Alcohol Consumption and Risk of Parkinson's Disease: Data From a Large Prospective European Cohort.
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SUBMITTER: Peters S
PROVIDER: S-EPMC7496254 | biostudies-literature | 2020 Jul
REPOSITORIES: biostudies-literature
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Alcohol Consumption and Risk of Parkinson's Disease: Data From a Large Prospective European Cohort.
Peters Susan S Gallo Valentina V Vineis Paolo P Middleton Lefkos T LT Forsgren Lars L Sacerdote Carlotta C Sieri Sabina S Kyrozis Andreas A Chirlaque María-Dolores MD Zamora-Ros Raul R Hansson Oskar O Petersson Jesper J Katzke Verena V Kühn Tilman T Mokoroa Olatz O Masala Giovanna G Ardanaz Eva E Panico Salvatore S Bergmann Manuela M MM Key Timothy J TJ Weiderpass Elisabete E Ferrari Pietro P Vermeulen Roel R
Movement disorders : official journal of the Movement Disorder Society 20200501 7
<h4>Background</h4>Parkinson's disease (PD) etiology is not well understood. Reported inverse associations with smoking and coffee consumption prompted the investigation of alcohol consumption as a risk factor, for which evidence is inconclusive.<h4>Objective</h4>To assess the associations between alcohol consumption and PD risk.<h4>Methods</h4>Within NeuroEPIC4PD, a prospective European population-based cohort, 694 incident PD cases were ascertained from 209,998 PD-free participants. Average al ...[more]
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Project description:BackgroundStudies regarding whether light to moderate alcohol consumption is associated with a lower risk of cardiovascular diseases (CVD) have generated mixed results. Further, few studies have examined the potential impact of alcohol consumption on diverse disease outcomes simultaneously. We aimed to prospectively study the dose-response association between alcohol consumption and risk of CVD, cancer, and mortality.MethodsThis study included 83,732 adult Chinese participants, free of CVD and cancer at baseline. Participants were categorized into 6 groups based on self-report alcohol consumption: 0, 1-25, 26-150, 151-350, 351-750, and > 750 g alcohol/wk. Incident cases of CVD, cancers, and mortality were confirmed by medical records. Hazard ratios (HRs) for the composite risk of these three outcomes, and each individual outcome, were calculated using Cox proportional hazard model.ResultsDuring a median follow-up of 10.0 years, there were 6411 incident cases of CVD, 2947 cancers and 6646 deaths. We observed a J-shaped relation between alcohol intake and risk of CVD, cancer, and mortality, with the lowest risk at 25 g/wk., which is equivalent to ~ 2 servings/wk. Compared to consuming 1-25 g/wk., the adjusted HR for composite outcomes was 1.38 (95% confidence interval (CI):1.29-1.49) for non-drinker, 1.15 (95% CI: 1.04-1.27) for 26-150 g/wk., 1.22 (95% CI: 1.10-1.34) for 151-350 g/wk., 1.33 (95% CI: 1.21-1.46) for 351-750 g/wk., and 1.57 (95% CI: 1.30-1.90) for > 750 g/wk., after adjusting for age, sex, lifestyle, social economic status, and medication use.ConclusionsLight alcohol consumption at ~ 25 g/wk was associated with lower risk of CVD, cancer, and mortality than none or higher consumption in Chinese adults.
