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What is the Natural Health Products Directorate (NHPD)? –
The NHPR (Natural Health Products Regulations) came into full effect in January 2010. It is federal legislation through which Health Canada would legislate the sale of natural health products as it does “drugs” through the Food and Drug Act and the Food and Drugs Regulation. With the classification as drugs, the intent is to have all natural products develop a body of evidence based on science. The fact that natural ingredients can not be patented poses a dilemma for manufacturers. Natural ingredients can be isolated and purified and even chemically altered, but does this change the properties? Are they still natural? —For the quarterly reporting periods (2008/2009 and the first three quarters of 2009/2010) which represents 37.9% of the product licensing applications received since the start of the NHPR in 2004, a total of 19,402 applications have been processed of which 11,195 were licensed, 2,493 were withdrawn and 5,714 were refused. (Source: Clash of the Regulatory Bodies by Andrew Waldie, Integrated health Practitioner, Special Report, Vol 10-2) This represents just a small fraction of natural products on the market. These are products already currently on the shelves, and does not count products in development. Already, many suppliers have stopped shipping to Canada and many small companies who cannot afford to comply are waiting in anticipation of what will happen.
 
Health Canada has far-reaching powers and in protecting the public interest can enter any private or business property and enforce the Act. Since 2004, there has been a growing backlog of applications and the CHFA (Canadian Health Food Association) has described the backlog as alarming. Bill C-36 will further enhance the ability of Health Canada to enforce their powers.—In January 2010, NAPRA, the National Association of Pharmacy Regulatory Authorities, of which the College of Pharmacists of BC is a member, issued a position statement advising pharmacies to stop selling any products that do not have a DIN ( Drug Identification Number), an NPN ( Natural Product Number) or a DIN-HM (Homeopathic Medicine DIN). This has been adopted by some provincial College of Pharmacists and is now being implemented through the removal of products at the retail level.
 
Where does Marigold fit in?
 
Marigold does not fit in neatly into any category. Although we are a full service pharmacy with prescription services, we are very different from a traditional drugstore. Our expertise is in natural medicine, but we also understand the language and complexity of pharmaceutical drugs. Since we are not a health food store, Health Canada sees us as falling under the auspices of the College of Pharmacists. –Marigold Compounding and Natural Pharmacy creates its own line of chemical- free products. In our formulations, we consciously and carefully select natural ingredients and avoid toxic chemicals. As much as possible, we try to stay close to the natural state of the medicine. We avoid using parabens, petroleum distillates, artificial colours, triethanolamine, magnesium stearate, butylated hydroxyanisole, butylated hydroxytoluene, PABA, sodium lauryl sulfate, artificial flavours and clay fillers. We formulate our capsules using alfalfa as the filler, rather than lactose or magnesium stearate.—Authorities from Health Canada have advised us in the past that as a compounding pharmacy, we have the ability to prepare products without an NPN registration as long as it fulfills the following criteria:
 
1. It is prepared in a proper laboratory with good manufacturing processes.
2. It is delivered directly to the end-user, the patient.
3. There exists a professional relationship between a health practitioner and the patient.
 
Our ability to deliver professional advice is unparalleled in the industry. We have the following ten accredited practitioners on our staff:
 
Janette Cormier, AA, RH, R.Ac. Registered Herbalist, Registered Acupuncturist
 
Michel Duhaime, R.Ac,, DTCM Registered Acupuncturist, Transformation Acupuncture, EFT
 
Raje Harwood Registered Reflexologist, Auricular Therapy
 
Dr. Erika Kneeland, B.Sc., ND Naturopathic Physician with a specialty in obstetrics, pediatrics and women’s health
 
Dr. Lise Maltais, FCAH, ND Naturopathic Physician, Registered Homeopathic Physician, Bowen Practitioner
 
Charlese Nan, RMT Registered Massage Therapist, Injury Specialist
 
Kira Neumann, RNCP Registered Holistic Nutritionist, Nutrition Consultant
 
Sharon Niscak, M.Sc., RH Registered Herbalist
 
Carol Smith, BA Reiki Master
 
Rudy Sanchez, B.Sc. Pharm. Consulting Pharmacist, Formulator
 
Raid by Health Canada and the College of Pharmacists:
 
On June 14, 2010, the store was inspected by four inspectors from Health Canada, two inspectors from the College of Pharmacists, accompanied by two RCMP officers. Products that did not contain NPN’s were removed from the shelves and taken away. —The store was closed and has been closed since, as we comply with the requirements set out by the College and Health Canada. —Here are some of the products that were removed from the shelves:
 
All Natural Sunscreens containing zinc oxide in various concentrations
Buttspackle containing calendula, peru balsam and zinc oxide
Arthrotopik Cream for inflammation, containing devil’s claw, calendula and arnica
Jocamu Ointment containing arnica and Rhus tox
Wild Oregano Oil, pure oil
Arnica Ointment 10%
Shatavari Ayurvedic Powder
Oil of Lavender pure essential oil
Grapefruit Seed Extract, pure
Colloidal Silver
Goldenseal Powder in Manuka 16+ Medicinal Honey
Health Canada has seized inventory which does not bear NPN’s. Part of this inventory are products that we make based on our own formulas. Part of this inventory is from suppliers who have not complied with NPN regulations. The store is closed by the College of Pharmacists of BC pending compliance with regulations.
 
These are the steps that are being done at this time:
1. Institution of individualized professional practitioner consultations prior to sale of products without NPN. This will require that we record patient name, date of purchase and practitioner information, This will allow us to sell these products and continue preparing them if needed.
2. Installation of a service counter to remove public access to Marigold Products.
3. Initiation of the procedure to register a site license for Marigold and allow us eventually to file for NPN’s for our products.
4. Meeting the compliance issues set out by the College of Pharmacists of BC
regarding labeling, compounding registers, etc.
 
We are using this opportunity to input our inventory into a POS system and make these improvements to allow us to continue serving your health needs.
 
