Disorders
    Cataract formation in rats. Top left (control lens): The lenses in this group were found to contain no detectable cataracts. (BSO-only lens): All lenses in this group developed very distinct cataracts, with most being nearly completely opaque (NACA-only lens): Results similar to those in the control group were obtained, with no detectable signs of cataract formation. (NACA+BSO lens): The lens depicted has a Grade 1 opacity which was evident by the amount of scattering light.
    ScienceDaily (Oct. 9, 2012) — Researchers at Missouri University of Science and Technology are working with an antioxidant that could prevent or cure cataracts, macular degeneration and other degenerative eye disorders.—The research group, headed by Dr. Nuran Ercal, the Richard K. Vitek/Foundation for Chemical Research Endowed Chair in Biochemistry at Missouri S&T, is studying eye drops prepared with the antioxidant N-acetylcysteine amide (NACA) as a treatment for these eye conditions.–Ercal says NACA is an improvement over another experimental treatment, the antioxidant N-acetylcysteine (NAC), because it passes more easily across cell membranes, allowing the medication to be used in lower doses.–“NACA’s characteristics as a drug were improved over NAC by neutralizing the carboxylic group of NAC, which makes the NACA pass cellular membranes easily,” says Ercal. “And because NACA can be administered at a lower dose, the drug has a greater therapeutic index and lowers the risk of side effects traditionally associated with NAC.—“NACA is also an excellent source of glutathione, a cell’s main antioxidant power, which is diminished during degenerative eye disorders,” she adds.—Vision loss from age-related eye disorders affects more than 30 million people in the United States and is expected to double in the coming decades, Ercal says.—In addition, more than $9 billion is spent annually in the U.S. on cataract surgery alone. The total annual cost of all services related to vision problems exceeds $20 billion, she says.—“NACA eye drops could drastically reduce these costs and represent an alternative to costly surgery, while greatly improving the quality of life for those afflicted,” says Ercal.—Ercal and her team have been testing NACA on HIV-related problems, lead poisoning and other toxicities for 10 years. About four years ago they began testing it on eye disorders.–Ercal recently received a $378,000 three-year research grant from the National Eye Institute of the National Institutes of Health. The preliminary data submitted for the funding was based on research by her former Ph.D. student, Joshua Carey.–Carey’s dissertation involved preliminary studies of the effects of NACA to slow down cataract growth on rats that had been given L-buthionine-S,R-sulfoximine (BSO), a solution that causes cataracts to form. “The NACA solution prevented cataracts from forming,” says Ercal. “Our research will build on Josh’s research, to see if NACA can actually reverse the degeneration as well.”—Ercal, who is also an M.D., says further testing will help establish appropriate dosage and frequency, as well as possible side effects and other factors. She says successful results using animal subjects may eventually support the viability of human usage.–Ercal works closely with Dr. Shakila Tobwala, a post-doctoral fellow in Missouri S&T’s chemistry department. Others in the research group include the grant’s co-investigator, Dr. Humeyra Karacal from the ophthalmology department at Washington University in St. Louis, and Missouri S&T graduate and undergraduate students.—Story Source-The above story is reprinted from materials provided by Missouri University of Science and Technology.
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    Caffeine May Block Inflammation Linked to Mild Cognitive Impairment
    ScienceDaily (Oct. 8, 2012) — Recent studies have linked caffeine consumption to a reduced risk of Alzheimer’s disease, and a new University of Illinois study may be able to explain how this happens.–“We have discovered a novel signal that activates the brain-based inflammation associated with neurodegenerative diseases, and caffeine appears to block its activity. This discovery may eventually lead to drugs that could reverse or inhibit mild cognitive impairment,” said Gregory Freund, a professor in the U of I’s College of Medicine and a member of the U of I’s Division of Nutritional Sciences.—Freund’s team examined the effects of caffeine on memory formation in two groups of mice — one group given caffeine, the other receiving none. The two groups were then exposed to hypoxia, simulating what happens in the brain during an interruption of breathing or blood flow, and then allowed to recover.–The caffeine-treated mice recovered their ability to form a new memory 33 percent faster than the non-caffeine-treated mice. In fact, caffeine had the same anti-inflammatory effect as blocking IL-1 signaling. IL-1 is a critical player in the inflammation associated with many neurodegenerative diseases, he said.—“It’s not surprising that the insult to the brain that the mice experienced would cause learning memory to be impaired. But how does that occur?” he wondered.—The scientists noted that the hypoxic episode triggered the release of adenosine by brain cells.–“Your cells are little powerhouses, and they run on a fuel called ATP that’s made up of molecules of adenosine. When there’s damage to a cell, adenosine is released,” he said.–Just as gasoline leaking out of a tank poses a danger to everything around it, adenosine leaking out of a cell poses a danger to its environment, he noted.—The extracellular adenosine activates the enzyme caspase-1, which triggers production of the cytokine IL-1β, a critical player in inflammation, he said.—“But caffeine blocks all the activity of adenosine and inhibits caspase-1 and the inflammation that comes with it, limiting damage to the brain and protecting it from further injury,” he added.—Caffeine’s ability to block adenosine receptors has been linked to cognitive improvement in certain neurodegenerative diseases and as a protectant against Alzheimer’s disease, he said.–“We feel that our foot is in the door now, and this research may lead to a way to reverse early cognitive impairment in the brain. We already have drugs that target certain adenosine receptors. Our work now is to determine which receptor is the most important and use a specific antagonist to that receptor,” he said.–The study appears in the Journal of Neuroscience. Co-authors are Gabriel Chiu, Diptaman Chatterjee, Patrick Darmody, John Walsh, Daryl Meling, and Rodney Johnson, all of the U of I. Funding for the study was provided by the National Institutes of Health.–Story Source-The above story is reprinted from materials provided by University of Illinois College of Agricultural, Consumer and Environmental Sciences. The original article was written by Phyllis Picklesimer. -Journal Reference-G. S. Chiu, D. Chatterjee, P. T. Darmody, J. P. Walsh, D. D. Meling, R. W. Johnson, G. G. Freund. Hypoxia/Reoxygenation Impairs Memory Formation via Adenosine-Dependent Activation of Caspase 1. Journal of Neuroscience, 2012; 32 (40): 13945 DOI: 10.1523/JNEUROSCI.0704-12.2012
