Letter by Hoenselaar Regarding Article, “Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies”
To the Editor:
Using meta-analyses, Farvid et al1 showed that higher intakes of linoleic acid (LA) and substitutions of LA for carbohydrates or saturated fatty acids were associated with lower risk of coronary heart disease (CHD). On the basis of this finding, the authors concluded, “These data provide support for current recommendations to replace saturated fat with polyunsaturated fat for primary prevention of CHD.”
Effects found were largely driven by results from 2 cohorts: the Nurses’ Health Study and the Health Professional Follow-Up Study. Few significant associations were found in other cohorts in any of the analyses.
Because the authors did not include the necessary data, I could not perform meta-analyses excluding these 2 cohorts. However, based on the percent weight given to the individual cohorts, the weighted means for the categorical analysis increased from a relative risk of 0.85 to 0.96 for CHD events and from 0.79 to 0.90 for CHD death. For a continuous 5% energy increase in LA intake, the weighted means increased from a relative risk of 0.90 to 0.94 for CHD events and from 0.87 to 0.91 for CHD death. The mean differences between highest and lowest intakes of LA intake were 2.9% and 3.2% of energy for CHD events and CHD death, respectively. However, the relative risks found in the categorical analyses were stronger than in the continuous analyses. CHD effects from incremental intakes of 5% of energy from LA were identical to substitutions of 5% of energy from LA for 5% of energy from carbohydrates or saturated fatty acids, showing that LA effects seem to be independent of intake of saturated fatty acids or carbohydrates.
In a comprehensive literature review, the World Cancer Research Fund2 included predefined criteria to assess causality using different grades of evidence. To be a convincing cause of the disease, the “relationship should be robust enough to be highly unlikely to be modified in the foreseeable future as new evidence accumulates.”
Currently, dozens of cohorts are being followed up for future results. Several of them include the same amount of participants as cohorts found by Farvid et al. Some even use hundreds of thousands of participants. This shows that the results published by Farvid et al are fragile and driven by a small amount of the cohorts included.
Nutrient effects are based on dietary intakes of whole foods, different foods with probably heterogeneous effects on CHD. Nutrient effects are then translated back to a homogeneous dietary advice based on all sources of this nutrient. We should ask ourselves how different dietary sources of LA influence CHD. Do different oils have various effects? Are they the same as for nuts and margarines?
Robert Hoenselaar, BSc
- © 2015 American Heart Association, Inc.
- Farvid MS,
- Ding M,
- Pan A,
- Sun Q,
- Chiuve SE,
- Steffen LM,
- Willett WC,
- Hu FB.
- 2.↵World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global Perspective. Washington, DC: AICR; 2007.