• Chapter 37: C Reactive Protein is Predictive of the Severity of Active Formation of Atherosclerosis
• Chapter 38: Testing Your Homocysteine and CRP Levels

Chapter Excerpts

Accordingly, an elevated CRP level is an indirect indication of inflammation in the body and that atherosclerosis, including heart disease, is actively developing.

The greater the homocysteine level, the greater the oxidation of both LDL cholesterol and the arterial lining (endothelium). The greater the inflammation, the higher the CRP level.

However, using statin drugs to lower CRP when it can be lowered more effectively through exercise, proper diet, weight loss, and vitamins and minerals, without any health risks makes the non-pharmacological route much more attractive and wise.

Ladd McNamara, M.D.

Chapter References

• 176: Guetta J, Fuselli J, Boissonnet C, Fairman E, et al. Pognostic value of C-reactive protein in diabetic patients with unstable angina. Am Coll Cardiol. 2003 41:346.
• 177: Wang TJ, et al. C-reactive protein is associated with subclinical epicardial coronary calcification in men and women: the Framingham Heart Study. Circulation 2002 Sep 3;106(10):1189-1191.
• 178: Ziaris M, et al. C-reactive protein and multiple complex coronary artery plaques in patients with primary untstable angina. Atherosclerosis 2002 Oct;164(2):355.
• 179: Pradhan AD, et al. Inflammatory biomakers, hormone replacement therapy, and incident coronary heart disease: propective analysis from the Women’s Health Initiative observational study. JAMA 2002 Aug 28;288(8):980-987.
• 180: Ridker PM, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. NEJM 1997 Apr 3;336(14):973-979.
• 181: Kaplan RC, Frishman WH. Systemic inflammation as a cardiovascular disease risk factor and as a potential target for drug therapy. Heart Dis 2001 Sep-Oct;3(5):326-332.
• 182: Blake CJ, Ridker PM, Kuntz KM. Projected life-expectancy gains with statin therapy for individuals with elevated C-reactive protein levels. J Am Coll Cardiol 2002 Jul 3;40(1):49-55.
• 183: Upritchard JE, Suterhland WH, Mann JI. Effect of supplementation with tomato juice, vitamin E, and vitamin C oxidation and products of inflammatory activity in type 2 diabetes. Diabetes Care. 2000 Jun;23(6):733-738.
• 184: Block G, Jensen C, Dietrich M, Norkus EP, Hudes M, Paker L. Plasma C-reactive protein concentrations in active and passive smokers: influence of antioxidant supplementation. J Am Coll Nutr. 2004 Apr;23(2):141-147.
• 185: Devaraj S, Jialal I. Alpha tocopherol supplementation decreases serum C-reactive protein and monocyte interleukin-6 levels in normal volunteers and type 2 diabetic patients. Free Radic Biol Med 2000 Oct 15;29(8):790-792.
• 186: Hertog MGS, et al. Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly study. Lancet 1993;342:1007-1011.
• 187: Keli SO, et al. Dietary flavonoids, antioxidant vitamins, and incidence of stroke: the Zutphen study. Arch Intern Med 1996 Mar 25;156?6):637-642.
• 188: Yoshizumi M, et al. Quercetin inhibits Shc- and phosphatidylinositol 3- kinase-mediated c-jun N-terminal kinase activation by angiotensin II in cultured rat aortic smooth muscle cells. Mol Pharmacol 2001 60:656-665.
• 189: Pignatelli P, et al. The flavonoids quercetin and catechin synergistically inhibit platelet function by antagonizing the intracellular production of hydrogen peroxide. Am J Clin Nutr 2000 72:1150-1155.
• 190: Koufaki M, et al. Novel potent inhibitors of lipid peroxidation with protective effects against reperfusion arrhythmias. J Med Chem 2001 Nov 22;44(24):4300-4303.
• 191: Munch G, Mayer S, Michaelis J, et al. Influence of advanced glycation end-products and AGE-ingivitors on nucleation-dependent polymerization of beta-amyloid peptide. Biochim Biophys Acta. 1997 1360(1):17-29.
• 192: Hipkiss A, Michaelis J, Syrris P. Non-enzymatic glycosylation of the dipeptide L-carnosine, a potential anti-protein-cross-linking agent. FEBS Lett. 1995 371(1):81-85.
• 193: Brownson C, Hipkiss A. Carnosine reacts with a glycated protein. Free Radic Biol Med. 2000 28(10):1564-1570.
• 183: Upritchard JE, Suterhland WH, Mann JI. Effect of supplementation with tomato juice, vitamin E, and vitamin C oxidation and products of inflammatory activity in type 2 diabetes. Diabetes Care. 2000 Jun;23(6):733-738.
• 184: Block G, Jensen C, Dietrich M, Norkus EP, Hudes M, Paker L. Plasma C-reactive protein concentrations in active and passive smokers: influence of antioxidant supplementation. J Am Coll Nutr. 2004 Apr;23(2):141-147.
• 194: Jialal I, Devaraj S. Inflammation and atherosclerosis: the value of the high-sensitivity C-reactive protein assay as a risk marker. Am J Clin Pathol 2001 Dec;116 Suppl:S108-115.
• 195: Nestel P, et al. The n-3 fatty acids eiosapentaenoid acid and docosahexaenoic acid increase systemic arterial compliance in humans. Am J Clin Nutr 2002 Aug;76(2):326-330.
• 196: Morrison H, et al. Serum folate and risk of fatal coronary heart disease. JAMA 1996 Jun 26;275:1893-1896.
• 197: Graham I, Daly L, Refsum H, et al. Plasma homocysteine as a risk factor for vascular disease. The European Concerted Action Project. JAMA. 1997 277:1775-1781.
• 198: McCully K. Homocysteine, folate, vitamin B6, and cardiovascular disease (Editorial). JAMA. 1998 279:392-393.
• 199: Wald N, Watt H, Law M, Weir D, McPartlin J, Scott J. Homocysteine and ischemic heart disease: results of a prospective study with implications regarding prevention. Arch Intern Med. 1998 158:862-867.
• 200: Nygard O, Nordrehaug J, Refsum H, et al. Plasma homocysteine levels and mortality in patients with coronary artery disease. NEJM 1997 337:230-236.
• 201: Luc G, Bard J, Juhan-Vague I, et al. C-reactive protein, interleukin-6, fibrinogen as predictors of coronary heart disease. The PRIME study. Arterioscler Thromb Vasc Biol. 2003 Jul 1;23(7):1255-1261.
• 202: Ridker P, Brown N, Vaughan D, Harrison D, Mehta J. Established and emerging plasma biomarkers in the prediction of first atherothrombotic events. Circulation 2004 109: IV-6-IV-19.