Marigold is a very unique and progressive pharmacy that happens to be right here in Courtenay. We appreciate your support during this period and ask you to participate as much as you can in the protection of natural health not just for this store, but for all natural health retailers and practitioners. —1. For more information about Health Canada regulations regarding the requirement of NPN’s, please go to the website for NHPPA (Natural Health Products Protection Association) and watch some of the videos of Shawn Buckley, constitutional lawyer and advocate for protection of natural health products. nhppa.org
2. Visit the site of CHFA (Canadian Health Food Association) and click on regulations to get information of the NHPD. chfa.ca
 
3. If you want to write a letter of support for Marigold, (especially if you have had a chance to use our services and have a story you want to share about outcomes), please send emails to:
[email protected]
 
4. All media enquiries are directed to :
250 338 9623 or [email protected]
 
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TOP H
[U1]The concept her eis that something would be disrupting the gut flora—with child obesity it would be something that they would be definiting eating such as a genetically modifief grown food or even soy—chemicals and artificial food additives and plastics would also contribute to the diminishing of the flora as well as alcohol from starches that may not be digestible or be broken down
[U2]Remember one year in dog years is 7 so that would equate to almost 14 years!!!
[U3]Not sure I would call this a bad thing for some of us getting Older
 
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Show of the Week July 26 2010
Astragulus—1 2 3
 
Conjugated Linoleic Acid
CLA may ease airways for asthmatics—Recipe CLA
Creatine at low doses promotes resistance to fatigue
Creatine—what it can do
 
How to take Creatine
 
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1-Chinese medicinal herb Radix Astragali suppresses cardiac contractile dysfunction and inflammation in a rat model of autoimmune myocarditis.
Toxicol Lett. 2008 Nov 10;182(1-3):29-35–Authors: Zhao P, Su G, Xiao X, Hao E, Zhu X, Ren J
Radix Astragali, a Chinese medicinal herb, consists of polysaccharides and flavonoids as its main active ingredients. It has been widely used for treatment of cardiovascular diseases such as heart failure, angina pectoris, myocardial infarction and stroke in Asian countries. This study was designed to evaluate the effect of Radix Astragali on myocardial dysfunction, cardiac remodeling and morphological alteration in an experimental model of autoimmune myocarditis, a clinical condition often resulting in dilated cardiomyopathy. Experimental autoimmune myocarditis was established with a subcutaneous injection of porcine cardiac myosin into rear footpad in Lewis rats. Radix Astragali treatment was delivered via an intravenous injection (0.2 ml/100g body weight, daily) for 3 weeks. Results from transthoracic echocardiography indicated that experimental autoimmune myocarditis led to impaired myocardial contractile function which was reconciled by Radix Astragali. The experimental autoimmune myocarditis triggered profound inflammation and fibrosis in myocardium as assessed by hematoxylin and eosin (H and E) and Masson’s trichrome staining. Interestingly, Radix Astragali significantly attenuated autoimmune myocarditis-induced myocardial inflammation and fibrosis. Similarly, Radix Astragali treatment alleviated autoimmune myocarditis-triggered overt lymphocyte proliferation. Furthermore, Radix Astragali significantly attenuated elevated levels of the Th1 cytokines (IFN-gamma and IL-2), and increased the Th2 cytokines (IL-4 and IL-10) in autoimmune myocarditis. Collectively, our data revealed that Radix Astragali effectively protected against cardiac functional and morphological aberrations in experimental autoimmune myocarditis.—-PMID: 18782607 [PubMed – indexed for MEDLINE]
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2-Novel herbal flavonoids promote apoptosis but differentially induce cell cycle arrest in human colon cancer cell.
Invest New Drugs. 2009 Jan 13;–Authors: Auyeung KK, Ko JK
Formononetin is a novel herbal isoflavonoid isolated from Astragalus membranaceus, a medicinal plant that possesses antitumorigenic property. We attempted to compare the anticarcinogenic mechanism of formononetin with that of the known proapoptotic flavonoid isoliquiritigenin (ISL) in human cancer cells. We first evaluated the effects of formononetin and ISL on HCT 116 colon cancer cell viability. Immunofluorescence staining was then performed to observe the morphological changes of cancer cells undergoing apoptosis, which had been substantiated using Annexin V-FITC/propidium iodide staining. Western immunoblotting and flow cytometry were also employed to study parameters associated with apoptosis and cell proliferation. Our data show that formononetin and ISL both inhibited the growth of colon cancer cells and promoted apoptosis. These processes were accompanied by caspase activation and downregulation of the antiapoptotic proteins Bcl-2 and Bcl-x(L). Besides, the novel proapoptotic protein NSAID-activated gene (NAG-1) and its upstream regulator were overexpressed in drug-treated cells. Nevertheless, only ISL was found to induce a G2 arrest. These findings exemplify that both formononetin and ISL could cause growth inhibition and facilitate apoptosis in colon cancer cells, while only ISL is capable of inducing phase-specific cell cycle arrest. This suggests that the anticarcinogenic activities of different herbal flavonoids may involve both common and differential mechanisms of action, which could be developed as potential anticancer drugs.PMID: 19139819 [PubMed – as supplied by publisher
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3-Astragalus polysaccharides inhibited diabetic cardiomyopathy in hamsters depending on suppression of heart chymase activation.
J Diabetes Complications. 2010 May-Jun;24(3):199-208–Authors: Chen W, Li YM, Yu MH
Diabetic cardiomyopathy is associated with high morbidity and mortality of heart failure. Overactivation of the local chymase-Ang II system plays a dominant role in diabetic cardiomyopathy. Astragalus polysaccharide (APS) is used in traditional Chinese medicine to boost immunity. To study the effect of APS on local system of chymase-Ang II in diabetic cardiomyopathy, we investigated APS/normal saline (NS)-administrated streptozotocin-induced diabetic hamsters. After APS/NS administration at a dose of 1 g/kg per day for 10 weeks, hemodynamic parameters, levels of insulin (INS), C-peptide (C-P), glycosylated serum protein (GSP), lipoproteins, myocardial enzymes, and Ang II (plasma and myocardial) were tested; myocardial collagen (type I and III), myocardial ultrastructure, and activities of matrix metalloproteinase (MMPs) were measured; activities and expression of cardiac chymase and ACE were detected by using quantitative real-time RT-PCR and RIA; protein expression of cardiac phosphoric extracellular signal-regulated kinase 1/2 (p-ERK1/2) was measured by Western blot. AP-administrated diabetic hamsters had lower levels of GSP, lipoproteins, myocardial enzymes, myocardial Ang II, expression of collagen I and I/ III, activities of pro-MMP-2 and MMP-2, activities and expression of chymase, and expression of p-ERK1/2 than NS-administrated diabetic hamsters and could better protect the myocardial ultrastructure. There was no difference in hemodynamic parameters between two groups. These results indicate that APS could inhibit diabetic cardiomyopathy in hamsters depending on the suppression of the local cardiac chymase-Ang II system.—PMID: 19230716 [PubMed – indexed for MEDLINE]
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Conjugated Linoleic Acid
 
