New kid on the block

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 research amassed over the past decade suggests that a diet-related substance, 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 methionine, itself derived from protein in the diet. Homocysteine helps to build and maintain tissues, but in excess has the capacity to injure the lining of the arteries. Many scientists believe that such damage is the first step in the process in which cholesterol causes artery narrowing - a common factor in heart disease and stroke. Homocysteine can also thicken the blood, which is likely to increase the risk of blood clots in the leg, or deep vein thromboses (DVTs).

Homocysteine levels in the bloodstream are measured in micromols per litre (mmol/l) of blood. It is not clear what values represent 'healthy' levels, though research suggests that less than 10 mmol/l is worth aiming for. Homocysteine can be converted in the body into a harmless substance, cystanthionine, and 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 800-1,000mcg of folic acid each day. Adding 10mg of vitamin B6 and 400mcg of vitamin B12 to this each day is likely to facilitate homocysteine reduction.

Despite the avalanche of evidence pointing to homocysteine as a causative factor in disease and contracted longevity, this issue receives scant attention in the 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. 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.

Dear John

In the New Year, I started a fitness campaign comprising regular running and some lightweight training. Despite all the stretching, I suffer from muscle soreness for a day or two after exercise. Do you know how I might prevent this?
Peter Barnes, by email

Soreness and perhaps even muscular strains are common side-effects of physical activity. During exercise our demands for oxygen go up, causing us to generate more damaging free-radical molecules than normal. Free-radical damage is thought to be one reason our muscles may feel sore and achy a day or so after exercise.

Antioxidant nutrients such as vitamin C and E may offset the damage that muscles endure during exercise, and may reduce activity-related muscle soreness. Try taking 1,000mg of vitamin C twice a day along with 400 IU (about 250mg) of vitamin E each day.

Another nutrient which may help is magnesium. Magnesium is essential for muscle health. In clinical practice, a deficiency of this mineral can manifest as a tendency to muscle soreness and injury, too. If you suffer from muscle cramp, then this is quite a strong sign that you may be magnesium deficient. I suggest you take 250-500mg of magnesium a day.

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