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From the Townsend Letter for Doctors & Patients
August/September 2004


Therapeutic Nutrition
by Gina L. Nick, PhD, ND

Whole Food Therapeutics and Lifestyle Change in the Treatment of Cardiovascular Disease in Men
Guest Author, David Minzel, PhD, CNC

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"Functional foods," "nutraceuticals," "designer foods" and "medicinal foods" are terms that describe foods, and key ingredients isolated from foods, that have non-nutritive or tertiary functional properties. Researchers, healthcare practitioners, laypersons, and the popular media use these words interchangeably. The purpose of this article is to detail valid scientific and pertinent clinical information on whole foods and accompanying lifestyle modifications recognized for their ability to prevent and treat cardiovascular disease in men.

Whole Food Therapeutics and Lifestyle Change in the Treatment of Cardiovascular Disease in Men
Guest Author, David Minzel, PhD, CNC

An Enormous Problem
Simply and tragically, there are no statistics in health care today more staggering than those for cardiovascular disease (CVD). According to current estimates, 61.8 million Americans have one or more types of cardiovascular disease.1 Thirty million men, or one in five, suffer from high blood pressure, coronary artery disease, myocardial infarction, angina pectoris, stroke, congenital cardiovascular defects, or congestive heart failure.
CVD claimed 958,775 American lives in 1999, according to the American Heart Association.2 That is the equivalent of more than 2,600 deaths each day from CVD, or an average of one death every 33 seconds; 46.5% of these deaths, about one every minute, were in men. Deaths associated with CVD are by far the number one cause of death, not only in the US, but globally as well. CVD claims more lives annually than the next seven leading causes of death combined.

Since 1900, CVD has been the top killer in the United States every year except 1918 (when World War I was the top killer).2 Although the death rate (number of deaths per 100,000 people) from CVD declined from 1989 to 1999, the total number of deaths actually increased by over 2% during that period.

Based on data from the National Heart, Lung, and Blood Institute,3 there has been an alarming increase in sudden cardiac deaths – 50% of men with CVD die suddenly from heart failure, without any previous symptoms of disease,3 making it difficult to diagnose and prevent. A large number of men who are diagnosed with CVD require long-term medical care and hospitalization. Although 25% of these men will die within the first year following an initial recognized myocardial infarction,3 the annual direct and indirect costs of treatment for cardiovascular diseases in the U.S. were estimated to be $329.2 billion dollars in 2002.2 (This figure includes the cost of physicians and other professionals, hospital and nursing home services, medications, home health care and other medical durables, and lost productivity resulting from morbidity and mortality). By comparison, the estimated medical costs for all cancers in 2001 was $156.7 billion and the estimated costs for treating HIV infection was $28.9 billion.

Conventional Medical Intervention
Medical intervention for these coronary diseases has focused on downstream treatment with cardiovascular procedures like cardiac catheterization, coronary artery bypass surgery, heart transplants, and percutaneous transluminal coronary angioplasty (so-called "balloon angioplasty"). Additionally, CVD symptoms are treated with targeted pharmaceutical drug interventions. The number of cardiovascular operations and procedures performed each year has increased over 400% from 1979-1999,2 and of the top 25 prescribed medications in 2001, seven were for the treatment of problems associated with CVD, such as high cholesterol and high blood pressure.4 The National Committee for Quality Assurance has emphasized prevention and treatment of cardiovascular diseases by advising smokers to quit, promoting the use of beta blocking medications following a heart attack, and recommending cholesterol and high blood pressure control in patients with coronary artery disease.5 Yet clearly the enormous number of deaths associated with CVD warrants more investigation into the prevention and treatment of CVD.

Answers to reducing the overall incidence of cardiovascular disease and death cannot lie only in developing costly complex technological treatments and procedures to alleviate the symptoms and end results of the disease state. The health care profession must focus its attention on prevention of CVD before it begins, and assist individuals in taking deeper responsibility for their health through lifestyle, diet, and education.

