Folic acid ‘could save lives’. This article refers to an article in today’s British Medical Journal. The original article describes a meta-analysis of the data on homocysteine and 3 diseases – stroke, ischemic heart disease and DVT/pulmonary embolism. The authors conclude that indeed homocysteine qualifies as an important modifiable risk factor. They present more data defining the risk than on proving the benefit from folate alone.
Dr David Wald and colleagues at Barts and the London School of Medicine reviewed 72 studies looking at the link between homocysteine levels and heart disease.
They found a strong link between high levels of the chemical and an increased risk of heart disease.
Folic acid is known to reduce levels of homocysteine.
The doctors suggested that people at high risk of heart disease or stroke should take folic acid supplements.
These include people with existing heart disease and everyone over the age of 55.
“Our results indicate that an estimated 16% of heart attacks and about 24% of strokes can be prevented just by taking a folic acid supplement everyday,” Dr Wald said in a statement.
“Everyone over 55 years of age, and in particular anyone with diabetes and existing cardiovascular disease should consider this. It would be ineffective, inexpensive and safe.”
The article, while quite complex, does make a strong case for homocysteine levels correlating with risk. I am somewhat skeptical of the conclusion that we should fortify our food with folate though. Quoting from the BMJ article,
Evidence of risk reduction
A placebo controlled randomised trial of treatment with B vitamins (folic acid, B-6, and B-12) to lower serum homocysteine concentration in patients with ischaemic heart disease has shown a rapid reduction of risk. There were 13 major cardiac events (coronary death, non-fatal myocardial infarction, or revascularisation procedure) over six months in 102 vitamin treated patients and 23 events in 94 placebo treated patients (P=0.04). Studies of patients with homocystinuria treated with B vitamins have also shown reduction in risk. In one study treatment with B vitamin led to two vascular events when 30 would have been expected (from previous observation in untreated patients), and in another study there were two events when 21 would have been expected.
Note that in that one study a market basket of B vitamins (folic acid, B-6 & B-12) decreased risk and homocysteine levels. Some would argue that indiscriminant folate use may mask the diagnosis of pernicious anemia (B 12 deficiency). Somehow we must consider that possibility when making policy. I believe that someone must test the hypothesis that folate supplementation will decrease the disease burden. We should not go down the road of extrapolating epidemiologic data to policy. We must understand that epidemiological studies generate hypotheses; randomized controlled trials test the validity of those hypotheses.
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