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    Cannabis Extract Eases Muscle Stiffness Typical of Multiple Sclerosis
    ScienceDaily (Oct. 8, 2012) — Cannabis seems to ease the painful muscle stiffness typical of multiple sclerosis (MS), indicate phase III trial results, published in the Journal of Neurology Neurosurgery and Psychiatry.—Up to 90 per cent of MS patients endure painful muscle stiffness at some point during the course of their disease, which reduces their mobility and interferes with daily routine activities and sleep quality. But current treatments often fail to resolve symptoms fully, and can be harmful, as a result of which many MS patients have experimented with alternative therapies, including cannabis.—Adult MS patients with stable disease, from 22 different specialist centres across the UK, were either randomly assigned to cannabis extract (tetrahydrocannabinol) daily (144) or a dummy pill (placebo) (135) for a period of 12 weeks.—The treatments were given in gradually increasing doses from 2.5 mg up to a maximum of 25 mg for two weeks, followed by maintenance doses for the remaining 10 weeks. The aim was to see if cannabis extract alleviated or improved muscle stiffness, associated pain, muscle spasms, and sleep quality, using a validated 11 point rating scale. After the first two weeks of treatment, 87 per cent of those taking the placebo were on the maximum daily dose compared with just under half of those (47%) taking the cannabis extract.—After 12 weeks, one in four patients treated with cannabis extract was taking the maximum daily dose compared with over two thirds (69.4%) of those taking the placebo.—At the end of the study period, the rate of relief from muscle stiffness was twice as high among those given the cannabis extract as those given the placebo. Muscle stiffness was alleviated in just under 30 per cent of those given cannabis compared with just under 16 per cent of those treated with the placebo. This difference was evident after 4 and 8 weeks, and also extended to pain, muscle spasms and sleep quality, at all time points, the results showed. The differences were most noticeable among patients not already using antispasmodic treatment, among whom almost 40 per cent of those taking the cannabis extract gained relief compared with just over 16 per cent of those taking placebo. -The rate of side effects was higher among those taking the cannabis extract and highest during the first two weeks of treatment. Nervous system disorders and gut problems were the most commonly reported side effects, but none was severe.–The authors conclude that the results of their trial indicate that cannabis extract could be a useful treatment for the muscle problems typical of MS, and could provide effective pain relief, particularly for those in considerable pain. Story Source-The above story is reprinted from materials provided by BMJ-British Medical Journal. –Journal Reference-J. P. Zajicek, J. C. Hobart, A. Slade, D. Barnes, P. G. Mattison. MUltiple Sclerosis and Extract of Cannabis: results of the MUSEC trial. Journal of Neurology, Neurosurgery & Psychiatry, 2012; 83 (11): 1125 DOI: 10.1136/jnnp-2012-302468
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    Cannabis as Painkiller
    ScienceDaily (Aug. 7, 2012) — Cannabis-based medications have been demonstrated to relieve pain. Cannabis medications can be used in patients whose symptoms are not adequately alleviated by conventional treatment. The indications are muscle spasms, nausea and vomiting as a result of chemotherapy, loss of appetite in HIV/Aids, and neuropathic pain.—This is the conclusion drawn by Franjo Grotenhermen and Kirsten Müller-Vahl in issue 29-30 of Deutsches Ärzteblatt International. –The clinical effect of the various cannabis-based medications rests primarily on activation of endogenous cannabinoid receptors. Consumption of therapeutic amounts by adults does not lead to irreversible cognitive impairment. The risk is much greater, however, in children and adolescents (particularly before puberty), even at therapeutic doses.—Over 100 controlled trials of the effects of cannabinoids in various indications have been carried out since 1975. The positive results have led to official licensing of cannabis-based medications in many countries. In Germany, a cannabis extract was approved in 2011 for treatment of spasticity in multiple sclerosis. In June 2012 the Federal Joint Committee (the highest decision-making body for the joint self-government of physicians, dentists, hospitals and health insurance funds in Germany) pronounced that the cannabis extract showed a slight additional benefit for this indication and granted a temporary license until 2015. Story Source-The above story is reprinted from materials provided by Deutsches Aerzteblatt International, via AlphaGalileo. –Journal Reference-Grotenhermen, F; Müller-Vahl, K. The Therapeutic Potential of Cannabis and Cannabinoids. Dtsch Arztebl Int, 2012; 109(29-30): 495-501 DOI: 10.3238/arztebl.2012.0495
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    Mushroom Compound Suppresses Prostate Tumors
