Text Size

Site Search powered by Ajax




Atherosclerosis is a degenerative condition of the arteries characterized by deposits, called plaques, within the walls of the artery. These plaques consist largely of lipids (mainly cholesterol, usually complexed to proteins, and cholesterol esters), connective tissue, and smooth muscle cells shed from the artery wall. The atherosclerotic plaque, or atheroma, represents the endpoint of a complex, insidious process. Its complications lead to the major causes of death in the United States and have reached epidemic proportions throughout the Western world.

Due to the insidious nature of the disease, an atheromatous plaque will develop quietly over a period of several years. It is usually not diagnosed until there is an interruption in the normal flow of blood. As the plaques increase in size, they narrow the channel permitting blood flow (the lumen of the arteries), progressively compromising blood flow, leading to vascular insufficiency or thrombosis.

Although any artery may be affected, the aorta, and the coronary and cerebral vascular systems are most frequently involved. The tissue area serviced by the diseased artery is deprived of its vital oxygen and nutrient supply. If the artery involved supplies the heart, the result is a heart attack or myocardial infarction. If the artery supplies the brain, the result is a stroke or cerebral vascular accident. Myocardial infarction alone accounts for 20% of all deaths in the U.S., while degenerative and arteriosclerotic heart disease account for a total of 33%. Cerebral vascular disease or stroke is the third most common cause of death. It has been estimated that the health care costs attributable to atherosclerosis have reached 56 billion dollars per year in the U.S.

The best treatment of atherosclerosis, appears to be a comprehensive prevention program involving diet, exercise and lifestyle modification. This contention is well supported by the well accepted fact that the major risk factors (hyperlipidemia, hypertension, cigarette smoking and diabetes mellitus) are all induced by the "typical" American diet and lifestyle, and most of the other risk factors are also related to lifestyle (obesity, stress, personality type, and physical inactivity).

Advanced conditions are visible on x-ray because the calcification is so intense, notably the major abdominal artery, the aorta.


No single theory of the cause of the processes of atherosclerosis has been formulated to satisfy all investigators. The most widely accepted theory is the "Reaction to Injury Hypothesis," which theorizes that the atherosclerotic plaques are initiated as a response to injury to the arterial endothelium, the cells lining the inner wall of the artery.

Immunological, physical, mechanical, hemodynamic, viral, chemical and drug factors have all been shown to induce endothelial damage leading to plaque formation in experimental studies. Sites of injury become more permeable to plasma constituents, especially lipoproteins, allowing platelets to adhere to the connective tissue underneath the endothelial cells where they aggregate and release the contents of their granules. This local concentration of lipoproteins and platelet constituents leads to the migration of smooth muscle cells from the outer layer of the artery to the middle layer, where they undergo proliferation. This results in the formation of a fibrous cap (consisting of collagen, elastin and glycosaminoglycans) over the intimal surface upon which lipid deposits accumulate.

The reaction to injury hypothesis is not the only theory on the cause of atherosclerosis. Of particular interest to the nutritionally oriented is the "Homocysteine Theory" of atherosclerosis. Similar to the reaction to injury hypothesis, the homocysteine theory states there is a mechanical form of endothelial damage due to a vitamin B6 deficiency.

Since the first report in 1948 by Rinehart and Greenberg of an association of atherosclerosis with pyridoxine deficiency, numerous studies have further substantiated the role of pyridoxine in preventing atherosclerosis and vascular thrombosis. Homocysteine is derived from the amino acid methionine during protein catabolism and converted, via pyridoxine-dependent enzymes, to cystathionine. A deficiency of pyridoxine leads to the accumulation of homocysteine, which is extremely damaging to endothelial cells, leading to atherosclerosis. Another hypothesis worth mentioning is the "Monoclonal Hypothesis." This hypothesis states that intimal plaque originates as the result of benign cancerous growth of the smooth muscle cells initiated by mutation. The mutagens may be environmental chemicals (e.g., hydrocarbons), cholesterol metabolites (e.g., cholesterol oxidation products), or viruses. The aryl hydrocarbons, including benzypyrene and methylcholanthrene, found in cigarette smoke are potent mutagens and both directly damage and evoke benign cancerous growth of vascular endothelium and smooth muscle cells.

