A Low-Enough LDL May Reduce Cardiovascular Risk to Nearly Nonexistent

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 9 No. 2 • April 2006


A Low-Enough LDL May Reduce Cardiovascular Risk to Nearly Nonexistent

A number of studies suggest that excess LDL plays a major role in the endothelial dysfunction found in patients with coronary artery disease (CAD). For example, one recent study,1 looking at 188 patients (135 males, 53 females) found that, in comparison with 51 healthy controls (22 males, 29 females), the relaxation in response to calcium ionophore of saphenous veins (removed during varicose vein surgery) was decreased. Total superoxide production was increased, and LDL-cholesterol was “a major determinant of endothelial dysfunction and oxidative stress in these patients.”

Other papers have reported that normal humans with genetic polymorphisms that result in unusually low LDL levels (below 70) rarely have cardiovascular disease. One paper2 reports that “the plasma concentration of LDL-cholesterol must exceed 2 mmol/L (80 mg/dL) for atherogenesis, even at sites of high shear stress [such as bifurcation points in arteries].” For avoiding cardiovascular disease, therefore, it would appear to be useful to reduce LDL to 80 or below. For those who do not have the advantageous low-LDL-producing genes, you will need to try a combination of diet modification, exercise, and supplements (such as moderate alcohol consumption, niacin, antioxidant vitamins, fish oils, and policosanol with CoQ10, to name just a few). For those who have high risk or already have cardiovascular disease, you may wish to try a statin to achieve this very low LDL level; be sure also to take a supplement of CoQ10 of at least 30 mg three to four times a day.3 But keep in mind that not all statins, though they all reduce cholesterol and LDL-cholesterol, have actually been shown to reduce all-cause or cardiovascular deaths.4 For example, in the IDEAL study (results published in the Nov. 16, 2005 JAMA), 80 mg/d of atorvastatin, compared with 20–40 mg/d of simvastatin, resulted in a 23-mg/dL lower LDL-C (by the 80-mg atorvastatin) with an 11% trend (not statistically significant) in reduction in coronary heart disease death, myocardial infarction, or cardiac arrest.

References

  1. Al-Benna et al. Low-density lipoprotein cholesterol determines oxidative stress and endothelial dysfunction in saphenous veins from patients with coronary artery disease. Arterioscler Thromb Vasc Biol 26:218-23 (2006).
  2. Williams and Tabas. The response-to-retention hypothesis of early atherogenesis. Arterioscler Thromb Vasc Biol 15:551-61 (1995).
  3. Lamperti et al. Muscle coenzyme Q10 level in statin-related myopathy. Arch Neurol 62:1709-12 (2005).
  4. Cannon. The IDEAL cholesterol. JAMA 294:2492-4 (2005).

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