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Dr. Bernard Presser D.C.
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Each year about 15 young athletes -- ranging in age from 12 to 40 - suddenly collapse and die. From 1985 through 1995 there were 158 such deaths, 134 of cardiovascular origin. The cause is usually hypertrophic cardiomyopathy, thought to be genetically transmitted, in which the wall of the heart's main pumping chamber, (left ventricle) is abnormally thick. During strenuous activity the heart cannot obtain sufficient blood for itself. i
Exercise supposedly benefits the cardiac muscle and blood vessels. Shouldn't athletes have the strongest, most efficient hearts? Since such occurrences are a recent phenomenon, could there be more to this than a genetic tendency? And what of all the avid joggers and others who regularly exercise? Are they strengthening their hearts or not?
The death rate from cardiovascular disease has been falling (almost 25% between 1982 and 1992) primarily due to advanced medical technologies that keep heart attack victims alive. However, cases of congestive heart failure (CHF) have more than doubled between 1979 and 1992 -- from 377,000 to 822,000 (requiring hospitalization). In 1990 alone, there were over 38,000 deaths. An estimated one to two million adults in the U.S. are affected, with more than 400,000 cases diagnosed each year. About 85% are age 65 or older. Sudden death is six to nine times more likely than among the general populace. ii
CHF results from a gradual loss of the heart's pumping ability involving both or either the left and/or right ventricles. The amount of blood pumped out with each contraction diminishes as the condition deteriorates. For a while, the heart may compensate for its inefficiency by enlarging as well as increasing the pulse rate, thus maintaining almost normal circulation. Shortness of breath, breathing difficulties, sensitivity to cold, chest pains with any activity, wheezing and coughing are common. The slightest efforts become overwhelming. Reduced cardiac output (decreased blood flow) brings about complex changes in the kidneys, nervous system, endocrine gland system, liver, brain, and other areas. Blood pressure elevates. Fluid accumulates in the legs, feet, lungs, and abdomen. As heart failure progresses, the amount of blood that the heart must pump increases. The cardiac muscle is further weakened and stressed so that the heart eventually fails.
It is believed CHF is on the rise because heart attack victims live long enough now to develop the disease. Sections of cardiac muscle damaged by the heart attack cause loss of contractile ability. However, there is much more to this story. Injury may result from toxins (e.g., alcohol, cytotoxic drugs), parasites (e.g. Chagas' disease), or prolonged cardiovascular stress (e.g. hypertension, valvular disease). "In many cases, the cause of the injury is unknown." (Emphasis added)
About 25 or 30 years ago persons with CHF invariably had a history of heart attack. But today, many have no history of heart attack. One possible reason is the overuse of beta blockers (beta-adrenergic-receptor blocking agents), medications prescribed to millions of people, not only following heart attack, but more so to treat hypertension. Beta blockers inhibit the ability of heart nerves to respond to epinephrine, a hormone and neurotransmitter. Epinephrine stimulates the sympathetic nervous system, heart muscle, and thus pulse rate and cardiac output (including blood pressure) as needed. Beta blockers are designed to weaken the heart so blood pressure is lowered and heart pain or pressure is reduced. Frequently, they are taken indefinitely. Listed adverse effects and warnings include heart failure for persons with AND without a history of cardiac failure. iii
Calcium-channel blockers (CCBs), the largest selling family of blood pressure lowering drugs, prevent calcium particles from entering the muscle cells that line blood vessels in order to keep arteries from constricting. And they prevent calcium from entering heart muscle cells, reducing "inappropriate" ventricular contractions. So these drugs, too, purposefully weaken the heart. Because of these effects, CCBs are prescribed for hypertension, angina, arrhythmias, and CHF. Recent studies have shown that patients on these drugs -- particularly the short-acting calcium antagonists -- were at "significantly greater risk" for CHF, heart attack, stroke, gastrointestinal bleeding, and cancer. Some experts believe the long-acting CCBs are safer, though researchers such as Michael J. Alderman, M.D., Albert Einstein College of Medicine, caution that this opinion "...is based on hope (or hype) and not evidence." The National Heart, Lung, and Blood Institute stated that the short acting CCBs should be used with "great caution if at all." Authorities recommend that CCBs "clearly should be avoided in the vast majority of patients with cardiovascular diseases, including hypertension." iv
Further complicating the picture is the current opinion that CHF is not simply a disorder in which the ventricles fail to pump adequate blood, but is a disorder of circulation. Yet, it is admitted that the "precise way" in which this works "remains undefined." Dr. Milton Packer of Columbia University, though endorsing the new hypothesis, admits: "A lot of heart failure is due to the progressive loss of cardiac cells that just die. You have to ask: What makes these cells die?" v
Allopathic medicine seeks to "manage" the symptoms with medication, most frequently diagoxin (digitalis) such as Lanoxin. It is assumed that diagoxin prevents heart failure. But researchers find that it does not prolong the life of heart patients; it only controls some symptoms. It is known that digitalis intoxication is one of the most common undiagnosed causes of death in the U.S. Patients are rarely if ever checked for over-dosage. vi
Digoxin was the sixth most frequently dispensed drug in the U.S. during 1995, with over 21 million new and refill prescriptions sold. Almost half of the older persons taking it were found to be receiving it inappropriately. One out of five people using it develops obvious signs of toxicity. vii
Other drugs are also used to treat patients with CHF, yet despite the considerable research and experimentation with various pharmacologic agents over the past 20 or more years, CHF continues to be a condition with a high and rising mortality.
