The International Network of Cholesterol Skeptics



Summaries of the talks given by members of THINCS at the Fourth Annual Conference of The Weston A. Price Foundation, WISE TRADITIONS, held May 3-5, 2003 in Arlington, VA, USA: 

Exposing the Fallacy That Cholesterol and Saturated Fat Cause Heart Disease

Mary G. Enig


Dietary Guidelines, Trans Fat and Heart Disease

Duane Graveline


Transient Global Amnesia – A Side Effect of Statin Treatment

Leslie Klevay


The Copper Deficiency Theory of Ischaemic Heart Disease

Peter H. Langsjoen


CoQ10 Depletion. The Achilles Heel of the Statin Crusade.
A review of Published Animal and Human Trials. 

Kilmer S. McCully


Homocysteine, Vitamins and Vascular Disease

Uffe Ravnskov


High Cholesterol May Protect Against Infections And Atherosclerosis

Paul Rosch


Cholesterol Does Not Cause Coronary Heart Disease, Statins Don´t Work by Lowering Lipids. The Role of Inflammation and Stress.




Dietary Guidelines, Trans Fat and Heart Disease

Mary G. Enig, Ph.D. Nutritional Sciences Division, Enig Associates, Inc., 12501 Prosperity Drive, Suite 340,  Silver Spring, MD 20904, USA

In this review, I attempted to address the major issues concerning fat in US diet and to clarify the problems many people seem to be having in understanding and accepting what is happening.

The issues addressed included: why low fat diets are not appropriate; why there is a dangerous lack of natural fats in the typical US diet; why there is too much trans fat, too much omega-6 fat, and too little omega-3 fat in the average diets; just who is it that promotes the wrong fat intake; who started the anti-saturated fat agenda; and why there have been so many problems with bringing about appropriate trans fat labeling.

The answers to the "whys" of these issues are based on how fats and oils in US diet have changed over the past 100 years. These changes have resulted in the loss of many natural protective fats from most diets over time and the gradual introduction of fats that are not protective, and, in fact, are detrimental to the health of the populace.

Careful evaluation of the historical food record tells us when these inappropriate changes came about, and just how much the food industry and/or the federal government agencies and others were a cause of many changes. The food industry influence played a major roll in the years following the end of World War II.

In the 1920s, a 2400 kcal diet was recommended in medical and dietetic text books and 35 percent of the calories were measured as fat, which included cream, butter and other animal fat.

In the 1940s, a 2700 kcal diet was being recommended to maintain and promote adequate growth and health, especially for young people and 53 percent of the calories were fat with 35 percent coming from dairy products. Thus during this period, the changes were not problematic.

However, at some point between the 1940s and the 1960s, there had been a shift in medical recommendations to consuming twice a much fat as polyunsaturates rather than saturates. The reason for these recommendations were to sponsor the edible oil industry’s need to promote its processed vegetable fats and oils. These fats were big money makers and the industry with the help of parts of the science establishment developed a false "science" that blamed all the current health problems on natural fats and promised benefit from the polyunsaturates. This was the beginning of the era where the coronary heart disease and cancer epidemics were blamed on natural saturated fats. This type of diet had to be abandoned because the danger of excess polyunsaturates was gradually becoming apparent.

By the 1980s, there was another shift in recommendations; this time to the replacement of the excess polyunsaturates by monounsaturates, but the natural saturates were still being blamed for the continued epidemics in spite of the many studies that continued to give scientific proof to the innocence of saturates.

By the 2000s, the controlling interests were recommending 30 to 35 percent of calories as fat, but still trying to maintain the anti-saturate agenda, while recognizing the danger of excess omega-6 polyunsaturates, the newly recognized need for omega-3 polyunsaturates, and at the same time trying to promote the monounsaturates.

These latter recommendations always ignored the real changes in dietary fat intake, which were basically replacements of whatever good fat there had been in the typical diet 60 or more years earlier; and the replacement was with large amounts of the trans fatty acids.



