FROM THE JOURNAL OF THE AMERICAN HEART ASSOCIATION
Insufficient omega-6 polyunsaturated fatty acids (n-6 PUFA), excess trans fat and, to a lesser extent, excess saturated fat, are significant causes of coronary heart disease, suggests a global study published online Jan. 20.
“Our analysis provides, for the first time, a rigorous comparison of global CHD burdens attributable to insufficient n-6 PUFA versus higher saturated fat. In 80% of nations, n-6 PUFA–attributable CHD burdens were at least twofold higher than saturated fat–attributable burdens. This suggests that focus on increasing healthful n-6 rich vegetable oils may provide important public health benefits,” Qianyi Wang, Sc.D., and her colleagues said.
The researchers estimated national intakes of saturated fat, n-6 PUFA, and trans fat based on country-specific dietary surveys, food availability data, and for trans fat, industry reports on fats/oils and packaged foods. The effects of dietary fats on CHD mortality were derived from meta-analyses of prospective cohorts, and CHD mortality rates were derived from the 2010 Global Burden of Diseases Study . Absolute and proportional attributable CHD mortality were computed using a comparative risk assessment framework.
The researchers estimated insufficient n-6 PUFA consumption having been replaced by carbohydrate or saturated fat consumption was responsible for 711,800 CHD deaths per year, accounting for 10% of total global CHD mortality and for 187 CHD deaths per year per 1 million adults. The most absolute CHD deaths per year – 547 per 1 million adults – attributable to insufficient n-6 PUFA occurred in Eastern Europe, while Oceania had the highest proportion of n-6 PUFA–attributable CHD deaths. East Asia had both the fewest absolute – 74 per 1 million adults – and lowest proportion – 6.7% – of CHD deaths attributable to inadequate consumption of n-6 PUFA.
Excess consumption of saturated fat as a replacement for n-6 PUFA caused an estimated 250,900 CHD deaths per year, accounting for 3.6% of CHD deaths and 66 CHD deaths per year per 1 million adults.
The researchers estimated that excess trans fat consumption caused 537,200 CHD deaths per year, representing 7.7% of global CHD mortality and 141 CHD deaths per year per 1 million adults. High-income nations generally had higher trans fat–attributable CHD mortality than lower-income nations. The highest trans fat–attributable absolute CHD mortality occurred in Egypt, with 1,120 deaths per year per 1 million adults. Canada, Pakistan, and the United States all had more than 475 deaths per year per 1 million adults because of excess consumption of trans fat. Such deaths accounted for more than 17% of corresponding national CHD mortality.
Sub-Saharan Africa and the Caribbean had the lowest estimated trans fat–attributable CHD mortality, with excess consumption of trans fat accounting for less than 5% of CHD deaths in these regions.
Additional findings of this study included mean global changes in dietary intakes of saturated fat, n-6 PUFA, and trans fat, and corresponding changes in CHD deaths occurring between 1990 and 2010. Specifically, global proportional CHD mortality attributable to insufficient n-6 PUFA and higher saturated fat consumption decreased by 9% and 21%, respectively. Such decreases occurred in concert with a 0.5% increase in consumption of n-6 PUFA and a 0.2% decrease in consumption of saturated fat. In high-income countries, trans fat consumption declined in parallel with policy strategies to reduce industrial trans fat production. In contrast, global proportional CHD deaths attributable to higher trans fat increased by 4% as global mean dietary intakes of trans fat increased by 0.1%.
“Growing evidence indicates that lowering saturated fat provides convincing cardiovascular benefits only when replaced by PUFA, whereas cardiovascular benefits of n-6 PUFA are similar whether replacing saturated fat or total carbohydrates,” said Dr. Wang of the Harvard T.H. Chan School of Public Health, Boston.
Read the study in the Journal of the American Heart Association ( doi: 10.1161/JAHA.115.002891 ).