| S-EPMC7852289 | biostudies-literature
Project description:BackgroundIn epidemiologic studies where physician-based case adjudication is not feasible, Parkinson's disease (PD) case ascertainment is often limited to self-reports which may not be accurate. We evaluated strategies to identify PD cases in the Agricultural Health Study (AHS).MethodsDoctor-diagnosed PD was self-reported on all cohort-wide surveys; potential cases were also identified from death certificates. Follow-up surveys asked about PD-related motor and non-motor symptoms. For PD confirmation, we collected additional diagnosis, symptom, and treatment data from 510 potential PD cases or their proxy (65% of those contacted) in a supplemental screener and obtained medical records for a subset (n = 65). We classified PD cases using established criteria and screener data.ResultsOf 510 potential PD cases, 75% were considered "probable" or "possible"; this proportion increased among participants diagnosed by a specialist (81.2%), taking PD medication (85.2%), or reporting ≥5 motor symptoms (86.8%) in a regular AHS survey. Of those with medical records, 93% (57 of 61) of probable or possible PD was confirmed. Never-smoking and non-motor and motor symptoms reported in prior AHS surveys were more common with probable/possible PD than unconfirmed PD.ConclusionIn this retrospective PD case ascertainment effort, we found that PD self-report with information on motor symptoms or medications may be a reasonable alternative for identifying PD cases when physician exam is not feasible. Because of intervening mortality, screeners could not be obtained from about one-third of those contacted. Thus, findings warrant replication.
| S-EPMC8133399 | biostudies-literature
Project description:BackgroundThe epidemiologic evidence on alcohol consumption and Parkinson's disease (PD) is equivocal. We prospectively examined total alcohol consumption and consumption of specific types of alcoholic beverage in relation to future risk of PD.MethodsThe study comprised 306,895 participants (180,235 male and 126,660 female) ages 50-71 years in 1995-1996 from the NIH-AARP Diet and Health Study. Consumption of alcoholic beverages in the past 12 months was assessed in 1995-1996. Multivariate odds ratios (OR) and 95% confidence intervals (CI) were obtained from logistic regression models.ResultsA total of 1,113 PD cases diagnosed between 2000 and 2006 were included in the analysis. Total alcohol consumption was not associated with PD. However, the association differed by types of alcoholic beverages. Compared with non-beer drinkers, the multivariate ORs for beer drinkers were 0.79 (95% CI: 0.68, 0.92) for <1 drink/day, 0.73 (95% CI: 0.50, 1.07) for 1-1.99 drinks/day, and 0.86 (95% CI: 0.60, 1.21) for ?2 drinks/day. For liquor consumption, a monotonic increase in PD risk was suggested: ORs (95% CI) were 1.06 (0.91, 1.23), 1.22 (0.94, 1.58), and 1.35 (1.02, 1.80) for <1, 1-1.99, and ?2 drinks/day, respectively (P for trend <0.03). Additional analyses among exclusive drinkers of one specific type of alcoholic beverage supported the robustness of these findings. The results for wine consumption were less clear, although a borderline lower PD risk was observed when comparing wine drinkers of 1-1.99 drinks/day with none drinkers (OR?=?0.74, 95% CI: 0.53, 1.02).ConclusionsOUR RESULTS SUGGEST THAT BEER AND LIQUOR CONSUMPTION MAY HAVE OPPOSITE ASSOCIATIONS WITH PD: low to moderate beer consumption with lower PD risk and greater liquor consumption with higher risk. These findings and potential underlying mechanisms warrant further investigations.
| S-EPMC3686735 | biostudies-literature
Project description:We performed this meta-analysis to explore the precise quantification relationship between alcohol consumption and gastric cancer and to provide evidence for preventing gastric cancer. We searched PubMed, Embase, and Web of Science for articles published up to December 2016, and identified 23 cohort studies that included a total population of 5,886,792 subjects. We derived meta-analytic estimates using random-effects models, taking into account correlations between estimates. We also investigated the dose-response relationship between gastric cancer risk and alcohol consumption. We found that alcohol consumption increased gastric cancer risk, where the summary risk ratio was 1.17 (95% confidence interval (CI): 1.00-1.34; I2 = 79.6%, p < 0.05. The dose-response analysis showed that every 10 g/d increment in alcohol consumption was associated with 7% increased gastric cancer risk (95% CI 1.02-1.12; I2 = 28.9%, p = 0.002). This meta-analysis provides evidence that alcohol consumption is an important risk factor of the incidence of gastric cancer.