– An Update
Denver Office Chicago Office Washington D.C. Office
P.O. Box 3469 444 North Michigan Avenue 1301 Pennsylvania Avenue, N.W.
Englewood, CO 80155 Chicago, Illinois 60611 Suite #300
(303) 694-0305 (312) 467-5520 Washington, DC 20004
(202) 347-0228 11-424 1995.0
Conjugated linoleic acid (CLA), a natural derivative of the fatty acid linoleic acid, has received increasing attention in recent years. Starting with anticarcinogenic effects, the potential benefits of this unique fatty acid have extended to antiatherogenic properties, anti-diabetic properties, enhanced immune response and positive effects on energy partitioning and growth.–These effects have been documented in numerous reviews (1-4) as well as in extensive scientific literature that has grown exponentially since the late 1980’s (5). As a naturally occurring compound in foods from–ruminant animal sources, CLA’s anticarcinogenic properties are unique. Of the vast number of naturally occurring substances, demonstrated to have anti-carcinogenic activity, all but a very few are of plant origin (1).
 
Chemistry/Structure
CLA is a collective term used to describe a mixture of positional and geometric isomers/forms of linoleic acid. Linoleic acid is an 18-carbon unsaturated fatty acid with two double bonds in positions 9 and 12, both
in the “cis” (on same side) configuration. Thus, the “chemical name” of linoleic acid is cis-9, cis-12-octadecadienoic acid. In contrast, the two double bonds in CLA are primarily in positions 9 and 11, and 10 and 12 along the carbon chain with the designation of a conjugated-diene. In addition to these “positional” changes of the double bonds, there can also be geometric changes (cis(c) or trans(t) [on opposite sides] configuration). Thus, at least eight different CLA isomers of linoleic–acid have been identified. Of these isomers, the c9, t11 form is believed to be the most common natural form of CLA, with biological activity. However, in recent years, biological activity has been proposed for–other forms, especially the t10, c12 isomer. Although not widely accepted, the name “rumenic acid” has been proposed as a “common name” for the major CLA isomer found in natural products (6). For a comparison of these CLA isomer “forms” with linoleic acid. Additional potentially active isomers are also being identified and studied (2,7). Figure 1. Chemical Structures of Linoleic Acid and Two Isomers of Conjugated Linoleic Acid (CLA). * Linoleic acid (c-9, c-12) Conjugated linoleic acid Conjugated linoleic acid octadecadienoic acid c-9, t-11 isomer t-10, c-12 isomer [U1]* Adapted from: Steinhart, C. Conjugated Linoleic Acid The Good News about Animal Fat. J.Chem.Educ. 73:A302; 1996. 2 Table 1. Representative/Relative Concentrations of CLA in Uncooked Foods [adapted from Chin et al. (12)].
Total CLA c9, tll-isomer
Food (mg/g fat) (%)
Meat
Fresh ground beef 4.3 85
Beef round 2.9 79
Beef frank 3.3 83
Beef smoked sausage 3.8 84
Veal 2.7 84
Lamb 5.6 92
Pork 0.6 82
Poultry
Chicken 0.9 84
Fresh ground turkey 2.5 76
Seafood
Salmon 0.3 n.d.*
Lake trout 0.5 n.d.
Shrimp 0.6 n.d.
Dairy Products
Homogenized milk 5.5 92
Butter 4.7 88
Sour cream 4.6 90
Plain yogurt 4.8 84
Ice cream 3.6 86
Sharp cheddar cheese 3.6 93
Mozzarella cheese 4.9 95
Colby cheese 6.1 92
Cottage cheese 4.5 83
Reduced fat swiss 6.7 90
Am. Processed cheese 5.0 93
Cheez whizTM 5.0 92
Vegetable Oils
Safflower 0.7 44
Sunflower 0.4 38
Canola 0.5 44
Corn 0.2 39
* n.d. => not detectable
History/Identification/Sources
CLA is a naturally occurring fatty acid found in food products from ruminants (cattle and sheep). Although identified much earlier, increased interest in CLA occurred when it was isolated and identified by Pariza
and coworkers as an anticarcinogenic substance from grilled ground beef (8-10). It was also found to be present in a variety of dairy products (11).–The total CLA content in foods may vary widely. Representative and relative concentrations of CLA in a variety of foods are summarized in Table 1. CLA concentrations are highest in foods from ruminants (including beef, lamb and dairy products). Seafoods, pork, most poultry products and vegetable oils are not notable sources of CLA (12). CLA has been found in triglycerides, lipoproteins and cell membrane phospholipids in various tissues of rodents, rabbits and humans (2). As a normal isomerization product of linoleic acid metabolism by rumen bacteria, CLA is synthesized from free linoleic acid through biohydrogenation pathways and enzymatic isomerization. Early studies suggested that CLA content could be increased in foods that are heat processed (dairy pasteurization, pan frying of meats, etc.) (11). However, later studies (13) suggest that CLA is not increased by cooking, but rather with water loss, CLA remains constant on a per gram of fat basis. Additionally, CLA is stable and not destroyed by cooking or storage. Foods from ruminant sources (beef and dairy) generally have CLA levels in the range of 3-7 mg/g fat; although, recent studies have shown it may be possible to increase these “naturally” occurring levels (4,14-16). Multisite Anticarcinogen – Cell and Animal Studies Following the initial identification of CLA as a modulator of mutagenensis and carcinogenesis, research interest accelerated. Additional studies confirmed this anticarcinogen effect in a variety of tissues, especially skin and forestomach. Continuing work with a wide variety of cell cultures and cancer cell lines (including malignant melanoma, colorectal cancer, breast/mammary cancer, lung adenocarcinoma, prostate cancer, leukemia, ovarian and liver cancers) have demonstrated inhibition by CLA (3,17-20). In contrast, linoleic acid did not inhibit the growth of any cell line and in some cases stimulated tumor growth and metastasis (18,21). Perhaps the most significant early anticarcinogenic effects of CLA were described by Ip and co-workers (22,23) where CLA prevented mammary cancer in rodents given CLA in the diet, prior to administration of a carcinogen. This contrasted with earlier studies that used acute dosing by direct contact, gavage, or via cell culture additions. These dietary studies found a dose-dependent protection at levels of 1% CLA and below, but no further beneficial effect was evident at levels above 1%. In studies with dietary CLA at 0.05, 0.1, 0.25 and 0.5%, as little as 0.1% CLA was sufficient to cause a significant reduction in mammary tumors. This confirmed CLA as a powerful anticarcinogen, which could be administered safely via the diet to achieve cancer protection, in an animal model. To put in perspective, the effect of CLA (an animal fat) in cancer prevention is specific and is more powerful than for any other fatty acid in modulating tumor development (1). For instance, unlike linoleic acid (a 3 close relative of CLA) which sometimes stimulates carcinogenesis (21), CLA is inhibitory. Also, the n-3 fatty acids of fish oil, which generally are responsible for tumor suppression, require in excess of 10% in the diet to elicit the same tumor suppression responses. In contrast, CLA at levels as low as 0.1% in the diet produce a significant reduction in mammary tumor yield in animal studies. Further work by Ip and co-workers has shown that the timing of CLA feeding can be critical. For instance, when CLA is given during the time the mammary tissue is actively developing, you see a lasting protective effect. If CLA is given after carcinogen administration, a continual supply of CLA is needed for a preventive effect. CLA appears to have a major impact on the mammary gland, making the tissue less susceptible to tumor formation (4,23,24). Work continues to determine the exact mechanism by which CLA may effect carcinogen metabolism, activation or detoxification (2,3,25). Studies with mice given CLA, prior to administration of the heterocyclic amine IQ, have shown varying reductions in IQ-DNA adducts in the liver, lung, large and small intestine, kidneys and colon (26,27). CLA at levels equivalent to 0.5% of the diet, exerted inhibitory effects on the process of colon carcinogenesis (27). Other Beneficial Effects of CLA Antiatherogenic and
 
