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28-06-2011 | Cardiometabolic | Article

De novo lipogenesis of fatty acids linked to risk for sudden cardiac arrest

Abstract

Free abstract

MedWire News: Adults with elevated levels of the fatty acids 7-hexadecenoic acid (16:1n29) and cis-vaccenic acid (18:1n27) face an increased risk for sudden cardiac arrest (SCA) and possibly coronary heart disease (CHD), study results show.

Circulating concentrations of these fatty acids were associated with dietary carbohydrate, protein, and alcohol intake within normal population ranges, and the researchers suggest that de novo lipogenesis (DNL) is a major factor behind the observed cardiovascular risk.

"If confirmed, these findings could have potential public health relevance because prevailing dietary guidelines have produced a shift in overall energy intake from fat to carbohydrate," Jason Wu (Harvard School of Public Health, Boston, Massachusetts) and colleagues comment in the American Journal of Clinical Nutrition.

DNL is an endogenous pathway for lipid synthesis, whereby carbohydrates and proteins are converted to fatty acids.

Previous interventional studies have shown that DNL is upregulated in humans on relatively extreme diets, and influences circulating concentrations of several specific fatty acids.

However, the extent to which usual ranges of dietary and lifestyle exposures influence DNL or concentrations of these fatty acids has not been established. Furthermore, fatty acids are important cellular constituents that may directly affect biologic processes relevant for the development of CHD or SCA.

To investigate, Wu et al performed a community-based prospective study in 2890 men and women aged 65 years or older, who were free of known CHD at baseline and who were followed-up from 1992 to 2006.

Cardiovascular disease risk factors and plasma phospholipid fatty acids were measured at baseline using standardized methods.

During 29,835 person-years of follow-up there were 631 CHD and 71 SCA events. In multivariate analyses, elevated concentrations of 18:1n27 and 16:1n29 were associated with an increased risk for SCA with hazard ratios (HR) for the interquintile range (comparing the median of the first and fifth quintiles, ie, the 10th to 90th percentile) of 7.63 and 2.30, respectively.

In secondary analyses at the mid-follow-up of 7 years (to minimize the effects of changes in concentrations over time), 16:1n29 was also associated with a significantly higher risk for total CHD, with an interquintile HR of 2.11.

Considering potential stimulators of the DNL pathway, Wu et al found that consumption of carbohydrate or protein in place of fat and also alcohol use were each independent predictors of higher concentrations of these fatty acids.

"These findings highlight the need for experimental studies of the potential mechanistic link between SCA and 18:1n27 and 16:1n29 and the conditions that increase the concentrations of these fatty acids," Wu and team conclude.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Springer Healthcare Limited. © Springer Healthcare Ltd; 2011

By Andrew Czyzewski