What of the role of nutrition in CHF? A short review in biochemistry may assist:
Heart muscle cells are composed of 18 different amino acids, all of which must be supplied simultaneously and unaltered. Six of the 18 are heat labile. So when food is cooked, pasteurized, or otherwise heated, these six amino acids are denatured and then coagulated to an insoluble state which the body cannot use to form polypeptide chains needed for cellular repair or replacement.
Cardiac muscle cells are also rich in myoglobin (an oxygen carrier) and the enzymes of the electron transport chain and the Krebs citric acid cycle (a complicated series of reactions involving oxidative metabolism of pyruvic acid and liberation of energy). From the electron transport chain and citric acid cycle, heart muscle cells obtain energy for contraction by ATP (adenosine triphosphate). This energy system, located in the mitochondria of the cells, is oxidative phosphorylation.
During glycolysis (breakdown of sugars to pyruvic acid or lactic acid), during fatty acid oxidation (breakdown), and citric acid cycling, two energy-rich molecules are formed: (1) NADH (nicotinamide adenine dinucleotide) for which niacinamide (B3) is the basic micronutrient needed, and FADH2 (flavin adenine dinucleotide for which riboflavin (B2) is the basic micronutrient needed. When NADH is oxidized, it yields 3 ATP. When FADH2 is oxidized, it yields 2 ATP. ATP is the chief provider of energy for muscle work.
The constant needed energy for muscle work, muscle repair, and muscle tone depends upon:
(1) Proper glycolysis.
(2) Oxidative phosphorylation requiring:
(a) Phosphorylative enzymes -- proteins -- in the mitochondria.
(b) Coenzyme Q and cytochromes (which play an important role in cellular
respiration to release energy).
(c) All 18 amino acids in a biologically active form.
(d) Thiamin (B1), riboflavin (B2), and niacinamide (B3).
(e) Oxygen and hydrogen.
(f) Unimpaired citric acid cycling of carbohydrates.
(g) Unimpaired fatty acid metabolism.
(h) Myoglobin as a transporter of iron-containing heme into the cytoplasm
and cytochromes of muscle cells.
BOVINE HEART SUPPLEMENTATION
Beef heart mitochondria was found to contain a structure called electron transport particle (ETP) which contains the entire electron transport chain from NAD+ to oxygen. ETP contains two hemes, one red and one green, the latter containing tyrosinase (organic copper-containing enzyme). ETP also contains a flavin (B2), a copper-flavin, and a lipid which apparently is a source of vitamin K and coenzyme Q (CoQ).
Since beef heart mitochondria contain the complete electron transport particle plus the cofactors of the citric and fatty acid cycles, then -- if the proteins of the beef heart cells have not been denatured by heat -- ingestion of such food could greatly benefit human heart function.
CoQ, chemically similar to vitamin K, is found in the chloroplasts of green plants as well as beef heart cells. The chloroplasts provide a chlorophyll/ vitamin E complex which is involved in the electron transport system. This type of vitamin E is rich in selenium, the trace mineral activator of vitamin E complex and a factor needed for the synthesis of CoQ in the body.
