Cholesterol: A Patient-Specific Nutritional Approach
by Guy R. Schenker, D.C.
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(This article has been published by: Today's Chiropractic March/April 1989,
and by Healthcare Rights Advocate June, 1990, the Journal of the Coalition for
Alternatives in Nutrition and Healthcare.)
Introduction
When asked how he had been so successful in blazing a new path of thought
Einstein replied, "I did it solely by challenging axioms." It is the intent of
this article to challenge the universally accepted idea that dietary intake of
cholesterol is correlated directly with cholesterolemia and with myocardial
infarction. A patient-specific approach to the problem of hypercholesterolemia
and coronary artery disease is offered.
An axiom, though based upon scientifically verifiable facts, is not itself
provable. In other words, an axiom is an extrapolation of the facts, i. e.; it
involves "jumping to conclusions." From certain scientifically measurable facts
it was once axiomatically accepted that the earth was flat and the sun revolved
around the earth. An extrapolation of facts always involves making assumptions;
assumptions which in this case clearly were inaccurate.
A statistically significant correlation between hypercholesterolemia and
myocardial infarction has been demonstrated. From this irrefutable fact it is
accepted as self-evident the assumption that dietary cholesterol intake leads to
elevated cholesterol and thence to heart attack. It must be understood that this
is indeed an assumption. Nowhere, to the author's knowledge, has a cause and
effect relationship been established between cholesterol intake and either
cholesterolemia or atherosclerosis.
If high cholesterol and cardiovascular disease do not result from eating
cholesterol, then where do they come from? Numerous studies have shown that it
is aberrant lipid metabolism, not over-consumption, that causes cholesterol
problems. This knowledge allows the clinical nutritionist to approach patients
with something more than advice to quit eating cholesterol. By specific testing,
the biochemical imbalance that has deranged lipid metabolism in each individual
patient can be identified. Having defined the individual's underlying
biochemical imbalances, the clinician can prescribe a specific nutrition regimen
designed to restore normal metabolism, rather than treating high cholesterol as
a disease entity per se. Thus one can correct the cause of the problem, more
than merely minimizing it's effects.
RESEARCH REFUTING THE CHOLESTEROL AXIOM
Following are a number of little known facts regarding cholesterol which are
in direct conflict with commonly accepted assumptions.
Cholesterol is a requirement of every living cell and we cannot live without
it. It is the building block of sex hormones. Fifteen percent of the dry weight
of the human brain is cholesterol (5, 9).
The body synthesizes 2,000 mg. daily of this essential substance. In
comparison, even a high cholesterol diet provides only about 800 mg.
Furthermore, when large quantities of cholesterol are ingested the body simply
synthesizes less such that an excess is avoided. Animal studies which induced
atheroma with dietary cholesterol used the human equivalent of 15,000 mg. of
cholesterol a day (1).
Animals fed a diet consisting of 81% animal fat, but with concurrent high
levels of protein, vitamins and minerals showed no pathological changes in the
aorta or the heart (2, 8).
Studies of primitive African cultures have shown no correlation between
dietary intake and atherosclerosis even among 400 men of the Masai tribe who ate
meat and milk exclusively. A strong correlation did exist, however, between
atherosclerosis and consumption of refined sugar and flour (6, 7).
In 1914 only 15% of all heart disease was athero-sclerotic in nature; today
that has risen to over 90%. Over 50% of adult Americans now die of
cardiovascular disease. Yet the only significant change in dietary patterns in
Western countries over the last 100 years has not been in fat consumption but in
refined sugar and flour intake (15).
Hundreds of millions of dollars have been spent on research attempting to
prove that eating foods high in cholesterol increases the risk of heart attack.
No such evidence has been produced (3).
Even the existence of a statistical correlation between hyper-cholesterolemia
and myocardial infarction does not necessarily establish a cause and effect
relationship. How does one explain the countless patients in our practices whose
x-rays show arteriosclerosis of the aorta, yet who have normal serum
cholesterol? How does one explain the patients who have cholesterol levels over
300 yet show no evidence of cardiovascular disease? How does one explain to the
heart attack victim with normal cholesterol that he is a statistical fluke?
To conclude, based on epidemiological studies, that serum cholesterol and
heart attack are cause and effect seems a careless assumption. But to
extrapolate from those statistics that dietary cholesterol causes cardiovascular
disease represents a rather blatant "jumping to conclusions."
UNDERSTANDING HYPERCHOLESTEROLEMIA
So what does it actually mean when a patient has high serum cholesterol? The
answer to this question lies in a study not of cholesterol, but of the
individual and his or her unique body chemistry. Hypercholesterolemia is merely
a symptom of one of two possible underlying biochemical imbalances.
Nutri-Spec Laboratory has developed the means by which a clinician can obtain
complete evaluation of a patient's body chemistry using objective test
procedures. Urine and saliva chemistries as well as clinical tests are employed
in putting together the patient's biochemical profile (11). The Nutri-Spec
system represents a radical departure from disease-specific methods of diagnosis
and treatment, in favor of a purely patient-specific approach.
Nutri-Spec has defined five fundamental biochemical imbalances, the
operations of which are involved in maintaining homeostasis of all physiological
processes. All pathology reflects a loss of homeostasis associated with
aberration in one or more of the four fundamental balances (12). Every patient's
symptoms, therefore, have a nutritional component and will benefit from
restoration of biochemical balance (13, 14).
