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.

26 August 2022 In Cardiovascular System

AIMS: The association between low-to-moderate alcohol consumption and atrial fibrillation (AF) has yet to be fully elucidated. The main purpose of this meta-analysis was to estimate the risk of incident AF related to low-to-moderate alcohol consumption.

METHODS AND RESULTS: A meta-analysis was performed on 13 publications discussing the estimated risk for AF with habitual low-to-moderate alcohol intake in 10 266 315 participants. Graphical augmentations to the funnel plots were used to illustrate the potential impact of additional evidence on the current meta-analysis. Thirteen eligible studies were included in this meta-analysis. We found that moderate alcohol consumption was associated with an increased risk of incident AF in males [hazard ratio (HR) 1.09, 95% confidence interval (CI): 1.07-1.11, P < 0.00001], Europeans (HR 1.32, 95% CI: 1.23-1.42, P < 0.00001), and Asians (HR 1.09, 95% CI: 1.07-1.11, P < 0.00001). Moderate beer consumption was associated with an increased risk of developing AF (HR 1.11, 95% CI: 1.02-1.21, P = 0.01). Low alcohol consumption conferred an increased risk of AF in males (HR 1.14, 95% CI: 1.01-1.28, P = 0.04) and Europeans (HR 1.12, 95% CI: 1.07-1.17, P < 0.00001).

CONCLUSIONS: This analysis represents the increased risk of incident AF in males, Europeans, and Asians at moderate alcohol consumption levels and in males and Europeans at low alcohol consumption levels. Those who drink any preferred alcohol beverage at moderate levels should be cautious for incident AF. More studies are warranted to find those factors that influence alcohol's effect on predisposing AF.

23 November 2020 In General Health

A previous meta-analysis provided convincing evidence for an inverse association between adherence to a Mediterranean diet (MedDiet) and the risk of all-cause mortality. Since then, 19 prospective studies have been published. We updated the evidence from these prospective studies and conducted a dose-response meta-analysis to test the linear and potential nonlinear dose-response associations between adherence to a MedDiet and the risk of all-cause mortality.

The PubMed, Scopus, ISI Web of Knowledge, and Embase bibliographic databases were systematically searched up to August 24, 2018. Summary HRs were estimated with the use of a random-effects meta-analysis to assess the association between a 2-point increment in MedDiet adherence and the risk of all-cause mortality. Sensitivity and subgroup analyses were performed and potential publication bias was tested. Twenty-nine prospective studies with 1,676,901 participants and 221,603 cases of all-cause mortality were included in the final analysis.

The pooled HR of all-cause mortality was 0.90 (95% CI: 0.89, 0.91; I2 = 81.1%) for a 2-point increment in adherence to a MedDiet. Subgroup analyses showed that a significant inverse association was stronger in participants who lived in the Mediterranean region compared with non-Mediterranean areas (HRs: 0.82 compared with 0.92, respectively), and in studies that used the Panagiotakos MedDiet score.

A nonlinear dose-response meta-analysis indicated that the risk of all-cause mortality linearly decreased with the increase in adherence to a MedDiet. The robustness of findings was confirmed in the sensitivity analyses. In conclusion, low-quality evidence from prospective cohort studies suggests an inverse association between adherence to a MedDiet and the risk of all-cause mortality, especially in Mediterranean regions. An inverse linear dose-response relation was also observed between adherence to a MedDiet and the risk of all-cause mortality.

25 August 2020 In General Health

BACKGROUND:AIMS: Gallstone disease (GSD) is a common gastrointestinal disorder. Clinical epidemiological studies revealed that alcohol consumption has a preventive effect on the development of GSD. This study aimed to evaluate the relative risks of drinking for GSD development and investigate the dose-response relationships.

METHODS: A systematic search of the MEDLINE, EMBASE, and Cochrane Library databases for studies published up to 2018 was performed. All studies that satisfied the following eligibility criteria were included: patients with GSD with or without cholecystitis; and cohort or case-control studies investigating the association between alcohol consumption and GSD development.

RESULTS: Sixteen case-control studies including 24,401 gallstone cases and 76,185 controls, and eight cohort studies with 14,693 GSD cases among 2,432,471 person-years were enrolled. Alcohol consumption presented a decreased overall risk of GSD (pooled relative ratio [RR], 0.84; 95% confidence interval [CI], 0.79 to 0.89; p=0.02). Subgroup analyses according to drinking levels indicated a gradual risk reduction for GSD compared to nondrinkers (light: RR, 0.96; 95% CI, 0.94 to 0.99; p=0.75; moderate: RR, 0.80; 95% CI, 0.75 to 0.85; p=0.27; high: RR, 0.66; 95% CI, 0.56 to 0.79; p0.01). A nonlinear risk reduction was observed in a dose-response meta-analysis of all the studies (n=14, p0.01 for nonlinearity).

CONCLUSIONS: In this systematic review with meta-analysis, alcohol consumption could decrease the risk of GSD, and the dose-response analysis revealed a dose-dependent linear risk reduction and a weakened linear trend between alcohol consumption levels less than and greater than 28 g/day.

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