| S-EPMC5669963 | biostudies-literature
Project description:ObjectiveTo investigate whether alcohol consumption and raised body mass index (BMI) act together to increase risk of liver disease.DesignAnalysis of data from prospective cohort studies.SettingScotland.ParticipantsData were from two of the Midspan prospective cohort studies (9559 men): "Main" study 1965-8, participants from workplaces across central belt of Scotland, population of island of Tiree, and mainland relatives, and "Collaborative" study, 1970-3, participants from 27 workplaces in Glasgow, Clydebank, and Grangemouth. Follow-up was to 31 December 2007 (median 29 years, range 0.13-42). We divided participants into nine groups based on measures of body mass index (BMI) (underweight/normal weight <25, overweight 25 to <30, and obese >or=30) and alcohol consumption (none, 1-14, and >or=15 units per week).Main outcome measuresLiver disease morbidity and mortality.Results80 (0.8%) men died with liver disease as the main cause and 146 (1.5%) with liver disease as any cause. In the Collaborative study, 196 men (3.3%) had liver disease defined by a death, admission, or cancer registration. BMI and alcohol consumption were strongly associated with liver disease mortality in analyses adjusted for other confounders (P=0.001 and P<0.0001 respectively). Drinkers of 15 or more units per week in any BMI category and obese drinkers had raised relative rates for all definitions of liver disease, compared with underweight/normal weight non-drinkers. Drinkers of 15 or more units per week had adjusted relative rates for liver disease mortality of 3.16 (95% confidence interval 1.28 to 7.8) for underweight/normal weight men, 7.01 (3.02 to 16.3) for overweight, and 18.9 (6.84 to 52.4) for obese men. The relative rate for obese men who consumed 1-14 units per week was 5.3 (1.36 to 20.7). The relative excess risk due to interaction between BMI and alcohol consumption was 5.58 (1.09 to 10.1); synergy index=2.89 (1.29 to 6.47).ConclusionsRaised BMI and alcohol consumption are both related to liver disease, with evidence of a supra-additive interaction between the two. The occurrence of both factors in the same populations should inform health promotion and public health policies.
| S-EPMC2837144 | biostudies-literature
Project description:Identification of blood biomarkers that prospectively predict progression of Mycobacterium tuberculosis infection to tuberculosis disease might lead to interventions that combat the tuberculosis epidemic. We aimed to assess whether global gene expression measured in whole blood of healthy people allowed identification of prospective signatures of risk of active tuberculosis disease. RESULTS:Between July 6, 2005, and April 23, 2007, we enrolled 6363 from the ACS study and 4466 from independent South African and Gambian cohorts. 46 progressors and 107 matched controls were identified in the ACS cohort. A 16 gene signature of risk was identified. The signature predicted tuberculosis progression with a sensitivity of 66·1% (95% CI 63·2â68·9) and a specificity of 80·6% (79·2â82·0) in the 12 months preceding tuberculosis diagnosis. The risk signature was validated in an untouched group of adolescents (p=0·018 for RNA sequencing and p=0·0095 for qRT-PCR) and in the independent South African and Gambian cohorts (p values <0·0001 by qRT-PCR) with a sensitivity of 53·7% (42·6â64·3) and a specificity of 82·8% (76·7â86) in 12 months preceding tuberculosis. Interpretation: The whole blood tuberculosis risk signature prospectively identified people at risk of developing active tuberculosis, opening the possibility for targeted intervention to prevent the disease. In this prospective cohort study, we followed up healthy, South African adolescents aged 12â18 years from the adolescent cohort study (ACS) who were infected with M tuberculosis for 2 years. We collected blood samples from study participants every 6 months and monitored the adolescents for progression to tuberculosis disease. A prospective signature of risk was derived from whole blood RNA sequencing data by comparing participants who developed active tuberculosis disease (progressors) with those who remained healthy (matched controls). After adaptation to multiplex qRT-PCR, the signature was used to predict tuberculosis disease in untouched adolescent samples and in samples from independent cohorts of South African and Gambian adult progressors and controls. Participants of the independent cohorts were household contacts of adults with active pulmonary tuberculosis disease.
