OTHER TESTING NOTES
The little manual that came with the charger stated that alkaline batteries can be charged to 75 – 90% of their original capacity. It further said that the batteries should be fully drained before recharging but I found that as a practical matter, the fully drained batteries came up “BAD” and could not be recharged at all.
There is one more rather important note that I want to make. I checked on my recharged batteries about two weeks after storing them in a box in my utility cupboard. Much to my surprise there were some new leakers. Now whether these were overlooked initially (had I wiped away the residue not realizing they were compromised) or a byproduct of the charging process – I do not know. Even more curious, they were all the Costco Kirkland brand batteries.
The manual also indicates that alkaline batteries should not be recharged more than 30 times. 30 times – holy moly – that seems like a lot of charging to me. For now, I will charge them once until I go through the pile and then start anew. But 30 times? I am going to play it safe and protect my devices by recharging no more than a dozen times if that.
SO REALLY, HOW DID THEY WORK?
Using the recharged batteries on low power devices such as mini LED flashlights and of course, my computer mouse, worked great. As a matter of fact, I can not tell the difference between the recharged Alkalines and standard rechargeables. On the other hand, the Survival Husband uses wireless headphones to watch TV and the recharged alkalines only last abut 8 hours as opposed to the typical 15 to 20 hours with standard Ni-mh rechargeables.
STORING THE BATTERIES
I purchased these inexpensive storage cases for my recharged batteries. They are really quite handy and I like that the six individual cases interlock and connect together to make a larger case. The rest of my spares are in the plastic pencil case you see pictured above.
THE FINAL WORD
For a total investment of about $34 I now have what for all intents and purposes, a lifetime of free batteries. The reason I say “lifetime” is that my friends have indicated an willingness to give me all of their dead batteries and you can bet that many will still be either good as is or eligible for recharging.
Would I trust these recycled batteries in a survival situation – sure, if that is all I had, But of course, that is not the case. I still have a large supply of brand new alkaline batteries in all sizes plus a good supply of standard rechargeables (you know how I love those eneloop rechargeables).
But as spare batteries to use day to day, heck, these are great. As my tests have proven, a recharged alkaline battery can keep a small LED flashlight going to over a week and a computer mouse for much longer than that. As a matter of fact, you might say I have become obsessed with using these recharged alkaline batteries. But that, of course, is a story for another time
Treating Skin Blemishes
Hot steaming towels then are applied to the afflicted area at least three times and, afterward, the afflicted area is patted dry.
One tablespoon of common table salt is dissolved in one measuring cup of very hot water having a temperature of not more than 120° F. The salt is completely dissolved in the water and a facecloth is immersed and soaked in the salt water. Sea salt with naturally occurring substances may have antibacterial characteristics that are superior to ordinary table salt and thus, sea salt water may be preferable for use in this step of the treatment process. The salt kills, it is believed, through osmosis.
A towel is folded lengthwise and then across. One side of the towel is thoroughly saturated with ordinary tap water and then folded into thirds in order to keep the wetted side of the towel on the inside of the folds. The towel is heated, preferably in a toaster oven or dryer, for several minute in order to heat the water in the wetted interior until it steams.
With the subject’s head slightly inclined to prevent inhalation of water from the towel (when treating facial acne), the hot salt water soaked facecloth is placed over the affected area, the saline water soaked facecloth then being covered by the unfolded steaming towel. Preferably, a second steaming towel can be placed over the first towel to maintain the facecloth’s heat for a longer period of time. Care must be taken, however, to make sure that these hot applications are sufficiently cool to avoid burning the skin that is undergoing treatment. With respect to this step in the treatment, it is thought that the hot applications help to further open the pores and gravity promotes flow of the saline water from the facecloth into the pores.
The heat, it seems, also promotes an increase in capillary blood flow that not only increases the supply of white and red blood cells to advance the healing process, but also removes waste products from the afflicted area. The effect of the heat applied to the subject’s skin also might destroy at least some of the bacteria that are related to the acne condition. As a general matter, heat may aid in the process in several ways. It may denature proteins, cause membrane damage and also may cause enzymatic cleavage of DNA. Moist heat, moreover, sterilizes at a lower temperature than dry heat because water serves to disrupt noncovalent bonds (hydrogen bonds) which hold protein chains together in their secondary and tertiary structures.
The steaming towel is replaced at least one more time, this replacement being repeated when the subject feels that the applied towel is no longer hot or has a noticeably elevated temperature. In this instance, the towel may actually be very warm, but the subject has at this point in the treatment become so conditioned to heat that the sensation of heat fails to register with the patient as being significant. The process temperatures need to be continually increased to and maintained at the desired levels to cause morbidity of proionibacterium acnes, dilation of the body’s own vascular structures to bring in the body’s own defensive mechanisms, remove waste through the dilated structures, and allow the salt to enter deep into the affected pilosebaceous unit. The salt will, but is not limited to, deprive the bacterium of water needed to survive, and the sodium that enters the bacterium’s membrane can not be excreted (it is a one-way trap for sodium, much like a diode is in electricity), but more water has to be brought into the bacteria to dilute the absorbed sodium until the bacteria actually ruptures.
