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CHOLESTEROL:
A PATIENT-SPECIFIC
NUTRITIONAL
APPROACH
by
Guy R. Schenker, D.C.
(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 its 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
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 five 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 the cellular level.
This means that serum cholesterol levels say absolutely nothing
about a patient's cholesterol status (10).
Hypercholesterolemic patients 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:
negative valence sulfur, vitamin B6,
magnesium (orotate or aspartate), L-carnitine, copper, 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, 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 (--- yes the diet must include high-cholesterol
foods such as eggs).
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 mineral dispensing agents 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
1)
Anitschow, N: "Changes
in the Rabbit Aorta in Experimental Cholesterol Steatose,"
Beitr Pathol Anat 56; 379-404, 1913.
2)
Barboriak, J J: "Influence
of High-fat Diets; Growth and Development of Obesity in the Albino
Rat," J Nutr 64:
241-249, 1958.
3)
Bundlie, E: "Egg Nutrition Group Has Active First Year," Feedstuffs
Sept. 11,1972, p 21.
4)
Cabot, R C: "The
Four Common Types of Heart Disease," JAMA 63: 1461-1463, 1914.
5)
Clausen, J: "Gray-White
Matter Differences," Handbook of Neurochemistry, Vol 1. edited by
Lajtha. New York, Plenum,
1969, 273-300.
6)
Cleave, TL: "The Saccharine Disease," Bristol, John Write
& Sons, 1974.
7)
Mann, G V, Shaffer, R D: "Cardiovascular
Disease in the Masai," Atheroslerosis
Res 4:289-312, 1964.
8)
Naimi, S "Cardiovascular Lesions, Blood Lipids, Coagualation
and Fibrinolysis in Butter-induced Obesity in the Rat,"
J Nutr 86: 325-332. 1965.
9)
National Commission on Egg Nutrition, Eggs and Cholesterol, A
position paper, Chicago, 1972.
10)
Revici, E: "Research in Physiopathology as a Basis of Guided
Chemotherapy," 453-457, New York 1961.
11)
Schenker, GR: "Nutritional Specificity and Laboratory Testing,
Part
I, "Digest of Chiropractic Economics, Vol. 27, Number
1, July/August, 1984.
12)
Schenker, GR: "Nutritional Specificity and Laboratory Testing,
Part
II," Digest of Chiropractic Economics, Vol. 27, Number
1, July/August, 1984.
13)
Schenker, GR: "Pain Control: A Specific Nutritional
Approach,"
Digest of Chiropractic Economics, Vol. 28, Number 3,
Nov/Dec,
1985.
14)
Schenker, GR: " Nutrition for Athletes: Anabolic and Erogenic,"
Digest of Chiropractic Economics, Vol. 30, Number 3,
Nov/Dec, 1987.
15)
Yudkin, J: "Sugar
Consumption and Myocardial Infarction,"
Lancet 1: 296-297, 1971.
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