Transient Global Amnesia – A Side Effect Of Statin Treatment

Duane Graveline, MD, former NASA Astronaut, USAF Flight Surgeon, Space Medicine Research Scientist, Family Doctor. 4414 Cormorant Ln., Merritt Island, FL 32953. Homepage

 Try to imagine the complete inability to formulate new memory. This condition is known as transient global amnesia, now known to be associated with statin drug use. My first encounter occurred six weeks after my annual astronaut physical at Johnson Space Center. Despite regular exercise, weight maintenance and proper diet my total serum cholesterol had risen to 250 mg and the recommendation of the flight surgeons there was to start Lipitor, 10 mg daily. My wife noticed me walking aimlessly about the yard after my return from my usual walk. I did not know who she was and would not enter our house. Our family doctor referred me immediately to a  neurologist and finally, in the office of the neurologist, my senses returned to normal. Following a negative MRI the following day, the diagnosis of transient global amnesia was made. I discontinued Lipitor because I suspected it was the cause. 

At my next NASA physical I was assured that statin drugs do not do this. Reluctantly I started again with 5 mg, daily, one-half my previous dose. Six weeks later I descended again into the black pit of amnesia, this time for an extraordinary 12 hours. In addition to the mainly antegrade amnesia which characterized my first attack, this time I had a retrograde element all the way back to my high school days. Gone was my medical school training, USAF flight surgeon career, my marriage and four children and even my selection as scientist astronaut. Again the same doctors made the same diagnosis, transient global amnesia. Again I stopped Lipitor on my own knowing it was the cause but I was the only one convinced. 

Several months later I got in contact with the statin drug study at UCSD's College of Medicine. There, Dr. Beatrice Golomb reported she had several cases just like mine. A few days later, thanks to the Graedons of the radio program Peoples Pharmacy, thousands of case reports of memory dysfunction started flooding in from patients across the country, all with the same common thread - association with statin drug use. And the amnesia is just the tip of the iceberg of the true incidence of memory impairment associated with Lipitor, Mevacor and Zocor. For every case of amnesia, thousands of cases of extreme forgetfullness, incapacitating confusion and profound disorientation have been and are being reported. Neither patients nor doctors are aware of this side effect.



The Copper Deficiency Theory of Ischemic Heart Disease

Leslie M. Klevay, MD, SD, Professor, University of North Dakota School of Medicine and Health Sciences, Research Medical Officer at the Grand Forks Human Nutrition Research Center, PO Box 9034, University Station, Grand Forks,  North Dakota, 58202, USA.

 In brief, the Western diet often is low in copper. Copper deficiency is the only nutritional insult that elevates cholesterol, blood pressure and uric acid, has adverse effects on electrocardiograms and arteries, impairs glucose tolerance, promotes thrombosis and oxidative damage, and to which
males respond differently than females. More than 80 anatomical, chemical and physiological similarities between animals deficient in copper and people with ischemic heart disease have been identified.



CoQ10 Depletion.  The Achilles Heel of the Statin Crusade. A Review of Published Animal and Human Trials. 

Peter H. Langsjoen, M.D., F.A.C.C., Cardiovascular Diseases. Research in Biomedical Aspects of Coenzyme Q10. Tel (903) 595-3778, Fax (903) 595-4962 1107 Doctors Dr., Tyler, Texas 75701,USA. 

The depletion of the essential nutrient coenzyme Q10 (CoQ10) by the increasingly popular cholesterol lowering drugs, HMG-CoA reductase inhibitors (statins) has grown from a level of concern to one of alarm.  With ever higher statin potencies and dosages, and with a steadily shrinking target LDL cholesterol, the prevalence and severity of CoQ10 deficiency is increasing noticeably to the physicians in the trenches of front line patient care.  An estimated 36 million Americans are now candidates for statin drug therapy.

CoQ10 serves as the coenzyme for mitochondrial enzyme complexes I, II and III and is essential for mitochondrial ATP production.  CoQ10 is also a clinically relevant fat-soluble antioxidant and is the only fat soluble antioxidant that is known to be synthesized de novo.  It is found normally in the diet, predominantly in organ meats and is biosynthesized in all cells with peak capabilities in late teens and early twenties with a gradual age-related decline in blood and tissue CoQ10 levels after the age of 30 years.

