• Chapter 39: Conclusion
• Chapter 40: Specific Daily Supplement Considerations

Chapter Excerpts

The best treatment to prevent heart disease and stroke is NOT to simply lower cholesterol with statin drugs as much as it is to PROTECT LDL cholesterol… NO MATTER the level… from OXIDATION (according to the opinion of Dr. Ladd McNamara). Even among people with higher levels of cholesterol, those whose LDL cholesterol is NOT oxidized, along with a LOW homocysteine level (less than 6.5), will have a lower risk of heart disease and stroke than those that simply have a “normal” LDL cholesterol level (which IS oxidized).

Shall we risk serious and permanent side effects, including disease and possible death from statin drugs, or shall we enjoy all the positive benefits of nutrition, including longer life, less disease and no harm from the use of vitamins and minerals? The choice is in our hands …literally!

Ladd McNamara, M.D.

• 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 12: Conflicting Studies?
• Chapter 13: The Pharmaceutical Industry’s Money Influences the Treatment of Disease

Chapter Excerpts

In this study they never lowered homocysteine to what research has shown to be a safe and effective level, which is 6.5 or less. In fact, for every 3 points above 6.5 there is a 35% increase risk of heart disease.

Ladd McNamara, M.D.

Chapter References

• 11: Bonaa KH, et al. Homocysteine lowering and cardiovascular events after acute myocardial infarction. N Engl J Med. 2006. Apr 13;354(15):1578-88.

Ladd McNamara, M.D.

• Chapter 9: Homocysteine Oxidizes Both LDL Cholesterol and the Arterial Walls
• Chapter 10: Pharmaceutical Companies Conspire to Hide the Truth
• Chapter 11: The Discovery of the Association Between Homocysteine and Heart Disease

Chapter Excerpts

Inasmuch as the medical dogma was that high cholesterol caused heart disease, naturally Dr. McCully’s research and findings showing otherwise were blackballed by the pharmaceutical industry.

Homocysteine is second only to cigarette smoking in its oxidative destruction. The combination of oxidized LDL cholesterol and damaged arterial lining (the endothelium) is what causes LDL cholesterol to stick to the arteries, independent of whether the LDL cholesterol level is normal or not.

The Cholesterol Conspiracy includes ignoring one of the major causes of heart disease; thus doctors are unaware of the necessity to test for and reduce homocysteine levels …… Ladd McNamara, M.D.

"I realized immediately that this was a critical case because if this boy had arteriosclerosis, it would prove that no matter what the enzyme defect and no matter what the metabolic pattern, patients with inherited diseases causing homocystinuria also developed arteriosclerosis. Because of this I could attribute formation of the plaques to elevated homocysteine levels."
Kilmer McCully, M.D.

"They told me later they didn’t want to have Harvard or Massachusetts General Hospital associated with my theory because it appeared to contradict the conventional wisdom that cholesterol and fats were the causes of heart disease."
Kilmer McCully, M.D.

Ladd McNamara, M.D. on Dr. McCulley.

Chapter References

• 10: Haim M, et al. Serum Homocysteine and Long-Term Risk of Myocardial Infarction and Sudden Death in Patients with Coronary Heart Disease. Cardiology. 2006 Jun 6;107(1):52-56.

Ladd McNamara, M.D.