Browsing by Subject "Alcohol drinking"

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  • Sipila, Pyry; Rose, Richard J.; Kaprio, Jaakko (2016)
    AimsTo determine if associations of alcohol consumption with all-cause mortality replicate in discordant monozygotic twin comparisons that control for familial and genetic confounds. DesignA 30-year prospective follow-up. SettingPopulation-based older Finnish twin cohort. ParticipantsSame-sex twins, aged 24-60years at the end of 1981, without overt comorbidities, completed questionnaires in 1975 and 1981 with response rates of 89 and 84%. A total of 15607 twins were available for mortality follow-up from the date of returned 1981 questionnaires to 31December 2011; 14787 twins with complete information were analysed. MeasurementsSelf-reported monthly alcohol consumption, heavy drinking occasions (HDO) and alcohol-induced blackouts. Adjustments for age, gender, marital and smoking status, physical activity, obesity, education and social class. FindingsAmong twins as individuals, high levels of monthly alcohol consumption (259g/month) associated with earlier mortality [hazard ratio (HR)=1.63, 95% confidence interval (CI)=1.47-1.81]. That association was replicated in comparisons of all informatively drinking-discordant twin pairs (HR=1.91, 95% CI=1.49-2.45) and within discordant monozygotic (MZ) twin pairs (HR=2.24, 95% CI=1.31-3.85), with comparable effect size. Smaller samples of MZ twins discordant for HDO and blackouts limited power; a significant association with mortality was found for multiple blackouts (HR=2.82, 95% CI=1.30-6.08), but not for HDO. ConclusionsThe associations of high levels of monthly alcohol consumption and alcohol-induced blackouts with increased all-cause mortality among Finnish twins cannot be explained by familial or genetic confounds; the explanation appears to be causal.
  • Pena, Sebastian; Mäkelä, Pia; Laatikainen, Tiina; Härkänen, Tommi; Männistö, Satu; Heliövaara, Markku; Koskinen, Seppo (2021)
    Background and aims Lower socio-economic status (SES) is associated with higher alcohol-related harm despite lower levels of alcohol use. Differential vulnerability due to joint effects of behavioural risk factors is one potential explanation for this 'alcohol harm paradox'. We analysed to what extent socio-economic inequalities in alcohol-mortality are mediated by alcohol, smoking and body mass index (BMI), and their joint effects with each other and with SES. DesignCohort study of eight health examination surveys (1978-2007) linked to mortality data. Setting Finland.ParticipantsA total of 53 632 Finnish residents aged 25+ years.MeasurementsThe primary outcome was alcohol-attributable mortality. We used income as an indicator of SES. We assessed the joint effects between income and mediators (alcohol use, smoking and BMI) and between the mediators, adjusting for socio-demographic indicators. We used causal mediation analysis to calculate the total, direct, indirect and mediated interactive effects using Aalen's additive hazards models. Findings During 1 085 839 person-years of follow-up, we identified 865 alcohol-attributable deaths. We found joint effects for income and alcohol use and income and smoking, resulting in 46.8 and 11.4 extra deaths due to the interaction per 10 000 person-years. No interactions were observed for income and BMI or between alcohol and other mediators. The lowest compared with the highest income quintile was associated with 5.5 additional alcohol deaths per 10 000 person-years (95% confidence interval = 3.7, 7.3) after adjusting for confounders. The proportion mediated by alcohol use was negative (-69.3%), consistent with the alcohol harm paradox. The proportion mediated by smoking and BMI and their additive interactions with income explained 18.1% of the total effect of income on alcohol-attributable mortality. Conclusions People of lower socio-economic status appear to be more vulnerable to the effects of alcohol use and smoking on alcohol-attributable mortality. Behavioural risk factors and their joint effects with income may explain part of the alcohol harm paradox.
  • Dudek, Mateusz; Canals, Santiago; Sommer, Wolfgang H.; Hyytiä, Petri (2016)
    The nonselective opioid receptor antagonist naltrexone is now used for the treatment of alcoholism, yet naltrexone's central mechanism of action remains poorly understood. One line of evidence suggests that opioid antagonists regulate alcohol drinking through interaction with the mesolimbic dopamine system. Hence, our goal here was to examine the role of the nucleus accumbens connectivity in alcohol reinforcement and naltrexone's actions using manganese enhanced magnetic resonance imaging (MEMRI). Following long-term free-choice drinking of alcohol and water, AA (Alko Alcohol) rats received injections of MnCl2 into the nucleus accumbens for activity-dependent tracing of accumbal connections. Immediately after the accumbal injections, rats were imaged using MEMRI, and then allowed to drink either alcohol or water for the next 24 h. Naltrexone was administered prior to the active dark period, and the second MEMRI was performed 24 h after the first scan. Comparison of signal intensity at 1 and 24 h after accumbal MnCl2 injections revealed an ipsilateral continuum through the ventral pallidum, bed nucleus of the stria terminalis, globus pallidus, and lateral hypothalamus to the substantia nigra and ventral tegmental area. Activation was also seen in the rostral part of the insular cortex and regions of the prefrontal cortex. Alcohol drinking resulted in enhanced activation of these connections, whereas naltrexone suppressed alcohol-induced activity. These data support the involvement of the accumbal connections in alcohol reinforcement and mediation of naltrexone's suppressive effects on alcohol drinking through their deactivation. (C) 2016 Elsevier B.V. and ECNP. All rights reserved.