Hypocholesterolemic
Based on the possibility that CLA would exhibit antioxidant activity, both in vivo and in vitro (22,28), studies were initiated to examine the effect of CLA on experimental atherogenesis in rabbits (29). When CLA, was
added at 0.5% to an atherogenic diet, for 12 weeks, the aortas of the CLA fed rabbits exhibited less atherosclerosis. Also, LDL (low-density lipoprotein) cholesterol and triglycerides (TG) were lower in the CLA fed group (29). This observation was later supported by studies in hamsters
where CLA feeding resulted in lower plasma total and LDL cholesterol and TG levels (30). The CLA fed animals also had less aortic streak formation.
 
Fat Partitioning and Metabolism
One of the most interesting effects of CLA appears to be its influence on body fat levels and the proportion of lean to fat, especially in young growing animals. CLA induces a relative decrease in body fat levels and an increase in lean muscle. This observation has been noted in several studies with mice, rats, chicks and pigs (4,31-33). In a study with growing pigs, the results were quite dramatic. Backfat thickness was reduced up to 27% in CLA fed pigs and there was a 6.8% increase in percent lean (33). Such results have generated considerable interest as to whether humans will experience similar fat reductions and increases in proportion of muscle mass if CLA is consumed in the diet. Studies in humans are currently underway (4). Effects on Immune Response and Bone Formation The effects of CLA on fat partitioning may be at least partially the result of modulation of the immune system. Ordinarily, stimulation of the immune system produces cytokines (proteins released by a cell, upon contact with an antigen, acts as a mediator) which can cause breakdown of muscle cells. CLA can modulate (decrease) the production of cytokines and thus prevent muscle degradation. Experiments in chicks, rats, and mice show that CLA increases feed efficiency and counteracts immune-induced cachexia or malnutrition–(4,31,34). Through this effect on cytokines, CLA may also have positive effects on bone health (4,35,36). Diets rich in fats containing CLA, compared to soybean oil, caused a greater rate of bone formation (4).
 