When studied in this light, atherosclerosis is seen as a dysfunction in two
of the fundamental balances, namely, water/electrolyte balance and anaerobic/dysaerobic
balance. While a discussion of water/electrolyte balance lies outside the theme
of this article, anaerobic/dysaerobic imbalance fully explains the vast majority
of high cholesterol problems.
Anaerobic/dysaerobic balance concerns not only the problems of oxidative
energy production, but also represents the two opposite abnormalities of lipid
metabolism. An anaerobic patient has insufficient fatty acid activity and excess
sterols; the dysaerobic patient has excess fatty acids and insufficient sterols.
Cholesterol is a sterol fat. An excess, therefore, represents an anaerobic
imbalance, while low levels correspond to a dysaerobic condition. However, there
is a vital fact about cholesterol of which most are not cognizant; its
biological role is played only at cellular level. This means that serum
cholesterol levels say absolutely nothing about a patient's cholesterol status
(10).
The hypercholesterolemic patient can be either anaerobic or dysaerobic. If
anaerobic, their cells are so saturated with cholesterol that it has now begun
to accumulate in the serum. A dysaerobic patient actually has low cellular
cholesterol due to excess fatty acid activity there. Serum levels rise as the
cholesterol is unable to penetrate the cells.
Clinically this means that there is no treatment for high cholesterol per se.
Effective therapy is contingent upon determining the patient's fundamental
biochemical imbalance. Having done so, the clinician can confidently prescribe
the diet and supplements specific to the individual patient's needs.
The anaerobic patient responds to one or more of the following supplements:
omega-3 and omega-6 fatty acids (fish, flax, primrose oil), vitamin B6,
magnesium (orotate or aspartate), L-carnitine, copper, sulfur (negative
valence), and proteolytic enzymes (bromelaine, pancreatin). Dietary
recommendations include avoidance of sugar, alcohol, fermented foods, and sterol
fats.
If dysaerobic, the patient's supplemental needs will be met from the
following: glycerol (lecithin, etc.), choline, inositol, potassium (orotate or
citrate), bioflavenoids, and niacin. The diet must avoid free fatty acids and
trans fatty acids (vegetable oils, margarine, salad dressing, fried foods,
canned meats), and include sterol fats in moderation.
CASE HISTORY
A 45-year old male presented with serum cholesterol of 324, and a blood
pressure of 138/94. Nutri-Spec testing revealed a dysaerobic imbalance as well
as a water/electrolyte imbalance. He was put on a salt restricted diet and
supplemented with necessary minerals for his water/electrolyte imbalance. Being
dysaerobic, he was given the appropriate diet and supplementation.
In five weeks his cholesterol had dropped to 184. His blood pressure had
dropped to 121/77.
This case history reiterates our point that there is no disease-specific
nutritional treatment for hypercholesterolemia. The patient was treated not for
his disease, but per his biochemical imbalances. His cholesterol, being merely
an effect of underlying causes, responded dramatically when those causes were
corrected.
SUMMARY
Objective clinical testing procedures are the only consistently efficacious
means to implement patient-specific diagnosis and treatment. The familiar cliche'
applies, "One must treat the patient and not the disease."
This couldn't be more true of hypercholesterolemia. Routine prescription of a
low cholesterol diet and not much else is woefully inadequate case management,
and allows what is a reversible condition to progress to the stage of life
threatening tissue degeneration.
The cholesterol axiom stands without foundation. The true causative factors
of hypercholersterolemia can be reliably determined and effectively treated.
REFERENCES
- Anitschow, N: "Changes in the Rabbit Aorta in Experimental Cholesterol
Steatose," Beitr Pathol Anat 56; 379-404, 1913.
- Barboriak, J J: "Influence of High-fat Diets; Growth and Development of
Obesity in the Albino Rat," J Nutr 64: 241-249, 1958.
- Bundlie, E: "Egg Nutrition Group Has Active First Year," Feedstuffs Sept.
11,1972, p 21.
- Cabot, R C: "The Four Common Types of Heart Disease," JAMA 63: 1461-1463,
1914.
- Clausen, J: "Gray-White Matter Differences," Handbook of Neurochemistry, Vol 1. edited by Lajtha. New York, Plenum, 1969, 273-300.
- Cleave, TL: "The Saccharine Disease," Bristol, John Write & Sons, 1974.
- Mann, G V, Shaffer, R D: "Cardiovascular Disease in the Masai,"
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- Naimi, S "Cardiovascular Lesions, Blood Lipids, Coagualation and
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- National Commission on Egg Nutrition, Eggs and Cholesterol, A position
paper, Chicago, 1972.
- Revici, E: "Research in Physiopathology as a Basis of Guided
Chemotherapy," 453-457, New York 1961.
- Schenker, GR: "Nutritional Specificity and Laboratory Testing, Part I,
"Digest of Chiropractic Economics, Vol. 27, Number 1, July/August, 1984.
- Schenker, GR: "Nutritional Specificity and Laboratory Testing, Part II,"
Digest of Chiropractic Economics, Vol. 27, Number 1, July/August, 1984.
- Schenker, GR: "Pain Control: A Specific Nutritional Approach," Digest of
Chiropractic Economics, Vol. 28, Number 3, Nov/Dec, 1985.
- Schenker, GR: " Nutrition for Athletes: Anabolic and Erogenic," Digest of
Chiropractic Economics, Vol. 30, Number 3, Nov/Dec, 1987.
- Yudkin, J: "Sugar Consumption and Myocardial Infarction," Lancet 1:
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