Ladd McNamara, M.D.

• Chapter 33: Vitamins, Minerals, Antioxidants, and Essential Fatty Acids: The Real Way to Reduce the Risk of Death from Heart Disease and Stroke – Part 3

Chapter Excerpts

Alpha-Lipoic Acid works in many ways to protect against disease and maintain health. ALA protects LDL cholesterol from oxidation, reduces the inflammatory reaction of the arteries, along with magnesium helps to maintain a health blood pressure. Alpha-Lipoic Acid works together with co-enzyme Q10 in the metabolism of sugar into energy.

Olive Oil and Olive Oil Extracts contain polyphenol antioxidants that are in part responsible for the benefits of the Mediterranean diet. Studies have shown those who consume more of these antioxidant compounds have a greatly reduced risk of heart disease and cancer, let alone a prolongation of life.

Fish oil supplements (containing DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) have been shown to decrease the risk of cardiac death greater than the use of statin drugs, …and without any toxic side-effects. Thus, more evidence of the Cholesterol Conspiracy.

In addition to magnesium supplementation, researchers are finding promise in the higher rates of survival after heart attacks when high-dose antioxidants are commenced shortly after such an attack.

Diets high in both soluble and insoluble fiber help reduce blood lipid levels, cholesterol, and insulin intolerance.

Ladd McNamara, M.D.