 
Anti-diabetic Effects
CLA has been found to help normalize or reduce blood glucose levels and possibly prevent diabetes (37). Using a laboratory animal model for diabetes, CLA was found to prevent the onset of diabetes. CLA appears to
work as well as a new class of diabetes-fighting drugs (thiazolidinediones) and may provide the added advantage of weight reduction, as drug treatments often result in weight gain. These initial findings with diabetic
rats are very encouraging and are the basis for continuing studies in human diabetics.
Other Human Studies – Epidemiology/ BREAST MILK IN WOMEN
Epidemiological studies support the hypothesis that there is some factor in whole milk that exerts a protective effect against breast cancer and coronary heart disease (4,38,39). Lower incidences of these diseases were
related to greater consumption of whole milk but not to intakes of low fat milk. The presence of CLA in milkfat may be a protective factor. In a recent report the incidence of breast cancer was significantly lower in women with higher breast tissue levels of CLA (40). It is clear that the CLA content of blood serum and breast milk can be modified by diet (41-43). In earlier studies in Australia, it had been found that breast milk from women of the Hare Krishna religious sect contained twice as much CLA as milk from Australian mothers on conventional diets (11.2 vs. 5.8 mg/g) (44). This 4 was attributed to the large amount of butter and ghee -(a clarified butter) consumed by the Hare Krishna. Park and coworkers (43) have also confirmed that CLA levels in human milk can be enhanced by increasing the CLA content of the maternal diet. Effective Intake/Dose Levels For any compound that produces the dramatic effects noted for CLA, an immediate question concerns the minimally effective dose level. Does it vary for different health and disease conditions, tissue sites and response levels? Is a “chronic” dose level required, or can an “acute” dose be effective and if so, when should it be consumed? Are food sources adequate or are supplemental sources required? If only some of the isomers of CLA are biologically effective, which ones are they? If so, dose levels of CLA should be “corrected” for the active isomer. Whether from food sources or supplements, any comparisons of effects should be sure to equate levels of the active isomer. These are just some of the many questions about CLA which require further research. Usual Dietary Intakes Current measures of usual or actual dietary intakes of CLA are very limited, most being only estimates. A listing of published reports based on estimates and data analysis is presented in Table 2. (10,45-49).–A variety of factors can influence estimates of CLA intake. Food composition and frequency of intake of particular foods affect dietary intake of any food component. For CLA, there may be the added variable of level of the biologically active form/isomer of CLA consumed. Also, men usually consume more meat than women do; dairy foods generally provide a higher percentage of dietary CLA than beef; and individuals may be beef or dairy users or non-users. In addition, intake estimates may be based on assumptions of dietary proportions, such as in the German studies of meat/meat products (40/60) and pork/beef (80/20) (47). In another study (48), available data on CLA content of foods has been applied to consumption data from the USDA CSFII 94-96 (Continuing Survey of Food Intake of Individuals). Based on intake data from this large dataset it is estimated that approximately 36% of total CLA intake is from beef and approximately 52% from dairy products. Dietary Beef as a Source Can a reasonable diet, containing beef, provide beneficial levels of CLA, considering that the minimal effective dose response is still unknown? At present, the answer would be “probably”, but more studies are needed to determine minimally effective levels of CLA. Animal studies have shown benefits at dietary levels as—low as 0.1-0.5%. Also, the potential for CLA enhanced, (but still “natural”), dietary sources of beef and dairy products is just now being explored (4). It has been shown that a number of dietary components for cattle can increase CLA levels in milk and beef. These include: plants consumed in pasture, forage in feeds, and unsaturated plant oils (with sunflower oil resulting in the most CLA). CLA concentrations in milk have been increased up to four fold by various dietary manipulations (4,14). Increases in the CLA content of beef tissue–is currently being explored, with preliminary indications that elevations in CLA content are possible via feeding practices (16). Table 2. Estimates of CLA Intake in Humans. Reference Population Studied Males Females All mg/day 10 Not specified — — “several hundred mg/day” 45 Australian (not specified) — 500-1500 46 German men 310
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CLA may ease airways for asthmatics
Daily supplements of CLA (conjugated linoleic acids) may improve the airway hyper-reactivity in asthmatics, suggests a new study.
A daily dose of 4.5 grams of CLA produced significant reduction in airway hyper-responsiveness as well as favorable effects on body weight and adipokine levels – cytokines produced in fat tissue – according to findings published in this month’s journal Clinical & Experimental Allergy. —CLA (conjugated linoleic acid) is a fatty acid naturally present in ruminant meat and dairy products. Due to changes in the Western diet, average intake of CLA has fallen[U2]; if the fat is removed from a dairy product to make a low fat version that will be acceptable to consumers, CLA is removed along with it. —The researchers used Cognis’ Tonalin branded CLA, and the study was funded by Cognis. The CLA oil used is a mixture of isomers: cis-9, trans-11 (36.4 percent) and trans-10, cis-12 (37.0 percent). —A significant body of science supports the potential of the ingredient to enhance lean body mass and aid in body sculpting. The new study, by scientists from the University of British Columbia in Vancouver, is the first to report that the ingredient may also have benefits for overweight asthmatics. —. —Commenting on the potential mechanism, the researchers note two possibilities: “Whether the improvement in AHR was due to direct effects on airway inflammation (likely cis-9, trans-11 mediated) or perhaps related to altered body composition and adipocytokine levels (likely trans-10, cis-12 mediated) in our overweight population is not clear,” they stated. —Indeed, talking to NutraIngredients-USA at the IFT Annual Meeting and Expo in Chicago, David Cai, PhD, science and regulatory manager, North America and Asia for Cognis concurred that it was too early to make conclusions.
Study details
The researchers recruited 28 overweight mild asthmatics aged between 19 and 40 to participate in their prospective, randomized, double-blind, placebo-controlled study. Subjects were randomly assigned to receive either 4.5 grams per day of CLA or placebo for 12 weeks. –At the end of the study the researchers noted significant improvements in airway hyper-responsiveness (AHR) and this was accompanied by a significant improvement in their ability to tolerate strenuous exercise. —In addition, subjects in the CLA group experienced significant improvements in the BMI, with an average reduction of 0.5 kg/m2, compared to a 0.8 kg/m2 increase in the placebo group.
Potential asthma alternative
The authors stressed however that care should be taken in extending the results to other sections of the population. “However, we believe our demonstrated efficacy is such that additional studies in these groups are warranted,” they said. —“A huge number of asthma patients seek complementary therapies, and a wide array of products are marketed as ‘asthma treatments’, frequently with no evidence. CLA is safe, clinically effective and may be considered for overweight mild asthmatics seeking natural remedies as part of their asthma management plan,” wrote the researchers. “We encourage further studies to elucidate the role of CLA in a broader asthma population,” they concluded.
Source: Clinical & Experimental Allergy
July 2010, Volume 40, Pages 1071-1078
“Conjugated linoleic acid improves airway hyper-reactivity in overweight mild asthmatics”–Authors: R. MacRedmond, G. Singhera[1], S. Attridge, M. Bahzad, C. Fava, Y. Lai, T. S. Hallstrand, D. R. Dorscheid
Recipe—Make your own CLA—all you need is butter—take it and put ½ pd ( 225 grams) in a frying pan or pot —at low heat warm up this butter til the cream separates Spoon out the cream and you have butter oil which has now had an elevated level of CLA Add 1 drop of the essential oil of Rosemary or Sage or both and this will preserve this
 