2016-03-22 | E-GEOD-79362 | biostudies-arrayexpress
Project description:Animal studies demonstrated that paternal alcohol exposure before conception increases the risk of adverse neurodevelopment in offspring, but limited evidence is known in humans. Based on Shanghai-Minhang Birth Cohort Study, we aimed to examine associations between preconceptional paternal alcohol consumption and child behavioral problems. Paternal alcohol consumption during the last 3 months before conception was obtained by maternal report. Children born to fathers who drank alcohol at least once a week were classified as exposed. Child behavioral problems were assessed using the Child Behavior Checklist (CBCL) at age of 2, 4, and 6. Negative binomial regression was used to estimate the rate ratio (RR) of CBCL raw scores in 796 offspring. The risks of rating scores on anxious/depressed were increased by 33% (RR 1.33, 95% CI 1.09, 1.61) and 37% (RR 1.37, 95% CI 1.02, 1.84) among boys in the exposed group at age of 4 and 6, respectively. We also found that risks of somatic complaints were increased by 18% (RR 1.18, 95%CI 1.00, 1.40) and 65% (RR 1.65, 95%CI 1.14, 2.38) among girls in the exposed group at age of 4 and 6. The increased risks of sleep problems (RR 1.25, 95% CI 1.00, 1.55) in girls at age 4, thought problems (RR 1.32, 95% CI 1.01, 1.73) in girls at age 6, rule-breaking behaviors (RR 1.35, 95% CI 1.09, 1.67) in boys at age 6 were also found. The risks of CBCL scores on anxious/depressed and sleep problems in girls at age 4, as well as the risks of somatic complaints and rule-breaking behaviors in boys at age 6 increased with the level of exposure to paternal alcohol consumption. Our findings provided preliminary evidence that preconceptional paternal alcohol consumption may increase risks of child behavioral problems.
| S-EPMC8795263 | biostudies-literature
Project description:BackgroundInverse associations have been observed between coffee consumption and liver cancer, but associations for other digestive cancers are unclear. Few previous studies have investigated coffee type (specifically instant or ground coffee) or a range of digestive cancer types within one cohort. We therefore investigated coffee consumption by type and digestive cancer risks in a population-based cohort.MethodsThe UK Biobank captured self-reported coffee consumption and cancer-registry recorded incident digestive cancers. Hazard ratios (HRs) and 95% CIs were calculated using Cox regression. The risk of every type of digestive cancer was investigated in association with coffee consumption by dose-response and by coffee type (decaffeinated, instant and ground).ResultsOver 7.5 years of follow-up, 3567 developed digestive cancer among 471,779 participants. There were 88 cases of hepatocellular carcinoma and a marked association was observed for hepatocellular carcinoma in coffee drinkers (HR 0.50, 95% CI 0.29, 0.87), which was similar for instant (HR 0.51, 95% CI 0.28, 0.93) and ground coffee (HR 0.47, 95% CI 0.20, 1.08). We did not observe significant consistently reduced risks of other individual digestive cancers amongst coffee drinkers.ConclusionsWe found some evidence that coffee consumption was inversely associated with hepatocellular carcinoma which was similar by coffee type.