Chapter References

• 130: Zhang WJ, Frei B. Alpha-lipoic acid inhibits TNF-alpha-induced NFkappa B activation and adhesion molecule expression in human aortic endothelial cells. FASEB J 2001 Nov;15(13):2423-2432.
• 131: El Midaoui A, de Champlain J. Prevention of hypertension, insulin resistance, and oxidative stress by alpha-lipoic acid. Hypertension 2002 Feb;39(2):303-307.
• 132: Takaoka M, et al. Effects of alpha-lipoic acid on deoxycorticos-terone acetate-salt-induced hypertension in rats. Eur J Pharmacol 2001 Jul;20;424(2):121-129.
• 133: Koufaki M, et al. Novel potent inhibitors of lipid peroxidation with protective effects against reperfusion arrhythmias. J Med Chem 2001 Nov 22;44(24):4300-4303.
• 134: Gonzalez-Perez O, Gonzalez-Castaneda R, Huerta M, et al. Beneficial effects of -lipoic acid plus vitamin E on neurological deficit, reactive gliosis and neuronal remodeling in the penumbra of the ischemic rat brain. Neuroscience Letters, 2002 March 15, 321(5);1:100-104.
• 135: Chen C et al. Endogenous sex hormones and prostate cancer risk: a case-control study nested within the carotene and retinal efficacy trial. Cancer Epidimeiol Biomarkers Prev. 2003 Dec;12(12):1410-1416.
• 136: Upritchard J, Suterhland W, Mann J. Effect of supplementation with tomato juice, vitamin E, and vitamin C oxidation and products of inflammatory activity in type 2 diabetes. Diabetes Care. 2000 Jun;23(6):733-738.
• 137: Decker E, et al. Inhibition of low-density lipoprotein oxidation by carnosine histidine. J Agric Food Chem 2001 Jan;49(1):511-516.
• 138: Owen RW, et al. Olive oil consumption and health: the possible role of antioxidants. Lancet Oncol, 2000, Oct., 1:107-12.
• 139: Visioli F, et al. Antioxidant and other biological activities of phenols from olives and olive oil. Med Res Rev. 2002 Jan;22(1):65-75.
• 140: Simopoulos Ap. The traditional diet of Greece and cancer. Eur J Cancer Prev. 2004 Jun;13(3):219-30.
• 141: Visioli F., et al. Low density lipoprotein oxidation is inhibited in vitro by olive oil constituents. Atherosclerosis. 1995 Sep;117(1):25-32.
• 142: Cullinen K. Olive oil in the treatment of hypercholesterolemia. Med Health R.I. 2006 Mar;89(3):113.
• 143: Nagyova A, et al. Effects of dietary extra virgin olive oil on serum lipid resistance to oxidation and fatty acid composition in elderly lipidemic patients. Bratisl Lek Listy. 2003;104(7-8):218-21.
• 144: Martinez-Gonzalez MA. The SUN cohort study (Seguimiento University of Navarra). Public Health Nutr. 2006 Feb;9(1A):127-31.
• 145: Bogani P., et al. Postprandial anti-inflammatory and antioxidant effects of extra virgin olive oil. Atherosclerosis. 2006 Feb 17; [Epub ahead of print].
• 146: Fito M., et al. Antioxidant effect of virgin olive oil in patients with stable coronary heart disease: a randomized, crossover, controlled, clinical trial. Atherosclerosis. 2005 Jul;181(1):149-58.
• 147: Fernandez-Jarne E., et al. Risk of first non-fatal myocardial infarction negatively associated with olive oil consumption: a case-control study in Spain. Int J Epidemiol. 2002, Apr;31(2):474-80.
• 148: Visioli F., Galli C. Antiatherogenic components of olive oil. Curr Atheroscler Rep. 2001. Jan;3(1):64-7.
• 149: Visioli F., et al. Low density lipoprotein oxidation is inhibited in vitro by olive oil constituents. Atherosclerosis. 1995 Sep;117(1):25-32.
• 150: Nestel P, et al. The n-3 fatty acids eiosapentaenoid acid and docosahexaenoic acid increase systemic arterial compliance in humans. Am J Clin Nutr 2002 Aug;76(2):326-330.
• 151: McLennan O. Myocardial membrane fatty acids and the antiarrhythmic actions of dietary fish oil in animal models. Lipids 2001 36 Suppl: S111-S114.
• 152: Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italian per lo Studio dells Soprvvivenza nell’Infarto Micardico (GISSI)-Prevenzione. Circulation. 2002 Apr 23;105:1897-1903.
• 56: Rosenson RS. Statins in atherosclerosis: lipid-lowering agents with antioxidant capabilities. Atherosclerosis. 2004. Mar;173(1):1-12.
• 57: Tsimikas S, et al. High-dose atorvastatin reduces total plasma levels of oxidized phospholipids and immune complexes present on apolipoprotein B-100 in patients with acute coronary syndromes in the MIRACL trial. Circulation. 2004 Sep 14;110(11):1406-12.
• 152: Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italian per lo Studio dells Soprvvivenza nell’Infarto Micardico (GISSI)-Prevenzione. Circulation. 2002 Apr 23;105:1897-1903.
• 154: Bernier M, et al. Reperfusion-induced arrhythmias and oxygen-derived free radicals. Circulation Res. 1986 58:331-340.
• 203: Studer M, et al. Effect of different antilipidemic agents and diets on mortality: a systematic review. Archives of Internal Medicine, 2005 Apr 11;165(7):725-30.
• 153: Grech E, et. al. Reperfusion injury after acute myocardial infarction. Brit Med J 1995 310:477-478.
• 154: Bernier M, et al. Reperfusion-induced arrhythmias and oxygen-derived free radicals. Circulation Res. 1986 58:331-340.
• 155: Chamiec T, et al. Effects of antioxidant vitamins C and E on signalaveraged electrocardiogram in acute myocardial infarction. Am J Cardiol. 1996 77:277-281.
• 156: Dzizinskii AA, et al. Effects of antioxidants and membrane protectors on clinical course and hemodynamics of patients of myocardial infarct. Ross Med Zh. 1992 1:32-34.
• 157: Kramer J, et al. Magnesium-deficiency potentiates free radical production associated with post-ischemic injury to rat hearts: vitamin E affords protection. Free Rad Bio Med. 1994 16:6:713-723.
• 158: Altura BM. Cardiovascular risk factors and magnesium: relationships to atherosclerosis, ischemic heart disease and hypertension. magnesium and trace elements. Switzerland, S. Karger AG, Basel, 1991-92;10:182-192.
• 159: Van Leer EM, et al. Dietary calcium, potassium, magnesium and blood pressure in the Netherlands. Internation J Epidem. 1995 24:6:1117-23.
• 160: Bernier M, et al. Reperfusion-induced arrhythmias and oxygen-derived free radicals. Circulation Res. 1986 58:331-340.
• 161: Chamiec T, et al. Effects of antioxidant vitamins C and E on signalaveraged electrocardiogram in acute myocardial infarction. Am J Cardiol. 1996 77:277-281.
• 162: Dzizinskii AA, et al. Effects of antioxidants and membrane protectors on clinical course and hemodynamics of patients of myocardial infarct. Ross Med Zh. 1992 1:32-34.