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Creatine at low doses promotes resistance to fatigue
Low dose supplementation of creatine could help combat fatigue, according to the results of a new study.
Published in the journal Nutrition, the study set out to test whether low dose creatine supplements could improve muscle function. —Creatine, an amino acid-like compound, was first identified in 1832 for its presence in muscle. It has been the subject of about 70 randomized, controlled trials over the last 12 years or so, with the majority investigating creatine’s performance-enhancing benefits. –However, according to the authors of the current study, there was a gap in the literature regarding the effects of low-dose creatine ingestion on high-intensity exercise performance and body composition when dosing was based on body size and administered over a period of time that would allow sufficient muscle uptake.
Tests
The trial involved twenty health men and women, who were randomized to receive creatine supplements or placebo. Participants were given 0.03 g of creatine (provided by NutraSense Company, Shawnee Mission, KS, USA) or placebo per kilogram of body weight per day for 6 weeks (range 1.7–2.9 g/d). Before supplementation participants were tested twice for anthropometric/body composition, muscle strength, and muscle fatigue, and they also provided blood samples to test plasma creatine concentration. They were then tested again after supplementation.
Results
At the end of the six week period, researchers found that the supplementation did not result in any significant differences in body mass, fat-free mass, fat mass, body fat —percentage, total body water, or maximal strength[U3]. –However, plasma creatine increased significantly in the creatine group. In addition, this group was found to be more resistant to fatigue in some of the tests. —“Our data indicate that the ingestion of approximately 2.3g of creatine per day for six weeks can increase body creatine retention and enhance fatigue resistance during repeated sets of high-intensity contractions with no increase in body mass,” wrote the researchers. “An additional unique finding of the present study is the absence of weight gain or increases in total body water[U4]. These may be viewed as beneficial effects in athletic populations for whom weight gain is undesirable. Future research should examine the effects of different doses of creatine supplementation with body composition and muscle function outcomes assessed at multiple time points in an effort to determine the minimal effective dose,” they concluded. —Source: Low-dose creatine supplementation enhances fatigue resistance in the absence of weight gain–Nutrition (2010), –doi:10.1016/j.nut.2010.04.001
Authors : Rawson ES, et al.
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What Creatine Can Do
Fibromyalgia patients have significantly lower levels of Creatine than healthy people (and supplemental Creatine Monohydrate may help to restore endogenous Creatine levels to normal in Fibromyalgia patients) – studies to determine whether supplemental Creatine Monohydrate could alleviate Fibromyalgia have not yet been performed.
Creatine concentrates in the Muscles (and supplemental forms of Creatine concentrate in the Muscles):
Creatine improves the condition of Muscle Fibers.
95% of the body’s Creatine reserves are stored in Skeletal Muscles.
Muscular Dystrophy patients often excrete excessive amounts of Creatine (a condition known as Creatinuria) in their Urine – this indicates that supplemental Creatine may alleviate Muscular Dystrophy.
Rheumatoid Arthritis patients have significantly lower levels of Creatine than healthy people (and supplemental Creatine Monohydrate may help to restore endogenous Creatine levels to normal in Rheumatoid Arthritis patients) – studies to determine whether supplemental Creatine Monohydrate could alleviate Rheumatoid Arthritis have not yet been performed. research
 
Nervous System—Some of the body’s Creatine pool is stored in the Brain
 
Creatine may reduce homocysteine levels
Homocysteine has been recognized as an important independent risk factor of heart disease, more so than cholesterol levels according to some studies. Creatine biosynthesis has been postulated as a major effector of homocysteine concentrations,2 and oral creatine supplements may reduce levels of homocysteine. Many studies have found that methyl donors (such as trimethylglycine (TMG) reduce levels of homocysteine, which also reduces the risk of heart disease. Conversely, pathways that demand large amounts of methyl groups may hinder the body’s ability to reduce homocysteine levels. The methylation of guanidinoacetate to form creatine consumes more methyl groups than all other methylation reactions combined in the human body. Researchers have postulated that increasing or decreasing methyl demands on the body may increase or decrease homocysteine levels. In one study researchers fed rats either guanidinoacetate- or creatine-supplemented diets for two weeks.3 According to the researchers “plasma homocysteine was significantly increased (~50%) in rats maintained on guanidinoacetate-supplemented diets, whereas rats maintained on creatine-supplemented diets exhibited a significantly lower (~25%) plasma homocysteine level.” These results suggest that homocysteine metabolism is sensitive to methylation demand imposed by physiological substrates such as creatine.
Creatine and chronic fatigue/fibromyalgia
Because of creatine’s apparent abilities to improve the symptoms of other pathologies involving a lack of high energy compounds (e.g., congestive heart failure, etc.) as well as the aforementioned afflictions outlined in the introduction to this article, it has been suggested that creatine may help with chronic fatigue syndrome and fibromyalgia (some researchers now post that they are in fact the same syndrome). Although the causes of both pathologies is still being debated, a lack of high energy compounds (e.g. ATP) at the level of the mitochondria and general muscle weakness exists. For example, people with fibromyalgia have lower levels of creatine phosphate and ATP levels compared to controls.4 No direct studies exist at this time showing creatine supplementation improves the symptomology of either chronic fatigue or fibromyalgia. Considering, however, the other data that finds that creatine supplementation increases creatine and ATP levels consistently in other pathologies where low levels of creatine and ATP are found, it stands to reason that people suffering from either syndrome may want to peruse the use of creatine. Another similar syndrome to chronic fatigue and fibromyalgia, is Multiple Chemical Sensitivity Syndrome, which may also be potentially improved by the use of creatine supplements, though more research is clearly needed.
 
Recipe-How to take Creatine—best way I have seen to take it is in either a Hot beverage like coffee or tea or to use a glycocarb ( sugar based carbohydrate ) found in health food stores using about 25 grams to a 5 gram dose( warning this can offset insulin and pancreas) if training and using this for recovery and increase ATP then this would be a good way to utilize this—But for those who are working and living a life of long hours and work this can be used at a 3-5 gram dose everyday in a warm beverage—add a sweetner like honey or maplesyrup to the warm beverage—this will bee seen to be effective in about 3 weeks at this dose—USED to have everyone do a 20 gram dose for 5 days—all it did for most is give everyone a bloated stomach at that dose—unless you were deficient in this.—This kind of dosing was designed to sell more product especially at that time when it was introduced—it never lived up to the hype on performance but it has been used therapeutically and it appears to have a strengthening effect especially among the elderly—it can be used with CLA ( above ) to increase Health –Strenght_ and Energy.
 