After the last steaming towel is felt to be cool by the subject, the steaming towels and the underlying saline water soaked facecloth are removed.
The afflicted area then is further treated by being washed with a castile soap. For the purpose of the invention, the soap marketed as “Dr. Bronner’s Magic Soaps 18-in-1 Hemp Peppermint Pure-Castile Soap” has been found to be particularly efficacious. The Dr. Bronner’s soap that is used in the invention is a compound of water, saponified coconut-hemp-olive oils (with retained glycerin), olive fatty acids, peppermint oil (boosted with menthol), vitamin E, and citric acid.
The treated area is rinsed and dried, having on visual inspection a rosy appearance that will disappear in about twelve hours.
Within three days after treatment, the red pustules will be gone from the afflicted area, leaving only a few circular, dark brown freckle-like areas in those portions of the skin that were most seriously afflicted. To post treat these residual marks, a cotton applicator, soaked in either turpentine or in honey, is touched to the dark areas.—
Research suggests that the term “turpentine” is used imprecisely to describe either the oleoresin obtained from the longleaf pine (Pinus palustris Mill.) or the slash pine (P. elliottii Engelm.) along with other Pinus species that yield exclusively terpene oils, or the essential oil obtained from the above oleoresin. More than a half-dozen additional Pinus species have been used in the production of turpentine. The oleoresin is sometimes referred to as “gum turpentine” while turpentine or its oil (also known as spirits of turpentine) are terms for the essential oil. Following steam distillation, gum turpentine yields turpentine oil and a resin called colophony (also known as rosin). Alternately, rosin is collected by scarring the tree trunk, and various grades of material are then refined. Turpentine and rosin also are obtained by the steam distillation of wood chips of that are by-products of the lumber and paper industries, and these sources account for the bulk of the production of these compounds. In terms of volume, turpentine is the largest volume essential oil product in the world, with the bulk of production occurring in the United States. The labor-intensive production of rosin, however, occurs to a greater extent in Spain, Greece, India, and Morocco.—-Turpentine is composed primarily of monoterpene hydrocarbons, the most prevalent of which are the pinenes, camphene, and 3-carene. Rosin contains mostly diterpene resin acids such as abietic acid, dehydroabietic acid, palustric acid and isopimaric acid. Numerous other compounds are present in small quantities in all turpentine products.—Canada turpentine or Canada balsam is an oleoresin obtained from the stems of the balsam fir, Abies balsamae (Family Pinaceae).
Terebinthina.—It is an exudation from different species of Pines. It is a valuable remedy, either externally or internally. Sprinkled on flannel dipped in hot water, wrung out, and then locally applied, it is a powerful counter-irritant, acting like mustard, and even blistering. It is useful for local pains, for lumbago, sciatica, and for inflammatory diseases in the abdomen. As an external application to burns, turpentine has been much used. ———Internally turpentine is anthelmintic[I1] , diaphoretic, diuretic, purgative and stimulant, It is also given as an astringent. As a destroyer of worms, it should be given in combination with Castor Oil, lest failing to purge it should over-stimulate the urinary organs. As a diuretic, it is prescribed in dropsy, and suppression of urine. As a purgative, it is useful in cases of tympanitic distension of the abdomen, and in acute stages of puerperal fever. As a stimulant to the nervous system, in neuralgia and epilepsy.
Uses of Turpentine
Turpentine has been used experimentally in a bath for the treatment of disseminated sclerosis and sexual dysfunction. It also has been studied for its antibacterial activity and inhibition of osteoclast activity. Turpentine is utilized in experimental models of inflammation to induce a systemic inflammatory immune response in animals.
One study from Russia documents the use of turpentine white emulsion baths in patients with sexual dysfunctions, but the safety of this treatment has not been established***** Karpukhin IV, Li AA, Gusev ME. Turpentine white emulsion baths in the rehabilation in patients with sexual dysfunctions [in Russian]. Vopr Kurortol Fizioter Lech Fiz Kult . 2000;32-33.******** –Application of yellow turpentine baths in patients with chronic prostatitis complicated by sexual dysfunctions].
[Article in Russian]-[No authors listed]
Abstract—Patients with chronic prostatitis complicated by sexual dysfunction took turpentine baths with yellow solution in concentration rising from 5 to 55 ml solution per 200 l water, temperature 35-40 degrees C, duration 5-16 min, daily, 12-15 procedures. Yellow turpentine baths raise efficacy of treatment of patients with copulative dysfunction to 64% due to intensive arterial blood inflow to the sexual organs including the cavernous bodies of the penis.
Turpentine white emulsion baths in the rehabilation in patients with sexual dysfunctions].
[Article in Russian]
Karpukhin IV, Li AA, Gusev ME.
