Background Alterations in the brain cortical structures of patients with chronic kidney disease (CKD) have been reported; however, the cause has not been determined yet. Herein, we used Mendelian randomization (MR) to reveal the causal effect of kidney damage on brain cortical structure. Methods Genome-wide association studies summary data of estimated glomerular filtration rate (eGFR) in 480,698 participants from the CKDGen Consortium were used to identify genetically predicted eGFR. Data from 567,460 individuals from the CKDGen Consortium were used to assess genetically determined CKD; 302,687 participants from the UK Biobank were used to evaluate genetically predicted albuminuria. Further, data from 51,665 patients from the ENIGMA Consortium were used to assess the relationship between genetic predisposition and reduced eGFR, CKD, and progressive albuminuria with alterations in cortical thickness (TH) or surficial area (SA) of the brain. Magnetic resonance imaging was used to measure the SA and TH globally and in 34 functional regions. Inverse-variance weighted was used as the primary estimate whereas MR Pleiotropy RESidual Sum and Outlier, MR-Egger and weighted median were used to detect heterogeneity and pleiotropy. Findings At the global level, albuminuria decreased TH (β = −0.07 mm, 95% CI: −0.12 mm to −0.02 mm, P = 0.004); at the functional level, albuminuria reduced TH of pars opercularis gyrus without global weighted (β = −0.11 mm, 95% CI: −0.16 mm to −0.07 mm, P = 3.74×10 −6 ). No pleiotropy was detected. Interpretation Kidney damage causally influences the cortex structure which suggests the existence of a kidney-brain axis. Funding This study was supported by the Science and Technology Planning Project of Guangdong Province (Grant No. 2020A1515111119 and 2017B020227007), the National Key Research and Development Program of China (Grant No. 2018YFA0902803), the National Natural Science Foundation of China (Grant No. 81825016, 81961128027, 81772719, 81772728), the Key Areas Research and Development Program of Guangdong (Grant No. 2018B010109006), Guangdong Special Support Program (2017TX04R246), Grant KLB09001 from the Key Laboratory of Malignant Tumor Gene Regulation and Target Therapy of Guangdong Higher Education Institutes, and Grants from the Guangdong Science and Technology Department (2020B1212060018).
Background and Aims Alcohol use disorders (AUD) are often comorbid with depressive symptoms. Cohort studies on the association between AUD and subsequent depressive symptoms have produced inconsistent results. Moreover, regarding alcohol intake, the risk of developing depressive symptoms might vary with alcohol intake level. We aimed to investigate the association between AUD, alcohol intake and subsequent depressive symptoms. Design and Setting We conducted a systematic search in PubMed, Embase and PsycINFO for cohort studies on the association between AUD or alcohol intake and subsequent depressive symptoms. Participants We included 338 426 participants from 42 studies. Six and four studies analyzed only females and males, respectively. Measurements We combined risk estimates for developing depressive symptoms using a random‐effects model. We divided alcohol intake into abstinence, light (0–84 g/week), moderate (85–168 g/week) and heavy drinking (> 168 g/week or > 48 g/day at least weekly). We conducted a categorical analysis to compare the risk of depressive symptoms between abstinence and different intake categories. Further, we conducted a dose–response analysis to investigate the alcohol–depression association. Findings We analyzed 42 studies (follow‐up time: 1–40 years). AUD was associated with significantly increased risk of subsequent depressive symptoms [relative risk (RR) = 1.57, 95% confidence interval (CI) = 1.41–1.76]. Regarding alcohol intake, heavy drinking had an increased risk of depressive symptoms; however, the association was only significant when controls were limited to non‐heavy drinkers (RR = 1.13, 95% CI = 1.05–1.22). Taking into consideration the possibility of publication bias and confounding factors made the association non‐significant. We observed J‐shaped associations in both categorical and dose–response analyses where light‐moderate drinking had a significantly decreased risk of depression, while heavy drinking did not show a significant association with depressive symptoms compared with non‐drinkers. Conclusion Alcohol use disorders are associated with increased the risk of subsequent depressive symptoms. Heavy drinking does not significantly predict occurrence of depressive symptoms after adjusting for potential confounders.
Alcohol use disorders (AUD), including alcohol abuse and alcohol dependence, are common psychiatric disorders contribute greatly to the burden of society. 1 Alcohol-related diseases are one of the leading risk factors of disability and mortality, causing about 3.3 million deaths around the world and taking account for 5.1% of the global burden of disease according to the report of WHO. 2 Depression is a highly prevalent mental illness and is one of the important causes of premature deaths. About 350 million people around the world suffer from depression and nearly one million of
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