Dr. Royal Lee formulated a method of extracting the heart nucleus material - the blueprint of the cell which contains the mitochondria -- for use as a food supplement. He found that it (protomorphogen) worked as a "heart muscle tonic according to cardiograph tests." It increased cardiac muscle tone and thus increased capacity for exertion. It promoted the disappearance of discomfort in breathing, pulmonary congestion, and edema. Essentially, it replaced or supplemented digitalis in decompensated cases. Comparative heart graphs (acoustic cardiographs) initially show myocardial atonicity (lack of heart muscle tone) and fatigue, and then show the same patient five minutes after ingesting the heart glandular supplement with MUCH stronger first sounds (muscle contraction) and less accentuated second sounds (relaxation).
In a previous paper we established that intact polypeptides (protein particles) cross the gastrointestinal barrier and influence target organ tissue responses. Thus, a heart muscle extract can cause a positive manifestation on the acoustic cardiograph as well as subjective response. There are at least three potential biochemical mechanisms to explain why the extract assists in rapid, measureable, heart strengthening effects:
(1) Provision of the concentrated cellular ‘control center' (protomorphogen) for production of essential amino acids in proper sequence and configuration for cellular repair and maintenance.
(2) The presence of ETP to potentiate cytoplasm, physiological oxidations and oxidative phosphorylations within the mitochondria. The left ventricle of the heart, due to greater work demand, contains higher concentrations of creatine, phosphorus, potassium, and adenine, than the right ventricle. This means the left heart muscle function requires large amounts of biologically ready ATP and creatine phosphate. ETP would provide these essential physiological activators. Phosphate bonds are energy rich, so these compounds can activate or energize the muscle cell receptors of cardiac muscle tissue. The result is improved contractile strength.
(3) The presence of carnitine, an amine synthesized in the liver from the amino acid, lysine. Lysine, an essential amino acid (cannot be manufactured in the body; but must be obtained in the diet), is heat labile -- denatured and coagulated by heat. The requirement for lysine (at least 1% of the diet) is greater than any other amino acid.
Both glycogen (stored glucose) and lipids (fats) are needed for muscle energy. Free fatty acids, once inside the cellular cytoplasm, are converted to acyl-CoA (acylcoenzyme A). To enter into beta oxidation (degradation of fatty acids into acetyl-CoA) in the mitochondria, the acyl-CoA must be transported by carnitine via the enzyme carnitine acyltransferace. "A deficiency of carnitine impairs fatty acid oxidation, and triglycerides (triacylglycerol) accumulate in the muscle cytoplasm." Carnitine deficiency results in progressive muscle weakness and abnormal lipid storage in the muscle.
A deficit of carnitine can develop from a lack of lysine in the diet, by lysine in foods being made biochemically unfit by cooking, or by a problem in the liver's ability to synthesize carnitine. Whatever the cause, loss of free fatty acid beta-oxidation from a lack of carnitine transport into the mitochondria results in the loss of low intensity, prolonged work efficiency -- crucial to the heart! A properly processed heart muscle supplement can provide both lysine and carnitine. viii
Several double-blind clinical studies have shown that carnitine improves cardiac function in patients with CHF. The longer the carnitine is used, the more dramatic the improvement, as demonstrated by maximum exercise time and the amount of blood pumped by the heart in one stroke. Carnitine supplied by a food concentrate -- as bovine heart muscle substance -- with all synergists naturally present, would no doubt bring even more impressive results. ix
Italian researchers gave a total extract of heart muscle to patients with CHF and found it to greatly benefit "the regulation of the metabolism of the myocardial fibers," improve coronary circulation, and - when used with digitalis -- help the drug to be better utilized, increase its action, and reduce or neutralize some of its toxic effects. x