100 patients with sexual dysfunction (SD) and 20 SD patients took turpentine white emulsion baths and sodium chloride baths, respectively. The turpentine baths were given with step-by-step rise in turpentine concentration from 20 to 50 ml per 200 l of water, temperature 36-37 degrees C, duration of the procedure 10-15 min. The course consisted of 10-12 procedures which were conducted daily or each other day. The turpentine baths were more effective than sodium chloride baths (85 vs 50%, respectively).-PMID: 11247146 -[PubMed – indexed for MEDLINE]
Use of white turpentine bath emulsion and yellow turpentine solution for the treatment of chronic prostatitis complicated by excretory pathospermia].
[Article in Russian]
Karpukhin IV, Li AA, Gusev MA.
The paper reports a review of up-to-date methods for the use of white turpentine bath emulsion and yellow turpentine solution in the treatment of chronic prostatitis complicated by excretory pathospermia. The results of bath therapy are presented. It is shown that the efficiency of white turpentine bath emulsion amounted to 69.7% compared with 88.3% in patients treated with the use of yellow turpentine solution.—Preliminary reports from Russia suggest that turpentine baths may assist in the treatment of disseminated sclerosis, but the safety of this treatment has not been established.******** . Ludianskii EA. The extension of the use of physical methods of treatment to patients with disseminated sclerosis [in Russian]. Vopr Kurortol Fizioter Lech Fiz Kult . 1992;34-37.*******
Turpentine possesses antibacterial activity in vitro and has been applied topically to debride severe wounds infested with fly larvae***** Leung AY. Encyclopedia of Common Natural Ingredients Used in Food, Drugs, and Cosmetics . New York, NY: John Wiley & Sons, Inc., 1980*******Benign skin tumors have been observed in animal models following chronic topical application of turpentine
[I1]Internal USES— anthelmintic [I1], diaphoretic, diuretic, purgative and stimulant, It is also given as an astringent. As a destroyer of worms- As a diuretic, it is prescribed in dropsy, and suppression of urine. As a purgative, it is useful in cases of tympanitic distension of the abdomen, and in acute stages of puerperal fever. As a stimulant to the nervous system, in neuralgia and epilepsy.
[I2]Turpentine for ED
Johann Wolfgang von Goethe
Speech on Hidden Truth
None are so hopelessly enslaved, as those who falsely believe they are free. The truth has been kept from the depth of their minds by masters who rule them with lies. They feed them on falsehoods till wrong looks like right in their eyes.”
Show of The Month April 20 2013
Myths & Truths About Soy
Doctors Not Informed of Harmful Effects of Medicines During Sales Visits
THE BENFITS OF HIGH CHOLESTEROL
Summary of latest data on antibiotic resistance in the European Union
Recipe for Insulin Regulating
Eggs Prevent Heart Disease and Cancer
Eggs’ Antioxidant Properties May Help Prevent Heart Disease and Cancer,
Myths & Truths About Soy
Myth: Use of soy as a food dates back many thousands of years.
Truth: Soy was first used as a food during the late Chou dynasty (1134-246 BC), only after the Chinese learned to ferment soy beans to make foods like tempeh, natto and tamari.
Myth: Asians consume large amounts of soy foods.
Truth: Average consumption of soy foods in Japan and China is 10 grams (about 2 teaspoons) per day. Asians consume soy foods in small amounts as a condiment, and not as a replacement for animal foods.
Myth: Modern soy foods confer the same health benefits as traditionally fermented soy foods.
Truth: Most modern soy foods are not fermented to neutralize toxins in soybeans, and are processed in a way that denatures proteins and increases levels of carcinogens.
Myth: Soy foods provide complete protein.
Truth: Like all legumes, soy beans are deficient in sulfur-containing amino acids methionine and cystine. In addition, modern processing denatures fragile lysine.
Myth: Fermented soy foods can provide vitamin B12 in vegetarian diets.
Truth: The compound that resembles vitamin B12 in soy cannot be used by the human body; in fact, soy foods cause the body to require more B12
Myth: Soy formula is safe for infants.
Truth: Soy foods contain trypsin inhibitors that inhibit protein digestion and affect pancreatic function. In test animals, diets high in trypsin inhibitors led to stunted growth and pancreatic disorders. Soy foods increase the body’s requirement for vitamin D, needed for strong bones and normal growth. Phytic acid in soy foods results in reduced bioavailabilty of iron and zinc which are required for the health and development of the brain and nervous system[F1]. Soy also lacks cholesterol, likewise essential for the development of the brain and nervous system. Megadoses of phytoestrogens in soy formula have been implicated in the current trend toward increasingly premature sexual development in girls and delayed or retarded sexual development in boys.
Myth: Soy foods can prevent osteoporosis.
Truth: Soy foods can cause deficiencies in calcium and vitamin D, both needed for healthy bones. Calcium from bone broths and vitamin D from seafood, lard and organ meats prevent osteoporosis in Asian countries—not soy foods.
Myth: Modern soy foods protect against many types of cancer.
Truth: A British government report concluded that there is little evidence that soy foods protect against breast cancer or any other forms of cancer. In fact, soy foods may result in an increased risk of cancer.
Myth: Soy foods protect against heart disease.