Statin-induced CoQ10 depletion has been documented in 15 animal studies in six different animal species and has been shown to correlate with decreased ATP production, increased ischemia reperfusion injury, skeletal muscle injury and increased mortality. 

There are 15 published trials on statin-induced CoQ10 depletion in humans. Of these 15 trials, nine were controlled trials, eight of which documented significant CoQ10 depletion.  Statin-induced CoQ10 depletion has been shown to be associated with a fall in left ventricular function, an elevation of lactate to pyruvate ratio and an enhancement of LDL cholesterol oxidation.  The current data on diastolic dysfunction further confirms the clinical importance of this drug-nutrient interaction.

Statin-induced CoQ10 depletion is well documented in animal and human studies with detrimental cardiac consequences in both animal models and human trials.  Furthermore, this drug-induced nutrient deficiency is dose-related and more notable in settings of pre-existing CoQ10 deficiency such as in the elderly and in heart failure.  Finally, statin-induced CoQ10 deficiency is completely preventable with supplemental CoQ10 with no adverse impact on the cholesterol lowering or anti-inflammatory properties of the statin drugs.

We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear.  As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide-spread deficiency of a nutrient critically important for normal heart function. 



Homocysteine, Vitamins and Vascular Disease

Kilmer S. McCully, M.D., Chief, Pathology & Laboratory Medicine, Veterans Affairs, Medical Center, VA Boston Healthcare System, 1400 Veterans of Foreign Wars Parkway, West Roxbury, Massachusetts 02132 USA. 

Within the past four decades the efforts of investigators worldwide have established homocysteine as an important factor in vascular disease, diseases of aging and other fundamental processes in biology and medicine.  Homocysteine was discovered by the American biochemist, Vincent DuVigneaud, in 1932.  Subsequent biochemical and nutritional investigations established homocysteine as an important intermediate in sulfur amino acid metabolism and transmethylation reactions.

Little was known, however, about the biomedical significance of homocysteine until 1962, when children with mental retardation, accelerated growth, dislocated ocular lenses, and propensity to thrombosis of arteries and veins were found to excrete homocysteine in the urine.  In 1968 my analysis of an archival case of homocystinuria from 1933 disclosed widespread arteriosclerotic plaques and thrombosis of carotid artery with death from stroke in an 8-year-old boy.  The cause of homocystinuria in most cases is deficiency of cystathionine synthase, a pyridoxal phosphate-dependent enzyme.  Later in 1968 my analysis of a second case of homocystinuria caused by deficiency of methionine synthase, a folate and cobalamin-dependent enzyme, was critical in the discovery of the atherogenic potential of homocysteine.  This 2-month-old boy was demonstrated to have advanced arteriosclerotic plaques in arteries throughout the body.  Because of the difference in enzyme abnormality in these two cases, it was possible for me to conclude that homocysteine causes arteriosclerosis by a direct effect of the amino acid on the cells and tissues of the arteries.  Several years later, arteriosclerotic plaques were demonstrated in a third major type of homocystinuria caused by deficiency of methylenetetrahydrofolate reductase, independently corroborating this conclusion.

The conclusion that homocysteine is atherogenic is supported by my demonstration of arteriosclerotic plaques in experimental animals with hyperhomocysteinemia produced by injection or feeding of the amino acid.  The homocysteine theory of arteriosclerosis attributes the underlying cause of the disease to dietary deficiencies of vitamin B6 and folic acid, which lead to hyperhomocysteinemia in the general population.  Dietary deficiencies of these B vitamins are caused by losses of these sensitive vitamins through important methods of food processing, including milling of grains, canning, extraction of sugar and oils, radiation, and chemical additives.  When introduced in the early 1970s this revolutionary view of the underlying cause of arteriosclerosis appeared to contradict the conventional dietary cholesterol and fat hypothesis, placing these factors in a secondary role.  Within the past decade, hundreds of major prospective and retrospective clinical and epidemiological studies have proven the underlying validity of the homocysteine theory by showing that hyperhomocysteinemia is a potent independent risk factor for vascular disease.