Much has been written concerning cholesterol and atherosclerosis. Evidence from population studies overwhelmingly associates high cholesterol levels with atherosclerosis and ischemic heart disease. In men and women 33 to 44 years of age, those with serum cholesterol levels of 256 mg/dl or over have a five times greater risk of developing coronary artery disease than those whose levels are below 220 mg/dl. Further analysis of serum lipoproteins has refined this risk to show the serum levels of low density lipoproteins (LDL) and very low density lipoproteins (VLDL) are directly related to risk in both men and women, while high density lipoprotein levels (HDL) are inversely related. Lowering serum cholesterol levels is a primary objective in the prevention of atherosclerosis. Most authorities now agree the level of plasma cholesterol is largely determined by the dietary intake of total calories of cholesterol, saturated fat, and polyunsaturated fat.

Cholesterol oxidative derivatives are potent lipid peroxides and are capable of significantly damaging arterial endothelium via free-radical formation, and indirectly via incorporation into the membranes. This results in increased fragility and permeability of endothelial and other cells. Cholesterol-rich fried foods are high in these toxic cholesterol derivatives and should be eliminated from the diet.

LDL, containing approximately 79% of the total plasma cholesterol, transports it to fibroblasts and smooth muscle, lymphoid and endothelial cells. HDL, however, transports cholesterol to the liver for metabolism and excretion. Therefore the HDL-to-LDL ratio determines the cholesterol catabolism-to-tissue deposition ratio. The HDL-to-LDL ratio also affects other balances in the body; for instance, platelet adhesiveness is inversely proportional to the HDL/LDL ratio.

The development of the atheromatous plaque can be prevented by inhibition of platelet function. The importance of platelet activity in development of the plaque cannot be overemphasized. Once platelets aggregate, they release a potent compound causing local cell proliferation. Saturated fats increase platelet aggregation, while polyunsaturated fats, particularly linoleic, linolenic and eicosapentaenoic acids, have the opposite effect. These effects are mediated through prostaglandin metabolism.

Prostaglandins and related compounds are derived from 20 carbon chain fatty acids containing three, four or five double bonds. 8,11,14-eicosatrienoic acid (di-homo-linolenic acid) contains three double bonds and is known as the prostaglandin-1 (PG1) series; 5,8,11,14-eicosatetraenoic acid (arachidonic acid) contains four double bonds and is known as the PG2 series; and 5,8,11,14,17-eicosapentaenoic acid (EPA) contains five double bonds and is known as the PG3 series. Subdivision into various prostaglandin classes is made according to changes in the cyclopentane ring incorporated in the structure of these fatty acid chains.

The prostaglandin I class (PGI or prostacyclin) is produced by the vascular endothelium and has anti-aggregating effects, while thromboxane A2 (a product of arachidonic acid metabolism) is produced by platelets and stimulates aggregation. The balance of these compounds is greatly affected by dietary fatty acids. Arachidonic acid increases aggregation while linoleic and linolenic acids inhibit the conversion of arachidonic acid to thromboxane. Prostacyclin synthesis is significantly impaired by lipid peroxidation.

There has been considerable research into the effects of EPA on prostaglandin metabolism and platelet function. Eskimo and Japanese diets are rich in EPA (from fish oils) and are associated with a lower incidence of cardiovascular disorders, more favorable plasma lipid and lipoprotein levels, and reduced platelet aggregation. In contrast, Western diets are rich in arachidonic acid and linoleic acid and are relatively poor in EPA and linolenic acid.

Decreasing platelet aggregation (particularly excessive aggregation) is an extremely important factor in the prevention and treatment of atherosclerosis. An increased consumption of oils containing linolenic and linoleic acids and EPA (PG3 prostaglandin series precursors) and a decreased consumption of arachidonic acid (PG2 series precursor), found only in animal products, will significantly reduce platelet aggregation and hence atherosclerosis.

Lack of Physical Exercise
Many studies have shown a direct relationship between physical activity and lipoprotein composition. One study, investigated various lipoprotein parameters in middle-aged marathon runners, joggers and inactive men. It demonstrated that HDL increases and cholesterol decreases in direct proportion to the distance run. Physical exercise is also associated with a decreased incidence of ischemic heart disease (IHD).

