In Reply: Dr Yu points out the influence of alcohol on IGFs as a potential mechanism by which alcohol consumption may increase the risk of breast cancer. This hypothesis was based on evidence regarding the potential effect of IGF on breast cancer risk, the association between IGF and alcohol consumption, and the observation in some,1- 3 but not all,4 epidemiologic studies that breast cancer risk plateaus at high alcohol intakes. For example, in our combined analysis of 6 cohort studies, we found that, compared with nondrinkers, women who consumed 60 g/d of alcohol (relative risk [RR], 1.31; 95% confidence interval [CI], 0.86-1.98) did not show a further increase in risk in comparison with women who consumed between 30 g/d and 60 g/d (RR, 1.41; 95% CI, 1.18-1.69). However, we had limited power to detect associations in the high-intake group; only 30 of the 4335 breast cancer cases identified across the 6 studies reported alcohol intakes of 60 g/d or more. In addition, self-reported alcohol intakes may be less reliable at higher alcohol intakes, which may contribute to the appearance of a plateau at these higher levels. Therefore, we are cautious in interpreting this result, even though other studies have reported similar results.1- 3 As noted by Yu, if breast cancer risk truly plateaus at high intake levels, this finding may be important in elucidating the mechanisms underlying the alcohol and breast cancer association. However, further research in populations with higher alcohol intakes than those included in the Pooling Project is necessary to examine the effects of these high alcohol intakes.