INTRODUCTION: Chronic pain represents a global health problem with a considerable economic burden. The relation of alcohol intake and chronic pain conditions was assessed in several studies with conflicting results. We used dose-response meta-analysis techniques to answer the question of whether alcohol intake is related to chronic pain occurrence.
METHODS: We searched MEDLINE, Embase, and other databases to identify cohort and case-control studies on alcohol consumption and chronic pain. Sixteen studies were eligible with a total population of 642 587 individuals. Fixed-effects and random-effects pooled estimates were obtained by weighting log odds ratios (ORs) in case-control studies and log incidence rate ratios in cohort studies by the inverse of their variance. A heterogeneity assessment and a dose-response analysis were carried out. Quality scoring was also performed.
RESULTS: Our results show that any alcohol consumption was related to lower odds of chronic pain (pooled OR=0.76; 95% confidence interval [CI], 0.61-0.95). The association was non-linear. The ORs by quartile of alcohol doses were as follows: OR2nd quartile=0.74; 95% CI, 0.64-0.87; OR3rd quartile=0.67; 95% CI, 0.53-0.86; and OR4th quartile=0.75; 95% CI, 0.50-1.14. This association was observed for cohort studies (OR=0.77; 95% CI, 0.61-0.98) and European studies (OR=0.65; 95% CI, 0.48-0.87) only. Studies with complete adjustment for confounding factors showed a stronger relation than those with incomplete adjustment (OR=0.69; 95% CI, 0.48-0.99 and OR=0.85; 95% CI, 0.65-1.11, respectively).
CONCLUSION: Alcohol consumption presents a non-linear inverse association with the occurrence of chronic pain. Although plausible mechanisms could explain this protective effect, other explanations, including reverse causation, are probable.
INTRODUCTION: Chronic pain represents a global health problem with a considerable economic burden. The relation of alcohol intake and chronic pain conditions was assessed in several studies with conflicting results. We used dose-response meta-analysis techniques to answer the question of whether alcohol intake is related to chronic pain occurrence.
METHODS: We searched MEDLINE, Embase, and other databases to identify cohort and case-control studies on alcohol consumption and chronic pain. Sixteen studies were eligible with a total population of 642 587 individuals. Fixed-effects and random-effects pooled estimates were obtained by weighting log odds ratios (ORs) in case-control studies and log incidence rate ratios in cohort studies by the inverse of their variance. A heterogeneity assessment and a dose-response analysis were carried out. Quality scoring was also performed.
RESULTS: Our results show that any alcohol consumption was related to lower odds of chronic pain (pooled OR=0.76; 95% confidence interval [CI], 0.61-0.95). The association was non-linear. The ORs by quartile of alcohol doses were as follows: OR2nd quartile=0.74; 95% CI, 0.64-0.87; OR3rd quartile=0.67; 95% CI, 0.53-0.86; and OR4th quartile=0.75; 95% CI, 0.50-1.14. This association was observed for cohort studies (OR=0.77; 95% CI, 0.61-0.98) and European studies (OR=0.65; 95% CI, 0.48-0.87) only. Studies with complete adjustment for confounding factors showed a stronger relation than those with incomplete adjustment (OR=0.69; 95% CI, 0.48-0.99 and OR=0.85; 95% CI, 0.65-1.11, respectively).
CONCLUSION: Alcohol consumption presents a non-linear inverse association with the occurrence of chronic pain. Although plausible mechanisms could explain this protective effect, other explanations, including reverse causation, are probable.
AIMS/HYPOTHESIS: The aim of this study was to evaluate the prospective association between baseline and 9 year change in alcohol consumption and long-term risk of diabetes and whether these associations might be modified by sex and/or BMI.
METHODS: We conducted a prospective analysis of 12,042 Atherosclerosis Risk in Communities (ARIC) study participants without prevalent diabetes (55% women, 78% white, mean age 54 years). Alcohol consumption was assessed at visit 1 (1987-1989) and visit 4 (1996-1998). We used Cox models to estimate hazard ratios for diabetes risk by baseline drinking categories and change in alcohol consumption, stratified by sex and obesity status.
RESULTS: During a median follow-up of 21 years, there were 3795 incident cases of diabetes. Among women, consuming 8-14 drinks/week was associated with a significantly lower risk of diabetes (HR 0.75, 95% CI 0.58, 0.96) compared with current drinkers consuming ≤1 drink/week. Among men, consuming 8-14 drinks/week was associated with a borderline significant lower risk of diabetes (HR 0.84, 95% CI 0.70, 1.00) and consuming >14 drinks/week was associated with a significantly lower risk of diabetes (HR 0.81, 95% CI 0.67, 0.97) (p(interaction) < 0.01 for sex). For both sexes, among current drinkers, there was a significant decreasing trend in diabetes risk as the alcohol consumption increased. The association was modified by BMI (p(interaction) = 0.042 for women, p(interaction) < 0.001 for men). In women, the inverse association was only seen among overweight and obese participants. In men, the inverse association was more pronounced among obese participants. On average, drinking status did not change substantially over the 9 year period. For men with alcohol intake ≥7 drinks/week at baseline, decreasing alcohol intake was associated with higher risk of diabetes (HR per daily drink decrease 1.12, 95% CI 1.02, 1.23).
CONCLUSIONS/INTERPRETATION: In this community-based population, there was an inverse association between alcohol consumption and diabetes risk. The amount of the alcohol consumption associated with lower risk was different in women and men, and the association was more pronounced among participants with higher BMI.
BACKGROUND: Both alcohol use and weight status have been linked to increased mortality risk, but evidence of their joint effect is limited. The goal of this study was to examine the combined effects of alcohol and weight status (BMI classes: underweight, normal, overweight, obesity) on mortality using nationally representative data.
METHODS: Using data from public-use National Health Interview Survey-Linked Mortality Files (NHIS-LMF), 2001-2011, linked to prospective mortality follow-up through December 2015, we used age-period-cohort Cox proportional hazards models to examine all-cause and cause-specific mortality associated with the joint effects of alcohol use and BMI on 209,317 individuals aged 35-85.
RESULTS: Individuals with an underweight BMI status had higher all-cause and cause-specific mortality risks than those with a normal BMI status and light/moderate alcohol intake. All-cause mortality risks were 148% (hazard ratio [HR] 2.48, 95% CI 1.60-3.83) higher in underweight heavy drinkers than light/moderate drinkers with normal BMI status. Obese heavy drinkers had a 16% higher chance of dying from all-cause mortality (HR 1.16, 95% CI 1.00-1.35). Individuals in the unknown alcohol and BMI category have a higher chance of death from all-cause (HR 1.35, 95% CI 1.14-1.59) or cause-specific (CVD HR 1.75, 95% CI 1.14-2.69 and Cancer HR 1.33, 95% CI 1.01-1.76).
CONCLUSIONS: Alcohol drinking levels result in heightened all-cause and cause-specific mortality risks; the risks are compounded among underweight, obese, and unknown BMI individuals across all or cause-specific mortality.