In carrying out its risk assessment on trans fatty acids, EFSA’s NDA panel reviewed evidence concerning both TFAs naturally present in foods, such as in certain animal fats (e.g. dairy, beef, lamb and mutton fat), and those occurring as a result of manufacturing processes, for instance hydrogenation of oils (e.g. certain margarines and fat spreads).

The Panel found that the intake of trans fatty acids varies between countries, with lowest intakes found in the Mediterranean countries. The contribution of TFAs to daily energy intake (based on estimates for 1995/1996) is approximately 0.5-2.0% in comparison with that of saturated fats which ranges from 10.5 to 18%. Recent dietary surveys indicate that TFA intakes have decreased in a number of EU countries, mainly due to the reformulation of food products (e.g. fat spreads) to reduce the TFA content.

Evidence from many human studies indicates that --as for saturated fatty acids-- increasing dietary intake of trans fatty acids (when compared to cis-monounsaturated or cis-polyunsaturated fatty acids) raises blood levels of LDL cholesterol (Low Density Lipoprotein – considered as ‘bad’ cholesterol), thereby increasing the risk of coronary heart disease (CHD). The rise in LDL cholesterol is proportional to the amount of TFAs consumed. These studies also show that for equivalent dietary levels, TFAs may increase the risk of coronary heart disease more than saturates. This is because – unlike saturates – TFAs also reduce blood levels of HDL cholesterol (High Density Lipoprotein – considered as ‘good’ cholesterol) and increase blood levels of triglycerides. However, average intakes of TFAs in European diets are generally more than 10-fold lower than those of saturates.

Commenting on these conclusions, Professor Albert Flynn, Chair of EFSA’s NDA Panel stated: “Evidence from human intervention trials, strengthened by findings from epidemiological studies, supports the idea that the effect of trans fatty acids on heart health may be greater than that of saturated fats. However, given current intake levels of TFAs, their potential to significantly increase cardiovascular risk is much lower than that of saturates which are currently consumed in excess of dietary recommendations in many European countries.”

Concerning other health implications, human studies revealed no consistent evidence of any effect of TFAs on blood pressure or on other markers associated with risk of CHD (for instance, platelet aggregation), or on insulin sensitivity associated with diabetes. Epidemiological evidence for a possible relationship of TFA intake with cancer, type 2 diabetes, or allergy is weak or inconsistent. No causal link has been established for the suggested adverse effects of TFAs on foetal and infant development.

In most of the intervention studies, monounsaturated TFAs from hydrogenated vegetable oils were evaluated. It is not possible to determine whether there are differences in the health effects of TFAs according to the source (ie TFAs from ruminant fat in comparison with those found in hydrogenated vegetable oils). In addition, there is no method of analysis applicable to a wide range of foods which can distinguish between TFAs which are naturally present in foods (e.g. dairy and beef fat) and those formed during the processing of hydrogenated oils.