be detectable within high-resistance populations, while the alternative variant(s) is neutral: e.g., the ALDH2*2 allele (Goedde et al., 1983; Harada et al., 1981). The rest of ALDH2 variation only weakly, if at all, influences alcoholism risk (Macgregor et al., 2009). The distinction between the risk and resistance perspectives is nontrivial also because it entails differences in approaches to the identification of respective factors. Research that is focused on risk factors alone is likely to detect those with the strongest risk-increasing effects, aggregated, e.g., among the affected individuals, representing the high end of the liability distribution (5–10% of the population). In contrast, phenotypes carrying strongest resistance-increasing effects – genetic or environmental – are diluted by the heterogeneity of the typical unaffected control, sampled from 90–95% of the population. Symmetric to high-risk groups, factors conferring high resistance are aggregated among those with phenotypes at the low end of the liability scale, requiring high-resistance sampling for their detection.