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TOP I
[U1]These are the Isomers You want to SEE if they are not on here then leave it on the shelf
[U2]Wonder why—the Food pyramid has been changed so that the things that would up build the body are now at the other end and instead of getting the fats from butter or animal protein high in this you are eating grains that are loaded with cancer causing properties due to the starchy sugars further exasperating an already chronic condition for those with intestinal and respiratory issues
[U3]Again 30 mg does is not enough to do anything—if the studies were at the least 3 gram dose then there would have been a significant effect again depending if there was fist a deficiency to begin with—vegetarians would see a significant impact with a dose of 3 grams or even less due to the fact that they would be deficient in the 3 aminos making creatine
[U4]This true—and at this dose this will work and again taking it a coffee or tea will also make it more absorbable due to the fact this will dissolve more readily when it is warm—
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TOP J
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Show of the Week July 30 2010
Four Days Of REM Sleep Deprivation Affects Forebrain, Long-Term Memory In Rats
Natural Substance NT-020 Aids Aging Brains in Rats
Glycine Could Be Key To REM Sleep Behavior Disorder
Study Points to Molecular Origins of Celiac Disease
Recipe—Sleep Remedies—
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Four Days Of REM Sleep Deprivation Affects Forebrain, Long-Term Memory In Rats
ScienceDaily (Feb. 6, 2008) — Four days’ exposure to a REM sleep deprivation procedure reduces cell proliferation in the part of the forebrain that contributes to long-term memory of rats, according to a new study.—The study, authored by Dennis McGinty, PhD, of the V.A. Greater Los Angeles Healthcare System, focused on male Sprague-Dawley rats. REM sleep deprivation was achieved by a brief treadmill movement initiated by automatic online detection of REM sleep. A yoked-control (YC) rat was placed in the same treadmill and experienced the identical movement regardless of the stage of the sleep-wake cycle.—According to the results, REM sleep was reduced by 85 percent in REM sleep deprived rats and by 43 percent in YC rats. Cell proliferation was reduced by 63 percent in REM sleep deprived rats compared with YC rats. Across all animals, cell proliferation exhibited a positive correlation with the percentage of REM sleep.–“Several studies have shown that sleep contributes to brain plasticity in general, and to adult neurogenesis, in particular,” said Dr. McGinty. “Neurogenesis is a concrete example of brain plasticity, suppression of adult neurogenesis is thought to be important in pathologies such as depression. One current question has to do with the relative contribution of the two sleep states, non-REM and REM, which have very different, even opposite, physiological properties. This study showed that REM sleep has a critical role in facilitating brain plasticity. The study does not exclude an equally important role for non-REM sleep. In other recent work, we have shown that sleep fragmentation can also suppress adult neurogenesis. How sleep affects the molecular mechanisms underlying neurogenesis remains to be explored.”—The article “Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat” was published in the February 1 issue of the journal Sleep.Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Academy of Sleep Medicine.–
 
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Natural Substance NT-020 Aids Aging Brains in Rats
ScienceDaily (July 21, 2010) — A combination of nutrients called NT-020 promoted adult neural stem cell proliferation in aged rats and boosted their memory performance, reported University of South Florida researchers studying natural therapeutic approaches to promoting the health of neurons in the aging brain.–Researchers from the USF Department of Neurosurgery and Brain Repair tested two groups of aged laboratory rats; one group received NT-020 and another, the control group, did not. In the NT-020 group, the process by which neurons are generated — called neurogenesis — increased.–The study was published in the current issue of Rejuvenation Research (Vol. 13 No. 5, June, 2010). The NT-020 formula was patented by USF and licensed to Natura Therapeutics, Inc.–“Aging has been linked to oxidative stress, and we have previously shown that natural compounds made from blueberries, green tea, and amino acids, such as carnosine, are high in antioxidants and have anti-inflammatory and anti-oxidative activity,” said Sandra Acosta, MS, the study’s lead author and a PhD student in the USF Center of Excellence in Aging and Brain Repair . “The combination of these nutrients, called NT-020, creates a synergistic effect that promotes the proliferation of stem cells in the aged animals.”–Acosta and colleagues compared the NT-020 group to the control group by evaluating their performance on a variety of behavioral and memory tests, including a spatial navigation test. The NT-020 group demonstrated increased adult neural stem cell proliferation in the two main stem cell niches in the brains and improvement in learning and memory.–In past studies, NT-020 has been shown to have beneficial effects on animals with simulated stroke. NT-020 has also been shown to encourage the proliferation of adult stem cells, which have the potential to develop into tissue and bone cells and also migrate to areas of damage to help with repair.—That increased stem cell proliferation coincided with better cognitive performance is significant.–“The notion that aging is a stem cell disease has been gaining popularity,” said study senior author Paula Bickford, PhD, professor of neurosurgery and brain repair at USF and a senior research career scientist at the James A. Haley Veterans’ Hospital (Tampa). “Our hypothesis is that aging alters the local environment in the brain and other organs and can promote an environment that retards the growth of stem cells. For example, high glucose, which would be seen with diabetes, excessive alcohol and oxidative stress, can lead to reduced neurogenesis.”–The researchers concluded that increased inflammation in the brains of the aged animals led to reduced production of stem cells, but that stem cell renewal created a rejuvenating effect. They found that NT-020 treated animals had fewer activated inflammatory cells in the brain, reflecting a decrease in factors that reduced the production of stem cells.—“NT-020 may have not only a positive effect on the stem cell niche,” concluded Bickford. “NT-020 may have far-reaching effects on organ function beyond the replacement of injured cells, as demonstrated by cognitive improvement in the NT-020 group.”–Disclaimer statement: Paula Bickford and Paul Sanberg are co-founders of Natura Therapeutics, Inc.—Story Source:—The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of South Florida (USF Health). The original article was written by Randolph Fillmore, USF Center of Excellence for Aging and Brain Repair.—Journal Reference:—S. Acosta, J. Jernberg, C.D. Sanberg, P.R. Sanberg, Brent J. Small, Carmelina Gemma, Paula C. Bickford. NT-020, a Natural Therapeutic Approach to Optimize Spatial Memory Performance and Increase Neural Progenitor Cell Proliferation and Decrease Inflammation in the Aged Rat. Rejuvenation Research, 2010; 100629131832013 DOI: 10.1089/rej.2009.1011
 