    ScienceDaily (May 24, 2011) — A mushroom used in Asia for its medicinal benefits has been found to be 100 per cent effective in suppressing prostate tumour development in mice during early trials, new Queensland University of Technology (QUT) research shows.–The compound, polysaccharopeptide (PSP), which is extracted from the ‘turkey tail’ mushroom, was found to target prostate cancer stem cells and suppress tumour formation in mice, according to an article written by senior research fellow Dr Patrick Ling in the online journal PLoS ONE, published by the Public Library of Science.–Dr Ling, from the Australian Prostate Cancer Research Centre-Queensland and Institute for Biomedical Health & Innovation (IHBI) at QUT, said the results could be an important step towards fighting a disease that kills 3,000 Australian men a year.–“The findings are quite significant,” Dr Ling said.–“What we wanted to demonstrate was whether that compound could stop the development of prostate tumours in the first place.–“In the past, other inhibitors tested in research trials have been shown to be up to 70 per cent effective, but we’re seeing 100 per cent of this tumour prevented from developing with PSP.–“Importantly, we did not see any side effects from the treatment.”–Dr Ling said conventional therapies were only effective in targeting certain cancer cells, not cancer stem cells, which initiated cancer and caused the disease to progress.–During the research trial, which was done in collaboration with The University of Hong Kong and Provital Pty Ltd, transgenic mice that developed prostate tumours were fed PSP for 20 weeks.–Dr Ling said no tumours were found in any of the mice fed PSP, whereas mice not given the treatment developed prostate tumours. He said the research suggested that PSP treatment could completely inhibit prostate tumour formation.–“Our findings support that PSP may be a potent preventative agent against prostate cancer, possibly through targeting of the prostate cancer stem cell population,” he said.b He said PSP had been previously shown to possess anti-cancer properties, and ‘turkey tail’ mushrooms (known as Coriolus versicolor or Yun-zhi) had been widely used in Asia for medicinal benefits.–However, Dr Ling said it was the first time it had been demonstrated that PSP had anti-cancer stem cell effects.–Although ‘turkey tail’ mushrooms had valuable health properties, Dr Ling said it would not be possible to get the same benefit his research showed from simply eating them.–A fundraiser has been organised in September to support further tests for the therapeutic potential of PSP against prostate tumours either alone or in combination with other anti-cancer compounds.—Story Source-The above story is reprinted from materials provided by Queensland University of Technology. –Journal Reference-Sze-Ue Luk, Terence Kin-Wah Lee, Ji Liu, Davy Tak-Wing Lee, Yung-Tuen Chiu, Stephanie Ma, Irene Oi-Lin Ng, Yong-Chuan Wong, Franky Leung Chan, Ming-Tat Ling. Chemopreventive Effect of PSP Through Targeting of Prostate Cancer Stem Cell-Like Population. PLoS ONE, 2011; 6 (5): e19804 DOI: 10.1371/journal.pone.0019804
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    Show Of The Month October 26 2012
    Even Your Fat Cells Need Sleep
    Prebiotic May Help Patients With Intestinal Failure Grow New and Better Gut
    Special Note as to why not to Consume grains
    Non-Medical Prescription Drug Use More Common Among Rural Teens Than City Dwellers
    Research Reveals Decline in Illicit Drug Abuse- Prescription Drug Abuse On the Rise
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    Even Your Fat Cells Need Sleep
    ScienceDaily (Oct. 15, 2012) — In a study that challenges the long-held notion that the primary function of sleep is to give rest to the brain, researchers have found that not getting enough shut-eye has a harmful impact on fat cells, reducing by 30 percent their ability to respond to insulin, a hormone that regulates energy.—Sleep deprivation has long been associated with impaired brain function, causing decreased alertness and reduced cognitive ability. The latest finding — published by University of Chicago Medicine researchers in the Oct. 16 issue of the Annals of Internal Medicine — is the first description of a molecular mechanism directly connecting sleep loss to the disruption of energy regulation in humans, a process that can lead over time to weight gain, diabetes and other health problems. The study suggests that sleep’s role in energy metabolism is at least as important as it is in brain function.–“We found that fat cells need sleep to function properly,” said study author Matthew Brady, PhD, associate professor of medicine and vice-chair of the Committee on Molecular Metabolism and Nutrition at the University of Chicago.—-Brady said body fat plays an important role in humans.—“Many people think of fat as a problem, but it serves a vital function,” he said. “Body fat, also known as adipose tissue, stores and releases energy. In storage mode, fat cells remove fatty acids and lipids from the circulation where they can damage other tissues. When fat cells cannot respond effectively to insulin, these lipids leach out into the circulation, leading to serious complications.”–Esra Tasali, MD, assistant professor of medicine at the University of Chicago and co-senior author, led the recruitment of six men and one woman, all young, lean and healthy. Each volunteer went through two study conditions, at least four weeks apart. In one, they spent 8.5 hours a night in bed for four consecutive nights. In the other, they spent 4.5 hours in bed for four nights. Food intake, strictly controlled, was identical under both study conditions.—On the morning after the fourth night following both the long and short sleep conditions, each volunteer took an intravenous glucose tolerance test, which measures total-body insulin sensitivity. The researchers performed a biopsy, removing abdominal fat cells from the area near each volunteer’s navel. Then they measured how these fat cells responded to insulin.—The researchers assessed insulin sensitivity at the molecular level by measuring the phosphorylation of a protein called Akt within fat cells. Akt phosphorylation is a crucial early chemical step in the cell’s response to insulin.–After four nights of short sleep, total-body insulin response decreased by an average of 16 percent. The insulin sensitivity of fat cells decreased by 30 percent. This reduction is comparable to the difference between cells from obese vs. lean participants or from people with diabetes versus non-diabetic controls.—They found that the sleep-deprived study participants had a decreased response to a range of doses of insulin. It took nearly three times as much insulin to provoke half of the maximum Akt response in volunteers who had been deprived of sleep.
