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Assessing The Risk of Heart Disease


By John L. Wilson, M.D.


According to the American Heart Association, more than 2,600 Americans died of Cardiovascular (Heart) Disease each day in 1998. That is one death every 33 seconds. Considering that Cardiovascular Disease (CVD) has been the leading cause of death in the US since 1900 (except in 1918 when more deaths occurred from an influenza epidemic), it is becoming obvious that the prevention and treatment strategies have fallen short.


Factors that have long been thought to put an individual at risk for CVD include smoking tobacco products, sedentary lifestyle, obesity, high blood pressure, stress, abnormal blood fats including cholesterol and triglycerides, and a family history of heart disease. One’s inherited predisposition to heart disease does not mean that one is fated to get heart disease, as the expression of that genetic predisposition is strongly influenced by lifestyle. Lifestyle modification is critical to successful prevention and intervention of CVD.


For years, elevated cholesterol was the focus of thinking about the cause of CVD, and this decades long oversimplified and largely incorrect belief has been the basis of many ineffective recommendations. The British Medical Journal on March 31, 2001 analyzed 27 separate studies of dietary restriction of cholesterol and fats in reducing CVD risk and found it has no proven effect on total mortality rates.


So if heart disease isn’t a simple plumbing problem, what is it? New research reveals it to be the result of many complex chemical events in the body, that can include clotting, oxidation, inflammation, excess insulin levels, and inborn errors in metabolism that are aggravated by nutritional deficiencies. This more current information on the causes of heart disease has resulted in the development of blood testing that can more accurately identify individuals at risk for heart disease earlier in life, and, importantly, result in very specific interventions to reduce risk. Some of the most important tests are:

1. Lipoprotein (a) [Lp(a)] – Lp(a), a genetic risk factor thought to be the most dangerous of the “bad fats” in the blood stream, does not correlate with cholesterol or triglycerides, so it stands alone as a separate risk factor. Initially defined by Nobel Prize recipient Dr. Linus Pauling, N-acetyl cysteine is the treatment of choice for reducing elevated Lp(a) levels.

2. Fibrinogen – Elevated fibrinogen, involved in the formation of clots and plaque, can detect those at risk for abnormal clot formation. Increasing certain types of dietary fat, eating oily fish, taking Vitamin E, and taking anti-inflammatory natural enzymes may reduce elevated fibrinogen levels.

3. Homocysteine – When elevated, this sulfur-containing amino acid can be toxic to the body, including coronary arteries. High levels can be addressed with increased intake of vitamins B6, B12, and folic acid.

4. Antioxidant Status – Oxidation can damage the lining of arteries, and one’s ability to offset this damage can be measured in the laboratory. Treatment is lifestyle changes (specifically stopping smoking) and antioxidant nutrients.

5. High Sensitivity C-Reactive Protein (HSCRP) – This inflammatory marker can reveal if there is inflammation occurring in the lining of the coronary arteries, addressing the most recent theories on the origin of CVD that point to an infectious/inflammatory contributing cause.

6. Lipids – Recent research from Harvard suggests the Coronary Risk Ratio (Total cholesterol divided by the “good” cholesterol HDL), combined with HSCRP are the best early predictors of vascular disease.

7. 4-Hour Glucose-Insulin Tolerance Test (GITT) – Excess insulin causes a thickening of the lining of the arteries, setting the stage for CVD. It is also the definitive screen for early detection of diabetes that increases risk for CVD.

8. Ferritin – Hemochromotosis is the medical term for an elevated ferritin, a protein that stores iron. Just as iron can oxidize or rust when left exposed to the elements outside, excess iron is a major source of oxidation inside the body, notably to the blood vessels. We don’t age, we rust! Doctor-supervised blood donation or phlebotomy can often return ferritin levels to normal range.

9. Mineral Adequacy – Imbalances and deficiencies in mineral levels in the body can accelerate the damaging process of hardening of the arteries. Customized supplementation of minerals addresses this contributing cause of heart disease.


A comprehensive CVD risk assessment provides very specific information of exactly where one’s risk is, and provides opportunities for particularly effective prevention and customized early intervention to decrease that risk.