Despite similar recent alcohol use and post-consumption BrAC levels, individuals in this study with at least one ADH1B*3 allele reported experiencing greater sedation following a moderate dose of alcohol. This difference was most pronounced at the 60 minute assessment, when most participants were at their peak BrAC. A time x gene status interaction effect indicated that subjects with ADH1B*3 alleles also experienced a sharper increase in pulse rate immediately after consumption compared to those homozygous for ADH1B*1. An increase in pulse rate is consistently associated with alcohol-induced flushing and ADH/ALDH polymorphisms (Peng et al., 1999; Wall et al., 1992). The sharp elevation in pulse rate, followed by a rapid return, is consistent with the short-term acetaldehyde “burst” hypothesized to result from faster alcohol conversion (Quintanilla et al., 2007). The pattern of results is similar to studies comparing ADH1B*1 and ADH1B*2 in an Asian sample (Cook et al., 2005) as well as a mixed Caucasian and African American sample (Duranceaux et al., 2006). The isoenzymes encoded by ADH1B*2 and ADH1B*3 are fairly similar in their kinetic constants and should produce faster alcohol elimination rates compared to ADH1B*1 (Edenberg, 2007).