Ladd McNamara, M.D.

• Chapter 33: Vitamins, Minerals, Antioxidants, and Essential Fatty Acids: The Real Way to Reduce the Risk of Death from Heart Disease and Stroke – Part 2

Chapter Excerpts

Studies using levels of vitamin C, well above 700 mg per day have shown a decreased risk of diseases, including the risk of heart disease.

Ladd McNamara, M.D.

Bioflavanoids such as grape seed extract, resveratrol, & quercetin all have shown remarkable results in reducing the risk of heart disease and cancers. They work synergistically, as well as with other antioxidants to reduce the risk of disease.

L-carnosine may slow down the aging process, and protects the brain, skin, and arteries from damage. Furthermore, L-carnosine helps the heart to contract more effectively through enhancing the use of calcium.

Chapter References

• 95: Mehra M, et al. Prevention of atherosclerosis. Postgraduate Med. 1995 98:1:175-182.
• 96: Hoffman RM, et al. Antioxidants and the prevention of coronary heart disease. Arch Int Med. 1995 155:241-244.
• 97: Morrison H, et al. Serum folate and risk of fatal coronary heart disease. J Am Med Assoc. 1996 275:24:1893-1896.
• 98: Chasan-Taber L, et al. A prospective study of folate and vitamin B-6 and risk of myocardial infarction in U.S. physicians. J Am Coll Nutri. 1996 15:2:136-143.
• 99: Levine GN, et al. Ascorbic acid reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation. 1996 93:6:1107-1113.
• 100: Gatto LM, et al. Ascorbic acid induces a favorable lipoprotein profile in women. J Am Coll Nutri. 1996 15:2:154-158.
• 101: Hallfrisch J, et al. High plasma vitamin c associated with high plasma HDL (1) – and HDL (2) cholesterol. Am J Clin Nutri. 1994 60:100-105.
• 102: Osganian S, Stampfer M, Rimm E, Spiegelman D, et al. Vitamin C and risk of coronary heart disease in women. J Am Coll Cardiol. 2003 42:246-252.
• 103: Rifici V, Khachadurian A. Dietary supplementation with vitamins C and E inhibits in-vitro oxidation of lipoproteins. J Am Coll Nutri. 1993 12:6:6331-6337.
• 104: Gaziano J. Antioxidant vitamins and coronary artery disease risk. Am J Med. 1994 97:3A-18S-3A-21S.
• 105: Lagrue G, et al. A study of the effects of procyanidol oligomers on capillary resistance in hypertension and in certain nephropathies. Sem Hop Paris. 1981 57:1399-1401.
• 106: Detre A, et al. Studies on vascular permeability in hypertension: action of anthocyanosides. Clin Physiol Biochem. 1986 4:143-149.
• 107: Meunier MT, et al. Free-radical scavenger activity of procyanidolic oligomers and anthocyanosides with respect to superoxide anion and lipid peroxidation. Plant Medphytother. 1989 4:267-274.
• 108: Tixier J, et al. Evidence by in vivo and in vitro studies that binding of pycnogenols to elastin affects its rate of degradation by elastases. Biochem Parmacol. 1984 33:3933-3939.
• 109: Facino R, et al. Free-radical scavenging action and anti-enzyme activities of procyanidines from vitis vinifera; a mechanism for their capillary protective action. Arzneimittel-Forschung Drug Research. 1994 44(1):5:592-601.
• 110: Dartenuc JY, et al. Capillary resistance in the geriatric: study of a micro-angioprotector. Bordeaux Medicale. 1985 13:903.
• 111: Kuhnau J. The flavonoids, a class of semi-essential food components: their role in human nutrition. World Rev Nutr Diet. 1976 24:117-191.
• 112: Gabor M. Pharmacologic effects of flavonoids on blood vessels. Angiologica, 1972 9:355-374.
• 113: Knekt P, et al. Flavonoid intake and coronary mortality in finland: a cohort study. Brit Med J. 1996 312:478-481.
• 114: Stephens N, et al. Randomized Controlled Trial of Vitamin E in Patients with Coronary Disease: Cambridge Heart Anti-Oxidant Study (CHAOS). The Lancet. 1996 347:781-786.
• 115: Niki E, et al. Interaction among vitamin C, vitamin E, and beta carotene. Am J Clin Nutri. 1995 62(suppl):1322S-1326S.
• 116: Morrison H, et al. Serum folate and risk of fatal coronary heart disease. J Am Med Assoc. 1996 275:24:1893-1896.
• 117: Carr A, Frei B. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Am J Clin Nutr. 1999 69(6):1086-1107.
• 118: Enstrom J. Counterpoint–vitamin C and mortality. Nutr Today. 1993 28:28-32.
• 119: Osganian S, Stampfer M, Rimm E, et al. Vitamin C and risk of coronary heart disease in women. J Am Coll Cardiol. 2003 42(2):246-252.
• 120: Keli S, et al. Dietary flavonoids, antioxidant vitamins, and incidence of stroke: the Zutphen study. Arch Intern Med 1996 Mar 25;156?6):637-642.
• 121: Duarte J, et al. Antihypertensive effects of the flavonoids quercetin in spontaneously hypertensive rats. Br J Pharmacol 2001 133:117-24.
• 122: Maron D, Lu G, Cai N, et al. Cholesterol-lowering effect of a theaflavin-enriched green tea extract. A randomized controlled trial. Arch Intern Med. 2003;163:1448-1453.
• 123: Preston JE, Hipkiss AR, Himsworth DT, et al. Toxic effects of betaamyloid (25-35) on immortalized rat brain endothelial cell: protection by carnosine, homocarnosine and beta-alamine. Neurosci Lett. 1998 242(2):1-0-108.
• 124: Stadman ER. Protein oxidation and aging. Science. 1992 257(5074):1220-1224.
• 125: Munch G, Schinzel R, Loske C, et al. Alzheimer’s disease – synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts. Journal of Neural Transmission. 1998 105(4-5):439-461.
• 126: Bierhaus A, Hofmann MA, Ziegler R, et al. AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE Concept. Cardiovascular Research. 1998 37(3)586-600.
• 127: McFarland GA, Holliday R. Retardation of the senescence of cultured human diploid fibroblasts by carnosine. Exp Cell Res. 1994 212(2):167-175.
• 128: Zaloga GP, Roberts PR, Black KW. Carnosine is a novel peptide modulator of intracellular calcium and contractility in cardiac cells. Am J Physiol 1997 272(1 Pt 2):H462-468.
• 129: Roberts PR, Zaloga GP. Cardiovascular effects of carnosine. Biochemistry (Mosc) 2000 Jul;65(7):856-861.

