Testing multiple levels of influence in the intergenerational transmission of alcohol disorders from a developmental perspective: The example of alcohol use promoting peers and μ-opioid receptor M1 variation

Abstract

This study examined the interplay between the influence of peers who promote alcohol use and μ-opioid receptor M1 (OPRM1) genetic variation in the intergenerational transmission of alcohol use disorder (AUD) symptoms while separating the “traitlike” components of AUD symptoms from their age-specific manifestations at three ages from emerging adulthood (17–23 years) to adulthood (29–40 years). The results for males were consistent with genetically influenced peer selection mechanisms as mediators of parent alcoholism effects. Male children of alcoholics were less likely to be carriers of the G allele in single nucleotide polymorphism A118G (rs1799971), and those who were homozygous for the A allele were more likely to affiliate with alcohol use promoting peers who increased the risk for AUD symptoms at all ages. There was evidence for women of an interaction between OPRM1 variation and peer affiliations but only at the earliest age band. Peer influences had stronger effects among women who were G-carriers. These results illustrate the complex ways in which the interplay between influences at multiple levels of analysis can underlie the intergenerational transmission of alcohol disorders as well as the importance of considering age and gender differences in these pathways.

ALDH2*2 and peer drinking in East Asian college students

“…Genetic susceptibility for substance use and peer selection are correlated, but likely attributed to other genes than those for alcohol metabolism (40,41). For example, Chassin et al (42) and Mrug and Windle (43), respectively, studied dopamine receptor ( DRD4 ) and μ-opioid receptor M1 ( OPRM1 ) genes in association with alcohol use behaviors and found evidence for both genetically influenced peer selection and gene–environment interaction. These interactions, as with the current study, showed stronger risk allele effects with greater peer influences.…”

Interaction Between the μ‐Opioid Receptor Gene and the Number of Heavy‐Drinking Peers on Alcohol Use

“…Genotype frequencies did not deviate significantly from Hardy-Weinberg equilibrium, χ 2 (1, n = 116) = 2.92, p = .09. Participants were dichotomized as either G allele carriers (A/G, G/G; n = 37, 32%) or noncarriers (A/A; n = 79, 68%) consistent with previous research (Chassin et al, 2012; Miranda et al, 2013) and suggestions that a cross-product G×E interaction term using a three-category polymorphic genotype may increase false positive and negative findings (Aliev et al, 2014). Although social drinking conditions were not stratified by genotype due to random assignment, participants were generally evenly distributed across the 0 ( n = 13 for carriers, n = 25 for noncarriers), 1 ( n = 12 for carriers, n = 27 for noncarriers), and 3 ( n = 12 for carriers, n = 27 for noncarriers) confederate conditions.…”

“…In a cross-sectional study of European-American adolescents ( N = 104), G allele carriers were more likely to meet criteria for an alcohol use disorder when endorsing high relative to low deviant peer affiliation (Miranda et al, 2013). In a longitudinal observational study ( N = 238), OPRM1 ’s G allele magnified the influence of heavy drinking peer affiliation (i.e., perceived peer drinking norms) among Caucasian women, but not men, on alcohol use disorder symptoms at 17–23 (but not 23–40) years of age (Chassin et al, 2012). Existing research on OPRM1 -based susceptibility to peer environments has been inconclusive and exclusively correlational.…”

“…Participants were randomly assigned to voluntarily consume alcohol in the presence of none, one, or three heavy drinking peer confederates. Manipulating the number of heavy drinking peers allowed the current study to expand upon prior inconclusive correlational findings (Chassin et al, 2012; Miranda et al, 2013) as well as examine the influence of drinking group size (one versus three peers) and peer presence (versus absence) on alcohol consumption. We hypothesized a significant interaction between OPRM1 and the number of heavy drinking peers on alcohol consumption; specifically, carriers of a G allele were hypothesized to drink more than noncarriers as the number of drinking peers increased.…”

Gene-Environment Interplay and Substance Use: A Review of Recent Findings

“…In a case-control design of adolescents with alcohol use disorder (n=104), Miranda and colleagues [48] found that a higher proportion of the high-risk G allele carriers (AG/GG genotype) met criteria for alcohol use disorder compared to the low risk AA homozygotes and this effect was amplified when parental monitoring was low and deviant peer affiliation was high. Using a larger sample (n= 529), Chassin and colleagues [49] found that exposure to deviant peers was associated with higher levels of alcohol use disorder symptoms for women (but not men) who were G allele carriers, but women with the AA genotype were not as susceptible to deviant peer influences.…”