Cigarette smoking is a potent risk factor for atherosclerosis and ischemic heart disease. Statistical evidence reveals a mean increase of about 70% in the death rate and a three-to-fivefold increase in the risk of ischemic heart disease in smokers compared to non-smokers. Women over the age of 35 who smoke and who also take oral contraceptives are at very high risk for ischemic heart disease. In general, the increase in death rate of ischemic heart disease due to smoking is proportional to the amount and duration of smoking. Smoking also exacerbates other risk factors and increases platelet aggregation.

A strong association exists between coffee consumption (six cups a day) and serum cholesterol. The incidence of acute myocardial infarction has been found to correlate with coffee, but not tea (black) consumption.

Signs & Symptoms

Atherosclerosis is a quiet disease, significant symptoms only appear when the process as advanced to a stage where blood flow to a particular area has been greatly reduced. A simple physical finding, a crease in the ear lobe, may offer some warning atherosclerotic processes are occurring.

The ear lobe is richly vascularized, and a decrease in blood flow over a period of time is believed to result in collapse of the vascular bed. This leads to a diagonal ear lobe crease, which has been recognized as a sign of cardiovascular disease since 1973.

Since then, over 30 studies have been reported in the medical literature, with the largest to date involving 1,000 unselected patients. The crease is seen more commonly with advancing age, until the age of 80, when the incidence drops dramatically. However, the association with coronary heart disease is age-independent. The ear lobe crease appears to be a better predictor of heart disease than any other known risk factor including age, smoking, sedentary lifestyle, hyperlipidemia and others. While the presence of an ear lobe crease does not prove coronary artery disease, it strongly suggests it, and examination of the ear lobe should be a useful screening procedure. The correlation does not work with Orientals, native Americans and children with Beckwith's syndrome.

Nutritional Supplements

Structure & Function: Cardiovascular Support

General Supplements

Beta carotene*
Bromelain 750 mg
Carnitine1,500 mg
Chondroitin sulfate*
Chromium200 - 300 mcg
Copper2 - 3 mg
Fish Oils 4 - 10 g
Ginkgo biloba*
Magnesium 400 - 800 mg
Selenium 100 - 300 mcg
Vitamin C1,000 - 3,000 mg
Vitamin B-625 mg
Wheat germ*

* Please refer to the respective topic for specific nutrient amounts.


Certainly, in the industrialized world, virtually every adult suffers some degree of atherosclerosis. The array of nutrients used to reverse this trend is extensive. Unfortunately, a majority of the American population still consumes saturated fats, remains sedentary and cannot compensate for these factors simply with nutritional supplements, at any dosage.

Bee propolis is one of the more exotic products.

One of the largest groups is antioxidants: Beta Carotene, quercetin and rutin.

Another large group is composed of fibers, some of which are singled out: guar gum and oat bran. Fibers are believed to help cleanse the system, in which process it may also be helpful to boost the beneficial flora with L. acidophilus.

Other plants seem to be useful even without their fibers, in the form of juice, including: chlorella, chlorophyll and green barley. Also, garlic, ginkgo biloba and kelp , which are usually in capsule form, for convenience.

Oil from plant sources is also preferred by some people over fish oils e.g. evening primrose oil.

Several old favorites continue to be used: brewer's yeast and wheat germ, or the derivative from wheat germ: octacosonol.

Recent additions include: chromium picolinate, CoQ10, DHEA and lecithin (or its derivatives).

The listed nutrients are discussed individually.


Chromium chloride supplementation (200 mcg per day) results in a decrease in serum triglycerides and total cholesterol, while increasing HDL levels and improving glucose tolerance.

These results have also been duplicated with chromium-rich brewer's yeast, but not chromium-poor torula yeast. The chromium content of the U.S. diet is generally quite low.


Carnitine has been shown to be therapeutically effective in the treatment of ischemic heart disease. Since long chain fatty acids are the preferred metabolic substrate in well-oxygenated myocardial tissue, normal cardiac function is probably dependent on appropriate myocardial concentrations of carnitine. This is due to carnitine's role as a component of several enzymatic systems which are involved in the transport of fatty acids during energy production.

The normal myocardium stores more carnitine than it needs, but during decreased oxygen supply, carnitine levels quickly decrease.