Ladd McNamara, M.D.

• Chapter 33: Vitamins, Minerals, Antioxidants, and Essential Fatty Acids: The Real Way to Reduce the Risk of Death from Heart Disease and Stroke – Part 1

Chapter Excerpts

The answer to lowering the risk of arteriosclerosis, heart disease and stroke is to reduce the oxidative damage to the LDL cholesterol, triglycerides, and the arterial lining so that plaque does not form.

The Cholesterol Conspiracy is about the makers of statin drugs hiding the truth that antioxidants work better than the statin drugs to reduce the risk of cardiac death. Antioxidants appear to be much more effective in reducing the risk of death from heart disease than current treatments using aspirin or cholesterol-lowering drugs combined.

There is a balance of D-alpha tocopherol and gamma tocopherol that is required to protect the fat and the protein components, respectively, or LDL cholesterol from oxidation. LDL that is not oxidized does not stick to the arterial walls.

Ladd McNamara, M.D.

Chapter References

• 85: Aviram M. HDL–associated paraoxonase 1 (PON1) and dietaryantioxidants attenuate lipoprotein oxidation, macrophage foam cells formation and atherosclerosis development. Pathophysiol Haemost Thromb. 2006;35(1-2):146-51.
• 86: Hertog M, Feskens E, Hollman P, Katan M, Kromhout D. Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly study. Lancet 1993 Oct 23;342(8878):1007-1011.
• 87: Street D, et al. A population based case control study of the association of serum antioxidants and myocardial infarction. Am J Epidemiol. 1991 134:719-720.
• 88: Steinberg D, et al. Antioxidants in the prevention of human atherosclerosis. Circulation. 1992 85:6:2338-2343.
• 89: Gey K, et al. Inverse correlation between plasma vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology. Am J Clin Nutri. 1991 53:326S-334S.
• 90: Stampfer M, et al. Vitamin E consumption and the risk of coronary disease in women. New Engl J Med. 1993 328:1444-1449.
• 91: Rimm E, Stampfer M, et al. Vitamin E consumption and the risk of coronary artery disease in men. New Engl J Med. 1993 328:1450-1456.
• 92: Munteanu, A. et al. Anti-atherosclerotic effects of vitamin E – Myth or reality? J Cell Mol Med., 2004, Jan-Mar;8(1):59-76.
• 93: I-Min Lee, et al. Vitamin E in the Primary Prevention of Cardiovascular Disease and Cancer. JAMA. 2005, Vol. 294, 56-65.
• 94: Losonczy K, et al. Vitamin E and vitamin C supplement use and risk of all-cause and coronary heart disease mortality in older persons: the established populations for epidemiologic studies of the elderly. Am J Clin Nutri. 1996 64:190-196.

Ladd McNamara, M.D.

• Chapter 31: The Importance of LDL Cholesterol
• Chapter 32: The Role of Diabetes and High Blood Sugar in the Development of Coronary Artery Disease

Chapter Excerpts

Evidence supports the theory that when a person’s total cholesterol drops below 160, the immune system is weakened. Statin drugs, i.e., cholesterol-lowering drugs, are known to suppress the immune system.

Obesity leads to diabetes through oxidation of insulin receptors, and along with the oxidation of lipids (including cholesterol) and inflammation of the arterial wall leads to heart disease, stroke, and eventually death.

