-IBIS-1.7.6-
tx
cardiovascular system
atherosclerosis
Nutrition
dietary guidelines
eating principles:
Lifestyle Heart Trial by Dean Ornish, et al: Intensive lifestyle changes consisting of 10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support for a period of 5 years. Researchers found more regression of coronary atherosclerosis occurred after 5 years than after 1 year in the experimental group. In contrast, in the control group, coronary atherosclerosis continued to progress and more than twice as many cardiac events occurred.
(Ornish D, et al. JAMA 1998 Dec 16;280(23):2001-2007.)
low sugar, low cholesterol
low fat diet of unsaturated fats
calorie percentages: 70% complex carbohydrates, protein 12-15%, fat 15-18%
high fiber
low Sodium/Sodium-restricted diet
vegetarian cleansing diet or short fasts
see Materia Medica: Diet for Lowering Cholesterol, Fasting, General Sample Diet, General Guidelines for Eating, Sample Vegetarian Diet
therapeutic foods:
Garlic, onions and ginger exert a beneficial effect on platelet aggregation
garlic, wheat germ, liquid chlorophyll, alfalfa sprouts, buckwheat, watercress, rice polishings, apple, celery, cherries (Ni, 120.)
foods high in water-soluble fiber: flax seed, pectin, guar gum, oat bran
onions, beans, legumes, soy, ginger, alfalfa, yogurt (Marz)
increase omega-3 and omega-6 fatty acids: vegetable, nut, seed oils, salmon, herring, mackerel, sardines, walnuts, flaxseed oil, evening primrose oil, black currant oil
fresh juices:
carrot and pineapple with honey
liquid chlorophyll (Jensen, 51.)
parsley, alfalfa, and pineapple (Jensen, 51.)
carrot, celery, parsley, and spinach (Walker, p. 123.)
carrot and spinach (Walker, 123.)
carrot, beet, and celery (Walker, 123.)
celery, lettuce, and spinach (Walker, 123.)
asparagus and honey (Ni, 120.)
avoid:
trans-fatty acids, hydrogenated oils (margarine, vegetable shortenings, imitation butter spreads, most commercial peanut butters) oxidized fats (deep fried foods, fast food, ghee, barbequed meats)
simple carbohydrates: sucrose, refined flours
supplements
Folic acid 5 mg per day exerts a beneficial effect on homocysteine metabolism.
Vitamin B3 100 mg three times per day, working up to 6 g per day (POSSIBLE LIVER PROBLEMS with some forms)
- best form for treating hypercholesterolemia is inositol hexoniacinate: 500 mg three times per day, for two weeks, then increase to 1,000 mg three times per day. (Murray M, Pizzorno J, 1998, 354.) Or if you use niacin, 1-6 g per say, start out with 100 mg three times per day, with meals. Niacinamide is not effective for lowering cholesterol.
(Grundy J. Lipid Research 1981;22:24-36; Carlson, Oro. Atherosclerosis 18:9,1973; Canner. J Am Coll Cardiol. 1985;5:442.)
Pantothenic acid 600-1200 mg per day.
Vitamin B6, 50 mg per day, exerts a beneficial effect on homocysteine metabolism.
Vitamin B12, 400 mg per day, exerts a beneficial effect on homocysteine metabolism.
Vitamin B-complex
Vitamin C, 1 g three times per day, has antioxidant effect as well as other potential benefits, including protecting LDL, reversing the dysfunction associated with elevated homocysteine levels, and enhancing thickness and pliability of endothelium.
(Frei B. Am J Clin Nutr 1991;54:1113S-1118S; Chambers JC, et al. Circulation 1999;99:1156-1160; Carr AC, et al. Biochem J 2000 Mar 1;346 Pt 2:491-499.)
Vitamin E, 400-600 IU twice daily: antioxidant effect protects LDL from oxidative damage; double blind research has confirmed value in prevention of heart disease. Caution: possible problems in some individuals with hypertension)
(Steiner, 1976; Belcher JD, et al. Arterioscler Thromb 1993;13:1779-1789; Stephens NG, et al. Lancet 1996;347:781-786; Rimm E. 60th Annual Biology Colloquium, 1999.)
Calcium 1.5 mg per day.
Chromium picolinate 200-400 mcg per day; preventive role in modulating blood sugar levels; may facilitate plaque regression.
