Free Shipping on All Orders $75 Or More!

Your Trusted Brand for Over 35 Years

Life Extension Magazine

<< Back to May 2006

New Blood Test Better Predicts Heart Attack Risk

May 2006

By William Davis, MD, FACC

C-Reactive Protein

Inflammation is fuel for the fire that leads to coronary plaque rupture, resulting in heart attack. Inflammation may also contribute to other diseases, such as diabetes, cancer, and arthritis. A number of proteins circulate in the blood, signaling heightened states of inflammation. The most clinically studied of these is C-reactive protein (CRP).

Dr. Paul Ridker of Harvard University is the nation’s foremost authority on CRP. He has demonstrated that high CRP levels increase heart attack risk threefold, even when LDL level is low. When elevated CRP occurs in the company of small LDL particle size, a very high risk for heart attack can develop—a risk that is sixfold greater.17

Scientists have developed a way to measure CRP, called “high-sensitivity” CRP, that can detect low levels of inflammation. While highly elevated levels nearly always represent inflammation outside the heart (e.g., arthritis) and should not be used to prognosticate coronary risk, modestly elevated levels can be used to gauge low-grade inflammation that contributes to coronary plaque rupture.

Healthy lifestyle choices, such as restricting saturated fat, choosing low-glycemic-index foods, and engaging in regular exercise, are the best way to lower CRP. Fish oil can be a useful adjunct in your program for turning off inflammation and lowering CRP.44 Prescription agents like the cholesterol drug ezetimibe (Zetia®) and the diabetes drugs Actos® and Avandia® can lower CRP. Aspirin lowers CRP modestly,45 as does alpha tocopherol (vitamin E).46 Plant-based compounds called flavonoids, including olive oil polyphenols, are emerging as potentially important factors in lowering inflammation and CRP levels, though further investigation is warranted.46,47


Our blood maintains a precarious balance between being able to flow freely into the smallest capillaries and being capable of clotting in response to injury. Clotting proteins circulating in the blood help maintain this balance. Fibrinogen is a principal clotting protein. With the appropriate stimulation (injury or stress), fibrinogen is modified to form a smaller protein called fibrin. Thousands of strands of fibrin accumulate at an injury site to form a blood clot.

When greater blood levels of fibrinogen are present, the balance is tipped in favor of blood clot formation, even when it may not be appropriate. This can happen, for instance, at the site of a ruptured coronary plaque. The injured plaque surface causes fibrinogen to be converted to fibrin, forming a blood clot, which may result in heart attack. Fibrinogen can also promote atherosclerotic plaque growth, even without blood clot formation. Elevated fibrinogen levels are associated with an increased risk of heart attack.48-50

The modern American lifestyle of sedentary occupations and excessive intake of high-fat foods and refined starches increases fibrinogen. Estrogen raises fibrinogen levels, which may account for some of the increased blood-clotting tendency observed with estrogen replacement.

Fish oil at doses of 3000 mg or greater daily does a good job of lowering fibrinogen.51 Combine this with a diet rich in green vegetables and fiber, low in saturated and hydrogenated fat, and physical activity, and fibrinogen levels usually drop into a favorable range. For the occasional person who requires more intensive effort, the fibric acid class of drugs, especially fenofibrate, can lower fibrinogen by 15-40%. Niacin also helps by lowering fibrinogen by 10-30%.52

  • Oat bran, ground flaxseed, or ground psyllium seed: 2 tablespoons/day. Oat bran and flaxseed are the most versatile, great either in hot cereal or added to yogurt or fruit smoothies.53-56
  • Raw almonds, walnuts, or pecans: 1/4-1/2 cup/day.39
  • Soy protein powder: 3 tablespoons (25 gm)/day of this supplement added to yogurt or fruit smoothies is among the most effective nutritional methods for lowering LDL particle number, by suppressing the liver’s production of cholesterol.54 Other convenient sources of soy protein include soy cheese, low-carbohydrate pasta, and soy milk.
  • Stanol/sterol esters: found in some butter substitutes and fortified orange juice products.54
  • Beans: lima, Spanish, black, red, etc.: 1/2-1 cup/day.55
  • Chitosan: 1200 mg per day lowers LDL level by around 10%.57,58
  • Pectin: citrus fruit rinds can be an effective adjunct for lowering cholesterol.59 Pectin can also be taken as a supplement.
  • Glucomannan: this fiber from konjac root decreases LDL level by around 10%, while lowering blood sugar and promoting weight loss by providing a feeling of fullness.58 A dose of 1500 mg before meals works well, and should be consumed with plenty of water, since it is highly water-absorbing.