Chapter References

• 74: Rauchhaus M, Clark A, Doehner W, Davos C, et al. The relationship between cholesterol and survival in patients with chronic heart failure. J Am Coll Cardiol. 2003 Dec 3; 42(11):1933-1940.
• 75: Fuller C, Jialal I, et al. rrr-alpha-tocopherol acetate supplementation at pharmacologic doses decreases low-density-lipoprotein oxidative susceptibility but not protein glycation in patients with diabetes mellitus. Am J Clin Nutri. 1996 63:753-759.
• 76: Somogyi A, et al. Hypothetical connection between diabetes mellitus and free radical reactions in arteriosclerosis. Orvosi Hetilap [Hungarian] 1994 135:(33):1815-1818.
• 77: Jialal I. Effect of combined supplementation with alpha-tocopherol ascorbate and beta-carotene on low-density lipoprotein oxidation. Circulation. 1993 88:2780-2786.
• 78: Munch G, Mayer S, Michaelis J, et al. Influence of advanced glycation end-products and AGE-ingivitors on nucleation-dependent polymerization of beta-amyloid peptide. Biochim Biophys Acta. 1997 1360(1):17-29.
• 79: Hipkiss A, Michaelis J, Syrris P. Non-enzymatic glycosylation of the dipeptide L-carnosine, a potential anti-protein-cross-linking agent. FEBS Lett. 1995 371(1):81-85.
• 80: Brownson C, Hipkiss A. Carnosine reacts with a glycated protein. Free Radic Biol Med. 2000 28(10):1564-1570.
• 81: Yamano T, et al. Effect of L-carnosine on the hyperglycemia caused by intracranial injection of 2-deoxy-D-glucose in rats. Neurosci Lett 2001 Nov 2;313(1-2):78-82.
• 82: Heitzer T, et al. Beneficial effects of alpha-lipoic acid and ascorbic acid on endothelium-dependent, nitric oxide-mediated vasodilation in diabetic patients: relation to parameters of oxidative stress. Free Radic Biol Med 2001 Jul 1;31(1):53-61.
• 83: El Midaoui A, de Champlain J. Prevention of hypertension, insulin resistance, and oxidative stress by alpha-lipoic acid. Hypertension 2002 Feb;39(2):303-307.
• 84: Takaoka M, et al. Effects of alpha-lipoic acid on deoxycorticosterone acetate-salt-induced hypertension in rats. Eur J Pharmacol 2001 Jul;20;424(2):121-129.

• Chapter 30: The Combination of Antioxidant Supplements and Statin Drugs

Chapter Excerpts

The most significant risk factor for heart disease and stroke is not the level of LDL cholesterol, but the oxidation of LDL cholesterol, homocysteine and inflammation of arterial walls. If the oxidized LDL cholesterol, homocysteine and the C reactive protein had been measured in the study, the antioxidant use would most surely have shown a protective effect.

Do not be fooled by a study here or there that shows that "antioxidants are bad" because of the changes in cholesterol levels. It is only important to the pharmaceutical industry that wants to scare you from taking vitamins and minerals…

Chapter References

• 71: Brown B, Zhao X, Chait A, et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med. 2001 345(22):1583-1592.
• 72: Collins R, Peto R, Armitage J. The MRC/BHF Heart Protection Study: preliminary results. Int J Clin Pract. 2002 56(1):53-56.
• 73: Manuel-Y-Keenoy B, Vinckx M, Vertommen J, et al. Impact of Vitamin E supplementation on lipoprotein peroxidation and composition in Type 1 diabetic patients treated with Atorvastatin. Atherosclerosis 2004 Aug; 175(2):369-76.

• Chapter 28: Which Makes More Sense?
• Chapter 29: Adding Vitamins to Statin Drugs

Chapter Excerpts

Medications, even taken the way they’re prescribed, are the third leading cause of death in the United States after cardiovascular disease and cancer. Over 100,000 people die every year in the United States from taking prescription medications.

The drug manufacturers will never admit that it is the antioxidants that reduce disease and death. In order to make money, the industry needs to sell you patented drugs, …not convince you that you should be taking vitamins and minerals.