Time for a New Approach?
It seems reasonable to ask:
• If the conventional medical approach to CVD treatment is failing to stop the ravages of the disease, is there a better way?
• What do we know about the relationship of diet to the risk of heart disease?
• Can dietary and/or supplement therapies help lower the risks or reverse the progression of CVD?
• What part does genetics and family history play in CVD?
• Can dietary and nutrient therapeutics change the risk-associated genetic expressions of heart disease? Can we more effectively treat these diseases by affecting biochemical processes upstream of the genetic expression of disease?
• What part does lifestyle play in the development and prevention of CVD?

Smoking, Dietary Change, CVD, Deaths and Cost
Twenty-five million American men over 18 years of age are smokers, and therefore at increased risk for heart attacks and strokes. About one in five deaths from CVD is attributed to smoking with an annual estimated cost for medical care of $130 billion.6 This would suggest that a recommendation by health care practitioners for their patients to quit smoking would be a very high priority. Yet in 1996, only 61% of smokers were advised to quit smoking by their health care practitioners and that number had only increased to 65% in 1999.2

It has been estimated that reducing meat intake, increasing intake of antioxidant-rich fruits and vegetables, eating fiber-rich complex carbohydrates, and consuming low-fat dairy products can reduce CVD risk by as much as 90%.7,8 This suggests other recommendations that health care practitioners might make to their patients to alleviate the health care burden of CVD. At best, however, doctors promote the common "Food Pyramid," a dietary recommendation system where simple, low-fiber carbohydrates are the staple of the diet. The Food Pyramid, incidentally, was devised by General Mills, a company that manufactures food products consisting largely of refined, simple carbohydrates.

The impact of CVD is not limited to mortality. Thus, men in their prime productive years (40-60 years old) are often crippled by CVD, unable to work and enjoy life, resulting in enormous social and economic losses. CVD is the single largest contributor to permanent disability in male workers under the age of 65 and is responsible for more hospitalization days than any other illness.2

If dietary and lifestyle changes alone could prevent lives from being prematurely ruined or lost, and at the same time reduce the enormous health care costs of CVD, it would provide hope that this tragic disease could be prevented and possibly eliminated.

Dietary Nutrient Insufficiency
Data from the Third National Health and Nutrition Examination Survey of 1988-19949 clearly shows serious dietary and nutrient deficits in certain populations in the US. More than 10 million people in the US often do not have enough food to eat, leaving them at great risk for the development of nutrition-related health problems. The NHANES III study revealed many cardiovascular risks for the older population. Nearly 90% of Americans over the age of 65 have been found to have one or more nutrition-related cardiovascular risk factors.10 The future development of nutrition-related cardiovascular risk factors in children seems assured unless measures are taken to prevent it. Researchers studying over 3000 children in the U.S. ranging in ages from 2-19 found only 1% met all recommendations for food group and nutrient intake.11

Of the leading risk factors for the development of CVD, diet and lifestyle are at or near the top of the list. With clear dietary and nutrient insufficiency occurring, the place to begin prevention of CVD is with the intake of real, nutrient-rich foods.

Amino Acid Composition of Diet and CVD
The amino acid composition of dietary intake contributes to the modulation of arterial physiology. Soy protein intake containing a high arginine-to-lysine ratio has been shown to produce lower postprandial insulin-to-glucagon ratios and lower serum cholesterol than casein intake, higher in lysine that produces high insulin-to-glucagon ratios and an increase in serum cholesterol levels.12,13 More importantly, the arginine-rich protein intake modulated the concentration of low-density lipoprotein (LDL) which has been shown to increase the production of nitrous oxide (NO) that beneficially alters arterial compliance, LDL inhibiting the formation of NO.13,14 A change to a more plant-based diet then, higher in arginine, may contribute to improved arterial health and a reduction in CVD and hypertension.

Calcium and High Blood Pressure
Hypertension, or high blood pressure (HBP), was listed as a primary cause of death on the death certificates of over 42,000 Americans in 1999, and was a contributing cause of death in over 225,000. A higher percentage of men than women have HBP until the age of 55, when the percentage of women is slightly higher. The 1999 mortality numbers in the US showed 17,194 male deaths associated to HBP, 40% of the total deaths from HBP.2

Epidemiological studies show that people consuming low calcium-rich diets exhibit a higher incidence of HBP,15,16 and data from the Health and Nutrition Examination Survey I undertaken by the National Center for Health Statistics revealed that people with HBP consumed less dietary calcium than those with normal blood pressure.17