Copper 2-4 mg once daily avoid taking > 15 mg Zinc if no Copper being taken
Magnesium, 500 mg per day, decreases angina, arrhythmias and morbidity following infarction; best in combination with Potassium
Selenium 200 mcg per day. (Stead, 1984)
Bromelain 100-250 mg four times daily, away from meals: inhibits platelet aggregation; may facilitate plaque regression.
L-Carnitine, 750-1,500 mg twice daily, plays a key role in fatty acid metabolism; depleted in cardiac muscle during acute infarctions
Betaine, 200-1,000 mg per day, exerts a beneficial effect on homocysteine metabolism. Note: this is not the same as Betaine HCl.
Chondroitin sulfate: possible preventive role
Coenzyme Q10 30 mg per day, in divided doses
Alpha Lipoic Acid 50 mg two to three times daily: potent antioxidant, also recycles Vitamin C and Vitamin E
Omega-3 Fatty Acids 1,500 mg three times per day; most capsules are 300 mg EPA/DHA, but 500 mg are available; this equals 1.3/3.2 gms of EPA/DHA
(Childs, 1990; Saynor, 1984.)
Omega-6 Fatty Acids
Phosphatidyl choline
Quercitin: food sources associated with reduced risk of heart disease; protects LDL from damage
(Hertog MGL, et al. Lancet 1993;342:1007-1011; Hertog MGL, et al. Arch Intern Med 1995;155:381-386; Knekt P, et al. Brit Med J 1996;312:478-481; Rimm EB, et al. Ann Intern Med 1996; 125:384-389; Ronzio RA. Townsend Letter Oct 1996:34-35; Hertog MGL, et al. Am J Clin Nutr 1997;65:1489-1494.)
Resveratrol: antiplatelet activity. (Bertelli AA, et al. Drugs Exp Clin Res 1996;22(2):61-63.)
Rice bran oil 3.5 g per day.
» drug interactions:
Vitamin D and heparin: heparin interferes with renal hydroxylation of Vitamin D. Note: this could lead to osteopenia, check 1,25(OH)02 cholecalciferol levels.
footnotes
[No author listed.] Garlic powder for hyperlipidemia-analysis of recent negative results. Quart Rev Natural Med 1998;Fall:187-189.
Ascherio A, Willett WC. Health effects of trans fatty acids. Am J Clin Nutr 1997;66(suppl):1006S-1010S. (Review)
Balz F.Antioxidant Vitamins and Heart Disease. Presented at the 60th Annual Biology Colloquium, Oregon State University, February 25, 1999.
Belcher JD, Balla J, Balla G, et al. Vitamin E, LDL, and endothelium: Brief oral vitamin supplementation prevents oxidized LDL-mediated vascular injury in vitro. Arterioscler Thromb 1993;13:1779-1789.
Bertelli AA, Giovanninni L, Bernini W, et al. Antiplatelet activity of cis-resveratrol. Drugs Exp Clin Res 1996;22(2):61-63.
Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum lipoproteins and cholesterol metabolism. JAMA 1998;279:1900-1902.
Boberg M, Vessby B, Selinus I. Effects of dietary supplementation with n-6 and n-3 long-chain polyunsaturated fatty acids on serum lipoproteins and platelet function in hypertriglcyeridaemic patients. Acta Med Scand 1986;220:153-160.
Bordia A, Verma SK, Srivastava KC. Effect of ginger (Zingiber officinale Rosc) and fenugreek (Trigonella foenumgraceum L) on blood lipids, blood sugar, and platelet aggregation in patients with coronary artery disease. Prostagland Leukotrienes Essential Fatty Acids 1997;56:379-384.
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Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 1999;69:30-42.
Canner J. Am. Coll. Cardiol. 5:442,1985; The coronary drug project research group. JAMA 1975;213:360.
Abstract: Men with 1 or more MIs who took 3 g Vitamin B3 once dailyhad a lower incidence of nonfatal MIs and, for several years after the study ended, a lower mortality rate.
Carlson, Oro. Effect of treatment of nicotinic acid for one month on serum lipids in patients with different types of hyperlipidemia. Atherosclerosis 1973;18:9.
Abstract: 188 patients with various types of hyperlipoproteinemia were given 3 gms nicotinic acid daily. Most responsive were patients with Type V. Their cholesterols decreased 70% and triglycerides decreased 90%, followed by Type lll: decreases of 50% and 60% respectively. Both lipids were also reduced in the other types, and even patients with normal lipid levels showed a 10-20% reduction in serum lipids.
