Journal Name:
Arch. Intern. Med.
Article Title:
A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease
Date Written:
2009
Volume:
167
Number:
7
Page:
659
Author(s):
Mente, A.; de Koning, L.; Shannon, H.S.; Anand, S.S.
Article:
This publication describes a systematic review of the literature examining the association between nutrient intake, dietary components, and dietary patterns (exposures) and CHD and its related clinical outcomes. The objectives were (1) to systematically evaluate dietary exposures and CHD using the Bradford Hill criteria; (2) to determine which dietary exposures have been studied sufficiently in RCTs and found to support the findings of prospective cohort studies; and (3) to identify the dietary exposures deemed to have insufficient evidence to be conclusive.
A systematic search of MEDLINE was conducted including prospective cohort studies or randomized trials investigating dietary exposures in relation to CHD. The review used predefined criteria to evaluate the evidence of causation. High-quality or larger studies with sufficient outcome events were evaluated to minimize the potential for heterogeneity of effects across cohort studies and publication bias. The Bradford Hill guidelines were used to determine a causation score based on 4 criteria (strength, consistency, temporality, and coherence) for each dietary exposure in cohort studies and examined for consistency with the findings of randomized trials. Strong evidence supported valid associations when 4 criteria were satisfied, moderate evidence met 3 criteria and insufficient evidence met equal to or less than 2 criteria.
Strong evidence of a causal relationship for protective factors in CVD were found, including for intake of vegetables, nuts, and monounsaturated fatty acids and Mediterranean, prudent, and high quality dietary patterns, and harmful factors, including intake of trans– fatty acids and foods with a high glycemic index or load and a western dietary pattern. Modest evidence to support a causal relationship for intake of fish and marine omega-3 fatty acids and weak evidence of causation for intake of alpha-linolenic acid were reported. However, it was also noted that randomized clinical trials (RCTs) have sparse with regard to the effects of ALA on CVD and little direct evidence from RCTs supports a relationship between marine based omega 3 fatty acids and CHD risk factors.
For polyunsaturated fatty acid intake, most of the RCTs have not been adequately powered and did not find a significant reduction in CHD outcomes. Metabolic studies have however shown that the omega 3 fatty acid family exert beneficial effects on surrogate measures of CHD such as levels of serum triglycerides and thrombotic factors, markers of endothelial dysfunction, and prevention of cardiac arrhythmias. The findings though from cohort studies have been inconsistent. It must be emphasized that CHD is a complex condition involving numerous physiologic systems which makes it unlikely that modifying the intake of a few nutrients would alter these systems and influence clinical outcomes. Given the advantages of evaluating dietary patterns vs single nutrient components, future studies are recommended in sufficiently large populations which include a determination of the effects of these patterns on multiple health outcomes, including cardiovascular disease and cancer.
The authors call for large prospective studies, in which multiple health outcomes are evaluated, on the relationship of a number of dietary factors (including omega 3 fatty acids) and CHD.
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