Chapter References

• 56: Rosenson RS. Statins in atherosclerosis: lipid-lowering agents with antioxidant capabilities. Atherosclerosis. 2004. Mar;173(1):1-12.
• 57: Tsimikas S, et al. High-dose atorvastatin reduces total plasma levels of oxidized phospholipids and immune complexes present on apolipoprotein B-100 in patients with acute coronary syndromes in the MIRACL trial. Circulation. 2004 Sep 14;110(11):1406-12.
• 58: Sparks DL., et al. Statin therapy in Alzheimer’s disease. Acta Neurol Scand Suppl. 2006;185:78-86.
• 59: Wolozin B., et al. Re-assessing the relationship between cholesterol, statins and Alzheimer’s disease. Acta Neurol Scand Suppl. 2006;185:63-70.
• 60: Nunomura A, et al. Involvement of oxidative stress in Alzheimer disease. J Neuropathol Exp Neurol. 2006. Jul;65(7):631-41.
• 61: Harman D. Alzheimer’s disease pathogenesis: role of aging. Ann NY Acad Sci. 2006 May;1067:454-60.
• 62: Moreira PI, et al. Therapeutic options in Alzheimer’s disease. Expert Rev Neurother. 2006 Jun;6(6):897-910.
• 63: Ono K., et al. Anti-amyloidogenic effects of antioxidants: implications for the prevention and therapeutics of Alzheimer’s disease. Biochim Biophys Acta. 2006 Jun;1762(6):575-86.
• 64: Montiel T, et al. Role of oxidative stress on beta-amyloid neurotoxicity elicited during impairment of energy metabolism in the hippocampus: Protection by antioxidants. Exp Neurol. 2006 Apr 18; [Epub ahead of print].
• 65: Ono K, Yamada M. Antioxidant compounds have potent antifibrillogenic and fibril-destabilizing effects for alpha-synuclein fibrils in vitro. J Neurochem. 2006 Apr;97(1):105-15. Epub 2006 Mar 8.
• 66: Hajieva P, Behl C. Antioxidants as a potential therapy against age-related neurodegenerative diseases: amyloid Beta toxicity and Alzheimer’s disease. Curr Pharm Des. 2006;12(6):699-704.
• 38: Langsjoen P, Langsjoen A. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors. 2003 18(1-4):101-111.
• 67: Passi S, Stancato A, Aleo E, Dmitrieva A, Littarru GP. Statins lower plasma and lymphocyte ugiquinol/ubiqinone without affecting other antioxidants and PUFA. Biofactors 2003 18(1-4):113-124.
• 68: Mortensen S, Leth A, Agner E, Rohde M. Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors. Mol Aspects Med. 1997 18(suppl):S137-S144.
• 69: Folkers K, Langsjoen P, Willis R, et al. Lovastatin decreases coenzyme Q10 levels in humans. Proc Natl Acad Sci USA. 1990 Nov; 87(22):8931-8934.
• 70: Quiles J, Farquharson A, Ramirez-Tortosa M, et al. Coenzyme Q10 differentially moderates phospholipid hydroperoxide glutathionate peroxidase gene expression and free radicals production in malignant and non-malignant prostate cancer. Biofactors 2003 18(1-4):265-270.

• Chapter 20: The Effects of Lowering Co-Enzyme Q10 with Statin Drugs
• Chapter 21: Statin Drugs May Cause Muscle Weakness & Destruction
• Chapter 22: Statin Drugs May Cause Heart Disease, Heart Failure, and Death
• Chapter 23: Statin Drugs May Damage the Liver
• Chapter 24: Stain Drugs May Damage the Brain and Nerves

Chapter Excerpts

Since all organs and all cells rely on the ubiquitous Co-Q10, the depletion of it by statin drugs causes problems everywhere in the body.

Additionally, Co-Q10 was shown to increase blood levels of vitamin E and significantly increase the levels of protective HDL. As low HDL is a major risk factor for heart disease, increasing it is a definite benefit. Statin drugs were shown not to provide any benefit beyond supplementing with Co-Q10.

Co-Q10 depletion will become more and more of a problem as the pharmaceutical industry encourages doctors to lower cholesterol levels in their patients even more than ever. Is it possible that we are going to see an epidemic of congestive heart disease and cardiomyopathy, as well as cancer, among those taking cholesterol-lowering statin drugs?

So much denial exists within the cholesterol conspiracy that many doctors will not associate common side-effect symptoms and resultant diseases with the use of a statin drug… physicians and patients need to be educated regarding the symptoms of a statin drug are.

Chapter References

• 35: Cullen D, Bates D, Small S, et al. The incident reporting system does not detect adverse drug events: a problem for quality improvement. Joint Commission Journal on Quality Improvement, Oct. 1995 21(10):541-548.
• 37: Singh R, Neki N, Kartikey K, et al. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction. Mol Cell Biochem. 2003 Apr; 246(1-2):75-82.
• 38: Langsjoen P, Langsjoen A. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors. 2003 18(1-4):101-111.
• 39: Mortensen S. Perspectives on therapy of cardiovascular diseases with coenzyme Q10 (ubiquinone). Clin Investig 1993 71(8 Supp):S116-123 and S140-144.
• 40: Langsjoen P, Folkers K, Lyson K, et al. Pronounced increase of survival of patients with cardiomyopathy when treated with coenzyme Q10 and conventional therapy. Int J Tissue React 1990 12:163-168.
• 22: Schwartz G, Olsson A, et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes. JAMA 2001 285:1711-1718.
• 41: Gaist D, Jeppesen U, Andersen M, et al. Statins and risk of polyneuropathy: a case-control study. Neurology 2002 May 14; 58(9):1333-1337.

• Chapter 18: How Beneficial are Cholesterol-Lowering Statin Drugs?
• Chapter 19: Cholesterol-Lowering Statin Drugs Deplete Co-Enzyme Q10

Chapter Excerpts

Conclusion: Lipitor (R) did not reduce the number of deaths from heart attack even though it lowered LDL cholesterol… In other words, lowering LDL cholesterol made NO difference in reducing the risk of death from heart disease.