    “Sleeping four to five hours a night, at least on work days, is now a common behavior” said study author and sleep specialist Esra Tasali.–“Some people claim they can tolerate the cognitive effects of routine sleep deprivation,” said co-author Eve Van Cauter, PhD, the Frederick H. Rawson Professor of Medicine and director of the sleep, metabolism and health center at the University of Chicago. “In this small but thorough study, however, we found that seven out of seven subjects had a significant change in insulin sensitivity. They are not tolerating the metabolic consequences.”—The study was one of the first to bring together sleep research experts and biologists focused on energy regulation and metabolism in adipose tissue. The impetus came from a sleep-research graduate student, Josiane Broussard, PhD ’10, lead author of the study and now a Society in Science-Branco Weiss fellow at Cedars-Sinai Medical Center in Los Angeles. She wanted to combine her interest in sleep and metabolism with research at the molecular level.—So she pulled together a team for this project that included the two sleep researchers, Tasali and Van Cauter, plus two specialists from the University of Chicago Kovler Diabetes Center, David Ehrmann, MD, and Brady, who studies how insulin regulates energy storage in fat and liver cells.—They focused on fat cells because of their direct links to metabolic disruption and weight gain. These cells store energy for the body, are exquisitely sensitive to insulin and help regulate appetite.—Witnessing the direct effect of sleep deprivation on a peripheral tissue such as fat at the cellular level “was an eye-opener,” Broussard said. It helps cement the link between sleep and diabetes and “suggests that we could use sleep like diet and exercise to prevent or treat this common disease[U1] .” Brady said the study opens up many new questions.–“What signals from sleep loss affect the fat cell? What effect does dysfunctional fat have at the whole-body level?” Brady wondered. “And if we can deprive healthy people of sleep and make them worse, can we take sick people, such as those with the common combination of sleep apnea, obesity and diabetes, improve their sleep and make them better? That’s the missing link in the sleep-obesity-diabetes connection.”–This study is “a valuable contribution to the understanding of the causal pathways by which reduced sleep duration may directly contribute to diabetes and obesity,” according to an editorial in the journal by Francesco Cappuccio, MD, DSc, and Michelle Miller, PhD, of the University of Warwick, in Coventry, United Kingdom. “These results point to a much wider influence of sleep on bodily functions, including metabolism, adipose tissue, cardiovascular function, and possibly more.”–The paper, “Impaired Insulin Signaling in Human Adipocyes,” appears in the Oct. 16, 2012, issue of the Annals of Internal Medicine. Funding for this work was provided by the National Institutes of Health and Society in Science — The Branco Weiss Fellowship.–Story Source-The above story is reprinted from materials provided by University of Chicago Medical Center, via Newswise. –Journal Reference-Josiane L. Broussard, David A. Ehrmann, Eve Van Cauter, Esra Tasali, Matthew J. Brady. Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study. Annals of Internal Medicine, 2012; 157 (8): 549-557 [link]

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    Prebiotic May Help Patients With Intestinal Failure Grow New and Better Gut
    ScienceDaily (Oct. 15, 2012) — Adding the right prebiotic to the diets of pediatric patients with intestinal failure could replace intravenous feeding, says a new University of Illinois study. “When we fed the carbohydrate fructooligosacharide (FOS) as a prebiotic, the gut grew and increased in function,” said Kelly A. Tappenden, a U of I professor of nutrition and gastrointestinal physiology. “The study showed that using the correct pre- and probiotic in combination could enhance these results even more.”–When FOS enters the intestines, bacteria convert it into butyrate, a short-chain fatty acid that increases the size of the gut and its ability to digest and absorb nutrients, she said[U2] .—But today’s IV solutions don’t contain butyrate and adding it would entail drug development trials and regulatory red tape. She wanted to see if adding this carbohydrate to the diet while continuing to provide most nutrients intravenously would cause the gut to start producing butyrate on its own. It worked According to Tappenden, at least 10,000 U.S. patients are totally reliant on intravenous feeding because their intestines have been surgically shortened. Many of these patients are premature infants who develop necrotizing enterocolitis, a kind of gangrene of the intestine. In the U.S., one in eight infants is a preemie, and removing necrotized, or dead, intestine is the most common surgical emergency in these babies. “Surgery saves their lives, but with so much intestine removed, they’re unable to digest or absorb nutrients. These babies are also at risk for long-term complications, such as bone demineralization and liver failure. Our goal is to take kids who’ve had this resection and cause their gut to grow and adapt,” she said.—She tested her hypothesis about butyrate using newborn piglets, an excellent model for the human infant in metabolism and physiology. Piglets with intestinal failure were assigned to one of four groups: a control group; a group whose diet contained FOS, a carbohydrate given as a prebiotic to stimulate the production of butyrate by beneficial bacteria; a probiotic, or actual live bacteria; and a combination of pre- and probiotics. -“We believed that bacteria in the gut would use the prebiotic to make butyrate and support intestinal growth. But we thought that might only happen in the group that received both pre- and probiotics because we didn’t know if the newborn gut would have enough bacteria to make this important short-chain fatty acid.” Actually, the neonatal piglets did have enough bacteria in their guts, and the prebiotic alone was effective in increasing intestinal function and structure, she said. “In fact, the probiotic that we used in one of the groups eliminated the beneficial effect of the prebiotic. That shows us that we need to be exceptionally careful in selecting the probiotic we use, matching it to the specific disease,” she noted. Many consumers believe all probiotics are equal, but the effect of specific bacterial strains is different, she said. “At this point, we can only recommend consumption of the FOS[U3] prebiotic alone,” she added.