Experiments with cell cultures from a child with cystathionine synthase deficiency demonstrated a new biochemical pathway for conversion of the sulfur atom of homocysteine thiolactone to phosphoadenosine phosphosulfate and sulfated glycosaminoglycans.  This pathway is inactive in malignant cells, causing failure of sulfate synthesis, accumulation of homocysteine thiolactone, and homocysteinylation of cellular proteins.  Organic synthesis of derivatives of homocysteine thiolactone revealed the new compounds, thioretinamide and thioretinaco containing retinoic acid and cobalamin that are anticarcinogenic, antineoplastic, and antiatherogenic.  The results are explained by a theory of oxidative phosphorylation involving thioretinaco ozonide.  This theory relates accumulation of free radical oxygen species to deficiency of thioretinaco ozonide in aging, cancer, arteriosclerosis, and degenerative diseases of aging.



High Cholesterol May Protect Against Infections and Atherosclerosis
(The full paper is published in
Quarterly Journal of Medicine 2003;96:927-34.) 

Uffe Ravnskov, MD, PhD, independent researcher; Magle Stora Kyrkogata 9, S-22350 Lund, Sweden. Homepage

There is much evidence that blood lipids play a key role in the immune defence system. Bacterial endotoxin and  Staphylococcus aureus α-toxin bind rapidly to and become inactivated by low-density-lipoprotein (LDL). Exogenous and endogenous hypercholesterolaemia increase the survival of mice challenged with endotoxin or live bacteria; and  exogenous hypocholesterolaemia decreases it, unless the mice are injected with lipoprotein. Individuals with low LDL-cholesterol have significantly fewer circulating lymphocytes, total T cells, helper T-cells and CD8 + cells than individuals with high LDL-cholesterol; and  monocytes from hypercholesterolaemic individuals have greater phagocytic activity than monocytes from normal individuals.

These findings are supported by epidemiological and clinical observations. Total cholesterol is inversely associated with mortality caused by respiratory and digestive disease, the aetiology of which are mostly infectious. Total cholesterol is also inversely associated with the risk of being admitted to hospital because of an infectious disease. Carriers of hepatitis B antigen have lower cholesterol than non-carriers; individuals with low cholesterol are at higher risk of HIV and AIDS; and low cholesterol is a predictor for death due to intra-abdominal infections and chemotherapy-induced neutropenia.

Support is also available from inborn errors of cholesterol metabolism. Individuals with congenitally low cholesterol due to the Smith-Lemli-Opitz syndrome suffer from frequent and severe infections, that improve after substitution with dietary cholesterol, and  before year 1900, where most people died from infectious diseases, individuals with congenitally high cholesterol due to familial hypercholesterolaemia (FH) had a  lower mortality than the general population, as have old individuals with FH to-day. Young FH individuals run a greater risk of dying from cardiovascular disease, but the vascular changes seen in homozygotic FH have little resemblance with atherosclerosis and are most likely due to other factors than hypercholesterolemia.

Considering the mounting support of the hypothesis that the first step in atherosclerosis is an inflammatory response to injury of the arterial intima, these findings are suggestive of a protective role of high cholesterol against atherosclerosis, in  particular because they also explain the many observations that are at odds with the LDL receptor hypothesis. Thus, although the large majority of all cardiovascular diseases are seen after age 60, most studies of  this age group found no association between cholesterol and the risk of coronary disease, or all-cause mortality; indeed, in some of these studies high cholesterol was associated with longevity, and in the 30 year follow up of the Framingham population, those whose cholesterol fell had the highest coronary and total mortality. Furthermore, changes in cholesterol levels were inversely associated with atherosclerosis growth in two of five observational angiographic studies; in the only cholesterol lowering trial that included a post-mortem, atherosclerosis was more pronounced in the treatment group, and although statin treatment lowers coronary and total mortality and also has beneficial angiographic effects, these effects are independent of the initial cholesterol level and the degree of cholesterol reduction. This lack of exposure-response may be due to the negative effects of lowering cholesterol that counteract other and more beneficial effects of the statins on the cardiovascular system.