…both groups receiving Pravacol (R) suffered an increased incidence of cancer. In other words, not one life saved.
…LDL cholesterol levels did not correlate to their risk of death.
Statin drugs showed no benefit in reducing the number of overall deaths.

Statin drugs can lead to unpredictable chaos on the cellular level, interfering with proper cellular functions and breakdown, as well as preventing repair of damaged cells.

Chapter References

• 22: Schwartz G, Olsson A, et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes. JAMA 2001 285:1711-1718.
• 23: Arron M, member of The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in moderately hyper-cholesterolemic, hypertensive patients randomized to pravastatin vs. usual care: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT). JAMA 2002 288:2998-3007.
• 24: Heart Protection Study Collaborative Group (writing committee: Collins R, Armitage J, Parish S, Sleight P, Peto R). MRC/BHF heart protection study of cholesterol lowering in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002 360:7-22.
• 25: Medical Research Council/British Heart Foundation Heart Protection Study. Press release. Life-saver: World’s largest cholesterol-lowering trial reveals massive benefits for high-risk patients. Available at www.ctsu.ox.ac.uk/~hps/pr.shtml.
• 26: Ravnskov U. Statins as the new Aspirin. Conclusions from the heart protection study were premature. British Medical Journal 2002 324:789.
• 27: Shepherd J, Blauw G, Murphy M, et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomized controlled trial. Lancet 2002 Nov 23; 360(9346):1623-30.
• 28: Matsuzaki M, Kita T, Mabuchi H, Matsuzawa Y, Nakaya N, Oikawa S, Saito Y, Sasaki J, Shimamoto K, Itakura H; J-LIT Study Group. Japan Lipid Intervention Trial. Large scale cohort study of the relationship between serum cholesterol concentration and coronary events with low-dose simvastatin therapy in Japanese patients with hypercholesterolemia. Circ J. 2002 Dec; 66(12):1087-1095.
• 29: Newman CB, Palmer G, Silbershatz H, Szarek M. Safety of atorvastatin derived from analysis of 44 completed trials in 9,416 patients. Am J Cardiol. 2003 Sep 15; 92(6):670-676.
• 30: Hecht H, Harman S. Relation of aggressiveness of lipid-lowering treatment to changes in calcified plaque burden by electron beam tomography. Am J Cardiol. 2003 Aug 1; 92(3):334-336.
• 31: Sever P, Dahlof B, Poulter N, Wedel H, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo- Scandinavian Cardiac Outcomes Trial–Lipid Lowering Arm (ASCOTLLA): a multicenter randomized controlled trial. Lancet 2003 Apr 5; 361(9364):1149-58.
• 32: Jenkins A. Might money spent on statins be better spent? BMJ. 2003 Oct 18; 327(7420):933.
• 33: Liu Y, Coresh J, Eustace J, et al. Association Between Cholesterol Level and Mortality in Dialysis Patients: Role of Inflammation and Malnutrition. JAMA 2004 291:451-459.
• 34: Moore T, Psaty B, Furberg C. Time to act on drug safety. JAMA May 20, 1998 279(19):1571-1573.

• Chapter 16: Conspiracy to Have Everyone Taking Cholesterol-Lowering Drugs
• Chapter 17: The Cholesterol-Lowering Statin Drugs and the New Recommendations

Chapter Excerpts

Only 30-40% of people with blocked arteries and heart disease have elevated blood cholesterol levels, and posed the logical question: "How do you explain the other 60 to 70 %?"

The level at which LDL cholesterol is considered normal has continually been influenced by pharmaceutical companies, who pull the financial strings of research grants that keep medical schools and medical organizations running. The lower they can establish the level at which LDL cholesterol is considered normal, the more people automatically become victims of the dreaded disease of "high cholesterol."

The fact is eight of the nine panel members making the new LDL cholesterol recommendations were being paid by the statin-producing pharmaceutical companies. The panelists did not disclose their financial conflict of interest.

Chapter References

• 17: Rafai N, Ridker P. Inflammatory markers and coronary heart disease. Curr Opin Lipidol 2002 Aug; 13(4):383-389.
• 18: Albert C, et al. Prospective study of C-reactive protein, homocysteine, and plasma lipid levels as predictors of sudden cardiac death. Circulation 2002 Jun 4; 105 (22):2595-2599.
• 19: Bermudez E, Ridker P. C-reactive protein, statins, and the primary prevention of atherosclerotic cardiovascular disease. Prev Cardiol 2002 Winter; 5(1):42-46.
• 20: Blake C, Ridker P. Inflammatory mechanisms in atherosclerosis: from laboratory evidence to clinical application. Ital Heart J 2001 Nov; 2(11):796-800.
• 21: Grundy SM, Cleeman JI, Bairey Merz CN, Brewer HB, Clark LT, Hunninghake DB, Pasternak RC, Smith SC, Stone NJ; for the Coordinating Committee of the National Cholesterol Education Program. Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines. Circulation 2004 110:227-239.