The combined efforts of the pharmaceutical and food industries have done a good job of convincing us is that having too much cholesterol floating around our bloodstream is one factor that is sure to speed our demise: only 15 years ago practically no one had heard of cholesterol, and now many individuals seem as fluent with their cholesterol level as their golfing handicap or shoe size. However, a stack of researched amassed over the last decade suggests that a diet-related substance called homocysteine may be a critical factor that precedes the dumping of cholesterol on the inside of the body’s vessels. It appears that cholesterol’s reputation as the pre-eminent element in conditions such as heart disease and stroke is under threat.

Homocysteine (pronounced homo-sis-teen) is a breakdown product of a substance called methionine, itself derived from protein in the diet. Homocysteine helps to build and maintain tissues in the body, but in excess, has the capacity to injure the lining of the arteries in the body. Many scientists believe that such damage in the vessel wall is the first step in the process in which cholesterol causes artery narrowing that is a common underlying factor in heart disease and stroke. In addition, homocysteine can thicken the blood too, an effect which is likely to increase the risk of these conditions as well as blood clots in the leg known as deep vein thromboses (DVTs). Recently, UK researchers published a study in the British Medical Journal that reviewed data from a total of 92 studies assessing the relationship between homocysteine levels and disease. The authors of this study concluded that there is indeed strong evidence to suggest that homocysteine is a causative factor in heart disease, stroke and DVT.

Homocysteine levels in the bloodstream are generally measured in units known as micromols per litre (mol/l) of blood. It is not clear what values represent ‘healthy’ levels of homocysteine, though existing research suggests that less than 10 mol/l is worth shooting for. Homocysteine can be converted in the body into a harmless substance known as cystanthionine, and that this conversion is dependent on vitamins B6, B12 and folic acid. Upping our intake of these appears to be one simple way of quelling homocysteine levels in the body.

The recent BMJ study suggested that supplementation with 800 micrograms (mcg) of folic acid per day should reduce the risk of heart disease, stroke and deep vein thrombosis by 16, 24, and 25 per cent respectively. In addition to eating foods rich in folic acid such as spinach, asparagus and broccoli, individuals with high homocysteine levels are likely to benefit from supplementing with 800 – 1000 mcg of folic acid each day. Adding 10 mg of vitamin B6 and 400 mcg of vitamin B12 to this each day is likely to confer additional benefit in terms of homocysteine reduction.

Despite the avalanche of evidence that points to homocysteine as a causative factor in disease and contracted longevity, it seems that this issue receives scant attention in the popular press. The fact that neither the food nor pharmaceutical industry has anything to sell us for homocysteine reduction is perhaps one reason why this story has yet to be pushed by PR companies and marketeers. Personally, I wouldn’t wait for the development of foods or medications that promise to lower homocysteine before becoming familiar with your homocysteine level and popping a decent B-complex supplement each day if need be.

Print This Post