consumption (13). This overlap persists even when consumption data from alcohol dependent individuals are omitted from the analysis, to avoid an artefactual correlation due to escalating consumption secondary to the onset of alcoholism (14). Studies of alcohol metabolism genes (ALDH2, ADH gene family), initially in Asian samples, and then in those of Jewish, European or African ancestry, have shown how genetic variants can make important contributions to differences in risk of alcohol dependence, consumption, or other aspects of response to alcohol (15,16,17,18,19). Finally, a third approach using various forms of latent structure modeling has emphasized the quasi-continuous nature of alcoholism (20,21,22), drawing attention to the undesirability, for some research purposes, of dichotomizing into affected and unaffected.
