‘Trans-fatty acids’ can be formed in the processing of fats. They usually start out life as a vegetable oil, which is then treated in a multi-stage process to, say, solidify it and extend its shelf life. The word ‘trans’ refers to the chemical shape of these molecules. In general terms, these fats are a different shape to fats found naturally in nature, which usually have a different – ‘cis’ – shape. Trans fats have been linked with a variety of health issues including enhanced risk of cardiovascular disease [1-4] and diabetes [5-7].
However, trans fats can be found in nature too. For example, butter contains trans fatty acid. The food industry sometimes refers to this fact, I suspect in an attempt to suggest that the industrially-produced trans fats that they put in foods are somehow ’natural’ too. But are the trans-fats found in nature the same as those that are formed in a factory?
Actually, industrially produced and naturally occurring trans fats have different chemical structures: industrially-produced trans fats are predominantly monounsaturated trans fats of which something known as ‘elaidic acid’ is a major component. Trans fats found naturally in food, on the other hand, are mainly to be found in the form of very different fats known as ‘trans vaccenic acid’ and ‘conjugated linoleic acids’. Do these differences reflect on their impact on health?
This week saw the publication of a study that assessed the relationship between trans fats and heart disease in the form of a meta-analysis (lumping together of similar studies) [8]. The authors of this study amassed evidence from eight studies. Higher total trans fat intake was associated with an increased risk of heart disease and risk of death from heart disease.
Taken separately, neither natural nor industrial trans fat was associated with a statistically significant increased risk of heart disease. However, the trends were for industrial trans fat to be associated with an increased risk of heart disease, while natural trans fat was associated with a reduced risk of heart disease.
Taken as a whole, these results do point the finger of suspicion towards industrial trans fat, but away from those that are naturally occurring.
Previous evidence has also not found a link between naturally-occurring trans fat intake and enhanced risk of heart disease [9].
Overall, the evidence is consistent with the idea that food elements that have been in the diet a long time are going to be generally better for the body than new foods. Industrially produced trans fats have been in the diet in meaningful amounts for a few decades. Naturally occurring trans fats, on the other hand, have been in the diet forever.
References:
1. Pedersen JI, et al. Adipose tissue fatty acids and risk of myocardial infarc¬tion — A case-control study. Eur J Clin Nutr 2000:54:618-625
2. Ascherio A, et al. Dietary fat and risk of coronary heart disease in men: Cohort follow up study in the United States. BMJ 1996:313:84-90
3. Hu FB, et al. Dietary fat intake and the risk of coro¬nary heart disease in women. N EngI J Med 1997:337:1491-1499
4. Oomen CM, et al. Association between trans fatty acid intake and 10-year risk of coronary heart disease in the Zutphen Elder¬ly Study: A prospective population-based study. Lancet 2001357:746751
5. Christiansen E, et al. Intake of a diet high in trans monounsaturated fatty acids or saturated fatty acids. Effects on postprandial insulinemia and glycemia in obese patients with NIDDM. Diabetes Care l997;20:88l-887
6. Alstrup KK, et al. Differential effects of cis and trans fatty acids on insulin release from isolated mouse islets. Metabolism I 999:48:22-29
7. Salméron J, et al. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr 2001;73:1019-1026
8. Bendsen NT, et al. Consumption of industrial and ruminant trans fatty acids and risk of coronary heart disease: a systematic review and meta-analysis of cohort studies. Eur J Clin Nutr. 2011 Mar 23. [Epub ahead of print]
9. Jakobsen MU, et al. Intake of ruminant trans fatty acids and risk of coronary heart disease. Int J Epidemiol. 2008;37(1):173-82