    The article appears in the September 2012 issue of the Journal of Parenteral and Enteral Nutrition. Jennifer L. Barnes of the U of I and Bolette Hartmann and Jens J. Holst of the University of Copenhagen, Copenhagen, Denmark, are co-authors of the study, which was funded by grants from the National Institutes of Health.—Journal References-J. L. Barnes, B. Hartmann, J. J. Holst, K. A. Tappenden. Intestinal Adaptation Is Stimulated by Partial Enteral Nutrition Supplemented With the Prebiotic Short-Chain Fructooligosaccharide in a Neonatal Intestinal Failure Piglet Model. Journal of Parenteral and Enteral Nutrition, 2012; 36 (5): 524 DOI: 10.1177/0148607112444131-K. A. Tappenden. Probiotics Are Not a One-Species-Fits-All Proposition. Journal of Parenteral and Enteral Nutrition, 2012; 36 (5): 496 DOI: 10.1177/0148607112458407
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    Special Note as to why not to Consume grains— Amylose is the less easily digested component of Starch (only approximately 40% of dietary Amylose is digested via Amylase). Amylose that escapes digestion is known as Resistant Starch. Several factors influence the percentage of Amylose that escapes digestion— The physical structure of the Grain protects the starch from digestion (e.g. partly milled grains and pulses). The larger the Grain size, the higher the amount of Resistant Starch.
    – The natural chemical composition of the starch in foods influences the amount of resistant starch. The higher the Amylose content of Starch, the greater its resistance to digestion. Raw Potato, green Bananas, pulses and high amylose Maize starch have a high Amylose content.—When Starch is heated, Starch granules swell and are disrupted. This process, known as gelatinisation, makes the Starch much more accessible to digestive enzymes. Starch with a high Amylose content and Starch which is inaccessible due to the physical structure in which it is located, are less susceptible to gelatinisation and hence are more resistant to digestion.
    – When Starch that has been heated, is cooled, retrogradation occurs converting the Starch to a crystalline form which is resistant to digestion. Foods, such as bread, cornflakes, cold cooked potato, rice and pasta, contain retrograded starch which is resistant to digestion.
     
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    Non Medical Prescription Drug Abuse-Substance Abuse From Doctors
    Non-Medical Prescription Drug Use More Common Among Rural Teens Than City Dwellers
    ScienceDaily (Nov. 2, 2010) — Rural teens appear more likely than their urban peers to use prescription drugs for non-medical purposes, according to a report posted online that will appear in the March 2011 print issue of Archives of Pediatrics & Adolescent Medicine, one of the JAMA/Archives journals.–The non-medical use of prescription drugs is common among U.S. adolescents, with about one in eight reporting lifetime non-medical use of prescription opioids, according to background information in the article. “During adolescence, non-medical prescription drug use is particularly problematic given its association with use of other illicit drugs such as cocaine and heroin, as well as engagement in problem behaviors such as gambling, increased sexual activity and impulsivity,” the authors write. “Moreover, individuals who use prescription drugs earlier in life have a greater chance of later developing prescription drug dependence[U4] .” Previous studies have examined substance abuse among urban teens, but their conclusions may not apply to those from rural areas, the authors note. Jennifer R. Havens, Ph.D., M.P.H., of University of Kentucky College of Medicine, Lexington, and colleagues analyzed data from 17,872 12- to 17-year-olds participating in the 2008 National Survey on Drug Use and Health. Of these, 53.2 percent lived in urban areas, 51 percent were male and 59 percent were white.—There were no differences between urban and rural youth in rates of any illicit drug use, including marijuana, cocaine, heroin and hallucinogens. However, 13 percent of rural teens reported ever having used prescription drugs for non-medical purposes, compared with 10 percent of urban teens. When the researchers assessed specific medication types, they found rural teens were also more likely to have used pain relievers (11.5 percent vs. 10.3 percent) or tranquilizers (3.5 percent vs. 2.5 percent) non-medically[U5] . –After adjusting for sociodemographic factors, health status and the use of other substances, rural teens remained 26 percent more likely than urban adolescents to say they had used prescription drugs for non-medical purposes. “Data support that one reason for the higher prevalence of non-medical prescription drug use in rural areas may be the lack of availability of drugs such as heroin that are easily accessed in urban areas,” the authors write.—Rural teens were more likely to misuse prescription drugs if they reported poorer health, episodes of depression or other substance abuse. “Residing in a household with two parents was associated with a 32 percent reduction in the odds of non-medical prescription drug use,” the[U6] authors write. “These results suggest that interventions aimed at family involvement may be beneficial in preventing or reducing non-medical prescription drug use.” Enrollment in school was also a protective factor.