Truth: In some people, consumption of soy foods will lower cholesterol, but there is no evidence that lowering cholesterol with soy protein improves one’s risk of having heart disease.
Myth: Soy estrogens (isoflavones) are good for you.
Truth: Soy isoflavones are phyto-endocrine disrupters. At dietary levels, they can prevent ovulation and stimulate the growth of cancer cells. Eating as little as 30 grams (about 4 tablespoons) of soy per day can result in hypothyroidism with symptoms of lethargy, constipation, weight gain and fatigue.
Myth: Soy foods are safe and beneficial for women to use in their postmenopausal years.
Truth: Soy foods can stimulate the growth of estrogen-dependent tumors and cause thyroid problems. Low thyroid function is associated with difficulties in menopause.
Myth: Phytoestrogens in soy foods can enhance mental ability.
Truth: A recent study found that women with the highest levels of estrogen in their blood had the lowest levels of cognitive function; In Japanese Americans tofu consumption in mid-life is associated with the occurrence of Alzheimer’s disease in later life.
Myth: Soy isoflavones and soy protein isolate have GRAS (Generally Recognized as Safe) status.
Truth: Archer Daniels Midland (ADM) recently withdrew its application to the FDA for GRAS status for soy isoflavones following an outpouring of protest from the scientific community. The FDA never approved GRAS status for soy protein isolate because of concern regarding the presence of toxins and carcinogens in processed soy.
Myth: Soy foods are good for your sex life.
Truth: Numerous animal studies show that soy foods cause infertility in animals. Soy consumption enhances hair growth in middle-aged men, indicating lowered testosterone levels. Japanese housewives feed tofu to their husbands frequently when they want to reduce his virility.
Myth: Soy beans are good for the environment.
Truth: Most soy beans grown in the US are genetically engineered to allow farmers to use large amounts of herbicides.
Myth: Soy beans are good for developing nations.
Truth: In third world countries, soybeans replace traditional crops and transfer the value-added of processing from the local population to multinational corporations.
Doctors Not Informed of Harmful Effects of Medicines During Sales Visits
Apr. 10, 2013 — The majority of family doctors receive little or no information about harmful effects of medicines when visited by drug company representatives, according to an international study involving Canadian, U.S. and French physicians. —Yet the same doctors indicated that they were likely to start prescribing these drugs, consistent with previous research that shows prescribing behaviour is influenced by pharmaceutical promotion.–The study, which had doctors fill out questionnaires about each promoted medicine following sales visits, was published online today in the Journal of General Internal Medicine. It shows that sales representatives failed to provide any information about common or serious side effects and the type of patients who should not use the medicine in 59 per cent of the promotions. In Vancouver and Montreal, no potential harms were mentioned for 66 per cent of promoted medicines.—“Laws in all three countries require sales representatives to provide information on harm as well as benefits,” says lead author Barbara Mintzes of the University of British Columbia. “But no one is monitoring these visits and there are next to no sanctions for misleading or inaccurate promotion.”—Serious risks were mentioned in only six percent of the promotions, even though 57 per cent of the medications involved in these visits came with US Food and Drug Administration “black box” or Health Canada boxed warnings — the strongest drug warning that can be issued by both countries.—“We are very concerned that doctors and patients are left in the dark and patient safety may be compromised,” says Mintzes, an expert on drug advertising in UBC’s School of Population and Public Health.–Doctors in Toulouse were more likely to be told of a harmful effect in a promotional visit, compared to doctors in Canada and the U.S., according to the study. Researchers suggested that this may reflect stricter regulatory standards for promotion of medicines in France.
About the study
The UBC-led study is the most comprehensive to date of the quality of pharmaceutical sales representative promotions to family physicians.–Researchers recruited physicians to participate using random samples from lists of primary care physicians at four sites — Vancouver, Montreal, Sacramento and Toulouse. Among 704 eligible physicians contacted, 255 (36 per cent) chose to participate. Information was collected on 1,692 drug promotions at sales visits between May 2009 to June 2010.
Doctors were asked to fill out a questionnaire about the information provided for each promoted medicine following each visit they received from pharmaceutical sales representatives. Sales representatives regularly visit doctors’ offices to promote medicines by providing information, free samples and in some cases food and invitations to events. The study focused on how often information was provided about drug safety.–The team includes researchers from UBC, York University, University of Montreal, University of California, Davis and the University of Toulouse.
Story Source-The above story is reprinted from materials provided by University of British Columbia, via EurekAlert!, a service of AAAS. -Journal Reference—Barbara Mintzes, Joel Lexchin, Jason M. Sutherland, Marie-Dominique Beaulieu, Michael S. Wilkes, Geneviève Durrieu, Ellen Reynolds. Pharmaceutical Sales Representatives and Patient Safety: A Comparative Prospective Study of Information Quality in Canada, France and the United States. Journal of General Internal Medicine, 2013; DOI: 10.1007/s11606-013-2411-7
THE BENFITS OF HIGH CHOLESTEROL
People with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers. Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite. But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either. Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack. But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.