In a recent study, after prolonged and strenuous exertion, six out of 23 athletes had elevated blood levels of troponins -- proteins produced by injured heart muscle cells. Two of the six had concentrations as high as persons who had had heart attacks. Five of the six showed abnormal heart function. When the heart cannot produce a normal force or when stressed to perform more than its capacity, adaptive responses are triggered to increase the force of contraction. Cellular protein breakdown, indicating injury, is likely, with troponin or abnormal myosin (muscle protein) produced. Hence, persons not obtaining the nutrients required for normal or exertive workouts are draining or hurting their cardiac muscle tissues with activity. Exercise supposedly increases the strength and capacity of the cardiovascular system. Yet, if the heart muscle cells are not getting all the nutritive factors needed, exercise only further depletes, and stresses, those cells. As a result, young athletes may collapse with exertion. Older joggers and others dutifully exercising may hasten the onset of CHF, hypertrophy, arrhythmias, or other afflictions. xi
CoQ and OTHER NUTRIENTS
Within the ETP of beef heart cells is found a lipid source of CoQ. CoQ is essential to the electron transport system coupled to oxidative phosphorylation, needed for heart muscle tone and contractile strength. Dr. Richard Passwater observed: "Coenzyme Q (also called ubiquinone) is an aid in certain energy-producing enzymatic reactions and is indispensable to heart function. Since the normal human heart is higher in Coenzyme Q content than most other tissues, it follows that biopsy samples taken from the hearts of heart disease patients show a deficiency of Coenzyme Q." xii
CoQ functions as a fat-soluble vitamin (coenzyme) and is found in every cell of the body. Since it is synthesized by cells from required raw materials, it would not be categorized as a vitamin according to classical definition (that a vitamin can be acquired only in integral form through food). Nevertheless, many persons - particularly the elderly -- are found to be deficient.
CoQ-10 is an essential component in a fundamental biochemical process: conversion of fuel into cellular energy (ATP). The highest concentrations appear in the heart and liver, so animal heart and liver are excellent food sources. Eggs, green leafy vegetables, wheat berries, wheat germ oil, rice bran oil, some legumes, potatoes (white and sweet), corn, walnuts, almonds, chestnuts, and some fish contain much lesser amounts.
Ten common CoQs (Q-1 to Q-10) have been found so far in plants, animals, and humans, which the liver can break down and recombine to produce the CoQ needed. Nutritional deficiencies are known to impair CoQ-10 production. There are at least 17 reaction steps in human tissue to yield CoQ-10 from the amino acid phenylalanine and acetyl CoA. Many of these steps "indispensably require" certain nutrients including tetrahydrobiopterin (coenzyme in hydroxylating phenylalanine, tryptophan, and tyrosine); pyridoxal-5-phosphate (coenzymatic form of B6); riboflavin, folic acid, and vitamin B12 coenzymes; pantothenic acid, niacinamide, vitamin C complex, and other nutrients.
It is known that levels of CoQ decline in selenium deficiency and that selenium stimulates CoQ production. "Selenium appears to be the most important nutrient in the control of Coenzyme Q levels. Therefore, adequate selenium is required to produce the necessary coenzyme Q required for a healthy heart."
Selenium, the trace mineral activator of vitamin E complex, naturally occurs in foods rich in vitamin E complex. Evidence shows that CoQ-10 can help "recycle" vitamin E, that it protects lipoprotein lipids (including LDL and other fractions), and that it induces energy conservation.
Among the "basic functions" of vitamin E complex are "preventing muscle disintegration" (including heart muscle), strengthening muscle, conserving oxygen, and promoting oxygenation. Heart tissue from normal animals contains twice as much vitamin E as body fat. Oxygen consumption of heart muscle tissues from E-deficient animals will be as much as 40% above normal, indicating this vitamin is necessary to utilize oxygen efficiently. It can assist in ridding the body of excess fluid, reduce elevated blood pressure, and "has similar actions as digitalis."
A deficiency of selenium produces a variety of diseases, including cardiomyopathy and CHF. With its vitamin E coworkers, selenium protects cardiac and skeletal muscle from degenerative wasting and aids in replacement of functional muscle tissue. Plasma selenium decreases in many persons as they age.
Dozens of studies have demonstrated the value and effectiveness of CoQ-10 supplementation. One scientist listed 60 clinical studies assessing more than 1200 patients. In 42 studies concerned with heart muscle, 77% of the patients given CoQ-10 showed clinical improvement. In studies on CHF, patients often improved dramatically, resuming normal activities. Other cardiovascular areas, the immune system, other muscle tissues, nerve tissues, the retina, periodontal tissues, and general energy all have benefited from CoQ-10.