    “The cultural, structural and social realities of rural life can not only affect the prevalence of drug use but also exacerbate its consequences. The isolation and self-reliance of rural communities can negatively affect careseeking behavior, particularly regarding mental health and substance abuse services[U7] ,” the authors write. “While we were able to identify potential targets for intervention such as increased access to health, mental health and substance abuse treatment, this may be difficult for rural areas where such resources are in short supply or non-existent. Research into the causal mechanisms surrounding initiation of non-medical prescription drug use in rural adolescents is necessary to develop tailored interventions for this population.”–Story Source-The above story is reprinted from materials provided by JAMA and Archives Journals. —Journal Reference-Jennifer R. Havens; April M. Young; Christopher E. Havens. Nonmedical Prescription Drug Use in a Nationally Representative Sample of Adolescents: Evidence of Greater Use Among Rural Adolescents. Archives of Pediatrics & Adolescent Medicine, 2010; DOI: 10.1001/archpediatrics.2010.217
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    Research Reveals Decline in Illicit Drug Abuse- Prescription Drug Abuse On the Rise
    ScienceDaily (Oct. 15, 2012) — Research presented at the ANESTHESIOLOGY™ 2012 annual meeting showed while there has been an encouraging decline in illicit drug abuse across most major metropolitan areas in recent years, prescription drug abuse is climbing[U8] .–“Examining trends among various geographical areas, highlighting problem areas and possibly illuminating patterns that may remain otherwise hidden on a larger national level will help determine if we’ve stemmed the tide of prescription drug abuse or if a national epidemic has surfaced,” said study author Asokumar Buvanendran M.D., Rush University Medical Center and Professor, Department of Anesthesiology, Chicago.—About the Study—Emergency department drug abuse-related visits were extracted from the Drug Abuse Warning Network (DAWN) over three years (2007-09) for 11 major metropolitan areas (plus a combined “other” category of various smaller regions). Two types of drug abuse visits were examined; those associated with prescription drugs (e.g., pain medications such as OxyContin®) and those associated with illicit “street” drugs (e.g., heroin, cocaine, etc).—In 2007, the percentage of emergency department visits identifying the involvement of illicit drug abuse (36 percent) was consistently higher than prescription drug abuse (20 percent) for all metro areas except the Phoenix region. Among the metropolitan areas, rates of illicit drug abuse varied in magnitude considerably more than prescription drug abuse. Prescription drug abuse rates were more consistent across metropolitan areas but still displayed a few spikes, with higher rates in Houston (33 percent) and Phoenix (27 percent).
    Change over time from 2007-09, for illicit drug abuse, showed a consistent downward trend for all metro areas (8 percent overall), while prescription drug abuse rates over this same time period changed much less, showing a slightly increasing trend (2 percent) with some areas increasing while others decrease.–Overall, in the U.S. the percentage of visits for illicit drug abuse decreased (2007: 36 percent, 2008: 32 percent, 2009: 28 percent) while prescription drug abuse visits increased (2007: 20 percent, 2008: 21 percent, 2009: 22 percent) and the total number of “visits” were: 2007: 301,000; 2008: 352,000; and 2009: 280,000.–“The harsh reality is prescription drug abuse has become a growing problem in our society,” said Dr. Buvanendran. “We hope the results of this study will aid physicians in effectively treating patients who struggle with prescription drug abuse, as well as encourage widespread patient education about the safe use, storage and disposal of medications.”—Story Source-The above story is reprinted from materials provided by American Society of Anesthesiologists (ASA), via Newswise.
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    [U1]This is basically stating as well an over worked pancreas and liver—as a result of lack of sleep the other organs have to compensate for this excessive activity
    [U2]Dietary Carbohydrates (especially Polysaccharides) are fermented (by Beneficial Bacteria) within the Large Intestine resulting in the manufacture of Butyric Acid: references
    – Inulin may enhance the production of Butyric Acid in the Colon. references
    – Of all Carbohydrates, Starch produces the greatest concentration of Butyric Acid: references
    – The constituent of Starch that most contributes to the production of Butyric Acid is Amylose that escapes digestion (i.e. Resistant Starch). references
    Fructooligosaccharides (FOS) (by nourishing Beneficial Bacteria in the Intestines which produce Butyric Acid) may facilitate the endogenous production of Butyric Acid in the digestive tract. references
    Larch Arabinogalactan may stimulate the body’s production of Butyric Acid. references
    Psyllium may increase the production of Butyric Acid in the Intestines (especially in the Colon). This effect occurs from Beneficial Bacteria in the Intestines fermenting Psyllium. references
     
    Lipids
    Acetic Acid may enhance the ability of Butyric Acid to stimulate the absorption of Calcium and Magnesium in the Colon. references
    Beneficial Bacteria within the Large Intestine (especially the Colon) are responsible for the fermentation of dietary Carbohydrates that result in the production of Butyric Acid. references
    Aspirin may enhances the ability of Butyric Acid to prevent Colon Cancer. references
    Resveratrol may enhance the ability of Butyric Acid to prevent Colon Cancer. references
    [U3]Chicory (root) Burdock
    Vegetables: Leeks Onions
    Tomatoes Garlic
    Asparagus Jerusalem Artichoke
     
    These foods will increase FOS
    [U4]Now here’s a thought—what if in early infancy when Teachers working indirectly for the “State” tell you your offspring need a drug-ritalin—as you can see it will lead to an addictive state later on in life—or perhaps a Birth Control pill to offset pregnancy and then later on in life your taking HRT pills to regulate what was shut down
    [U5]This research is splitting hairs here –what we have is a stressed or taxed group of people –in this case Caucasians who are looking at these prescriptions to alleviate whatever they are dealing with and it would appear the access is easier to gain in the rural areas–
    [U6]In other words a specific level of security in regards not only to access but to the persons stability
    [U7]Isolation and the issues of rural living usually are not the issue it is the access —the more connected a community is the less likely of this kind of behaviour—the less attached a person is or if there is any type of rejection or osterization then this may exacerbate the abuse