Supplementation with carnitine normalizes myocardial carnitine levels and allows the ischemic heart muscle to utilize its limited oxygen supply more efficiently. Carnitine also increases HDL levels, while decreasing triglyceride and cholesterol levels.

Chondroitin sulfate:

Chondroitin sulfate, at a daily dose of 3 grams, has been shown to lower cholesterol and triglyceride levels and diminish thrombus formation.


Clinical studies have shown that the daily ingestion of 10-20 grams of commercially produced EPA results in reduced total cholesterol, increased HDL, reduced platelet aggregation, and increased bleeding time. These effects of EPA are due to its alteration of prostaglandin ratios and competition with arachidonic acid for binding enzyme sites. Increased consumption of EPA results in decreased production of PG2 series prostaglandins and increased levels of PG3 series. This is significant, due to the differing activities of the products of these series: prostacyclin (PGI3) has a greater anti-aggregating effect than PGI2, and thromboxane A3 is a less potent platelet-aggregating factor than thromboxane A2.


There is an inverse correlation between total body magnesium and atherosclerosis. Furthermore, it has been observed individuals dying suddenly of ischemic heart disease have significantly lower levels of myocardial magnesium and potassium than matched controls. Such a deficiency may be due to inadequate magnesium intake or excessive vitamin D intake, which intensifies magnesium deficiency. A magnesium deficiency has been shown to produce spasms of the coronary arteries and is thought to be a cause of nonocclusive sudden death ischemic heart disease. Intravenous magnesium is becoming a widely accepted procedure to halt heart attacks. Magnesium supplementation also increases HDL levels, decreases platelet aggregation and prolongs clotting time. Magnesium is also very effective in relieving many cardiac arrhythmias.


The daily administration of 800 mg elemental calcium has resulted in a 25% decrease in serum cholesterol in hypercholesterolemic men over a period of one year.


Lecithin provides phosphatidylcholine and the essential fatty acid linoleic acid. Lecithin has been used over 4 decades to lower blood levels of cholesterol and triglycerides in individuals with elevated levels. Reports in the medical literature are conflicting on the efficacy of lecithin. The dose that appears most effective is very large, i.e., 25 grams per day. However, most individuals tolerate this dose very well. As most commercially available lecithins are only 20% phophatidylcholine, administration of a more concentrated source of phosphatidylcholine could be at a lower dose.


Niacin has long been used as a cholesterol lowering agent. However, the dose required (2 to 9 grams) is quite high and usually produces significant side effects including flushing, gastrointestinal distress, gastric ulcer, glucose intolerance and damage to the liver. For these reasons, niacin's use as a cholesterol/triglyceride lowering compound should be reserved for individuals under the care of a physician.

Vitamin B-6

One of the theories of atherosclerosis is based on the idea that a vitamin B6 deficiency results in high levels of homocysteine which then damages the arterial wall. Vitamin B6 is indicated in a prevention program due to its role in normal collagen synthesis and platelet inhibiting action.


Low selenium levels are associated with an increased risk of ischemic heart disease. This observation is based on a study of 11,000 case-controlled pairs from Finland. Restricted selenium intake reduces the levels of glutathione peroxidase, a free radical scavenging enzyme. Deficiency of glutathione peroxidase may lead to increased lipid peroxide-induced vascular endothelial damage. These effects would be aggravated by a vitamin E deficiency as well. Selenium also influences prostaglandin metabolism and decreases platelet aggregation.

Vitamin C

Strong clinical and experimental evidence suggests a chronic latent vitamin C deficiency leads to hypercholesterolemia and the accumulation of cholesterol in certain tissues. Vitamin C helps prevent atherosclerosis by directly promoting the catabolism of triglycerides, and through its regulation of arterial wall integrity via its essential role in collagen formation.

Vitamin E

A tocopherol deficiency results in significantly higher levels of lipid peroxides; significantly reduced release of prostacyclin; and lower levels of superoxide dismutase (SOD), glutathione peroxidase and catalase, resulting in increased free radical damage, particularly of the vascular endothelium. Supplemental vitamin E has been shown to prevent atherosclerosis through its inhibition of the platelet-releasing reaction, which produces a marked rise in lipid peroxides; its actions as a free radical scavenger; inhibition of platelet aggregation; and its elevation of HDL levels.