In a large study of 2,664 CHF patients, improvement of at least three symptoms after only three months on CoQ-10 occurred in 54%. One study of heart patients found CoQ-10 deficiencies in 75% of the 132 patients involved. Confounding this situation is that some common "heart" drugs can aggravate a CoQ-10 deficiency. For example, lovastatin, used to lower cholesterol levels, inhibits the body's production of CoQ-10.
Cardiologist Peter Langsjoen, M.D., says that: "CoQ-10 is not specific to any type of heart failure. All forms of cardiomyopathy seem to respond..." including enlarged hearts and ischemic (reduced blood flow) types
Unfortunately, CoQ-10 has been synthesized as a "pure" (refined, artificially manufactured) compound by fermentation. This synthetic isolate is the supplement most often purchased. "It is not ethical to prescribe dosages of CoQ-10 without a medical evaluation by a health professional." This is because it is more of a drug than a food. Thus, several studies showed patients had an increased "feeling of wellbeing" (probably a foreign-substance euphoric effect) but no other improvements. The data on the synthetic version do not confirm that CoQ-10 is good therapy. Attempts to corroborate the observation of CoQ-10 deficiency with improvements by synthetic supplementation are, so far, "inconclusive." Mild adverse effects often occur since it is no longer an integral part of food. xiii
MINERALS AND MORE
The magnesium ion -- essential to over 300 known enzyme reactions, utilization of energy-rich ATP, optimum mitochondrial function including oxidative phosphorylation, and ionic regulation across cell membranes -- is needed for normal function of heart muscle cells, including contraction and relaxation. Tissues with the highest concentration of magnesium are those which are most metabolically active: heart, brain, liver, and kidney. Animal studies demonstrate that magnesium deficiency results in significant injury to the myocardium. The experiments also show that the severity of the damage is reduced with adequate vitamin E levels, pointing to the protective properties of vitamin E. "Nutrients work in the body as a team." In fact, among other consequences of magnesium deficits are hypocalcemia (low calcium levels), and hypokalemia (low potassium levels) -- minerals also imperative to cardiac health and function. Further, magnesium assists in regulating proper calcium metabolism by its actions on several hormones such as parathyroid hormone and calcitonin. Such natural regulation and balance must be far superior to calcium channel-blocker drugs.
Magnesium deficiency is known to contribute to cardiac arrhythmias and sudden death. Low levels of magnesium (particularly of white blood cells) are common in patients with CHF, though serum levels are depressed only in severe deficiencies. Survival rates have been directly correlated with magnesium levels. Supplementation has produced beneficial effects in CHF patients receiving conventional drug therapy even if serum magnesium levels are normal. Usual drug therapies (digitalis, diuretics, beta-blockers, calcium channel-blockers, etc.) cause magnesium depletion.
Decreased magnesium concentrations and resultant increased calcium concentrations in the heart may increase the risk for heart damage and acute heart failure, according to some research data. Yet, increasing the levels of heart cell calcium is also found to be beneficial in CHF -- "appropriate levels optimize cardiac function..." Calcium is functionally important to cardiac cells and is involved in the generation of electrical potential in the conducting system. Lack of sufficient potassium can paralyze or cramp muscle tissues and cause cardiac arrhythmia. A deficit of muscle potassium in patients with CHF cannot be corrected when there is a concomitant magnesium deficiency, magnesium loss leading to further loss of intracellular potassium. In CHF, myocardial sodium may be elevated, while serum sodium may be reduced. It is evident that mineral balance (especially alkaline-ash minerals) and attainment of food sources of organic mineral complexes are crucial to heart function and stability. xiv
