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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #234613
Title: Confounding by dietary pattern of the inverse association between alcohol consumption and type 2 diabetes risk

Author
item IMAMURA, FUMIAKI - JM USDA HNRCA @ TUFTS
item Lichtenstein, Alice
item Dallal, Gerald
item MEIGS, JAMES - MASS GENERAL HOSPITAL
item Jacques, Paul

Submitted to: American Journal of Epidemiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/25/2009
Publication Date: 4/1/2009
Citation: Imamura, F., Lichtenstein, A.H., Dallal, G., Meigs, J.B., Jacques, P. 2009. Confounding by dietary pattern of the inverse association between alcohol consumption and type 2 diabetes risk. American Journal of Epidemiology. 170(1):37-45.

Interpretive Summary: Habitual intake of alcohol is associated with a lower incidence of type 2 diabetes mellitus. However, it remains unclear whether the observed association is fully attributable to alcohol intake itself or is a consequence of confounding by differences in diet between those who do and do not consume alcohol. Confounding by diet is conventionally dealt with by statistical adjustment for a limited number of specific dietary factors, either nutrients or foods. Selection of these dietary factors is often subjective and may not adequately capture the differences in overall dietary patterns between drinkers and non-drinkers. If differences in diet are not fully controlled, then it is not possible to determine if the observed association between alcohol and diabetes is independent of alcohol-associated dietary patterns. To our knowledge, no study relating alcohol and risk of type 2 diabetes mellitus has addressed the issue of confounding by dietary patterns. We used the dietary pattern approach to adjust for potential confounding of the association between alcohol consumption and risk of type 2 diabetes mellitus by overall diet in 2,879 healthy adults enrolled in Framingham Offspring Study. The purpose of this study was to determine whether the previously reported protective association between alcohol and diabetes risk was attributable to alcohol itself or was a consequence of dietary patterns related to alcohol consumption. After adjusting for standard risk factors, the observed risk of type2 diabetes mellitus was 53% lower among consumers of >/=9.0 drink/week than among abstainers. Additional adjustment for selected nutrients associated with alcohol consumption had little effect on the observed risk. However, after adjustment for dietary pattern related to alcohol consumption, the observed risk among consumers of >/=9.0 drink/week was 67% lower than among abstainers. This significant 40% reduction in the observed risk indicates that the inverse association between alcohol intake and incidence of type 2 diabetes mellitus was confounded by dietary patterns, but not by individual nutrients. Furthermore, the presence of a strong inverse association between alcohol intake and type 2 diabetes mellitus risk after accounting for diet patterns suggests that alcohol intake, and not dietary patterns associated with alcohol intake, is responsible for the observed association with type 2 diabetes mellitus risk.

Technical Abstract: Epidemiology of dietary components and disease risk limits interpretability due to potential residual confounding by correlated dietary components. Dietary pattern analyses by factor analysis or partial least squares may overcome the limitation. To examine confounding by dietary pattern as well as standard risk factors and selected nutrients, the longitudinal association between alcohol consumption and 7-year risk of type 2 diabetes mellitus (T2DM) in 2,879 healthy adults enrolled in Framingham Offspring Study was modeled by Cox-proportional hazard models. After adjusting for standard risk factors, consumers of >/-9.0 drink/week had a significantly lower risk of T2DM compared to abstainers (hazard ratio [HR]: 0.47; 95% confidence interval [CI]: 0.27, 0.81). Adjustment for selected nutrients had little effect on the HR (=0.53), whereas adjustment for dietary pattern variables by factor analysis significantly shifted the HR away from null (=0.33, 95% CI: 0.17, 0.64) by 40.0% (95% CI: 16.8, 36.4%, P=0.002). Dietary pattern variables by partial least squares showed the similar results. Therefore, the observed inverse association, consistent with past studies, was confounded by dietary patterns, not adjustable by individual nutrients. The data suggest alcohol intake, and not dietary patterns associated with alcohol intake, is responsible for the observed inverse association with T2DM risk.