Zinc and Copper

A high zinc-to-copper ratio appears to be a causative factor in atherosclerosis. Zinc and copper compete for binding sites for absorption. High dose zinc administration (160 mg per day) has been shown to lower serum HDL levels in men (but not in women). Lower levels of supplemental zinc (50 mg/day), however, appear to have no ill effects on cholesterol and HDL levels.

High dose zinc supplementation may induce a relative copper deficiency. A deficiency of copper produces results in elevated cholesterol levels. Copper is important both in lipid metabolism and in production of normal connective tissue.

As copper levels are commonly marginal in U.S. diet, supplementation may be appropriate keeping in mind that a balanced zinc-to-copper ratio is necessary for optimal health.

Note: All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.

Dietary Considerations

Low Fat Diet (Pritikin)
Low Fat Diet (Non Pritikin)

Fatty Acids
Saturated fats, fats which have been heated at high temperatures in the presence of oxygen (deep frying) and processed trans-partially-saturated fats and oils (e.g. margarine) are all believed to contribute to various aspects of atherosclerosis. Sources of saturated fats are usually also sources of cholesterol; while processed, heated, or trans-partially-saturated fats and oils are sources of lipid peroxides which interfere with normal essential fatty acid metabolism and, as they are incorporated into cell membranes, alter membrane structure and function.

Instead, dietary fats should be composed of linoleic (18:2n6), linolenic (18:3n3) and eicosapentaenoic (EPA,20:5n3) acids. These fatty acids lower cholesterol and triglyceride levels and decrease platelet aggregation. Men with new coronary heart disease have significantly lower levels of linoleic acid in their diet, adipose tissue, and platelets.

In population studies, it has been demonstrated that fish consumption is inversely correlated with mortality from coronary heart disease, while meat consumption is positively correlated. Mortality due to coronary heart disease was 50% lower among those who consumed an average of 30 g of fish per day compared with those who ate meat daily, who had a 300% increase in risk for coronary heart disease.

Common sugar promotes increased concentrations of plasma cholesterol, triglycerides and uric acid; and increased platelet adhesiveness, all of which are known to be atherogenic.

Homeopathic Remedy

1.* Cholesterinum - 15C to 30C
2. Plumbum iodatum - 15C
3.* Polygonium aviculare - 6X to 15C
4.* Sumbul - 2X - best used every 3 hours daily for several days.
5.** Aurum metallicum - 15C
6. Aurum muriaticum natronatum - 15C
7.** Baryta carbonica - 15C
8. Stront. carb. tinct. - 15C

Treatment Schedule

Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.


X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency
Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.


Boericke, D.E., 1988. Homeopathic Materia Medica.

Coulter, C.R., 1986. Portraits of Homeopathic Medicines.

Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.

Koehler, G., 1989. Handbook of Homeopathy.

Shingale, J.N., 1992. Bedside Prescriber.

Smith, Trevor, 1989. Homeopathic Medicine.

Ullman, Dana, 1991. The One Minute (or so) Healer.

Herbal Approaches


Garlic Plant
Ginger Plant
Milk thistle
Onion Plant

Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.


Alfalfa decreases cholesterol levels and has a "shrinkage" effect on atherosclerotic plaque.


This proteolytic enzyme of the pineapple plant has been shown to inhibit platelet aggregation in vitro and in vivo, inhibit angina pectoris, reduce blood pressure in hypertensives and break down atherosclerotic plaques.


Cayenne prevents the formation of thrombi and platelet aggregation and also lowers cholesterol.

Garlic Plant

Garlic bulbs have been shown to significantly lower total serum cholesterol and triglycerides, while increasing HDL levels. Also, garlic is capable of lowering blood pressure and preventing thrombus formation. (500 mg t.i.d.)

Ginger Plant

Ginger has been shown to lower cholesterol levels, inhibit platelet aggregation and possess cardiotonic activity.

Ginkgo Tree

Gingko increases blood supply to the brain, prevents platelet aggregation, and improves metabolic processes during ischemic conditions. It is particularly indicated in cases of vascular insufficiency, e.g., cerebral vascular insufficiency, peripheral vascular insufficiency and angina pectoris. (40 mg t.i.d.)

Hawthorn berries

Hawthorn berries prevent and reverse atherosclerotic plaque formation, reduce serum cholesterol levels, dilates coronary arteries, increases blood flow to the heart muscle, increase the force of contraction of the heart and lowers high blood pressure. (100 mg t.i.d.)

