Chunk #34 — Explanations for Lower Alcohol Use among African Americans Compared to European Americans — Historical Perspective — Biological Vulnerability and Response to Alcohol
Similar effects have been found for some variants of ADH genes, such as ADH1B (Cook et al., 2005; Crabb, 1995; Duranceaux et al., 2006; McCarthy, Pedersen, Lobos, Todd, & Wall, 2010). Specifically, ADH1B*3 appears to metabolize alcohol more efficiently, especially at high blood alcohol concentrations, leading to a more rapid lowering of blood alcohol levels, and simultaneously causing transiently higher levels of acetaldehyde (Ehlers et al., 2007; Lee, Hong, & Yin, 2004). There is evidence that the ADH1B*3 allele is present almost exclusively within individuals of African descent and has been estimated to be present in up to one-third of African Americans (Ehlers, Carr, Betancourt, & Montane-Jaime, 2003; Ehlers, Glider, Harris, & Carr, 2001; Luo et al., 2006; Thomasson, Beard, & Li, 1995; Wall, 2005). There is also evidence for the protective effects of the allele against alcohol dependence among African Americans based on both national (the Collaborative Study of the Genetics of Alcoholism, or COGA: Edenberg et al., 2006) and smaller community samples (n=150; Luo et al., 2006). Studies, though smaller scale convenience samples, have shown that the ADH1B*3