High Cholesterol Protects Against Infection
Many studies have found that low cholesterol is in certain respects worse than high cholesterol. For instance, in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.3 Most gastrointestinal and respiratory diseases have an infectious origin. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection? To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.4,5 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered? Isn´t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.
Low Cholesterol and HIV/AIDS
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. The Minnesota researchers, now led by Dr. Ami Claxton, followed such individuals for 7-8 years. After having excluded those who became HIV-positive during the first four years, they ended up with a group of 2446 men. At the end of the study, 140 of these people tested positive for HIV; those who had low cholesterol at the beginning of the study were twice as likely to test postitive for HIV compared with those with the highest cholesterol.6 Similar results come from a study of the MRFIT screenees, including more than 300,000 young and middle-aged men, which found that 16 years after the first cholesterol analysis the number of men whose cholesterol was lower than 160 and who had died from AIDS was four times higher than the number of men who had died from AIDS with a cholesterol above 240.7
Cholesterol and Chronic Heart Failure
Heart disease may lead to a weakening of the heart muscle. A weak heart means that less blood and therefore less oxygen is delivered to the arteries. To compensate for the decreased power, the heart beat goes up, but in severe heart failure this is not sufficient. Patients with severe heart failure become short of breath because too little oxygen is delivered to the tissues, the pressure in their veins increases because the heart cannot deliver the blood away from the heart with sufficient power, and they become edematous, meaning that fluid accumulates in the legs and in serious cases also in the lungs and other parts of the body. This condition is called congestive or chronic heart failure. There are many indications that bacteria or other microorganisms play an important role in chronic heart failure. For instance, patients with severe chronic heart failure have high levels of endotoxin and various types of cytokines in their blood. Endotoxin, also named lipopolysaccharide, is the most toxic substance produced by Gram-negative bacteria such as Escherichia coli, Klebsiella, Salmonella, Serratia and Pseudomonas. Cytokines are hormones secreted by white blood cells in their battle with microorganisms; high levels of cytokines in the blood indicate that inflammatory processes are going on somewhere in the body. The role of infections in chronic heart failure has been studied by Dr. Mathias Rauchhaus and his team at the Medical Department, Martin-Luther-University in Halle, Germany (Universitätsklinik und Poliklinik für Innere Medizin III, Martin-Luther-Universität, Halle). They found that the strongest predictor of death for patients with chronic heart failure was the concentration of cytokines in the blood, in particular in patients with heart failure due to coronary heart disease.8 To explain their finding they suggested that bacteria from the gut may more easily penetrate into the tissues when the pressure in the abdominal veins is increased because of heart failure. In accordance with this theory, they found more endotoxin in the blood of patients with congestive heart failure and edema than in patients with non-congestive heart failure without edema, and endotoxin concentrations decreased significantly when the heart’s function was improved by medical treatment.9A simple way to test the functional state of the immune system is to inject antigens from microorganisms that most people have been exposed to, under the skin. If the immune system is normal, an induration (hard spot) will appear about 48 hours later at the place of the injection. If the induration is very small, with a diameter of less than a few millimeters, this indicates the presence of “anergy,” a reduction in or failure of response to recognize antigens. In accordance, anergy has been found associated with an increased risk of infection and mortality in healthy elderly individuals, in surgical patients and in heart transplant patients.10 Dr. Donna Vredevoe and her group from the School of Nursery and the School of Medicine, University of California at Los Angeles tested more than 200 patients with severe heart failure with five different antigens and followed them for twelve months. The cause of heart failure was coronary heart disease in half of them and other types of heart disease (such as congenital or infectious valvular heart disease, various cardiomyopathies and endocarditis) in the rest. Almost half of all the patients were anergic, and those who were anergic and had coronary heart disease had a much higher mortality than the rest.10 Now to the salient point: to their surprise the researchers found that mortality was higher, not only in the patients with anergy, but also in the patients with the lowest lipid values, including total cholesterol, LDL-cholesterol and HDL-cholesterol as well as triglycerides. The latter finding was confirmed by Dr. Rauchhaus, this time in co-operation with researchers at several German and British university hospitals. They found that the risk of dying for patients with chronic heart failure was strongly and inversely associated with total cholesterol, LDL-cholesterol and also triglycerides; those with high lipid values lived much longer than those with low values.11,12 Other researchers have made similar observations. The largest study has been performed by Professor Gregg C. Fonorow and his team at the UCLA Department of Medicine and Cardiomyopathy Center in Los Angeles.13 The study, led by Dr. Tamara Horwich, included more than a thousand patients with severe heart failure. After five years 62 percent of the patients with cholesterol below 129 mg/l had died, but only half as many of the patients with cholesterol above 223 mg/l. When proponents of the cholesterol hypothesis are confronted with findings showing a bad outcome associated with low cholesterol—and there are many such observations—they usually argue that severely ill patients are often malnourished, and malnourishment is therefore said to cause low cholesterol. However, the mortality of the patients in this study was independent of their degree of nourishment; low cholesterol predicted early mortality whether the patients were malnourished or not.