Milk thistle (Silymarin)

Is also recommended for hypertriglyceridemia, via improved liver function. (1 capsule of the extract t.i.d.)

Onion Plant

Onions have been shown to counteract the increased platelet aggregation seen after a high-fat meal as well as have antihypertensive and cholesterol lowering effects.

Aromatherapy - Essential Oils

Garlic Essence,
Juniper Essence,
Lemon Essence,
Onion Essence.


Related Health Conditions

Coronary heart disease
Insufficient blood circulation


Agarwal, O.P. Role of serum magnesium in development of spontaneous atherosclerosis in pigs. Ind J Exp Biol 20:262-3, 1982

Allen, K.G.D. & L.M. Klevay. Hyperlipoproteinemia in rats due to copper deficiency. Nutr Rep Int 22: 295-9, 1980

Ammon, H.P.T. & M. Handel. Crataegus, Toxicology & Pharmacology. Planta Medica 43:318-22, 1981.

Anonymous: Antioxidants in the Prevention of Human Atherosclerosis: Summary and Proceedings of a National Heart, Lung and Blood Institute Workshop, September, 1991;5-6, Circulation, June 1992;85(6):2338-2344.

Baggio, B. & G.F. Rizzoni. Juvenile Renal Stone Disease: A Study of Urinary Promoting and Inhibiting Factors. J. Of Urology, 130 1983.

Bauer, U. Six-Month double-blind randomized clinical trial of ginkgo biloba versus placebo in two parellel groups in patients suffering from peripheral artery insufficiency.

Bierenbaum, M.L., A.I. Fleischman, & R.I. Raichelson. Long term human studies on the lipid effects of oral calcium. Lipids 7:202-6, 1972

Bordia, A.K., H.K. Josh & Y.K. Sanadhya. Effect of garlic oil on fibrinolytic activity in patient with CHD. Atherosclerosis 28:155-9,1977

Chasroff, I.J. & J.W. Ellis. 1983. Family Medical Guide, William Morrow and Company Inc., Pub. 594 pp.

Cordova, C., A. Musca, F. Viola et al:Influence of ascorbic acid on platelet aggregation in vitro and in vivo. Atherosclerosis 41:15-9, 1982

Davis W.H., W.P. Leary, A.J. Reyes, & J.V. Olhaberry. Monotherapy with magnesium increases abnormally low high density lipoprotein cholesterol: A clinical essay. Curr Ther Res 36:341-5, 1984

Ed: Activation of lysyl oxidase by copper. Nutr Rev 37:330-1, 1979 Elliot W.J. Ear lobe crease and coronary artery disease. Am J Med 75:1024-32, 1983

Editor: Antibodies to Oxidize LDL in Atherosclerosis. The Lancet, April 11, 1992:339:899-900.

Freland-Graves J.H. et al., Effect of zinc supplementation on plasma high-density lipoprotein cholesterol and zinc. Am J Clin Nutr 35:988-92, 1982

Fromhout, D. et al.,The inverse relationship between fish consumption and 20-year mortality from coronary heart disease. N Eng J Med 312:1205-9, 1985

Gilman, A.G., L.S. Goodman & A. Gilman. The Pharmacological Basis of Therapeutics, 6th ed. MacMillan Publ Co., NY, NY, 1980, pp839-40.

Ginter, E. et al: Effect of ascorbic acid in the regulation of cholesterol metabolism and the pathogenesis of atherosclerosis. Int J Vit Nutr Res 47:, 1977

Gottfries-CG et al: The neurochemistry of vascular dementia. Dementia. 1994 May-Aug; 5(3-4): 163-7

Gujaral, S. et al.,Effect of ginger (zinger officinale roscoe) oleoresin on serum and hepatic cholesterol levels in cholesterol fed rats. Nutr Rep Int 17:183-9, 1978

Harris, W. S.: The Prevention of Atherosclerosis With Antioxidants. Clinical Cardiology, 1992;15:636-640.

Hattersley, J. G.: Acquired Atherosclerosis: Theories of Causation, Novel Therapies. Journal of Orthomolecular Medicine, 1991;6(2):83-98.

