Omega-3 may slash levels of heart disease risk factor

Supplements of omega-3 fatty acids are associated with lower levels of an amino acid called homocysteine, an amino acid linked to increased risks of heart disease and dementia, says a new meta-analysis of the scientific evidence.

Data from 11 trials including 720 people with doses of omega-3 ranging from 0.2 to 6 grams per day concluded that supplementation with omega-3s was associated with lower blood levels of homocysteine.

“Our systematic review provides, to our knowledge, the most comprehensive assessment to date of the effects of omega-3 PUFAs on plasma homocysteine,” wrote the researchers in Nutrition.

Researchers from China, Taiwan, and Australia added that a more comprehensive analysis would benefit from additional rigorous and long term trials. They also noted that such trials should also seek to measure whether the reduction in homocysteine levels actually produces an important health effect, such as a reduction in heart disease.

“The implications of [our] findings remain to be elucidated,” they added.

The homocysteine hypothesis

Previously, high levels of the amino acid, hyperhomocysteinemia, were said to be a marker for heart disease and thought to be a risk factor for atherosclerotic disease, which contributes to heart attacks.

The link was founded on the observation that children with homocystinuria – a rare genetic condition causing extreme elevations in homocysteine levels – have higher rates of cardiovascular disease. Such an observation was therefore generalized to the wider population. This has led to the hypothesis that supplementation with B vitamins may reduce blood homocysteine levels and reduce the risk of heart disease.

The link between homocysteine and cardiovascular events was questioned recently with results of a meta-analysis of eight folic acid trials involving 37,485 participants finding no benefits on the risk of major vascular events, cancer, or deaths, despite reducing homocysteine levels by 25 per cent (Archives of Internal Medicine, Vol. 170, pp. 1622-1631).

Commenting on a potential mechanism for omega-3 to reduce homocysteine, the researchers note that this “has not yet been fully elucidated”. They did propose, however, that omega-3 fatty acids may be related to a B vitamin-dependent enzyme called cystathionine-gamma-lyase (CSE). Data from various animal and in vitro studies suggests that omega-3s may affect the genes responsible for CSE activity: CSE catalyzes the conversion of cystathionine (an intermediate in the conversion of homocysteine to cysteine).

“Subsequently, the […] reaction moves in a direction beneficial for decreasing homocysteine,” they hypothesized.

Heart health and beyond

The heart health benefits of consuming oily fish, and the omega-3 fatty acids they contain, are well-documented, being first reported in the early 1970s by Dr Jorn Dyerberg and his co-workers in The Lancet and The American Journal of Clinical Nutrition. To date, the polyunsaturated fatty acids (PUFAs) have been linked to improvements in blood lipid levels, a reduced tendency of thrombosis, blood pressure and heart rate improvements, and improved vascular function.

Beyond heart health, omega-3 fatty acids, most notably EPA and DHA, have been linked to a wide-range of health benefits, including reduced risk of certain cancers, good development of a baby during pregnancy, joint health, and improved behavior and mood.

Despite such benefits there are still problems with ensuring adequate omega-3 intakes from fatty fish. This has led to a fleet of omega-3-rich concentrates becoming available. Projections by Frost & Sullivan set annual growth for the omega-3 market at an impressive 24 per cent, and the market is estimated to be worth $1.6bn by 2014.

Source: Nutrition

Published online ahead of print, doi: 10.1016/j.nut.2010.12.011

“High consumption of omega-3 polyunsaturated fatty acids decrease plasma homocysteine: A meta-analysis of randomized, placebo-controlled trials “

Authors: T. Huang, J. Zheng, Y. Chen, B. Yang, M.L. Wahlqvist, D. Li