THE LIPID HYPOTHESIS
Guidelines, Trans Fat and Heart Disease
G. Enig, Ph.D.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Global Amnesia – A Side Effect Of Statin Treatment
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.
Copper Deficiency Theory of Ischemic Heart Disease
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.
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
Depletion. The Achilles Heel of
the Statin Crusade. A Review of Published Animal and Human Trials.
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. www.coenzymeQ10.org
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
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.
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
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.
Cholesterol May Protect Against Infections and Atherosclerosis
is much evidence that blood lipids play a key role in the immune
defence system. Bacterial endotoxin and Staphylococcus
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.
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
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.
does not cause coronary heart disease and statins don´t work by lowering
lipids. The role of inflammation and stress