Carr AC, Tijerina T, Frei B. Vitamin C protects against and reverses specific hypochlorous acid- and chloramine-dependent modifications of low-density lipoprotein. Biochem J 2000 Mar 1;346 Pt 2:491-499.
Abstract: Activated phagocytes produce the highly reactive oxidant hypochlorous acid (HOCl) via the myeloperoxidase-catalysed reaction of hydrogen peroxide with chloride ions. HOCl reacts readily with a number of susceptible targets on apolipoprotein B-100 of low-density lipoprotein (LDL), resulting in uncontrolled uptake of HOCl-modified LDL by macrophages. We have investigated the efects of vitamin C (ascorbate), an effective water-soluble antioxidant, on the HOCl- and chloramine-dependent modification of LDL. Co-incubation of vitamin C (25-200 &mgr;M) with LDL resulted in concentration-dependent protection against HOCl (25-200 &mgr;M)-mediated oxidation of tryptophan and lysine residues, formation of chloramines and increases in the relative electrophoretic mobility of LDL. Vitamin C also partially protected against oxidation of cysteine residues by HOCl, and fully protected against oxidation of these residues by the low-molecular-mass chloramines, N(alpha)-acetyl-lysine chloramine and taurine chloramine, and to a lesser extent monochloramine (each at 25-200 &mgr;M). Further, we found that HOCl (25-200 &mgr;M)-dependent formation of chloramines on apolipoprotein B-100 was fully reversed by 200 &mgr;M vitamin C; however, the loss of lysine residues and increase in relative electrophoretic mobility of LDL were only partially reversed, and the loss of tryptophan and cysteine residues was not reversed. Time-course experiments showed that the reversal by vitamin C of HOCl-dependent modifications became less efficient as the LDL was incubated for up to 4 h at 37 degrees C. These data show that vitamin C not only protects against, but also reverses, specific HOCl- and chloramine-dependent modifications of LDL. As HOCl-mediated LDL modifications have been strongly implicated in the pathogenesis of atherosclerosis, our data indicate that vitamin C could contribute to the anti-atherogenic defence against HOCl.
Chambers JC, McGregor A, Jean-Marie J, et al. Demonstration of rapid onset vascular endothelial dysfunction after hyperhomocysteinemia. An effect reversible with vitamin C therapy. Circulation 1999;99:1156-1160.
Chen CK, Pace-Asciak. CR. Vasorelaxing activity of resveratrol and quercetin in isolated rat aorta. Gen Pharm 1996;27(2):363-366.
Corti M-C, Guralnik JM, Salive ME, et al. Serum iron level, coronary artery disease, and all-cause mortality in older men and women. Am J Cardiol 1997;79:120-127.
Danesh J, Appleby P. Coronary heart disease and iron status. Meta-analyses of prospective studies. Circulation 1999;99:852-854.
Folsom AR, Nieto FJ, McGovern PG, et al. Prospective study of coronary heart disease incidence in relation to fasting total homocysteine, related genetic polymorphisms, and B vitamins. Circulation 1998;98:204-210.
Franken DG, Boers GHJ, Blom HJ, et al. Treatment of mild hyperhomocysteinemia in vascular disease patients. Arterioscler Thromb 1994;14:465-470.
Frei B. Ascorbic acid protects lipids in human plasma and low-density lipoprotein against oxidative damage. Am J Clin Nutr 1991;54:1113S-1118S.
Grundy. Influence of nicotinic acid on metabolism of cholesterol and triglycerides in man. J. Lipid Research 22:24-36,1981.
Abstract: 12 hyperlipidemic patients were placed on nicotinic acid for 1 month. During treatment, triglycerides decreased 52%, VLDL decreased 36%, and total cholesterol decreased 22%.
Hertog MGL, Feskens EJM, Hollman PCH, et al. Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly Study. Lancet 1993;342:1007-1011.
Hertog MGL, Kromhout D, Aravanis C, et al. Flavonoid intake and long-term risk of coronary heart disease and cancer in the Seven Countries Study. Arch Intern Med 1995;155:381-386.
Hertog MGL, Sweetnam PM, Fehily AM, et al. Antioxidant flavonols and ischemic heart disease in a Welsh population of men: the Caerphilly Study. Am J Clin Nutr 1997;65:1489-1494.
