As I write this I have once again read the comments of a medical researcher regarding the use of B vitamins in preventing hardening of the arteries. Dr. Petra Verhoef of Wageningen University in the Netherlands, who was the senior researcher on a study looking at the effect of folic acid supplementation in elderly individuals with homocysteine levels equal to or greater than 13. The study showed that 800 mcg. of folic acid daily lowered homocysteine levels by an average of 26 %, but the lowering of homocysteine did not result in less thickening or stiffness of arterial walls.

Dr. Verhoef commented, “The findings suggest that folic acid is not effective in slowing down early stages of cardiovascular disease, as measured by accepted markers of atherosclerosis. More and more researchers are thinking that homocysteine does not directly contribute to heart disease and stroke after all.”

Homocysteine is a substance that is toxic to the lining of arteries. It has been fifteen years since the upper “safe” limit of homocysteine was found to be around 7 mmol/liter with the preferred level being less than 6.3 mmol/L. The Verhoef led team lowered homocysteine levels an average of 26 %; they did not lower homocysteine to a level generally regarded as safe. Since the study subjects began with homocysteines in excess of 13 mmol/L the ending levels would have been in excess of 9.62. I suspect the actual level was much higher, since 13 was the minimum level of homocysteine required for admission to the study.

The researchers began with a group of individuals who had dangerously high levels of homcysteine. They lowered homocysteine to an unsafe level, a level known to increase the risk of atherosclerosis, and then had the audacity to conclude that homocysteine is not directly associated with the atherosclerotic process and that B vitamins are of no value in preventing hardening of the arteries!

Contrast the attitude and thought process of the investigators toward B vitamins with the prevailing attitude toward cholesterol-lowering drugs. When focus was first placed upon the lowering of LDL cholesterol in 1993 the recommended target was 130 mg/dl. When significant reductions in heart disease deaths were not seen the target was lowered to 100 mg/dl in 2001. The target was further lowered to 70 mg/dl in 2004.

If one were to construct a study of a drug to lower LDL cholesterol along the lines of the Netherlands’ B vitamin/ homocysteine study one would begin with individuals with LDL cholesterol levels in excess of 146 mg/dl and lower them by 26 % to 108 mg/dl, far above the current target of 70 mg/dl. It is inconceivable that such as study would be taken seriously or that any medical researcher would use its findings to conclude that LDL cholesterol plays no role in the development of atherosclerosis and that cholesterol-lowering medications are of no benefit in preventing hardening of the arteries.

Medical researchers base their conclusions not on the basis of logic and objectivity, but rather on the basis of their personal biases against nutritional supplements and for pharmaceutical agents. It is important to keep this in mind when you read headlines proclaiming the ineffectiveness of vitamins in the prevention of illness.