How and When to Get These Tests

If you have already been diagnosed with coronary or vascular disease, or have a history of heart attack, coronary stent, angioplasty, or bypass surgery, your doctor may have failed to identify many of the underlying causes of your condition. Uncovering the hidden causes of your heart disease can make a profound difference to your future. After all, how can an effective prevention program be devised without identifying all causes of your heart disease? It is not unusual for lipoprotein assessment to identify three, four, or five risk factors of heart disease. The good news is that this information can help you and your doctor to implement new treatments to comprehensively reduce your risk.

If you do not have known heart disease but have reason to believe that you are at high risk—due to family history of the disease, diabetes in yourself or your family, being overweight or obese, or having had significant cholesterol or triglyceride abnormalities identified—strongly consider lipoprotein testing to shed more light on the extent of your risk factors. Better information can mean more effective prevention and thus better health. The same advice applies if a computed tomography (CT) heart scan has revealed that you suffer from arterial calcification.

Even if you are simply concerned about heart disease risk, you might consider lipoprotein testing. The blood draw is no different than that for a cholesterol panel and is performed at virtually no risk to you.

Thankfully, more and more physicians are recognizing the deficiencies of conventional lipid assessment and have turned to lipoprotein testing for better answers. Laboratories around the country are now offering advanced lipoprotein testing. Life Extension now offers the Vertical Auto Profile, or VAP™, method of advanced lipoprotein testing.


Advanced lipoprotein testing can help provide great insight into your risks for heart disease, filling the gaping deficiencies of mainstream cholesterol or lipid testing. The superior information provided by lipoprotein testing can help you and your physician to devise an effective program to prevent future heart attacks.

If you have a family history of heart disease, high blood pressure, diabetes, or any measure of coronary plaque, you should strongly consider lipoprotein testing. If you have had coronary disease already diagnosed—that is, if you have had a heart attack, angina, or a heart procedure like coronary angioplasty or bypass surgery—then lipoprotein testing can be a crucial part of your program to prevent future cardiac catastrophes, particularly if conventional lipid testing has failed to pinpoint the cause of your disease.


Being aware of the glycemic-index values of different foods is very important when you have small LDL particles, low total HDL, deficient large HDL, or increased triglycerides or VLDL. This means choosing foods that release sugars slowly, an effect that may help improve all of these risk factors. Abrupt spikes in sugar release help create these abnormalities and lead to both coronary plaque growth and diabetes. By contrast, foods that release sugars slowly or contain little or no sugar can help correct these patterns.60,61

The glycemic index is calculated by comparing a food’s ability to raise blood sugar to that of either white table sugar or white bread, two foods that are processed by the body like pure sugar. The height of the blood sugar peak is then measured. A glycemic index of 100 would be equal in sugar-release properties to sugar or white bread; an index below 100 would mean less sugar release. In general, proteins and fats have lower glycemic index values, while carbohydrates and refined foods have higher values.

Carbohydrates are a potential problem for glycemic index control. Processed foods like breakfast cereals, white bread, other white flour products, and sweets are clearly the worst culprits, causing big spikes in blood sugar after ingestion. Desirable carbohydrate sources with lower glycemic indexes include foods containing oats, whole fruits and vegetables (the pulp and fiber slow sugar release, unlike their juices), and beans.

Healthy oils, like canola, olive, and flaxseed oils, slow the sugar-release effect of other foods. Foods rich in fiber, such as oat bran, whole grains, and raw nuts (almonds, walnuts, pecans), tend to slow sugar release. Supplements containing glucomannan and other fibers are very viscous, which slows sugar release and also promotes satiety, thereby supporting weight loss.

A website managed by the University of Sydney ( has an excellent searchable database that allows you to enter the food in question and obtain its glycemic index. Dr. Jennie Brand-Miller has published extensively on the glycemic index, and the complete glycemic index tables generated by her research are also available in her book The Glucose Revolution (Marlowe and Company, 1999).