(Full paper published in Quarterly Journal of Medicine 2003;96:927-34.


Cholesterol does not cause coronary heart disease and statins don´t work by lowering lipids. The role of inflammation and stress

Paul Rosch;
MD, FACP, Clinical Professor of Medicine and Psychiatry, New York Medical College, President, The American Institute of Stress, Honorary Vice President, International Stress Management Association, 124 Park Ave.Yonkers, NY 10703, USA.

1.   Increased dietary fat intake does not significantly elevate cholesterol or lipid levels.  

2.   Elevated serum cholesterol and/or other lipids are not the cause of coronary heart disease.

3.   Statins can have significant side effects that have been overlooked or deliberately suppressed.  In addition to rhabdomyolysis and liver dysfunction, these include: muscle pain, weakness and fatigue and biopsy evidence of myopathy and tendinopathy in the absence of elevated CK, memory loss, global amnesia, difficulty in sleeping and concentration, erectile dysfunction, problems with temperature regulation, difficulty in managing diabetes, and peripheral neuropathy.  

4.   All statins have been shown to be carcinogenic in experimental animals in dosages that approximate those given to patients.  Although the lag time between exposure to a carcinogen and clinical detection is often a decade or more, a disturbing increase in breast cancer has already been reported in the CARE trial as well as certain skin malignancies in the simvastatin trials. Statins could initiate and/or accelerate malignant growth by a) blocking the production of Coenzyme Q10, which has been shown to have anti-cancer effects; b) stimulating the growth of new blood vessels that malignancies require to promote their propagation; c) decreasing the cytotoxicity of natural killer cells; d) blocking the production of squalene, an intermediate cholesterol metabolite with anti-cancer activities in animal studies and currently used as adjunctive therapy in treating cancer; e) reducing the production of DHEA, which has been shown to have anticancer and immune stimulating effects in experimental studies.  

5.   Cardioprotective effects are seen regardless of baseline cholesterol or LDL levels or the degree to which they are reduced and are achieved far too rapidly to be due to lowering LDL.  If statins worked by lowering LDL one would expect to see dose-response relationship, which has not been demonstrated in any statin trials.  Cardioprotective effects are seen in the elderly where LDL or other lipids are not a risk factor for coronary heart disease and in the HPS study statin treatment also prevented ischemic stroke although high LDL is not a risk factor for stroke. 

6.   There is abundant evidence that reducing inflammation, thrombotic factors and endothelial
damage may explain the statin effects. For example, in the CARE, the outcome was related to the degree of inflammation but independent of any lipid response.  

7.   Most coronary events are not due to progressive blockage of a vessel by gradual accumulation of lipid material but to thrombosis and disruption of an asymptomatic fibrous plaque with minimal protrusion. Human atherosclerotic plaque bears little resemblance to experimental atherosclerosis in animals force-fed high-fat and high cholesterol diets, but has all the hallmarks of an inflammatory response to infection and there is considerable evidence to support such an etiology, particularly for chlamydia pneumoniae.  Homocysteine, angiotensin II and a host of inflammatory agents have also been implicated.   

8.   Therefore, the current therapy goals of lowering LDL to arbitrary levels are not only inappropriate but also dangerous, since this will only lead to larger doses and more side effects.

Stress can contribute to the pathogenesis of coronary heart disease via a number of well documented neuroendocrine activities.  With respect to inflammation, it should also be noted that CRP levels correlate best with abdominal obesity, which has been shown to be largely due to increased cortisol activities that increase adipocyte production of inflammatory cytokines.  In addition to these chemical/molecular pathways there is an emerging paradigm of communication at a physical/atomic level that may help to explain other stress-related cardiovascular effects as well as the success of novel "energy treatment" effects.