Dataset Information

Lifetime employment, tobacco use, and alcohol consumption trajectories and cardiovascular diseases in old age.

ABSTRACT: Despite the great advances of life course epidemiology studies during the last decade in understanding the general health effects of employment trajectories, research has yet to evaluate the effects of employment trajectories along with other major risk factors, such as tobacco and alcohol consumption, on cardiovascular diseases (CVDs)-the main cause of deaths worldwide. This is highly relevant, since health advantages in one domain (e.g., being a permanent formal full-time worker) may offset health disadvantages in other domains (e.g., being a regular smoker or alcohol consumer); conversely, disadvantages in both domains may interact, leading to even greater health risks. Considering these knowledge gaps, this research has two main objectives: (1) to reconstruct simultaneous employment, tobacco use, and alcohol consumption trajectories over the life course (from birth to old age) and (2) to measure the association between these trajectories and CVD in old age. Drawing on a rich and comprehensive life history dataset and using multichannel sequence and regression analyses, we analyzed a cohort of individuals aged 65-75 in Chile, a Latin American country with high social inequalities and scarce research on this matter. Our study shows that following a trajectory of formal employment together with no tobacco and alcohol use reduces CVD risk by 36 percentage points relative to a similar employment trajectory but with regular tobacco and alcohol use. Even with an employment trajectory characterized by constant informal employment or permanent inactivity, a life course free of regular tobacco and alcohol use shows protective effects against CVD. This study stresses the importance of health policies that consider CVD as a condition that strongly depends on individual experiences in multiple life domains and across different life stages.

SUBMITTER: Madero-Cabib I

PROVIDER: S-EPMC7848642 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature

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Lifetime employment, tobacco use, and alcohol consumption trajectories and cardiovascular diseases in old age.

Madero-Cabib Ignacio I Azar Ariel A Bambs Claudia C

SSM - population health 20210125

Despite the great advances of life course epidemiology studies during the last decade in understanding the general health effects of employment trajectories, research has yet to evaluate the effects of employment trajectories along with other major risk factors, such as tobacco and alcohol consumption, on cardiovascular diseases (CVDs)-the main cause of deaths worldwide. This is highly relevant, since health advantages in one domain (e.g., being a permanent formal full-time worker) may offset he ...[more]

PMID: 33553569

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Project description:BackgroundAlcohol consumption and smoking, 2 major risk factors for cardiovascular disease (CVD), often occur together. The objective of this study is to use a wide range of CVD risk factors and outcomes to evaluate potential total and direct causal roles of alcohol and tobacco use on CVD risk factors and events.Methods and findingsUsing large publicly available genome-wide association studies (GWASs) (results from more than 1.2 million combined study participants) of predominantly European ancestry, we conducted 2-sample single-variable Mendelian randomization (SVMR) and multivariable Mendelian randomization (MVMR) to simultaneously assess the independent impact of alcohol consumption and smoking on a wide range of CVD risk factors and outcomes. Multiple sensitivity analyses, including complementary Mendelian randomization (MR) methods, and secondary alcohol consumption and smoking datasets were used. SVMR showed genetic predisposition for alcohol consumption to be associated with CVD risk factors, including high-density lipoprotein cholesterol (HDL-C) (beta 0.40, 95% confidence interval (CI), 0.04-0.47, P value = 1.72 × 10-28), triglycerides (TRG) (beta -0.23, 95% CI, -0.30, -0.15, P value = 4.69 × 10-10), automated systolic blood pressure (BP) measurement (beta 0.11, 95% CI, 0.03-0.18, P value = 4.72 × 10-3), and automated diastolic BP measurement (beta 0.09, 95% CI, 0.03-0.16, P value = 5.24 × 10-3). Conversely, genetically predicted smoking was associated with increased TRG (beta 0.097, 95% CI, 0.014-0.027, P value = 6.59 × 10-12). Alcohol consumption was also associated with increased myocardial infarction (MI) and coronary heart disease (CHD) risks (MI odds ratio (OR) = 1.24, 95% CI, 1.03-1.50, P value = 0.02; CHD OR = 1.21, 95% CI, 1.01-1.45, P value = 0.04); however, its impact was attenuated in MVMR adjusting for smoking. Conversely, alcohol maintained an association with coronary atherosclerosis (OR 1.02, 95% CI, 1.01-1.03, P value = 5.56 × 10-4). In comparison, after adjusting for alcohol consumption, smoking retained its association with several CVD outcomes including MI (OR = 1.84, 95% CI, 1.43, 2.37, P value = 2.0 × 10-6), CHD (OR = 1.64, 95% CI, 1.28-2.09, P value = 8.07 × 10-5), heart failure (HF) (OR = 1.61, 95% CI, 1.32-1.95, P value = 1.9 × 10-6), and large artery atherosclerosis (OR = 2.4, 95% CI, 1.41-4.07, P value = 0.003). Notably, using the FinnGen cohort data, we were able to replicate the association between smoking and several CVD outcomes including MI (OR = 1.77, 95% CI, 1.10-2.84, P value = 0.02), HF (OR = 1.67, 95% CI, 1.14-2.46, P value = 0.008), and peripheral artery disease (PAD) (OR = 2.35, 95% CI, 1.38-4.01, P value = 0.002). The main limitations of this study include possible bias from unmeasured confounders, inability of summary-level MR to investigate a potentially nonlinear relationship between alcohol consumption and CVD risk, and the generalizability of the UK Biobank (UKB) to other populations.ConclusionsEvaluating the widest range of CVD risk factors and outcomes of any alcohol consumption or smoking MR study to date, we failed to find a cardioprotective impact of genetically predicted alcohol consumption on CVD outcomes. However, alcohol was associated with and increased HDL-C, decreased TRG, and increased BP, which may indicate pathways through impact CVD risk, warranting further study. We found smoking to be a risk factor for many CVDs even after adjusting for alcohol. While future studies incorporating alcohol consumption patterns are necessary, our data suggest causal inference between alcohol, smoking, and CVD risk, further supporting that lifestyle modifications might be able to reduce overall CVD risk.