Dr. William Davis is an author, lecturer, and practicing cardiologist focusing on coronary disease regression. He is author of the book, Track Your Plaque: The only heart disease prevention program that shows you how to use the new heart scans to detect, track, and control coronary plaque. He can be contacted through


1. Law MR, Wald NJ. Risk factor thresholds: their existence under scrutiny. BMJ. 2002 Jun 29;324(7353):1570-6.

2. Akosah KO, Schaper A, Cogbill C, Schoenfeld P. Preventing myocardial infarction in the young adult in the first place: how do the National Cholesterol Education Panel III guidelines perform? J Am Coll Cardiol. 2003 May 7;41(9):1475-9.

3. Sharrett AR, Ballantyne CM, Coady SA, et al. Coronary heart disease prediction from lipoprotein cholesterol levels, triglycerides, lipoprotein(a), apolipoproteins A-I and B, and HDL density subfractions: The Atherosclerosis Risk in Communities (ARIC) Study. Circulation. 2001 Sep 4;104(10):1108-113.

4. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA. 1986 Nov 28;256(20):2823-8.

5. Castelli WP, Anderson K, Wilson PW, Levy D. Lipids and risk of coronary heart disease. The Framingham Study. Ann Epidemiol. 1992 Jan;2(1-2):23-8.

6. Sniderman AD, Pedersen T, Kjekshus J. Putting low-density lipoproteins at center stage in atherogenesis. Am J Cardiol. 1997 Jan 1;79(1):64-7.

7. Cheung MC, Brown BG, Wolf AC, Albers JJ. Altered particle size distribution of apolipoprotein A-I-containing lipoproteins in subjects with coronary artery disease. J Lipid Res. 1991 Mar;32(3):383-94.

8. Lamarche B, Despres JP, Moorjani S, et al. Prevalence of dyslipidemic phenotypes in ischemic heart disease (prospective results from the Quebec Cardiovascular Study). Am J Cardiol. 1995 Jun 15;75(17):1189-95.

9. Walldius G, Jungner I, Holme I, et al. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet. 2001 Dec 15;358(9298):2026-33.

10. van Lennep JE, Westerveld HT, van Lennep HW, et al. Apolipoprotein concentrations during treatment and recurrent coronary artery disease events. Arterioscler Thromb Vasc Biol. 2000 Nov;20(11):2408-13.

11. Gotto AM, Jr., Whitney E, Stein EA, et al. Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Circulation. 2000 Feb 8;101(5):477-84.

12. St-Pierre AC, Ruel IL, Cantin B, et al. Comparison of various electrophoretic characteristics of LDL particles and their relationship to the risk of ischemic heart disease. Circulation. 2001 Nov 6;104(19):2295-9.

13. Kwiterovich PO, Jr. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am J Cardiol. 2002 Oct 17;90(8A):30i-47i.

14. Lamarche B, Tchernof A, Moorjani S, et al. Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Quebec Cardiovascular Study. Circulation. 1997 Jan 7;95(1):69-75.

15. de Bruin TW. Lipid metabolism. Curr Opin Lipidol. 1998 Jun;9(3):275-8.

16. Krauss RM. Dietary and genetic effects on LDL heterogeneity. World Rev Nutr Diet. 2001;89:12-22.

17. St-Pierre AC, Bergeron J, Pirro M, et al. Effect of plasma C-reactive protein levels in modulating the risk of coronary heart disease associated with small, dense, low-density lipoproteins in men (The Quebec Cardiovascular Study). Am J Cardiol. 2003 Mar 1;91(5):555-8.

18. Morgan JM, Carey CM, Lincoff A, Capuzzi DM. The effects of niacin on lipoprotein subclass distribution. Prev Cardiol. 2004;7(4):182-7.

19. Guyton JR, Goldberg AC, Kreisberg RA, et al. Effectiveness of once-nightly dosing of extended-release niacin alone and in combination for hypercholesterolemia. Am J Cardiol. 1998 Sep 15;82(6):737-43.

20. Superko HR. Exercise and lipoprotein metabolism. J Cardiovasc Risk. 1995 Aug;2(4):310-5.

21. Berneis KK, Krauss RM. Metabolic origins and clinical significance of LDL heterogeneity. J Lipid Res. 2002 Sep;43(9):1363-79.