As discussed in The Cholesterol Myths (see sidebar), much evidence supports the theory that people born with very high cholesterol, so-called familial hypercholesterolemia, are protected against infection. But if inborn high cholesterol protects against infections, inborn low cholesterol should have the opposite effect. Indeed, this seems to be true. Children with the Smith-Lemli-Opitz syndrome produce very little cholesterol because the enzyme that is necessary for the last step in the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the central nervous system. Those who survive are imbecile, they have extremely low cholesterol and suffer from frequent and severe infections. However, if their diet is supplemented with pure cholesterol or extra eggs, their cholesterol goes up and their bouts of infection become less serious and less frequent.14
Laboratory studies are crucial for learning more about the mechanisms by which the lipids exert their protective function. One of the first to study this phenomenon was Dr Sucharit Bhakdi from the Institute of Medical Microbiology, University of Giessen (Institut für Medizinsche Mikrobiologie, Justus-Liebig-Universität Gießen), Germany along with his team of researchers from various institutions in Germany and Denmark.15 Staphylococcus aureus a-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy a wide variety of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in 0.9 percent saline, the blood is hemolyzed, that is the membranes of the red blood cells burst and hemoglobin from the interior of the red blood cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified a-toxin with human serum (the fluid in which the blood cells reside) and saw that 90 percent of its hemolyzing effect disappeared. By various complicated methods they identified the protective substance as LDL, the carrier of the so-called bad cholesterol. In accordance, no hemolysis occurred when they mixed a-toxin with purified human LDL, whereas HDL or other plasma constituents were ineffective in this respect. Dr. Willy Flegel and his co-workers at the Department of Transfusion Medicine, University of Ulm, and the Institute of Immunology and Genetics at the German Cancer Research Center in Heidelberg, Germany (DRK-Blutspendezentrale und Abteilung für Transfusionsmedizin, Universität Ulm, und Deutsches Krebsforschungszentrum, Heidelberg) studied endotoxin in another way.16 As mentioned, one of the effects of endotoxin is that white blood cells are stimulated to produce cytokines. The German researchers found that the cytokine-stimulating effect of endotoxin on the white blood cells disappeared almost completely if the endotoxin was mixed with human serum for 24 hours before they added the white blood cells to the test tubes. In a subsequent study17 they found that purified LDL from patients with familial hypercholesterolemia had the same inhibitory effect as the serum. LDL may not only bind and inactivate dangerous bacterial toxins; it seems to have a direct beneficial influence on the immune system also, possibly explaining the observed relationship between low cholesterol and various chronic diseases. This was the starting point for a study by Professor Matthew Muldoon and his team at the University of Pittsburgh, Pennsylvania. They studied healthy young and middle-aged men and found that the total number of white blood cells and the number of various types of white blood cells were significantly lower in the men with LDL-cholesterol below 160 mg/dl (mean 88.3 mg/l),than in men with LDL-cholesterol above 160 mg/l (mean 185.5 mg/l).18 The researchers cautiously concluded that there were immune system differences between men with low and high cholesterol, but that it was too early to state whether these differences had any importance for human health. Now, seven years later with many of the results discussed here, we are allowed to state that the immune-supporting properties of LDL-cholesterol do indeed play an important role in human health.
The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold at the Department of Medicine, University of California, San Francisco, and his group have published several interesting results from such research. In one of them they lowered LDL-cholesterol in rats by giving them either a drug that prevents the liver from secreting lipoproteins, or a drug that increases their disappearance. In both models, injection of endotoxin was followed by a much higher mortality in the low-cholesterol rats compared with normal rats. The high mortality was not due to the drugs because, if the drug-treated animals were injected with lipoproteins just before the injection of endotoxin, their mortality was reduced to normal.19
Dr. Mihai Netea and his team from the Departments of Internal and Nuclear Medicine at the University Hospital in Nijmegen, The Netherlands, injected purified endotoxin into normal mice, and into mice with familial hypercholesterolemia that had LDL-cholesterol four times higher than normal. Whereas all normal mice died, they had to inject eight times as much endotoxin to kill the mice with familial hypercholesterolemia. In another experiment they injected live bacteria and found that twice as many mice with familial hypercholesterolemia survived compared with normal mice.20
Other Protecting Lipids
As seen from the above, many of the roles played by LDL-cholesterol are shared by HDL. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more. triglycerides, molecules consisting of three fatty acids linked to glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by a lipoprotein named VLDL (very low-density lipoprotein) and by chylomicrons, a mixture of emulsified triglycerides appearing in large amounts after a fat-rich meal, particularly in the blood that flows from the gut to the liver. For many years it has been known that sepsis, a life-threatening condition caused by bacterial growth in the blood, is associated with a high level of triglycerides. The serious symptoms of sepsis are due to endotoxin, most often produced by gut bacteria. In a number of studies, Professor Hobart W. Harris at the Surgical Research Laboratory at San Francisco General Hospital and his team found that solutions rich in triglycerides but with practically no cholesterol were able to protect experimental animals from the toxic effects of endotoxin and they concluded that the high level of triglycerides seen in sepsis is a normal immune response to infection.21 Usually the bacteria responsible for sepsis come from the gut. It is therefore fortunate that the blood draining the gut is especially rich in triglycerides.