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Iribarren C, Sempos CT, Eckfeldt JH, Folsom AR. Lack of association between ferritin level and measures of LDL oxidation: the ARIC study. Atherosclerosis 1998;139:189-195.
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Janssen PLTMK, Meyboom S, van Staveren WA, de Vegt F, Katan MB. Consumption of ginger (Zingiber officinale Roscoe) does not affect ex vivo platelet thromboxane production in humans. Eur J Clin Nutr 1996;50:772-774.
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Kuller LH, Evans RW. Homocysteine, vitamins, and cardiovascular disease. Circulation 1998;98:196-199. (Review)
Lawson L. Garlic oil for hypercholesterolemia-negative results. Quart Rev Natural Med 1998; Fall:185-186.
Lumb AB. Effect of dried ginger on human platelet function. Thromb Haemost 1994;7:110-111.
Manson JB, Miller JW. The effects of vitamin B12, B6, and folate on blood homocysteine levels. Ann NY Acad Sci 1992;669:197-204. (Review)
McCrindle BW, Helden E, Conner WT. Garlic extract therapy in children with hypercholesterolemia. Arch Pediatr Adolesc Med 1998;152:1089-1094.
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Murray, M and Pizzorno, J, Encyclopedia of Natural Medicine. Revised Second Edition. Prima Publishing: Rocklin, CA: 1998, 354.
Neil HAW, Silagy CA, Lancaster T, et al. Garlic powder in the treatment of moderate hyperlipidaemia: A controlled trial and a meta-analysis. J R Coll Phys 1996;30:329-334.
Nelson GJ. Dietary fat, trans fatty acids, and risk of coronary heart disease. Nutr Rev 1998;250-252.
Olson BH, Anderson SM, Becker MP, et al. Psyllium-enriched cereals lower blood total cholesterol and LDL cholesterol, but not HDL cholesterol, in hypercholesterolemic adults: Results of a meta-analysis. J Nutr 1997;127:1973-1980.
Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-133.
Ornish D, Scherwitz LW, Billings JH, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ. Intensive lifestyle changes for reversal of coronary heart disease. JAMA 1998 Dec 16;280(23):2001-2007.
Abstract: CONTEXT: The Lifestyle Heart Trial demonstrated that intensive lifestyle changes may lead to regression of coronary atherosclerosis after 1 year. OBJECTIVES: To determine the feasibility of patients to sustain intensive lifestyle changes for a total of 5 years and the effects of these lifestyle changes (without lipid-lowering drugs) on coronary heart disease. DESIGN: Randomized controlled trial conducted from 1986 to 1992 using a randomized invitational design. PATIENTS: Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography. SETTING: Two tertiary care university medical centers. INTERVENTION: Intensive lifestyle changes (10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support) for 5 years. MAIN OUTCOME MEASURES: Adherence to intensive lifestyle changes, changes in coronary artery percent diameter stenosis, and cardiac events. RESULTS: Experimental group patients (20 [71%] of 28 patients completed 5-year follow-up) made and maintained comprehensive lifestyle changes for 5 years, whereas control group patients (15 [75%] of 20 patients completed 5-year follow-up) made more moderate changes. In the experimental group, the average percent diameter stenosis at baseline decreased 1.75 absolute percentage points after 1 year (a 4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the average percent diameter stenosis in the control group increased by 2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28 experimental group patients vs 45 events in 20 control group patients during the 5-year follow-up (risk ratio for any event for the control group, 2.47 [95% confidence interval, 1.48-4.20]). CONCLUSIONS: More regression of coronary atherosclerosis occurred after 5 years than after 1 year in the experimental group. In contrast, in the control group, coronary atherosclerosis continued to progress and more than twice as many cardiac events occurred.
Pace-Asciak CR, Rounova O, Hahn SE, et al. Wines and grape juices as modulators of platelet aggregation in healthy human subjects. Clin Chim Acta 1996;246(1-2):163-182.
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Rimm EB, Katan MB, Ascherio A, et al. Relation between intake of flavonoids and risk for coronary heart disease in male health professionals. Ann Intern Med 1996; 125:384-389.
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Srivastava KC, Tyagi OD. Effect of a garlic derived principle (ajoene) on aggregation and arachidonic acid metabolism in human blood platelets. Prostagl Leukotr Ess Fatty Acids 1993;49:587-595.
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