Magnesium and HBP
A number of studies have shown that increased dietary magnesium is associated with lower blood pressure.18-20 The principal source of magnesium is water and an inverse correlation has been found between water hardness due to magnesium and blood pressure. Additional dietary studies have looked at the association between HBP and magnesium intake from food. High blood pressure was found to be lower in segments of the population for which dietary magnesium levels were sufficient.21

Investigative trials on magnesium supplementation, however, have yielded mixed results, suggesting that food sources of magnesium may be more beneficial than supplements. There are likely numerous nutrients in whole foods that complement magnesium's anti-HBP role, making dietary magnesium more useful than elemental supplements in fighting the disease. Some of the richest food sources of magnesium are:
• Kelp
• Wheat Bran
• Wheat Germ
• Almonds
• Blackstrap molasses
• Brewer's yeast
• Buckwheat
• Dulse
• Millet
• Rye
• Tofu
• Beet greens

Potassium and HBP
Many studies show that potassium deficiency in the diet leads to HBP and ultimately CVD.22-28 Increasing dietary intakes of potassium-rich foods can lower blood pressure.22,28-30 A wide variety of foods are rich in potassium, particularly fruits and vegetables, suggesting that a diet rich in potassium may help decrease the risk of developing HBP.

Potassium has shown efficacy in treating and reducing HBP31,32 and the results compare favorably with drug treatments for HBP without the negative side effects often associated with these medications.33 Some of the richest food sources of potassium are:
• Dulse
• Kelp
• Sunflower seeds
• Wheat germ
• Raisins
• Avocado
• Swiss chard
• Garlic
• Millet
• Banana
• Chicken

Fish Oils & Coronary Artery Disease
Coronary artery disease (CAD) is the advanced form of atherosclerosis of the arteries that supply blood and oxygen to the heart muscle itself. Long-term damage to vascular biology leads to eventual blockage of these arteries, diminishing the blood and oxygen supply to the heart and damaging heart tissue. This damage further diminishes the supply of oxygen and nutrients to the heart, eventually leading to heart attack or myocardial infarction (MI). Whole food and nutrient therapies have been aimed at lowering platelet aggregation or interrupting the biochemical chain of events that leads to atherosclerosis. Many studies have clearly shown the beneficial effects of consuming fish, fish oils, and flaxseed oil.34-35 The antiatherosclerotic effect of these foods has been attributed to the high levels of omega-3 fatty acids they contain, which inhibit or delay thrombus formation by reducing platelet aggregation and oxidative stress-related arterial injury. Recent trials have shown a modest reduction in atherosclerotic plaque formation and hypertension with intake of omega-3 fatty acid-rich fish oils.36

Garlic & CAD
Dietary intake or supplementation with garlic has been effectively used to reduce the incidence of CAD by inhibiting platelet aggregation.37 Other so-called "functional foods," foods considered physiologically active, provide health benefits beyond basic nutrition and have been found to be potentially beneficial in the prevention and treatment of cardiovascular disease. These foods include soybeans, oats, Psyllium, flaxseed, garlic, tea, fish, grapes, and nuts, which act to improve arterial compliance, reduce low-density lipoprotein oxidation, decrease plaque formation, scavenge free radicals, and inhibit platelet aggregation.34

LDL Cholesterol
LDL, or low-density lipoprotein, cholesterol is one of three major lipoproteins in the body and is the primary way in which cholesterol manufactured in the liver and absorbed through the intestinal lining is transported to cells. LDL is the major source of cholesterol in atherosclerotic plaques. As a result, elevations in LDL-cholesterol are associated with the development of atherosclerosis and significant increases in the risk of developing CVD. Researchers in the Lipid Research Clinics Coronary Primary Prevention Trial38 found that with a 10-15% reduction in dietary LDL levels, the estimated incidence of heart attacks declined by approximately 20-30%.38

Oxidation of LDL plays a major role in the development of atherosclerosis because it is far more reactive than unaltered LDL. Oxidation of LDL is a significant step in the process of vascular damage. There are basically two ways to reduce the damaging effects of oxidized LDL. One is to reduce the amount of LDL in the bloodstream by decreasing dietary fat intake. The other way is to increase the intake of antioxidant-rich fruits and vegetables that have been shown in animal and human studies to reduce the oxidation of LDL by at least 30%.39-41

