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.
A synergistic effect between eNOS and Cav-1 polymorphisms on IS risk elevation was significantly influenced by alcohol drinking, heavy cigarette smoking (P-trend<0.01), and hypercholesterolemia (P-trend < 0.001).
Both additive and multiplicative interactions between heavy drinking and the CD14/-159C allele for total and specific serum IgE values was still present after adjusting for potential confounders.
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.
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.
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.
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.
Although NTX had no significant effect on relapse to heavy drinking in the overall sample in CSP 425, it significantly reduced relapse in the subgroup that provided DNA for analysis (i.e., the present study sample).
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.
Multiple regression analyses support the role of NS in mediating the relationship between DRD4 and heavy drinking in male adolescents but not in female adolescents.
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.
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.
The absence of an interaction between either current life stress or past-year trauma, and FKBP5 genotype on heavy drinking suggests that there exists a developmental period of susceptibility to stress that is moderated by FKBP5 genotype.
Drinking habits among adults during midlife affect the development of fatty liver, and sustained heavy drinking is associated with an increased FLI compared to stable low-risk drinkers.
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.