Funding: NIAAA R21AA026654
Project PI: Won Kim Cook
This study seeks to better understand the risk relationship between harmful drinking patterns and chronic health conditions—specifically, cardiovascular and cerebrovascular disease (CVD), the leading cause of death for Asian Americans, and three common conditions that increase CVD risk (diabetes, hypertension, and high cholesterol level).
No U.S.-based study has examined the relationship between drinking and these conditions in Asian Americans. This is an important gap as CVD risk profiles differ between Asians and non-Asians, and there are indications that drinking may pose a greater risk for Asians than whites.
In addition to addressing this key knowledge gap, we aim to examine the influences of alcohol metabolizing genes in the drinking-disease risk relationship, extending beyond the field’s usual focus on genotype-related protective effects against heavy drinking and alcohol dependence. Further, we will investigate synergistic effects of drinking pattern and other lifestyle risk factors on disease risk in an effort to identify under-explored factors that influence the relationship between drinking and chronic disease.
This study will draw upon a nationally-representative Asian American adult sample (Asian N=2,978) from the pooled National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) II and III. Logistic regression and structural equation modeling, and latent class analyses will be conducted to address three specific aims:
Aim 1: To test the hypothesis that lifetime drinking patterns are predictive of CVD-related conditions for Asian Americans and for their ethnic subgroups, and that this relationship is moderated by alcoholic beverage type.
Aim 2: To examine the roles alcohol-metabolizing genes play in the risk relationship between drinking and CVD-related conditions in two pathways. We will test: 1) the mediational hypothesis that Asian ethnic groups with higher prevalence of ALDH2*2 and ADH1B*2 have lower CVD-related risk via reduced drinking; and 2) the moderational hypothesis that ethnic groups with higher prevalence of ALDH2*2 and ADH1B*2 have a higher CVD-related risk, given the same pattern of drinking.
Aim 3: To test whether clustered lifestyle risk factors (i.e., harmful patterns of drinking, smoking, overweight, and physical inactivity) synergistically increase risk for CVD-related conditions and whether this risk is further elevated for low-SES individuals. Study findings will be used to develop a larger study that will examine drinking, other lifestyle factors, and alcohol-metabolizing genes to more fully understand these risk relationships prospectively and with greater precision.