Heinicke, R.M., L. van der Wal & M. Yokoyama. Effect of bromelain (Ananase) on human platelet aggregation. Experientia 28:844-5, 1972

Hermann, W.J., K. Ward & J. Faucett. Therapy effect of tocopherol on high-density lipoprotein cholesterol. Am J Clin Path 72:848-52,1979

Hodis HN et al., Intermediate-density lipoproteins and progression of carotid arterial wall intima-media thickness. Circulation, 1997 Apr 15, 95:8, 2022-6.

Hughes, A. & R.S. Tonks. Platelets, magnesium, and myocardial infarction. Lancet 1:1044-6, 1965

Jeppesen, B.B., A. Blach & B. Harvald. Serum magnesium in Greenland eskimos. Acta Med Scand 215:477-9, 1984

Kirschmann, J.D. 1990. Nutrition Almanac: Nutrition Search. McGrew-Hill: NY.

Kosolcharoen, P., J. Nappi, P. Peruzzi, et al:Improved exercise tolerance after administration of carnitine. Curr Ther Res 30:753-64, 1981.

Krumdieck, C. & C.E. Butterworth. Ascorbate-cholesterol-lecithin interactions: Factors of potential importance in the pathogenesis of atherosclerosis. Am J Clin Nutr 27:866-76, 1974.

Lam, SC-T et al., Investigation of possible mechanisms of pyridoxal 5-phosphate inhibition of platelet reactions. Thrombosis Res 20:633-45, 1980.

Louria, D.B et al: Onion extract in treatment of hypertension and hyperlipidemia: A preliminary communication. Curr Ther Res 37:127-31, 1985.

Manthey, J. Magnesium and trace metals: Risk factors for CHD. Circulation 64:722-9, 1981.

McCully, Kilmer S: Atherosclerosis, Serum Cholesterol and the Homocysteine Theory: A Study of 194 Consecutive Autopsies. The American Journal of The Medical Sciences, April 1990;299(4):217-221.

McCully, K.S. & R.B. Wilson. Homocysteine theory of arteriosclerosis. Atherosclerosis 22:215-27, 1975.

Mertz, W. Trace minerals and atherosclerosis. Fed Proc 41:2807-12, 1982.

Mower, R. & M. Steiner. Biochemical interaction of arachidonic acid and vitamin E in human platelets. Prostaglandins Med 10:389-403, 1983.

Murray, M.T., & J.E. Pizzorno. 1991. Encyclopedia of Natural Medicine. Rocklin, Ca; Prima Publishing.

Nakazawa, K. & K. Murata. The therapeutic effect of chondroitin polysulphate in elderly atherosclerotic patients. Journal of Internation Medical Research 1978: 6; 217-25

Nakamura, M. Effect of vitamin E deficiency on the level of SOD, glutathione peroxidase, catalase and lipid peroxide. Int J Vit Nutr Re 46:187-91, 1976

Nord, H.J., et.al. 1970. Treatment of congestive heart failure with glucagon. Annals of Internal Medicine, 72.

Offenbach, E. & F. Pistunyer. Beneficial effect of chromium-rich yeast on glucose tolerance and blood lipids in elderly patients. Diabetes 29:919-25, 1980.

Okuma, N., H. Takayama & H. Uchino. Generation of prostacyclin-like substance and lipid peroxidation in vitamin E deficient rats. Prostaglandins 19:527-536, 1980.

Pachotikarn, C., D.M. Medeiros & F. Windham. Effect of oral zinc supplementation upon plasma lipids, blood pressure, & other variables in young adult white males. Nutrition Reports International 32:373-82, 1985.

Petersdorf, R.G. & R.D. Adams. 1983. Harrison's Principles Of Internal Medicine. 10th ed. McGraw Hill Pub Co., New York. 2212 pp.

Petkov, V. Plants with hypotensive, antiatheromatous and coronarodilating action. Am Journal Chinese Med 3:197-236, 1979.

Pizzorno, Joseph E., Jr.,N.D. & Murray, Michael N.D. A Textbook of Natural Medicine. JBC Publications, Seattle, WA, 1985.

Pola, P., M. Savi, R. Grilli, et al: Carnitine in the therapy of dyslipidemic patients. Curr Ther Res 27:208-15, 1980.