22. Davy BM, Davy KP, Ho RC, et al. High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men. Am J Clin Nutr. 2002 Aug;76(2):351-8.

23. Griffin BA. The effect of n-3 fatty acids on low density lipoprotein subfractions. Lipids. 2001;36 SupplS91-7.

24. Gordon DJ, Rifkind BM. High-density lipoprotein—the clinical implications of recent studies. N Engl J Med. 1989 Nov 9;321(19):1311-6.

25. Miller NE. Associations of high-density lipoprotein subclasses and apolipoproteins with ischemic heart disease and coronary atherosclerosis. Am Heart J. 1987 Feb;113(2 Pt 2):589-97.

26. Syvanne M, Ahola M, Lahdenpera S, et al. High density lipoprotein subfractions in non-insulin-dependent diabetes mellitus and coronary artery disease. J Lipid Res. 1995 Mar;36(3):573-82.

27. Johansson J, Carlson LA, Landou C, Hamsten A. High density lipoproteins and coronary atherosclerosis. A strong inverse relation with the largest particles is confined to normotriglyceridemic patients. Arterioscler Thromb. 1991 Jan;11(1):174-82.

28. Bays H. Existing and investigational combination drug therapy for high-density lipoprotein cholesterol. Am J Cardiol. 2002 Nov 20;90(10B):30K-43K.

29. Thomas TR, Smith BK, Donahue OM, et al. Effects of omega-3 fatty acid supplementation and exercise on low-density lipoprotein and high-density lipoprotein subfractions. Metabolism. 2004 Jun;53(6):749-54.

30. Tsunoda F, Koba S, Hirano T, et al. Association between small dense low-density lipoprotein and postprandial accumulation of triglyceride-rich remnant-like particles in normotriglyceridemic patients with myocardial infarction. Circ J. 2004 Dec;68(12):1165-72.

31. Chung BH, Cho BH, Liang P, et al. Contribution of postprandial lipemia to the dietary fat-mediated changes in endogenous lipoprotein-cholesterol concentrations in humans. Am J Clin Nutr. 2004 Nov;80(5):1145-58.

32. Rivellese AA, Maffettone A, Vessby B, et al. Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects. Atherosclerosis. 2003 Mar;167(1):149-58.

33. Otvos J. Measurement of triglyceride-rich lipoproteins by nuclear magnetic resonance spectroscopy. Clin Cardiol. 1999 Jun;22(6 Suppl):II21-7.

34. Zilversmit DB. Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins. Clin Chem. 1995 Jan;41(1):153-8.

35. Chan DC, Barrett HP, Watts GF. Dyslipidemia in visceral obesity: mechanisms, implications, and therapy. Am J Cardiovasc Drugs. 2004;4(4):227-46.

36. Berglund L, Ramakrishnan R. Lipoprotein(a): an elusive cardiovascular risk factor. Arterioscler Thromb Vasc Biol. 2004 Dec;24(12):2219-26.

37. Maher VM, Brown BG, Marcovina SM, et al. Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a). JAMA. 1995 Dec 13;274(22):1771-4.

38. Sirtori CR, Calabresi L, Ferrara S, et al. L-carnitine reduces plasma lipoprotein(a) levels in patients with hyper Lp(a). Nutr Metab Cardiovasc Dis. 2000 Oct;10(5):247-51.

39. Jenkins DJ, Kendall CW, Marchie A, et al. Dose response of almonds on coronary heart disease risk factors: blood lipids, oxidized low-density lipoproteins, lipoprotein(a), homocysteine, and pulmonary nitric oxide: a randomized, controlled, crossover trial. Circulation. 2002 Sep 10;106(11):1327-32.

40. Marcovina SM, Koschinsky ML, Albers JJ, Skarlatos S. Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: recent advances and future directions. Clin Chem. 2003 Nov;49(11):1785-96.