So far, animal experiments have confirmed the hypothesis that high cholesterol protects against infection, at least against infections caused by bacteria. In a similar experiment using injections of Candida albicans, a common fungus, Dr. Netea and his team found that mice with familial hypercholesterolemia died more easily than normal mice.22 Serious infections caused by Candida albicans are rare in normal human beings; however, they are mainly seen in patients treated with immunosuppressive drugs, but the finding shows that we need more knowledge in this area. However, the many findings mentioned above indicate that the protective effects of the blood lipids against infections in human beings seem to be greater than any possible adverse effects.
Cholesterol as a Risk Factor
Most studies of young and middle-aged men have found high cholesterol to be a risk factor for coronary heart disease, seemingly a contradiction to the idea that high cholesterol is protective. Why is high cholesterol a risk factor in young and middle-aged men? A likely explanation is that men of that age are often in the midst of their professional career. High cholesterol may therefore reflect mental stress, a well-known cause of high cholesterol and also a risk factor for heart disease. Again, high cholesterol is not necessarily the direct cause but may only be a marker. High cholesterol in young and middle-aged men could, for instance, reflect the body’s need for more cholesterol because cholesterol is the building material of many stress hormones. Any possible protective effect of high cholesterol may therefore be counteracted by the negative influence of a stressful life on the vascular system.
Response to Injury
In 1976 one of the most promising theories about the cause of atherosclerosis was the Response-to-Injury Hypothesis, presented by Russell Ross, a professor of pathology, and John Glomset, a professor of biochemistry and medicine at the Medical School, University of Washington in Seattle.23,24 They suggested that atherosclerosis is the consequence of an inflammatory process, where the first step is a localized injury to the thin layer of cells lining the inside of the arteries, the intima. The injury causes inflammation and the raised plaques that form are simply healing lesions. Their idea is not new. In 1911, two American pathologists from the Pathological Laboratories, University of Pittsburgh, Pennsylvania, Oskar Klotz and M.F. Manning, published a summary of their studies of the human arteries and concluded that “there is every indication that the production of tissue in the intima is the result of a direct irritation of that tissue by the presence of infection or toxins or the stimulation by the products of a primary degeneration in that layer.”25 Other researchers have presented similar theories.26 Researchers have proposed many potential causes of vascular injury, including mechanical stress, exposure to tobacco fumes, high LDL-cholesterol, oxidized cholesterol, homocysteine, the metabolic consequences of diabetes, iron overload, copper deficiency, deficiencies of vitamins A and D, consumption of trans fatty acids, microorganisms and many more. With one exception, there is evidence to support roles for all of these factors, but the degree to which each of them participates remains uncertain. The exception is of course LDL-cholesterol. Much research allows us to exclude high LDL-cholesterol from the list. Whether we look directly with the naked eye at the inside of the arteries at autopsy, or we do it indirectly in living people using x-rays, ultrasound or electron beams, no association worth mentioning has ever been found between the amount of lipid in the blood and the degree of atherosclerosis in the arteries. Also, whether cholesterol goes up or down, by itself or due to medical intervention, the changes of cholesterol have never been followed by parallel changes in the atherosclerotic plaques; there is no dose-response. Proponents of the cholesterol campaign often claim that the trials indeed have found dose-response, but here they refer to calculations between the mean changes of the different trials with the outcome of the whole treatment group. However, true dose-response demands that the individual changes of the putative causal factor are followed by parallel, individual changes of the disease outcome, and this has never occurred in the trials where researchers have calculated true dose-response. A detailed discussion of the many factors accused of harming the arterial endothelium is beyond the scope of this article. However, the protective role of the blood lipids against infections obviously demands a closer look at the alleged role of one of the alleged causes, the microorganisms.
Is Atherosclerosis an Infectious Disease?
