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Funding of research by industry in general can lead to sponsorship bias. The aim of the current study was to conduct an initial exploration of the impact of sponsorship bias in observational alcohol research by focusing on a broad spectrum of health outcomes.
The purpose was to determine whether the outcome depended on funding source. We focused on moderate alcohol consumption and used meta-analyses that are the basis of several international alcohol guidelines. These meta-analyses included observational studies that investigated the association of alcohol consumption with 14 different health outcomes, including all-cause mortality, several cardiovascular diseases and cancers, dementia, and type 2 diabetes.
Subgroup analyses and metaregressions were conducted to investigate the association between moderate alcohol consumption and the risk of different health outcomes, comparing findings of studies funded by the alcohol industry, ones not funded by the alcohol industry, and studies with an unknown funding source. A total of 386 observational studies were included.
Twenty-one studies (5.4%) were funded by the alcohol industry, 309 studies (80.1%) were not funded by the alcohol industry, and for the remaining 56 studies (14.5%) the funding source was unknown. Subgroup analyses and metaregressions did not show an effect of funding source on the association between moderate alcohol intake and different health outcomes.
In conclusion, only a small proportion of observational studies in meta-analyses, referred to by several international alcohol guidelines, are funded by the alcohol industry. Based on this selection of observational studies the association between moderate alcohol consumption and different health outcomes does not seem to be related to funding source.
Adolescence is a particularly vulnerable neurodevelopmental period marked by high rates of engagement with risky alcohol use. This review summarizes the cognitive and neural consequences following alcohol use during adolescence from longitudinal design studies in humans and animals.
Findings from human adolescent studies suggest that binge drinking and heavy alcohol use is associated with poorer cognitive functioning on a broad range of neuropsychological assessments, including learning, memory, visuospatial functioning, psychomotor speed, attention, executive functioning, and impulsivity. Alcohol use during adolescence is associated with accelerated decreases in gray matter and attenuated increases in white matter volume, and aberrant neural activity during executive functioning, attentional control, and reward sensitivity tasks, when compared to non-drinking adolescents.
Animal studies in rodents and non-human primates have replicated human findings, and suggest cognitive and neural consequences of adolescent alcohol use may persist into adulthood. Novel rodent studies demonstrate that adolescent alcohol use may increase reward responsiveness of the dopamine system to alcohol later in life, as well as disrupt adolescent neurogenesis, potentially through neuroinflammation, with long-lasting neural and behavioral effects into adulthood.
Larger longitudinal human cognitive and neuroimaging studies with more diverse samples are currently underway which will improve understanding of the impact of polysubstance use, as well as the interactive effects of substance use, physical and mental health, and demographic factors on cognition and neurodevelopment.
The association between alcohol consumption and venous thromboembolism (VTE) risk has been investigated by various observational studies with inconsistent results. We examined this association by performing a meta-analysis of prospective studies.
A comprehensive literature search was carried out in the PubMed, EMBASE, and Web of Science from its inception to February 2020. Pooled effect estimates were calculated using a random effect model. Ten prospective studies (14 cohorts) were included in this meta-analysis with a total of 441,128 individuals and 10,221 VTE cases. Overall, the highest consumption of alcohol was not associated with the VTE risk compared with the lowest group [relative risk (RR), 0.96 (95% CI, 0.89-1.04), P = 0.293]. No obvious heterogeneity of RRs was observed across these studies (P = 0.249 for heterogeneity, I (2) = 18.8%). Egger's and Begg's tests showed no evidence of publication bias (Egger, P = 0.443; Begg, P = 0.730).
In the subgroup analysis by sex, a borderline significant association between alcohol consumption and VTE risk was observed in women [RR, 0.91 (95% CI, 0.82-1.00)]. In the dose-response analysis, we observed a linear decrease in VTE risk with increasing alcohol intake (P = 0.634 for nonlinearity). However, the reduced risk was not statistically significant.
In conclusion, the results from this meta-analysis suggest that alcohol intake is not related with the risk of VTE. Further large well-designed cohort studies are warranted to investigate a potential protective role of alcohol against VTE in women.