August 18, 2009

Higher vitamin B6 levels correlated with lower heart attack risk in women

In an article published online on August 10, 2009 in the American Heart Association journal Circulation, Harvard researchers report an association between higher plasma levels of vitamin B6 and a reduction in the risk of myocardial infarction (heart attack) in women.

The study included 144 participants in the ongoing Nurses' Health Study who were diagnosed with myocardial infarction. The women were each matched for age, smoking status and other factors with two participants in the same study who did not have a history of heart attack at the time of the heart attack cases' diagnoses. Stored fasting blood samples were analyzed for plasma pyridoxal 5' phosphate (PLP), which is the predominant form of vitamin B6 that exists in circulation, and homocysteine, an amino acid which, when elevated, has been associated with an increased risk of cardiovascular disease.

Higher levels of PLP were correlated with greater dietary intake of vitamin B6, lower body mass index and lower levels of homocysteine. The researchers uncovered a significant association between plasma PLP levels and reduced heart attack risk. Women whose PLP levels were among the top one-fourth of participants at greater than 70 picomoles per milliliter had a 78 percent lower adjusted risk of undergoing a heart attack compared to those whose levels were lowest at less than 27.9 pmol/mL. When the women were analyzed according to age, those aged 60 and older whose PLP levels were among the top quarter were found to have a 64 percent lower risk than those in the lowest quarter, while those who were under 60 in the top fourth of PLP had a 95 percent lower risk.

The authors remark that the study's findings are consistent with the role of vitamin B6 as a cofactor in the conversion of homocysteine to cysteine. The vitamin also plays a role in the transport of important minerals such as magnesium across cell membranes. The authors observe that the results of some research suggest that factors other than diet that control vitamin B6 levels could eventually be found to be more important in reducing heart attack risk.

The current prospective study is the first, to the authors' knowledge, to examine the relationship of vitamin B6 levels with heart attack in postmenopausal women. "Our investigation revealed that a lower fasting concentration of PLP is significantly associated with an increased risk of myocardial infarction in predominantly postmenopausal women, a relationship that may be causal," they write. "Future studies are needed to better understand both dietary and nondietary determinants of plasma and tissue vitamin B6 status and their role in the prevention of myocardial infarction and other chronic diseases."

Homocysteine reduction

Homocysteine is an intermediary amino acid; its role in the body is complex, but very important. Homocysteine is a necessary byproduct of a healthy metabolism. Homocysteine is produced as part of the methionine cycle, in which methionine is converted to S-adenosylmethionine (SAMe). SAMe is valuable because of its ability to donate methyl groups during chemical reactions throughout the body. Homocysteine is synthesized when SAMe donates its methyl group. In scientific terms, this means the SAMe has been methylated (lost a methyl group). Methylation is crucial to the health of our cells and tissues by regulating gene expression, protein function, and RNA metabolism.

The methionine cycle is responsible for the creation of all the homocysteine in the body. Most of the resulting homocysteine is bound to plasma and considered stored, or inactive. It may be released into the bloodstream as free homocysteine in response to adverse changes in the body's biochemistry. Thus, high levels of homocysteine are linked to specific health problems. There is also evidence that homocysteine itself causes damage to the cells within blood vessels.

Homocysteine in the bloodstream is metabolized through two principal pathways. It may be remethylated back into methionine through a process that involves folic acid (folate) and vitamin B12. This is called the remethylation pathway and is responsible for consuming most of the body's free homocysteine. The remethylation pathway creates more SAMe to support healthy methylation. (Some organs, namely the kidney and liver, are able to remethylate homocysteine directly back into SAMe, but only a fraction of homocysteine is processed in this way.)

Alternatively, some of the excess homocysteine may be used to create cysteine, which is then converted into glutathione. Glutathione is an important and powerful antioxidant. The conversion of homocysteine into glutathione may be accelerated when the body is under oxidative stress. This second process is called the transsulfuration pathway because it produces sulfate byproducts that are flushed from the body in urine. The transsulfuration pathway depends on vitamin B6 to work properly.

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Life Extension Update

• Study finds elevated homocysteine more than doubled heart attack risk in high risk patients
• Vitamin B12 emerges as strong determinant of homocysteine levels

What's Hot

• B complex supplements reduce atherosclerosis progression in individuals with elevated homocysteine
• Study finds reduced vitamin B6 and elevated homocysteine levels more prevalent in rheumatoid arthritis patients

Life Extension magazine

• Homocysteine as a risk factor for disease
• Nutritional therapies for managing homocysteine

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Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
954 766 8433 extension 7716
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