For many years scientists have suspected that viruses and bacteria, in particular cytomegalovirus and Chlamydia pneumonia (also named TWAR bacteria) participate in the development of atherosclerosis. Research within this area has exploded during the last decade and by January 2004, at least 200 reviews of the issue have been published in medical journals. Due to the widespread preoccupation with cholesterol and other lipids, there has been little general interest in the subject, however, and few doctors know much about it. Here I shall mention some of the most interesting findings.26 Electron microscopy, immunofluorescence microscopy and other advanced techniques have allowed us to detect microorganisms and their DNA in the atherosclerotic lesions in a large proportion of patients. Bacterial toxins and cytokines, hormones secreted by the white blood cells during infections, are seen more often in the blood from patients with recent heart disease and stroke, in particular during and after an acute cardiovascular event, and some of them are strong predictors of cardiovascular disease. The same is valid for bacterial and viral antibodies, and a protein secreted by the liver during infections, named C-reactive protein (CRP), is a much stronger risk factor for coronary heart disease than cholesterol Clinical evidence also supports this theory. During the weeks preceding an acute cardiovascular attack many patients have had a bacterial or viral infection. For instance, Dr. Armin J. Grau from the Department of Neurology at the University of Heidelberg and his team asked 166 patients with acute stroke, 166 patients hospitalized for other neurological diseases and 166 healthy individuals matched individually for age and sex about recent infectious disease. Within the first week before the stroke, 37 of the stroke patients, but only 14 of the control individuals had had an infectious disease. In half of the patients the infection was of bacterial origin, in the other half of viral origin.27 Similar observations have been made by many others, for patients with acute myocardial infarction (heart attack). For instance, Dr. Kimmo J. Mattila at the Department of Medicine, Helsinki University Hospital, Finland, found that 11 of 40 male patients with an acute heart attack before age 50 had an influenza-like infection with fever within 36 hours prior to admittance to hospital, but only 4 out of 41 patients with chronic coronary disease (such as recurrent angina or pervious myocardial infarction) and 4 out of 40 control individuals without chronic disease randomly selected from the general population.28 Attempts have been made to prevent cardiovascular disease by treatment with antibiotics. In five trials treatment of patients with coronary heart disease using azithromyzin or roxithromyzin, antibiotics that are effective against Chlamydia pneumonia,yielded successful results; a total of 104 cardiovascular events occurred among the 412 non-treated patients, but only 61 events among the 410 patients in the treatment groups.28a-e In one further trial a significant decreased progression of atherosclerosis in the carotid arteries occurred with antibiotic treatment.28f However, in four other trials,30a-d one of which included more than 7000 patients,28d antibiotic treatment had no significant effect. The reason for these inconsistent results may be that the treatment was too short (in one of the trials treatment lasted only five days). Also, Chlamydia pneumonia, the TWAR bacteria, can only propagate inside human cells and when located in white blood cells they are resistant to antibiotics.31 Treatment may also have been ineffective because the antibiotics used have no effect on viruses. In this connection it is interesting to mention a controlled trial performed by Dr. Enrique Gurfinkel and his team from Fundación Favaloro in Buenos Aires, Argentina.32 They vaccinated half of 301 patients with coronary heart disease against influenza, a viral disease. After six months 8 percent of the control patients had died, but only 2 percent of the vaccinated patients. It is worth mentioning that this effect was much better than that achieved by any statin trial, and in a much shorter time.
Does High Cholesterol Protect Against Cardiovascular Disease?
Apparently, microorganisms play a role in cardiovascular disease. They may be one of the factors that start the process by injuring the arterial endothelium. A secondary role may be inferred from the association between acute cardiovascular disease and infection. The infectious agent may preferably become located in parts of the arterial walls that have been previously damaged by other agents, initiating local coagulation and the creation of a thrombus (clot) and in this way cause obstruction of the blood flow. But if so, high cholesterol may protect against cardiovascular disease instead of being the cause! In any case, the diet-heart idea, with its demonizing of high cholesterol, is obviously in conflict with the idea that high cholesterol protects against infections. Both ideas cannot be true. Let me summarize the many facts that conflict with the idea that high cholesterol is bad. If high cholesterol were the most important cause of atherosclerosis, people with high cholesterol should be more atherosclerotic than people with low cholesterol. But as you know by now this is very far from the truth. If high cholesterol were the most important cause of atherosclerosis, lowering of cholesterol should influence the atherosclerotic process in proportion to the degree of its lowering. But as you know by now, this does not happen.If high cholesterol were the most important cause of cardiovascular disease, it should be a risk factor in all populations, in both sexes, at all ages, in all disease categories, and for both heart disease and stroke. But as you know by now, this is not the case I have only two arguments for the idea that high cholesterol is good for the blood vessels, but in contrast to the arguments claiming the opposite they are very strong. The first one stems from the statin trials. If high cholesterol were the most important cause of cardiovascular disease, the greatest effect of statin treatment should have been seen in patients with the highest cholesterol, and in patients whose cholesterol was lowered the most. Lack of dose-response cannot be attributed to the knowledge that the statins have other effects on plaque stabilization, as this would not have masked the effect of cholesterol-lowering considering the pronounced lowering that was achieved. On the contrary, if a drug that effectively lowers the concentration of a molecule assumed to be harmful to the cardiovascular system and at the same time exerts several beneficial effects on the same system, a pronounced dose-response should be seen. On the other hand, if high cholesterol has a protective function, as suggested, its lowering would counterbalance the beneficial effects of the statins and thus work against a dose-response, which would be more in accord with the results from the various trials. I have already mentioned my second argument, but it can’t be said too often: High cholesterol is associated with longevity in old people. It is difficult to explain away the fact that during the period of life in which most cardiovascular disease occurs and from which most people die (and most of us die from cardiovascular disease), high cholesterol occurs most often in people with the lowest mortality. How is it possible that high cholesterol is harmful to the artery walls and causes fatal coronary heart disease, the commonest cause of death, if those whose cholesterol is the highest, live longer than those whose cholesterol is low?
To the public and the scientific community I say, “Wake up!”