| S-EPMC6738036 | biostudies-literature
Project description:ObjectiveTo evaluate the association between egg intake and cardiovascular disease risk among women and men in the United States, and to conduct a meta-analysis of prospective cohort studies.DesignProspective cohort study, and a systematic review and meta-analysis of prospective cohort studies.SettingNurses' Health Study (NHS, 1980-2012), NHS II (1991-2013), Health Professionals' Follow-Up Study (HPFS, 1986-2012).ParticipantsCohort analyses included 83?349 women from NHS, 90?214 women from NHS II, and 42?055 men from HPFS who were free of cardiovascular disease, type 2 diabetes, and cancer at baseline.Main outcome measuresIncident cardiovascular disease, which included non-fatal myocardial infarction, fatal coronary heart disease, and stroke.ResultsOver up to 32 years of follow-up (>5.54 million person years), 14?806 participants with incident cardiovascular disease were identified in the three cohorts. Participants with a higher egg intake had a higher body mass index, were less likely to be treated with statins, and consumed more red meats. Most people consumed between one and less than five eggs per week. In the pooled multivariable analysis, consumption of at least one egg per day was not associated with incident cardiovascular disease risk after adjustment for updated lifestyle and dietary factors associated with egg intake (hazard ratio for at least one egg per day v less than one egg per month 0.93, 95% confidence interval 0.82 to 1.05). In the updated meta-analysis of prospective cohort studies (33 risk estimates, 1?720?108 participants, 139?195 cardiovascular disease events), an increase of one egg per day was not associated with cardiovascular disease risk (pooled relative risk 0.98, 95% confidence interval 0.93 to 1.03, I2=62.3%). Results were similar for coronary heart disease (21 risk estimates, 1?411?261 participants, 59?713 coronary heart disease events; 0.96, 0.91 to 1.03, I2=38.2%), and stroke (22 risk estimates, 1?059?315 participants, 53?617 stroke events; 0.99, 0.91 to 1.07, I2=71.5%). In analyses stratified by geographical location (P for interaction=0.07), no association was found between egg consumption and cardiovascular disease risk among US cohorts (1.01, 0.96 to 1.06, I2=30.8%) or European cohorts (1.05, 0.92 to 1.19, I2=64.7%), but an inverse association was seen in Asian cohorts (0.92, 0.85 to 0.99, I2=44.8%).ConclusionsResults from the three cohorts and from the updated meta-analysis show that moderate egg consumption (up to one egg per day) is not associated with cardiovascular disease risk overall, and is associated with potentially lower cardiovascular disease risk in Asian populations.Systematic review registrationPROSPERO CRD42019129650.
| S-EPMC7190072 | biostudies-literature
Project description:Background We aim to evaluate the association of within-individual changes in consumption of total and specific types of nuts and the subsequent risk of incident cardiovascular disease (CVD) in US men and women. Methods and Results We included 34 103 men from the HPFS (Health Professionals Follow-Up Study) (1986-2012), 77 815 women from the NHS (Nurses' Health Study) (1986-2012), and 80 737 women from the NHS II (1991-2013). We assessed nut consumption every 4 years using validated food frequency questionnaires. We used multivariable Cox proportional hazards regression models to examine the association between 4-year changes in nut consumption and risk of confirmed CVD end points in the subsequent 4 years. Per 0.5 serving/day increase in total nut consumption was associated with lower risk of CVD (relative risk [RR], 0.92; 95% CI, 0.86-0.98), coronary heart disease (RR, 0.94; 95% CI, 0.89-0.99), and stroke (RR, 0.89; 95% CI, 0.83-0.95). Compared with individuals who remained nonconsumers in a 4-year interval, those who had higher consumption of total nuts (≥0.5 servings/day) had a lower risk of CVD (RR, 0.75; 95% CI, 0.67-0.84), coronary heart disease (RR, 0.80; 95% CI, 0.69-0.93), and stroke (RR, 0.68; 95% CI, 0.57-0.82) in next 4 years. Individuals who decreased nut consumption by ≥0.50 servings/day had a higher risk of developing CVD (RR, 1.14; 95% CI, 0.99-1.32), coronary heart disease (RR, 1.06; 95% CI, 0.88-1.28), and stroke (RR, 1.28; 95% CI, 1.02-1.60) when compared with those who maintained their nut consumption. Conclusions Increasing total consumption of nuts and intake of individual types of nuts (eg, walnuts, other tree nuts, and peanuts) was associated with a subsequent lower risk of CVD. These data support the role of nut intake in the primary prevention of CVD. Registration URL: http://www.clinicaltrials.gov. Unique identifiers: NCT00005152 and NCT00005182.
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