Taurine is found in most body tissues and fluids as a free amino acid. In heart muscle, taurine increases the calcium available for contractions, yet protects against imbalance such as intracellular calcium overload when magnesium or potassium are low. Taurine in cardiac muscle "mediates contractility and workload to the extent that taurine has been considered effective therapy" in CHF. It is essentially absent from plants but is found in animal foods including muscle, brain, liver, and heart. It is the end product of sulfur amino acid metabolism. Methionine is one of the sulfur-bearing, essential amino acids which are denatured by heat and necessary for taurine biosynthesis. Enzymes involved in the pathway to taurine biosynthesis heavily depend on pyroxidine (B6) as a cofactor. xv
Intracellular creatine, another sulfur-bearing amino acid, serves as a tremendous source of energy for muscle contraction activity, and is decreased in patients with cardiac hypertrophy and CHF by approximately 20%. xvi
Animals fed diets low in copper will develop cardiac abnormalities including hypertrophy and cardiomyopathy. Copper is a cofactor in the activity of several key enzymes. Human studies document mitochondrial defects in various muscles, including heart (especially cardiomyopathy), with deficits of cytochrome oxidase, a copper-containing enzyme needed for energy production by the mitochondrial electron transport system. Organic copper as the enzyme tyrosinase is found in foods rich in vitamin C complex. Conversely, isolated ascorbic acid depletes the body of copper. xvii
It is well known that heart failure occurs with "wet" beriberi -- a severe deficit of thiamin (B1) and likely other B vitamin factors. The role of subclinical deficiencies of thiamin and the whole vitamin B complex in CHF is now receiving more interest. Such deficits are a consistent finding, especially when diuretics are used. Furosemide (Lasix) --the most widely prescribed diuretic -has been shown to cause thiamin deficiency in animals and in patients with CHF. xviii
Though frequently blamed on genetic mutations, particularly when affecting young people, CHF and cardiomyopathy have been indisputedly linked with inadequate supplies of many specific nutrients, and have been significantly aided and even overcome by dietary and supplemental assistance.
Dr. Royal Lee wrote that "correction of the deficiencies takes off the overload" on the heart which "alone means that the vicious cycle is broken and the improvement often is apparently miraculous..." On the other hand, he declared that, with cardiac depletion, it is "certainly a barbaric practice to try to stimulate the heart with drugs..." xix
To support the heart muscle and associated tissues, a diet of whole, natural foods -- avoiding processed and refined foods - can be supplemented with: heart glandular (e.g. protomorphogen); total, bioavailable protein; wheat germ oil and other sources of vitamin E complex and essential fatty acids; vitamin B complex: vitamin C complex with its organic copper; ionizable (phosphorus-free) calcium, magnesium, and other minerals and trace minerals, particularly alkaline-ash minerals.
i K. Fackelmann, Science News, Vol.150, No.5, 3 Aug. 1996, pp.76-77; B. Maron, JAMA, Vol.276, No.18, 13 Nov. 1996, p.1472.
ii R. Voelker, JAMA, Vol.273, No.8, 22 Feb. 1995, p.612; L. Katzenstein, Amer Health, Vol.XIV, No.3, April 1995, p.10; JAMA, Vol.271, No.11, 16 March 1994, pp.813-814.
iii Krause's Food, Nutrition & Diet Therapy, 8th Ed., ed., L. Mahan, M. Arlin, Phil: W.B. Saunders, 1992, pp.570-571; J. Whitaker, Health & Healing, Vol.5, No.4, April 1995, pp.1-2; Physicians' Desk Ref, 51 Ed., Montvale: Med Economics, 1997, pp.2834-2836.
iv Health Watch, Vol.1, No.7, Nov. 1996, p.1; M.H. Alderman, et al., Lancet, Vol.349, No.9052, 1 March 1997, pp.594-598; Worst Pills/Best Pills, Vol.2, No.5, May 1996, pp.17-19; A.A. Levin, Health Facts, Vol.XXI, No.207, Aug. 1996, p.2; JAMA, Vol.276, No.10, 11 Sept. 1996, pp.785-791, 829-830; Healthline, Vol.15, No.10, Oct. 1996, p.2.
v M. Packer, Lancet, Vol.340, No.8811, 11 July 1992, pp.88-95; M. McCarthy, Lancet, Vol.347, No.8994, 13 Jan. 1996, p.110.
vi New England J of Med, 20 Feb. 1997, cited in Second Opinion, Vol.VII, No.6, June 1997, pp.2-3.
vii Worst Pills/Best Pills, Vol.2, No.9, Sept. 1996, p.36.
viii R.P. Murray, Biomedical Critique, Vol.4, No.7, Aug. 1983, pp.1-5; and Vol.4, No.8, Sept. 1983, pp.1-3; R. Lee, Vitamin News, Sept. 1956, pp.188- 190; R. Roskoski, Biochemistry, Phil: W.B. Saunders, 1996, pp.111-117, 120-133; A.L. Lehninger, Principles of Biochemistry, NY: Worth Publishers, 1982, pp.512-523.