Pola, P., P. Tondi, A. Dal Lago, et al. Statistical evaluation of long-term L-carnitine therapy in hyperlipoproteinaemias. Drugs Exptl Clin Res IX:925-34, 1983.

Pola, P., L. Savi, M. Serricchio, et al. Use of physiological substance, acetyl-carnitine, in the treatment of angiospastic syndromes. Drugs Exptl Clin Res X:213-7, 1984.

Riales, R. & M. Albrink. Effect of chromium chloride supplementation on the glucose tolerance and serum lipids, including HDL, of adult men. Am J Clin Nutr 34:2670-8, 1981.

Robbins, S.L. & R.S. Cotran. 1979. Pathologic Basis of Disease, 2nd ed. Saunders Pub Co., Philadelphia. 1598 pp.

Rossi, C.S. & N. Siliprandi. Effect of carnitine on serum HDL-cholesterol Report of two cases. John Hopkins Med J 150:51-54, 1982.

Salonen, J.T. Association between cardiovascular death and myocardial infarction and serum selenium in a matched-pair longitudinal study. Lancet 2:175-9, 1982.

Sambiah, K. & M.N. Satyanarayana. Hypocholesterolemic effect of red pepper and capsaicin. ind J Exp Biol 18:898-9, 1980

Sanders, T.A.B. & F. Roshanai. The influence of different types of omega-3 polyunsaturated fatty acids on blood lipids and platelet function in healthy volunteers. Clin Sci 64:91-9, 1983

Seelig, M.S. & H.A. Heggtveit. Magnesium interrelationship in ischemic heart disease: A review. Am J CLin Nutr 27:59-79, 1974

Simons, L.A., J.B. Hickie, & S. Balasubramaniam. On the effects of dietary n-3 fatty acids (Maxepa) on plasma lipids and lipoproteins in patients with hyperlipidemia. Atherosclerosis 54:75-88, 1985

Snowdon, D.A., R.L. Phillips, G.E. Fraser. Meat consumption and fatal heart disease. Prev Med 13:490-500, 1984

Spittell-J.A.: Peripheral arterial disease. Dis-Mon. 1994 Dec; 40(12): 641-700.

Srivastava, K.C. Effects of aqueous extracts of onion, garlic and ginger on platelet aggregation & metabolism of arachidonic acid in the blood vascular system: In vitro study. Prostaglandins Med 13:227-35, 1984.

Steiner, M. & J. Anastasi. Vitamin E - An inhibitor of platelet release reaction. J Clin Invest 57:732-7, 1976.

Taussig, S.J. & H.A. Nieper. Bromelain: Its use in prevention and treatment of cardiovascular disease - present status. J Int Ac Prev Med VI:139-50, 1979.

Tur-E. et al: Cutaneous blood flow abnormalities in hypertriglyceridemia.. J-Invest-Dermatol. 1994 Oct; 103(4): 597-600.

Turlapaty, P.DMV & B.M. Altura. Magnesium deficiency produces spasms of coronary arteries. Relationship to etiology of sudden death ischemic heart disease. Sci 208:199-200, 1980

Valek, J., J. Hammer, M. Kohout, et al. Serum linoleic acid & cardiovascular death in postinfarction middle-aged men. Atherosclerosis 54, 1985.

Walji, Hasnain. 1994. Heart Health. A Self-help Guide to combining Orthodox & Complementary Approaches . Hodder Headline Plc.London.

Wang, J.P., M.F. Hsu & C.M. Teng. Antiplatelet effect of capsaicin. Thrombosis Res 36:497-507, 1984.

Watanabe, J., F. Umeda, H. Wakasugi, & H. Ibayashi. Effect of vitamin E on platelet aggregation in diabetes mellitus. Thromb Haemostas (Stuttgart) 51:313-6, 1984.

Watts-GF et al: Nutrient intake and progression of coronary artery disease. Am-J-Cardiol. 1994 Feb 15; 73(5): 328-32.

Wood, J.L. & Allison, R.G. Effects of consumption of choline and lecithin on neurological and cardiovascular systems. Fed Procs 1982 41;3015-21.


Follow Applied Health on FaceBook Follow Applied Health on Twitter Follow Applied Health on Pinterest Follow Applied Health on YouTube

cruelty free - tested only on humans
We test only on humans