This study examined the association of subjective responses with subsequent laboratory self-administration, also evaluating laboratory phenotypes in relation to putative genetic risk factors [family history (FH) of alcohol dependence and OPRM1 genotype] and subsequent heavy drinking.
Findings suggest no OPRM1-based susceptibility to the number of heavy-drinking peers, adding to the existing mixed findings from correlational studies.
Findings provide the first in vivo evidence that, among carriers of the DRD4-L allele, naltrexone blunts craving in real-world settings, and this effect in turn reduces the likelihood of heavy drinking.
OPRM1 genotype did not significantly moderate these effects, but G-allele carriers who received naltrexone had an accelerated return to heavy drinking after medication was stopped.
Moreover, one haplotype of the CHRNA4 (GGTG) was associated with increased body weight as compared to non-carriers of this haplotype, especially in the heavy consumers of alcohol (p=0.004).The present findings are the first to disclose a haplotype association between the CHRNA6 gene and heavy alcohol use as well as an association of the CHRNA4 gene with increased body mass in heavy consumers of alcohol.
This study compared self-reported alcohol use, via the AUDIT and CAGE, with levels of phosphatidylethanol (Peth), a phospholipid biomarker that forms with chronic, heavy drinking, among high-risk MSM and TW in Lima, Peru.
These findings provide first evidence in humans that the CRHR1 gene interacts with exposure to stressful life events to predict heavy alcohol use in adolescents.
These findings extend previous reports by demonstrating that the CRHR1 gene and stressful life events interact to predict both drinking initiation in adolescence and progression of heavy alcohol use in young adulthood.
The 'Identical By Descent' analysis provided significant evidence of an effect of the DRD2 locus on the liability to develop heavy drinking (P < 0.0016) and Research Diagnostic Criteria alcoholism (P < 0.0003) in the first sample of families studied.
We noted an effect on the percentage of days abstinent in the past 14 days (adjusted mean difference [AMD] 16·0% [8·1-24·1]; p<0·0001), but no effect on the percentage of days of heavy drinking (AMD -0·4% [-5·7 to 4·9]; p=0·88), the effect of drinking (Short Inventory of Problems score AMD-0·03 [-1·93 to 1·86]; p=0.97), disability score (WHO Disability Assessment Schedule score AMD 0·62 [-0·62 to 1·87]; p=0·32), days unable to work (no days unable to work adjusted odds ratio 1·02 [0·61-1·69]; p=0.95), suicide attempts (adjusted prevalence ratio 1·8 [-2·4 to 6·0]; p=0·25), and intimate partner violence (adjusted prevalence ratio 3·0 [-10·4 to 4·4]; p=0·57).
We have previously demonstrated that the GATA4 single nucleotide polymorphism (SNP) rs13273672 revealed stronger alcohol-specific amygdala activation associated with lowered relapse risk to heavy drinking at 90 days in the AA-homozygotes.
This decrease in plasma ACTH and beta-END levels with heavy drinking was more pronounced in female than male subjects of the 30-44 and 45-60 age groups.
Non-treatment-seeking underage drinkers who reported past-month heavy drinking (N = 167; ages 17 to 20; 42% female; 59% non-Hispanic White) were randomly assigned to receive a single session of BMI or REL.
We observed an increase in the global mean field power in the time window of 54- to 75-millisecond post-TMS, as well as significant topographical differences in the P60 and N100 in those with a history of heavy drinking.
Here, we describe research on the involvement of the transcription factor, Early Growth Response- 1 (Egr-1) in alcohol-induced liver injury, specifically, fatty liver (steatosis), one of the earliest and most frequent signs of liver injury that occurs after heavy drinking.
We observed an increase in the global mean field power in the time window of 54- to 75-millisecond post-TMS, as well as significant topographical differences in the P60 and N100 in those with a history of heavy drinking.