    [U8]In other words No Real Decline at all –the access is now easier through Doctors
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    Show Of The Week October 29 2012
     
    GM Crops Destroyed by US Drought but non-GM Varieties Flourish
    Contents of chemtrails jets have changed, it is now include plutonium
    6-shogaol-rich extract from ginger up-regulates the antioxidant defense
    Effect of dietary polyphenols on K562 leukemia cells- a Foodomics approach-Rosemary
    50 Reasons to Oppose Fluoridation
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    GM Crops Destroyed by US Drought but non-GM Varieties Flourish

    Non-GM varieties are more drought resistant, yet agritech giants ensure farmers are unable to access them. Dr Eva Sirinathsinghji—-The United States is suffering the worst drought in 50 years. But crop damage may well have been avoided if high quality non-GM varieties were available to farmers. Further evidence is emerging that glyphosate-tolerant crops are ill- equipped to deal with drought, while high quality non-GM varieties are flourishing. Monopoly of the seed industry has left farmers unable to get non-GM varieties, despite the drought having global repercussions including steep rises of cereal prices and reduced meat production in many countries. In a commentary circulated by GM Watch (UK), Howard Vlieger, a co-founder and agroecological farming advisor of Verity Farms in drought-stricken South Dakota the US, provides evidence from a farmer who has grown both GM and Verity Farms’ non-GM varieties of soybean and corn side by side [1]. Non-GM soybean, grown in agroecological conditions to promote soil biodiversity and nutritional content is shown next to Monsanto’s GM triple-stack GM corn, which is glyphosate- tolerant and additionally expresses two Bt insecticidal toxins, grown using conventional chemical industrial methods that include the use of Monsanto’s glyphosate-based herbicide, Roundup (Figure 1). As captured in the photograph, non-GM varieties appear greener, fuller, and healthier. These impressions are backed up by the far superior yield reported of non-GM corn, which averaged 100- 120 bushels per acre (BPA) compared to the 8-12 BPA to 30-50 BPA of GM corn. -The large yield differential was confirmed in a new set of harvest data provided by Vlieger (with accompanying photographic identification) for three fields surrounding Verity Farm, all growing Smart Stack RR corn [2]. All were harvested for corn silage as the yields were too poor to harvest the grain. The federal crop insurance adjuster appraised yields were respectively 12 bushels per acre (BPA), 27 BPA, and 28 BPA. The Non-GMO corn on Verity Farm across the road yielded 108 BPA.—The findings were replicated with soybean crops
    GM and non-GM soybean crops
    Previous studies found glyphosate tolerant crops require more water– Triple Stack RR corn may be especially drought intolerant, but the new evidence
    from the farm is consistent with previous laboratory findings that glyphosate- treated crops are less water efficient than untreated crops. One such study was performed in Brazil when farmers reported “injured-looking” glyphosate-tolerant soybean crops. The team, led by Luis Zobiole from State University of Maringá found that GM glyphosate-tolerant (GT) soybeans absorbed less water, which resulted in reduced water efficiency [3]. The volume of water that non-treated GT soybean plants required to produce 1 g of dry biomass was 204 % and 152 % less than required when the plant is exposed to 2 400 grams acid equivalent (a.e) of glyphosate per hectare, in single or sequential applications
    respectively. GT soybean plants receiving a single application of the currently
    recommended rates of glyphosate (600–1200 grams a.e per hectare) needed 13–20% more water to produce the same amount of dry biomass than non-glyphosate treated plants. A previous publication by the same lab showed GT soybeans to have reduced lignin content and photosynthesis rates, both possible mechanisms for the reduced water efficiency [4]. Lignin is an essential component of plant cell walls, and contributes to the compression strength of stems and to the efficient transport of water and solutes over long distances within the vascular system. Water deficiency is not the only physiological effect that glyphosate imposes on crops. It has been shown to reduce nutrient availability and immune responses and thus defence against plant diseases (see [5] Glyphosate Tolerant Crops Bring Death and Disease, SiS 47). At least 40 diseases are known to be increased in weed control programmes with glyphosate and the list is growing, affecting a wide range of species: apples, bananas, barley, bean, canola, citrus, cotton, grape, melon, soybean, sugar beet, sugarcane, tomato and wheat [6]. Monopolisation of the seed industry
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    Contents of chemtrails jets have changed, it is now incl. plutonium
    am hearing from all kind of friends who live in various parts of Europe that the contents from the Chemtrails what they used to spray on us has changed recently.
    Some of my friends who have a Geiger counter are measuring INCREDIBLE high radiation quickly after those chemtrail planes flew over. This has never happened before that they measured radiation coming from the chemtrail jets a few minutes after they passed !! I have friends in FRANCE, UK, NETHERLANDS, GERMANY, SWITZERLAND. And they all measure these readings !!! This means that the globalist are misusing the situation from Japan and started to bombard the whole world with PLUTONIUM and[U1] such…. NOT BROUGHT BY THE WIND, BUT BY PLANES !!!!! Look at California I mean I just cannot believe that the Wind took this super high concentration of Radiation to this place. Also what I heard in the Netherlands, the radiation in the air is going sky high a few minutes after those chemtrail planes just did their spraying . So high that is almost comparable to measurements close to the area of Fukushima !!
    IT IS NOT THE RADIATION COMING FROM JAPAN THAT IS INFECTING THE WORLD, IT IS THE RADIATION WHAT THEY ARE NOWADAYS DAILY LITERALLY SPRAYING ABOVE OUR HEADS. JUST LIKE WHAT THEY DID TO THE JEWS IN THE CAMPS !!! REMEMBER THOSE SHOWERS !!!!!!!!!
    California:
    http://blog.alexanderhiggins.com/2011/04/01/breaking-radiation-san-francisco-18100-drinking-water-limits-13014/
    People who I see walking on the streets in my neighborhood are coughing like crazy over here (area in FRANCE)
    Yesterday I helped an old woman to get up, she just dropped on the street, she forgot to take her rollator she told me. While she just had in her hand for god sake, it was laying next to her !!! But she did not realize it……
    http://www.tennessean.com/article/20110316/NEWS08/110316027/1969/NEWS/Group-warns-EPA-ready-increase-radioactive-release-guidelines-?odyssey=nav|head
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    6-shogaol-rich extract from ginger up-regulates the antioxidant defense systems in cells and mice.