41. Berglund L. Diet and drug therapy for lipoprotein (a). Curr Opin Lipidol. 1995 Feb;6(1):48-56.

42. Anon. Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA. 2002 Oct 23;288(16):2015-22.

43. Refsum H, Ueland PM, Nygard O, Vollset SE. Homocysteine and cardiovascular disease. Annu Rev Med. 1998;49:31-62.

44. Ciubotaru I, Lee YS, Wander RC. Dietary fish oil decreases C-reactive protein, interleukin-6, and triacylglycerol to HDL-cholesterol ratio in postmenopausal women on HRT. J Nutr Biochem. 2003 Sep;14(9):513-21.

45. Fredrikson GN, Hedblad B, Nilsson JA, et al. Association between diet, lifestyle, metabolic cardiovascular risk factors, and plasma C-reactive protein levels. Metabolism. 2004 Nov;53(11):1436-42.

46. Patrick L, Uzick M. Cardiovascular disease: C-reactive protein and the inflammatory disease paradigm: HMG-CoA reductase inhibitors, alpha-tocopherol, red yeast rice, and olive oil polyphenols. A review of the literature. Altern Med Rev. 2001 Jun;6(3):248-71.

47. Phillips T, Childs AC, Dreon DM, Phinney S, Leeuwenburgh C. A dietary supplement attenuates IL-6 and CRP after eccentric exercise in untrained males. Med Sci Sports Exerc. 2003 Dec;35(12):2032-7.

48. Chambless LE, Folsom AR, Sharrett AR, et al. Coronary heart disease risk prediction in the Atherosclerosis Risk in Communities (ARIC) study. J Clin Epidemiol. 2003 Sep;56(9):880-90.

49. Koenig W. Fibrin(ogen) in cardiovascular disease: an update. Thromb Haemost. 2003 Apr;89(4):601-9.

50. Palmieri V, Celentano A, Roman MJ, et al. Relation of fibrinogen to cardiovascular events is independent of preclinical cardiovascular disease: the Strong Heart Study. Am Heart J. 2003 Mar;145(3):467-74.

51. Vanschoonbeek K, Feijge MA, Paquay M, et al. Variable hypocoagulant effect of fish oil intake in humans: modulation of fibrinogen level and thrombin generation. Arterioscler Thromb Vasc Biol. 2004 Sep;24(9):1734-40.

52. de Maat MP. Effects of diet, drugs, and genes on plasma fibrinogen levels. Ann NY Acad Sci. 2001;936:509-21.

53. Berg A, Konig D, Deibert P, et al. Effect of an oat bran enriched diet on the atherogenic lipid profile in patients with an increased coronary heart disease risk. A controlled randomized lifestyle intervention study. Ann Nutr Metab. 2003;47(6):306-11.

54. Kerckhoffs DA, Brouns F, Hornstra G, Mensink RP. Effects on the human serum lipoprotein profile of beta-glucan, soy protein and isoflavones, plant sterols and stanols, garlic and tocotrienols. J Nutr. 2002 Sep;132(9):2494-505.

55. Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr. 1999 Jan;69(1):30-42.

56. Anderson JW, Allgood LD, Lawrence A, et al. Cholesterol-lowering effects of psyllium intake adjunctive to diet therapy in men and women with hypercholesterolemia: meta-analysis of 8 controlled trials. Am J Clin Nutr. 2000 Feb;71(2):472-9.

57. Bokura H, Kobayashi S. Chitosan decreases total cholesterol in women: a randomized, double-blind, placebo-controlled trial. Eur J Clin Nutr. 2003 May;57(5):721-5.

58. Gallaher DD, Gallaher CM, Mahrt GJ, et al. A glucomannan and chitosan fiber supplement decreases plasma cholesterol and increases cholesterol excretion in overweight normocholesterolemic humans. J Am Coll Nutr. 2002 Oct;21(5):428-33.

59. Anderson JW, Tietyen-Clark J. Dietary fiber: hyperlipidemia, hypertension, and coronary heart disease. Am J Gastroenterol. 1986 Oct;81(10):907-19.

60. Harbis A, Perdreau S, Vincent-Baudry S, et al. Glycemic and insulinemic meal responses modulate postprandial hepatic and intestinal lipoprotein accumulation in obese, insulin-resistant subjects. Am J Clin Nutr. 2004 Oct;80(4):896-902.

61. Pelkman CL. Effects of the glycemic index of foods on serum concentrations of high-density lipoprotein cholesterol and triglycerides. Curr Atheroscler Rep. 2001 Nov;3(6):456-61.