Our prediction that individuals homozygous for ADH1B*2 would report the most alcohol-related symptoms and heterozygotes would report more low-dose symptoms than those without the variant allele was partially supported by the trends in the data across the ADH1B-ALDH2 genotype combinations (as seen in the bottom two rows of Table 2); although only significant in the ALDH2 heterozygote group, sensitivity to alcohol increased within each ALDH2 genotype as the number of ADH1B*2 alleles increased. In a study of 4,597 Caucasian Australian twins who did not possess ALDH2*2, ADH1B*2 was associated with self-reported flushing and endorsing any of the six alcohol-related symptoms that were assessed in the current study (Macgregor et al., 2008). Thus, it seems reasonable that ADH1B*2 alone may heighten sensitivity to low doses of alcohol, and that this effect may emerge as significant in larger samples or in samples that have a greater proportion of individuals with no ADH1B*2 alleles. There is also evidence that the effects of ADH1B*2 on sensitivity may differ across type of alcohol (see Linneberg et al., 2009) and on alcohol dependence may differ across
