IJE Advance Access originally published online on January 9, 2008
International Journal of Epidemiology 2008 37(1):182-184; doi:10.1093/ije/dym263
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Commentary: Ruminant trans fatty acids and coronary heart disease—cause for concern?
Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, and Department of Epidemiology and Department of Nutrition, Harvard School of Public Health, Boston, MA, USA.
E-mail: dmozaffa{at}hsph.harvard.edu
Accepted 6 December 2007
In the beginning of the 20th century, the most common source in the modern food supply of trans fatty acids (TFA)—unsaturated fatty acids with at least one unsaturated double bond in the trans configuration—became industrial production of partially hydrogenated oils used for food manufacturing, baking and frying. Strongly concordant evidence from controlled dietary trials evaluating risk factors and observational studies evaluating clinical outcomes indicates that consumption of such industrial TFA significantly increases the risk of coronary heart disease.1
However, a ‘natural’ source of TFA preceded industrial hydrogenation. Bacteria present in stomachs of ruminants (e.g. cattle, sheep, goats) biohydrogenate a proportion of the unsaturated fatty acids consumed by these animals, resulting in small amounts of ‘natural’ or ruminant TFA in dairy products and meats from these animals (typically <5% of total fatty acids). Compared with industrial TFA, the impact of these ruminant TFA on CHD risk is less clear. Limited evidence from experimental feeding studies indicates that adverse effects of ruminant TFA on blood lipid levels, when consumed in high amounts (
2% of energy or more),2–4 may be qualitatively similar to those of industrial TFA in other studies. Conversely, in contrast to industrial TFA, prior epidemiological studies have not found positive associations with CHD risk of consumption of ruminant TFA, in the low amounts actually consumed (often <0.5% of energy).5–7
In this issue, Jakobsen and colleagues present important new evidence on the potential cardiovascular impact of ruminant TFA.8 Utilizing prospectively collected data from four Danish cohort studies, dietary habits were assessed in 3686 adults enrolled between 1974 and 1993 who were followed for a median of 18 years. After adjustment for other risk factors, no significant associations were found between ruminant TFA consumption and incidence of CHD: the multivariable-adjusted relative risk for a 0.5 g/day higher intake was 0.99 (95% CI 0.94–1.04) for absolute consumption and 1.05 (95% CI 0.97–1.13) for energy-adjusted consumption. These negative findings are noteworthy because, given the relatively high consumption of dairy products in Denmark, the range of ruminant TFA intake was relatively broad (median intake up to 1.1% of energy in the highest quintile). Thus, even at the upper ranges of ruminant TFA consumption seen in modern diets, little evidence existed for cardiovascular harm.
The authors highlight a trend toward lower CHD risk with ruminant TFA intake in women, seen only after simultaneous adjustment for saturated fat intake. The change in the risk estimates was relatively dramatic with vs without adjustment for saturated fat (Tables 3–4). When saturated fat consumption is added to the models, the interpretation of the risk estimate for ruminant TFA becomes the effect on CHD risk for differences in ruminant TFA intake for a fixed level of saturated fat intake. Given the strong correlation between dietary sources of ruminant TFA and saturated fat in this population, the meaning of these findings is unclear. The major sources of variation in ruminant TFA consumption in these individuals were differences in consumption of butter, followed by cheese, milk and meat products, that together accounted for 80–85% of the variation in ruminant TFA intake (Table 5). After adjusting for saturated fat intake (which accounted for two thirds of the variation in ruminant TFA), less than 25% of the variation in ruminant TFA intake was explained by consumption of all these ruminant products. It is this remaining relatively small proportion of the variation that was associated, in women, with trends toward lower CHD risk. Because this estimate no longer represents the majority of variation in consumption of ruminant products per se, its interpretation is problematic, and caution is warranted before concluding that ruminant TFA consumption may lower CHD risk in women.
Some other limitations were evident. Dietary habits were only assessed at baseline, and it is likely that the participants’ consumption (and relative rankings of their consumption) would have changed over time. Given the long duration of follow-up, such (likely random) misclassification would bias results toward the null, making it less likely to detect an association between ruminant TFA and CHD risk, if one were to exist. On the other hand, this study possessed several strengths, including the prospective cohort design, the careful assessment of baseline diet, adjustment for numerous other risk factors and dietary habits, and (as discussed) the relatively broad range of ruminant TFA consumption.
Overall, Jakobsen and colleagues provide additional evidence that ruminant TFA, in amounts actually consumed in diets, do not raise CHD risk. This neutral effect of ruminant TFA, compared with industrial TFA, could relate to presence of different TFA isomers in these two sources; to the lower amounts of ruminant TFA actually consumed, compared with industrial TFA (often >2% of energy); and/or to other potentially beneficial components of dairy or meat products that outweigh harmful effects of the TFA. Although ruminant and industrial sources do share many common TFA isomers, some differences exist. One example is higher levels of vaccenic acid (trans-18:1n-7) in ruminant fats, representing 30–50% of the trans isomers. In humans, vaccenic acid can be metabolized to conjugated linoleic acid (CLA), a conjugated TFA (i.e. with two trans double bonds separated by only one single bond). However, the controlled dietary studies that assessed blood lipid effects of relatively high amounts of ruminant TFA consumption were all CLA-enriched,2–4 providing little evidence that higher consumption of CLA has beneficial effects. The adverse effects of industrial, compared with ruminant TFA could also relate to specific harmful isomers in the former, rather than beneficial isomers in the latter. One set of candidates are the trans-18:2 (nonconjugated) TFA isomers that are present in partially hydrogenated oils (and, in smaller amounts, in deodorized oils and fried foods), but not in appreciable amounts in ruminant fats, and may have the strongest relationships with CHD risk.9–10 Further research on potentially different effects of specific TFA isomers is needed.
Ruminant TFA cannot be removed entirely from the diet, but their intake is already low and not significantly associated with CHD risk in this or prior studies.5–8 In contrast, consumption of TFA from partially hydrogenated oils adversely affects numerous cardiovascular risk factors and is strongly associated with increased risk of CHD events.1 Because TFA produced by partial hydrogenation have no health benefits and are industrial additives to food, their use and consumption should be avoided in food manufacturing, baking, restaurants, and homes. Potential health effects of TFA created during other industrial processes, such as deodorization or deep frying, also deserve further attention. The removal of partially hydrogenated oils from foods would result in substantial health benefits, with greatest health benefits obtained when replacement oils are rich in unsaturated fats.11
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This work was supported by a grant from the National Heart, Lung, and Blood Institute, National Institutes of Health (K08-HL-075628).
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8 Jakobsen MU, Overvad K, Dyerberg J, Heitmann BL. Intake of ruminant trans fatty acids and risk of coronary heart disease. Int J Epidemiol (2008) 37:173–82.
9 Lemaitre RN, King IB, Raghunathan TE, et al. Cell membrane trans-fatty acids and the risk of primary cardiac arrest. Circulation (2002) 105:697–701.
10 Lemaitre RN, King IB, Mozaffarian D, et al. Plasma phospholipid trans fatty acids, fatal ischemic heart disease, and sudden cardiac death in older adults: the cardiovascular health study. Circulation (2006) 114:209–15.
11 Mozaffarian D, Clarke R. WHO Scientific Update: Effects of replacing trans fatty acids with other fats and oils on blood lipids and coronary heart disease. Eur J Clin Nutr (2008) (in press).
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