ix M.T. Murray, Amer J of Natural Medicine, Vol.4, No.5, June 1997, p.6.
x A. Grigolato, et al., Minerva Med., Vol.47, 24 Jan. 1956, pp.178-182.
xi J. Fricker, Lancet, Vol.348, No.9042, 14 Dec. 1996, p.1647; Science News, Vol.150, No.22, 30 Nov. 1996, p.348.
xii R.A. Passwater, Selenium As Food & Medicine, New Canaan: Keats Publishing, 1980, p.57.
xiii A.R. Gaby, Acres, U.S.A., Vol.27, No.4, April 1997, pp.40-41; E.L. Knight, Med Update on Vitamins & Herbs, Vol.1, No.2, April 1996, pp.1-4; Passwater, Selenium as Food & Medicine, pp.57, 92, 124; Lee Foundation, Scope of Vitamin E, Report No.7, 1956, p.5; G.J. & J.D. Kirschmann, Nutrition Almanac, 4th Ed., NY: McGraw-Hill, 1996, p.241; J.D. Wallach, Acres, U.S.A., Vol.24, No.6, June 1994, pp.17-18; C. Berr, et al., J of Amer Geriatric Soc, Vol.41, 1993, pp.143-148; H. Santillo, Intuitive Eating, Prescott: Hohm Press, 1993, pp.123-125; Murray, Amer J of Natural Med, pp.16-17; M.R. Werbach, Nutritional Influences on Illness, Tarzana: Third Line Press, 1993, p.218; J. Challem, Natural Health, Vol.24, No.2, March/April1994, pp.44-50; D.Schardt, S. Schmidt, Nutrition Action Newsletter, Vol.22, No.2, March 1995, pp.8- 9; D. Bagchi, et al., Health Freedom News, Vol.16, No.1, Jan/Feb 1997, pp.50-56.
xiv K.L. Woods, Lancet, Vol.341, No.8838, 16 Jan. 1993, pp.155-156; A. Freedman, et al., Biochem & Biophys Research Comm., Vol.170, 1990, pp.1102- 1106; A.R. Gaby, Health News & Review, Vol.4, No.1, 1994, p.16; I.E. Dreosti, Nutrition Reviews, Vol.53, No.9, Sept. 1995, pp.523-527; M. T. Murray, Amer J of Natural Medicine, Vol.3, No.10, Dec. 1996, pp.8-19, and June 1997, p.15; R.B. Costello, J of Amer Coll of Nutrition, Vol.16, No.1, Feb. 1997, pp.22-31; H. Korpela, J of Amer Coll of Nutrition, Vol.10, 1991, pp.127-131; G.J. Kost, Archives in Pathological Laboratory Medicine, Vol.117, 1993, pp.890-896; Werbach, Nutritional Influences on illness, pp.216-218; C.C. Pfeiffer, Zinc & Other Micro-Nutrients, New Canaan: Keats, 1978, pp.97, 110.
xv Modern Nutrition in Health & Disease, 8th Ed., Philadelphia: Lea & Febiger, 1994, pp.477-482; Werbach, Nutritional Influences on Illness, p.219.
xvi M.L. Field, Cardiovascular Research, Vol.31, 1996, pp.174-175.
xvii D.M. Medeiros, The Nutrition Report, Vol.11, No.12, Dec. 1993, pp.89, 96; D. Medeiros, et al., J of Nutrition, Vol.121, 1991, pp.1026-1034.
xviii I. Shimon, et al., Amer J of Medicine, Vol.98, May 1995, pp.485-490; D. Leslie, M. Gheorghiade, Amer Heart J, Vol.131, 1996, pp.1248-1250; H.M. Seligmann, et al., Amer J of Medicine, Vol.91, Aug. 1991, pp.151-155.
xix Science News, Vol.152, No.4, 26 July 1997, p.55; R. Lee, Address to Annual Convention of International Assoc of Liberal Physicians, NY, 23- 24 Oct. 1943.
Originally published as an issue of Nutrition News and Views, reproduced with permission by the author, Judith A. DeCava, CNC, LNC.