Alcohol metabolism and disease risk in Asians: Examining the impact of personalized phenotypic/genotypic feedback on early drinking trajectories

About This Grant

The alcohol metabolizing gene ALDH2 encodes the enzyme that converts acetaldehyde into acetate during the metabolism of alcohol. The variant ALDH2*2 allele slows the conversion of acetaldehyde and results in heightened and protracted exposure to acetaldehyde, which is a known carcinogen. ALDH2*2 is found almost exclusively in individuals of east Asian descent (estimated in 560+ million people worldwide), and results in a flushing response from drinking (i.e., “Asian glow”). Although possession of ALDH2*2 is protective against heavy drinking and alcohol use disorders, for those who do drink, it is also associated with striking elevations in risk for several cancers, including esophageal and head and neck cancers. This cancer risk, however, is not widely known outside of the research community. The premise of this study is that we can affect early drinking trajectories through personalized communication about these cancer risks. This work builds upon two prior studies we conducted providing personalized feedback to Asian American college students, including an R21 exploratory/developmental study in which we developed and piloted interventions that we further investigate in this R01 study. These interventions showed sustained effects over a 10-month follow-up period on self-reported decreased frequency and quantity of alcohol use and increased use of protective behavior strategies (slowing pace, setting limits). In this study, we will assess 450 college students of northeast Asian descent, a high-risk group as college is a time of escalating alcohol consumption. It is also a context in which a risk-communications intervention, if successful, could be readily scaled-up. We will compare phenotypic risk communication with and without personalized genotype feedback by randomizing participants into one of three groups: 1) a group receiving information about cancer risk associated with alcohol consumption and alcohol metabolism genetic deficiencies that manifest as flushing, plus personalized flushing (i.e. phenotype) feedback (PHEN), 2) a group receiving the PHEN information plus personalized genotype (i.e. ALDH2) feedback (PHEN+GENE), or 3) a comparison attention CONTROL group. Post-intervention, participants will be followed for 3 years in annual surveys as well as quarterly surveys of retrospective drinking and 9-day "bursts" of daily reporting on past-day drinking behavior. In Aim 1, we will test whether the intervention reduces alcohol consumption. We also will test if genotype feedback results in a greater attenuation of drinking than general risk information and phenotype feedback only, and if the impact is stronger in those at greater risk based on their phenotype and/or genotype. In Aim 2, we will test if the interventions also increase the use of protective behavioral strategies and decrease the use of “flush cures” that reduce visible signs of flushing but not acetaldehyde levels. In Aim 3, we will examine potential mediators as underlying mechanisms of behavior change and explore possible moderators of intervention impact. Results of this work may inform intervention/prevention efforts on how to optimally target personalized feedback protocols for high-risk college samples and scale these at a national level.