27 October 2022 In General Health

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.

27 October 2022 In General Health

BACKGROUND: Research has long found 'J-shaped' relationships between alcohol consumption and certain health outcomes, indicating a protective effect of moderate consumption. However, methodological limitations in most studies hinder causal inference. This review aimed to identify all observational studies employing improved approaches to mitigate confounding in characterizing alcohol-long-term health relationships, and to qualitatively synthesize their findings.

METHODS: Eligible studies met the above description, were longitudinal (with pre-defined exceptions), discretized alcohol consumption, and were conducted with human populations. MEDLINE, PsycINFO, Embase and SCOPUS were searched in May 2020, yielding 16 published manuscripts reporting on cancer, diabetes, dementia, mental health, cardiovascular health, mortality, HIV seroconversion, and musculoskeletal health. Risk of bias of cohort studies was evaluated using the Newcastle-Ottawa Scale, and a recently developed tool was used for Mendelian Randomization studies.

RESULTS: A variety of functional forms were found, including reverse J/J-shaped relationships for prostate cancer and related mortality, dementia risk, mental health, and certain lipids. However, most outcomes were only evaluated by a single study, and few studies provided information on the role of alcohol consumption pattern.

CONCLUSIONS: More research employing enhanced causal inference methods is urgently required to accurately characterize alcohol-long-term health relationships. Those studies that have been conducted find a variety of linear and non-linear functional forms, with results tending to be discrepant even within specific health outcomes.

TRIAL REGISTRATION: PROSPERO registration number CRD42020185861.

22 September 2022 In General Health

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.

22 September 2022 In General Health

The association between alcohol intake and the risk of glioma has been widely studied, but these results have yielded conflicting findings. Therefore, we conducted this systematic review and updated meta-analysis to systematically evaluate the association between alcohol intake and the risk of glioma. A systematic literature search of relevant articles published in PubMed, Web of Science, CNKI and Wan fang databases up to December 2021 was conducted. Pooled estimated of relative risk (RR) and 95 % CI were calculated using fixed-effects models. A total of eight articles with three case-control studies involving 2706 glioma cases and 2 189 927 participants were included in this meta-analysis. A reduced risk of glioma was shown for the low-moderate alcohol drinking v. non-drinking (RR = 0.87; 95 % CI (0.78, 0.97); P = 0.014). In addition, there was no evidence of an increased risk of glioma in the heavy alcohol drinking compared with non-drinking (RR = 0.89; 95 % CI (0.67, 1.18); P = 0.404). The findings suggest an inverse association between low-moderate alcohol drinking and the risk of glioma, in the absence, however, of a dose-response relationship. More prospective studies are needed to provide further insight into the association between alcohol drinking and glioma risk.

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