Project description:Background and aimsAlcohol consumption changes markedly over the life course, with important implications for health and social development. Assessment of these patterns often relies on cross-sectional data, which cannot fully capture how individuals' drinking changes as they age. This study used data from 18 waves of a general population panel survey to measure drinking trajectories over the life course in Australia.Design and settingLongitudinal survey data from the Household, Income and Labour Dynamics in Australia (HILDA) survey between 2001 and 2018.ParticipantsA total of 20 593 individuals ages 15 or above in two samples assessing quantity-frequency (n = 20 569, 52.0% female) and risky single occasion drinking (RSOD), respectively, (n = 17 340, 52.5% female), interviewed as part of HILDA.MeasurementsUsual quantity of alcohol consumed per drinking occasion; frequency of drinking occasions per week; average daily consumption, calculated by combining reported usual quantity and frequency; and average reported frequency of RSOD per week.FindingsMultilevel, mixed effects models run with fractional polynomial terms found similar male and female alcohol consumption trajectories for quantity-frequency and RSOD measures. Usual quantity of alcohol consumed per drinking occasion (5.4 drinks for men, 3.8 for women) and RSOD frequency (0.56 occasions/week for men, 0.38 for women) peaked in young adulthood, whereas frequency of drinking occasions (2.5 occasions/week for men, 1.7 for women) peaked in middle age. Middle-age drinkers had the highest average daily consumption of alcohol (1.4 drinks/day for 54-year-old men, 0.6 drinks for 57-year-old women) and engaged in RSOD slightly less than young adults.ConclusionsAlcohol consumption in Australia appears to vary substantially over the life course, with usual quantity per drinking occasion and frequency of risky single occasion drinking peaking during early adulthood and average daily consumption and frequency of consumption peaking in middle age.

Project description:OBJECTIVE: First, to investigate and compare associations between alcohol consumption and variants in alcohol dehydrogenase (ADH) genes with incidence of cardiovascular diseases (CVD) in a large German cohort. Second, to quantitatively summarize available evidence of prospective studies on polymorphisms in ADH1B and ADH1C and CVD-risk. METHODS: We conducted a case-cohort study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam cohort including a randomly drawn subcohort (n?=?2175) and incident cases of myocardial infarction (MI; n?=?230) or stroke (n?=?208). Mean follow-up time was 8.2±2.2 years. The association between alcohol consumption, ADH1B or ADH1C genotypes, and CVD-risk was assessed using Cox proportional hazards regression. Additionally, we report results on associations of variants in ADH1B and ADH1C with ischemic heart disease and stroke in the context of a meta-analysis of previously published prospective studies published up to November 2011. RESULTS: Compared to individuals who drank >0 to 6 g alcohol/d, we observed a reduced risk of MI among females consuming >12 g alcohol/d (HR?=?0.31; 95% CI: 0.10-0.97) and among males consuming >24 to 60 g/d (HR?=?0.57; 95% CI: 0.33-0.98) or >60 g alcohol/d (HR?=?0.30; 95% CI: 0.12-0.78). Stroke risk was not significantly related to alcohol consumption >6 g/d, but we observed an increased risk of stroke in men reporting no alcohol consumption. Individuals with the slow-coding ADH1B*1/1 genotype reported higher median alcohol consumption. Yet, polymorphisms in ADH1B or ADH1C were not significantly associated with risk of CVD in our data and after pooling results of eligible prospective studies [ADH1B*1/1: RR?=?1.35 (95% CI: 0.98-1.88; p for heterogeneity: 0.364); ADH1C*2/2: RR?=?1.07 (95% CI: 0.90-1.27; p for heterogeneity: 0.098)]. CONCLUSION: The well described association between alcohol consumption and CVD-risk is not reflected by ADH polymorphisms, which modify the rate of ethanol oxidation.

Dataset Information

Lifetime employment, tobacco use, and alcohol consumption trajectories and cardiovascular diseases in old age.

Publications

Lifetime employment, tobacco use, and alcohol consumption trajectories and cardiovascular diseases in old age.

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