Can diabetes be prevented by vegetable fat?

The prevention of type 2 diabetes has become an important clinical and health policy issue around the globe because of the increasing rates of diabetes in developed as well as in developing countries. Evidence of successful programs concerning the primary prevention of diabetes has only very recently been provided. The Finnish Diabetes Prevention Study (1) was the largest randomized intervention study, which included 522 middle-aged overweight subjects with impaired glucose tolerance. The intervention consisted of individual counseling on reducing body weight, total fat intake, and intake of saturated fatty acids (SFAs) and increasing fiber intake and physical activity. After 4 years, the cumulative diabetes incidence was 11 vs. 23% in the control group (P , 0.001). The reduction in diabetes was highest in the group with the largest changes in lifestyle. An important feature of this study is that it resulted in a substantial decrease in diabetes risk despite an only modest difference in body weight (3 kg), which shows that other parts of the intervention played a role as well. In this light, it is worthwhile to pay close attention to the role of dietary composition in diabetes etiology. In this issue of Diabetes Care, Meyer et al. (2) report on the impact of various dietary fatty acids on the risk of type 2 diabetes in the Iowa Women’s Health Study. They studied 35,988 women, aged 55–69 years, free of diabetes, and followed them for 11 years, resulting in 1,890 new cases of type 2 diabetes. Intake of fat and fatty acids was assessed from a validated food-frequency questionnaire. After adjustments for main risk factors, including BMI, waist-to-hip ratio, physical activity, dietary fiber, magnesium, and other dietary fat subtypes, substituting polyunsaturated fatty acid (PUFA) intake for SFA was inversely associated with diabetes risk, with a 16% reduction in the highest quintile (median intake 16.6 g per day). The consumption of vegetable fat was associated with a 22% reduction in new cases of diabetes in the highest quintile (median 41.7 g per day). Other nutrients that have been implicated in the prevention of diabetes, such as vitamin E, cannot explain the vegetable fat finding. Results were similar for overand normal-weight women. This study can be well compared with the most recent results from the Nurses’ Health Study reported by Salmeron et al. (3). With a similar design and a similar food-frequency questionnaire, they followed a cohort of younger women (34–59 years of age) for 14 years. They observed a similar inverse association between diabetes risk and intake of vegetable fat and PUFAs, which strengthens the observations of Meyer et al (2). Other similar findings are the absence of clear associations with SFA and monounsaturated fatty acid (MUFA) intake but a positive association with dietary cholesterol. In contrast, trans–fatty acid intake is associated with increased diabetes risk in the Nurses’ Health Study but not in the Iowa Women’s Health Study. In the Iowa Women’s Health Study, no indication of a beneficial effect of n-3 PUFA (mostly from fish) on diabetes risk was observed, whereas in the Nurses’ Health Study, a reduced diabetes risk was observed in the highest one-fifth of intake (relative risk 0.8). Results of earlier epidemiological studies of various designs have been previously summarized (4). Inverse associations with intake of PUFAs, such as in the Iowa Women’s Study, have been previously shown, but the results were mixed. The two recent consistent findings support the evidence that PUFAs and vegetable fat may reduce the risk of type 2 diabetes. However, the general picture is that intake of SFAs and their associated dietary variables, dietary cholesterol, meat intake, and animal fat are associated with increased risk of diabetes. Only limited evidence is available on a potential detrimental effect of trans fatty acids on glucose metabolism. The absence of an association between SFA intake and diabetes in both cohorts is rather unexpected. Recently, the results of a large, well-designed, randomized intervention on fatty acids and insulin sensitivity have been published (5). The KANWU Study (5) included 162 healthy volunteers receiving a controlled isoenergetic diet containing either a high proportion of SFA (17.6% of energy) or MUFA (21.2% of energy) for 3 months. Within each group, there was a second random assignment to a supplement of n-3 PUFA from fish oil or a placebo. Introducing the SFA diet reduced insulin sensitivity by 10%, an effect not seen by introducing the MUFA diet (2%). Notably, the detrimental effect of SFA versus MUFA on insulin sensitivity was primarily seen in subjects with a total fat intake below the median value of 37% of energy. The addition of n-3 fatty acids did not influence insulin sensitivity or secretion. This well-conducted intervention study corroborates the suggestions of a detrimental effect of SFA intake from earlier epidemiological observations (4) and provides evidence for a more beneficial effect of MUFA intake, both of which were not seen in the Iowa Women’s Study (2) or in the Nurses’ Health Study (3). As for MUFA, the low intake of olive oil and the high intake of MUFA from milk products and meat in the cohorts (and thus the high correlation with SFA intake) may be responsible for this. Methodological factors may also play a role. Both studies used the same food-frequency questionnaire, and both studies were performed in a U.S. population, probably with similar sources of fatty acids. In both studies, a weak positive association between SFA and diabetes risk was seen, which disappeared after adjustments for other dietary factors, including MUFA and dietary cholesterol, possibly introducing problems with multicollinearity. Finally, no attempt was made to follow the KANWU suggestion of analyzing modification by total fat intake. A beneficial effect of n-3 fatty acids was not shown in the Iowa Women’s Study cohort or in the KANWU study. This is in contrast with animal experiE D I T O R I A L