    Molecules. 2012;17(7):8037-55 Authors: Bak MJ, Ok S, Jun M, Jeong WS
    Abstract—The rhizome of ginger (Zingiber officinale Roscoe) is known to have several bioactive compounds including gingerols and shogaols which possess beneficial health properties such as anti-inflammatory and chemopreventive effects. Based on recent observations that 6-shogaol may have more potent bioactivity than 6-gingerol, we obtained a 6-shogaol-rich extract from ginger and examined its effects on the nuclear factor E2-related factor2 (Nrf2)/antioxidant response element (ARE) pathway in vitro and in vivo. 6-Shogaol[U2] -rich extract was produced by extracting ginger powder with 95% ethanol at 80 °C after drying at 80 °C (GEE8080). GEE8080 contained over 6-fold more 6-shogaol compared to the room temperature extract (GEE80RT). In HepG2 cells, GEE8080 displayed much stronger inductions of ARE-reporter gene activity and Nrf2 expression than GEE80RT. GEE8080 stimulated phosphorylations of mitogen-activated protein kinases (MAPKs) such as ERK, JNK, and p38. Moreover, the GEE8080-induced expressions of Nrf2 and HO-1 were attenuated by treatments of SB202190 (a p38 specific inhibitor) and LY294002 (an Akt specific inhibitor). In a mouse model, the GEE8080 decreased the diethylnitrosamine (DEN)-mediated elevations of serum aspartate transaminase and alanine transaminase as well as the DEN-induced hepatic lipid peroxidation. Inductions of Nrf2 and HO-1 by GEE8080 were also confirmed in the mice. In addition, the administration of GEE8080 to the mice also restored the DEN-reduced activity and protein expression of hepatic antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and catalase. In conclusion, GEE8080, a 6-shogaol-rich ginger extract, may enhance antioxidant defense mechanism through the induction of Nrf2 and HO-1 regulated by p38 MAPK and PI3k/Akt pathway in vitro and in vivo.—PMID: 22763741 [PubMed – indexed for MEDLINE]—
    Recipe for ginger antioxidant -shogoal—either dehydrate ginger or buy the powder and add it to a alcohol base—if in the USA use ever clear—In Canada depending where you live utilize the polish version of everclear orr get a home made grappa—or buy a 90 proof if you can locate ( Canada has differering laws from province to province unfortunately in Ontario the gov’t still feels the need to control the dose of alcohol and access)—what you would do is take this and extract it in the alcohol medium by utilizing a mason jar and the bottom of a blender attachment—seal the jar with a tape and then place the powder and alcohol inside and then twist the bottom of the jar and seal it and proceed to blend this at medium to high speed—for 10-15 minutes then stop the blender and strain off the powder ginger—be careful this will be hot—this will give you this in it’s antioxidant levels at the rate they are explaining—if you cannot access the high alcohol then use the 40 or 50 proof it will still work but maybe 3 times stronger rather then 6 times
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    Effect of dietary polyphenols on K562 leukemia cells- a Foodomics approach-Rosemary
    Electrophoresis. 2012 Aug;33(15):2314-27
    Authors: Valdés A, Simó C, Ibáñez C, Rocamora-Reverte L, Ferragut JA, García-Cañas V, Cifuentes A
    Abstract– this work, a global Foodomics strategy has been applied to study the antiproliferative effect of dietary polyphenols from rosemary on two human leukemia lines, one showing a drug-sensitive phenotype (K562), and another exhibiting a drug-resistant phenotype (K562/R). To this aim, whole-transcriptome microarray together with an MS-based nontargeted analytical approach (via CE-TOF MS and UPLC-TOF MS) have been employed to carry out transcriptomics and metabolomics analyses, respectively. Functional enrichment analysis was done using ingenuity pathway analysis (IPA) software as a previous step for a reliable interpretation of transcriptomic and metabolomic profiles. Rosemary polyphenols altered the expression of approximately 1% of the genes covered by the whole transcriptome microarray in both leukemia cell lines. Overall, differences in the transcriptional induction of a number of genes encoding phase II detoxifying and antioxidant genes, as well as differences in the metabolic profiles observed in the two leukemia cell lines suggest that rosemary polyphenols may exert a differential chemopreventive effect in leukemia cells with different phenotypes. IPA predictions on transcription factor analysis highlighted inhibition of Myc transcription factor function by rosemary polyphenols, which may explain the observed antiproliferative effect of rosemary extract in the leukemia cells. Metabolomics analysis suggested that rosemary polyphenols affected differently the intracellular levels of some metabolites in two leukemia cell sublines. Integration of data obtained from transcriptomics and metabolomics platforms was attempted by overlaying datasets on canonical (defined) metabolic pathways using IPA software. This strategy enabled the identification of several differentially expressed genes in the metabolic pathways modulated by rosemary polyphenols providing more evidences on the effect of these compounds.—PMID: 22887152 [PubMed – indexed for MEDLINE]
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    [U1]I stated about a year ago that the chemtrails maybe different in different areas—it would appear I am right and with the newest dumping on the planet it will be used to heat and cause environmental imbalances we are see today
    [U2]Shogaol is a antioxidant that comes from the dehydrated part of the ginger—gingerol comes from the fresh part this can be made with both but in this case they are explaining how to make this with the dry form

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