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.
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.