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Glycine Could Be Key To REM Sleep Behavior Disorder
ScienceDaily (Mar. 28, 2008) — There is new promise on the horizon for those who suffer from REM Sleep Behaviour Disorder (RBD) according to researchers at the University of Toronto.–RDB, a neurological disorder that causes violent twitches and muscle contractions during rapid eye-movement (REM) sleep, can lead to serious injuries. John Peever, Assistant Professor at the University of Toronto, discovered that an inhibitory brain chemical called glycine is responsible for actively suppressing muscle twitches in REM sleep.—Deficiency in glycine levels in the brain cells that control muscles (motoneurons) was found to cause the violent muscle contractions that mimic the primary symptom of RBD.—“This study shows the mechanism that suppresses muscles twitches in REM sleep and this will lead to better treatments and potential cures for this disorder,” says Peever. “Treating REM sleep disorder may have much broader implications, since within five to eight years of being diagnosed with this disorder, 60-80% of individuals eventually develop Parkinson’s disease.”—The study findings are published in the March 26th edition of the Journal of Neuroscience.—Story Source:–The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Toronto, via EurekAlert!, a service of AAAS
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Study Points to Molecular Origins of Celiac Disease
3 protein fragments may drive immune response to gluten in those with genetic predisposition to the disorder—-WEDNESDAY, July 21 (HealthDay News) — Scientists believe they’ve identified the molecular triggers of celiac disease, a finding they say could lead to the first drugs to tame the chronic, painful gut disorder[U1].—People with celiac disease are intolerant to the protein gluten, which is found in wheat, barley and rye[U2]. Consuming these foods triggers an immune reaction that damages the lining of the small intestine, which can prevent the body from absorbing essential vitamins and nutrients.—Currently, the only treatment for celiac disease is adoption of a gluten-free diet, which means avoiding many types of bread, pasta, cereal and other foods. But gluten contamination in many foods makes it difficult to avoid and leads to long-lasting intestinal damage in some patients, said study senior author Robert Anderson, head of the celiac disease research laboratory at the Walter and Eliza Hall Institute of Medical Research in Parkville, Australia.—Regulating the aberrant immune response to gluten with a drug “would be a much more efficient way of dealing with celiac disease,” [U3]Anderson said, but an incomplete understanding of how the immune system responds to gluten has prevented researchers from developing such therapies.—Gluten actually consists of many different protein components, and it’s been unclear which of these fragments induces the immune response seen in celiac disease.—“You can’t design drugs for celiac disease until you know the parts of the gluten that are driving the condition,” Anderson explained.—During their investigation, he and his colleagues analyzed immune responses in the blood of more than 200 celiac disease patients after they had consumed meals containing gluten.—The researchers screened the blood samples for responses to thousands of different protein fragments (peptides) found in gluten, and they found that the patients’ immune systems seemed to be responding negatively to only three of them.—That suggests that “a very precise trigger is driving the immune response,” Anderson said. “The problem is not so much gluten, it’s really these three peptides.”—The authors also noted that most of the immune response to gluten appears tied to a single type of immune system cell, called the T cell.—The results are published in the July 21 issue of Science Translational Medicine.–According to Dr. Alessio Fasano of the University of Maryland School of Medicine in Baltimore, the evidence is indeed strong that these three protein fragments trigger the celiac immune response, but “I’m not sure that it’s the end of the story,” he added. It remains possible that the screen didn’t catch all the gluten components involved in the immune response, Fasano said.—The findings will also not be relevant to everyone with celiac disease, Anderson added, since his team studied patients with a particular genetic susceptibility to the disease. Although most people with the disease show this genetic background, some do not. Anderson and his colleagues are currently working to identify which gluten proteins induce the immune response in the remainder of celiac patients.—Through Anderson’s company, Nexpep, based in Ivanhoe, Australia, the researchers are also conducting phase I clinical trials on a drug based on the three gluten protein fragments they identified. The aim of the drug is to desensitize celiac patients to the offending proteins by presenting them in very controlled amounts[U4]. They expect results within the next couple of months.—The current study received funding from Nexpep, the Australian National Health and Medical Research Council, Coeliac UK, the Coeliac Research Fund, and others.—SOURCES: Robert Anderson, Ph.D., head, celiac disease research laboratory, Walter and Eliza Hall Institute, Parkville, Australia; Alessio Fasano, M.D., professor of pediatrics, medicine, and physiology and director of the Mucosal Biology Research Center, University of Maryland School of Medicine, Baltimore; July 21, 2010, Science Translational Medicine
 
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Recipe—Sleep Remedies—Glycine ( 500 mgs ) + Niacinamide ( 500mgs)-Inositol (500mgs) + Glycine ( 500mgs )—Glycine ( 500mgs) + Magnesium ( 100-200 mgs ) Creatine 3 grams + Magnesium ( 100-200 mgs )- Taurine ( 500 mgs) + Magnesium ( 100-200 mgs) –Gaba 500mgs ) + Niacinamide ( 500 mgs )- Tryptophan ( 500 mgs before bed ) + niacin ( 20 mgs )- Honey ( 1 tsp ) and Cocoa ( ½ tsp )- Melatonin ( 3 mgs-10 mgs )- Chamomile + St John’s Wort ( 1:1 ratio in 2 pint pot ) – Lavender Tea ( 1 tablespoon per 2 pint pot )- Passion Flower with any of the previous mentioned herbs again 1:1 will induce a solid state of sleep
 
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TOP J
[U1]Again they are going to use a drug to suppress the real problem—Genetic disposition did not come til we had GMO foods –the real problem here is that the grains are GMO and as a result are causing this intolerance not because people are eating wheat but because the wheat has been tampered and the food processing as well
[U2]The research on this is that the gluten has been genetically altered and as a result there is excess amount of proline and Glutamates –which will cause a high histamine release—an allergic response
[U3]Again Not a cure –just allowing the damage to be present while the person is unaware of the furthering damage of the colon
[U4]Desensitizing someone does not mean it will be safe—again this is all smoke and mirrors to get people to consume more of the eugenics foods that are being sold

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