A number of food substances have shown efficacy in reducing levels of LDL in human trials, including fish and flax seed oil,42-43 garlic,44-45 lecithin,46 and fiber.47-49 Increasing physical activity/exercise and decreasing smoking, excess alcohol, and coffee consumption have by far the greatest effect in lowering excess LDL and oxidative stress associated with vascular damage.50-57

In this author's opinion, optimal cardiovascular health lies not in post facto treatment of downstream biochemical events after a lifetime of poor diet and poor lifestyle, but in the early optimization and customization to the patient of the diet and lifestyle through education from those of us in the healing arts.

1. CDC/NCHS and AHA. 1994. National Health and Nutrition Examination Survey III (NHANES III), 1988-94. National Center for Health Statistics and the American Heart Association.
2. AHA. 2002. Heart and Stroke Statistical Update. Dallas, TX: American Heart Association.
3. NHLBI. 1987-1994. Framingham Heart Study.
4., 2002
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11. Munoz, K. A. et al. 1997. Food intakes of US children and adolescents compared with recommendations. Pediatrics 100(3 Pt 1): 323-329.
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22. Coruzzi, P. et al. 2001. Potassium depletion and salt sensitivity in essential hypertension. J Clin Endocrinol Metab 86(6): 2857-2862.
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29. Morris, R. C. et al. 1999B. Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications. Semin Nephrol 19(5): 487-93.
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31. Fotherby, M. D. and J. F. Potter. Potassium supplementation reduces clinic and ambulatory blood pressure in elderly hypertensive patients. J Hypertens 10(11): 1403-1408.
32. Oble, A. O. 1989. Placebo-controlled trial of potassium supplements in black patients with mild essential hypertension. J Cardiovasc Pharmacol 14:294-296.
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44. Kannar, D. et al. 2001. Hypocholesterolemic effect of an enteric-coated garlic supplement. J Am Coll Nutr 20(3): 225-231.
45. Slowing, K. et al. 2001. Study of garlic extracts and fractions on cholesterol plasma levels and vascular reactivity in cholesterol-fed rats. J Nutr 131(3 Suppl): 994S-999S.
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47. Jenkins, D. J. et al. 2002. Soluble fiber intake at a dose approved by the US Food and Drug Administration for a claim of health benefits: Serum lipid risk factors for cardiovascular disease assessed in a randomized controlled crossover trial. Am J Clin Nutr 75(5): 834-839.
48. Qureshi, A. A. et al. 2002. Effects of stabilized rice bran, its soluble and fiber fractions on blood glucose levels and serum lipid parameters in humans with diabetes mellitus Types I and II. J Nutr Biochem 13(3): 175-187.
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50. Fuller, C. J. et al. 2000. The effect of vitamin E and vitamin C supplementation on LDL oxidizability and neutrophil respiratory burst in young smokers. J Am Coll Nutr 19(3): 361-369.
51. Flesch, M. et al. 2001. Alcohol and the risk of myocardial infarction. Basic Res Cardiol 96(2): 128-135.
52. Spyridopoulos, I. et al. 2001. Alcohol enhances oxysterol-induced apoptosis in human endothelial cells by a calcium-dependent mechanism. Arterioscler Thromb Vasc Biol 21(3): 439-444.
53. Zima, T. et al. 2001. Oxidative stress, metabolism of ethanol and alcohol-related diseases. J Biomed Sci 8(1): 59-70.
54. Liu, C. S. et al. 2000. Autoantibody against oxidized low-density lipoproteins may be enhanced by cigarette smoking. Chem Biol Interact 127(2): 125-137.
55. Jee, S. H. et al. 2001. Coffee consumption and serum lipids: a meta-analysis of randomized controlled clinical trials. Am J Epidemiol 153(4): 353-362.
56. Nakanishi, N. et al. 2000. Association of lifestyle with serum lipid levels: a study of middle-aged Japanese men. J Epidemiol 10(4): 216-225.
57. De Roos, B. et al. 2000. Consumption of French-press coffee raises cholesteryl ester transfer protein activity levels before LDL cholesterol in normolipidaemic subjects. J Intern Med 248(3): 211-216.


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