Educational attainment and lifestyle risk factors associated with all-cause mortality in the US

Importance The US has experienced increasing socioeconomic inequalities and stagnating life expectancy. Past studies have not disentangled 2 mechanisms thought to underlie socioeconomic inequalities in health, differential exposure and differential vulnerability, that have different policy implications. Objective To evaluate the extent to which the association between socioeconomic status (SES) and all-cause mortality can be decomposed into a direct effect of SES, indirect effects through lifestyle factors (differential exposure), and joint effects of SES with lifestyle factors (differential vulnerability). Design, Setting, and Participants This nationwide, population-based cohort study used the cross-sectional US National Health Interview Survey linked to the National Death Index. Civilian, noninstitutionalized US adults aged 25 to 84 years were included from the 1997 to 2014 National Health Interview Survey and were followed up until December 31, 2015. Data were analyzed from May 1 to October 31, 2021. A causal mediation model using an additive hazard and marginal structural approach was used. Exposures Both SES (operationalized as educational attainment) and lifestyle risk factors (smoking, alcohol use, obesity, and physical inactivity) were assessed using self-reported questionnaires. Main Outcomes and Measures Time to all-cause mortality. Results Participants included 415 764 adults (mean [SD] age, 49.4 [15.8] years; 55% women; 64% non-Hispanic White), of whom 45% had low educational attainment and 27% had high educational attainment. Participants were followed up for a mean (SD) of 8.8 (5.2) years during which 49 096 deaths (12%) were observed. Low educational attainment (compared with high) was associated with 83.6 (men; 95% CI, 81.8-85.5) and 54.8 (women; 95% CI, 53.4-56.2) additional deaths per 10 000 person-years, of which 66% (men) and 80% (women) were explained by lifestyle factors. Inequalities in mortality were primarily a result of greater exposure and clustering of unhealthy lifestyle factors among low SES groups; with some exceptions among women, little evidence of differential vulnerability was identified. Conclusions and Relevance In this cohort study, differential exposure to lifestyle risk factors was an important mediator of socioeconomic inequalities in mortality. Public health interventions are needed, particularly among low SES groups, to address smoking, physical inactivity, alcohol use, and the socioenvironmental contexts within which these risk factors develop

Reducing alcohol use through alcohol control policies in the general population and population subgroups: a systematic review and meta-analysis.

We estimate the effects of alcohol taxation, minimum unit pricing (MUP), and restricted temporal availability on overall alcohol consumption and review their differential impact across sociodemographic groups. Web of Science, Medline, PsycInfo, Embase, and EconLit were searched on 08/12/2022 and 09/26/2022 for studies on newly introduced or changed alcohol policies published between 2000 and 2022 (Prospero registration: CRD42022339791). We combined data using random-effects meta-analyses. Risk of bias was assessed using the Newcastle-Ottawa Scale. Of 1887 reports, 36 were eligible. Doubling alcohol taxes or introducing MUP (Int$ 0.90/10 g of pure alcohol) reduced consumption by 10% (for taxation: 95% prediction intervals [PI]: -18.5%, -1.2%; for MUP: 95% PI: -28.2%, 5.8%), restricting alcohol sales by one day a week reduced consumption by 3.6% (95% PI: -7.2%, -0.1%). Substantial between-study heterogeneity contributes to high levels of uncertainty and must be considered in interpretation. Pricing policies resulted in greater consumption changes among low-income alcohol users, while results were inconclusive for other socioeconomic indicators, gender, and racial and ethnic groups. Research is needed on the differential impact of alcohol policies, particularly for groups bearing a disproportionate alcohol-attributable health burden. Research reported in this publication was supported by the National Institute on Alcohol Abuse and Alcoholism of the National Institutes of Health under Award Number R01AA028009

Improved estimates for individual and population-level alcohol use in the United States, 1984-2020

Aims: While nationally representative alcohol surveys are a mainstay of public health monitoring, they underestimate consumption at the population level. This paper demonstrates how to adjust individual-level survey data using aggregated alcohol per capita (APC) data for improved individual- and population-level consumption estimates. Design and methods: For the period 1984-2020 data on self-reported alcohol consumption in the past 30 days were taken from the Behavioral Risk Factor Surveillance System (BRFSS) involving participants (18+ years) in the US. Monthly abstainers were re-allocated into lifetime abstainers, former drinkers and 12-month drinkers using the 2005 National Alcohol Survey data. To correct for under-coverage of alcohol use, we triangulated APC and survey data by upshifting quantity (average grams/ day) and frequency (drinking days/week) of alcohol use based on national and state-level alcohol per capita data. Findings The corrections described above resulted in better correspondence between survey and APC data. Following our procedure, national estimates of alcohol quantity increased from 45% to 77% of APC estimates. Both quantity and frequency of alcohol use were upshifted; by upshifting to 90% of APC, we were able to fit trends and distributions in APC patterns for individual states and the US. Conclusions: An individual-level dataset which more accurately reflects the alcohol use of US citizens was achieved. This dataset will be invaluable as a research tool and for the planning and evaluation of alcohol control policies for the US. The methodology described can also be used to adjust individual-level alcohol survey data in other geographical settings

Trends in mortality from alcohol, opioid, and combined alcohol and opioid poisonings by sex, educational attainment, and race and ethnicity for the United States 2000–2019

Background The ongoing opioid epidemic and increases in alcohol-related mortality are key public health concerns in the USA, with well-documented inequalities in the degree to which groups with low and high education are affected. This study aimed to quantify disparities over time between educational and racial and ethnic groups in sex-specific mortality rates for opioid, alcohol, and combined alcohol and opioid poisonings in the USA. Methods The 2000–2019 Multiple Cause of Death Files from the National Vital Statistics System (NVSS) were used alongside population counts from the Current Population Survey 2000–2019. Alcohol, opioid, and combined alcohol and opioid poisonings were assigned using ICD-10 codes. Sex-stratified generalized least square regression models quantified differences between educational and racial and ethnic groups and changes in educational inequalities over time. Results Between 2000 and 2019, there was a 6.4-fold increase in opioid poisoning deaths, a 4.6-fold increase in combined alcohol and opioid poisoning deaths, and a 2.1-fold increase in alcohol poisoning deaths. Educational inequalities were observed for all poisoning outcomes, increasing over time for opioid-only and combined alcohol and opioid mortality. For non-Hispanic White Americans, the largest educational inequalities were observed for opioid poisonings and rates were 7.5 (men) and 7.2 (women) times higher in low compared to high education groups. Combined alcohol and opioid poisonings had larger educational inequalities for non-Hispanic Black men and women (relative to non-Hispanic White), with rates 8.9 (men) and 10.9 (women) times higher in low compared to high education groups. Conclusions For all types of poisoning, our analysis indicates wide and increasing gaps between those with low and high education with the largest inequalities observed for opioid-involved poisonings for non-Hispanic Black and White men and women. This study highlights population sub-groups such as individuals with low education who may be at the highest risk of increasing mortality from combined alcohol and opioid poisonings. Thereby the findings are crucial for the development of targeted public health interventions to reduce poisoning mortality and the socioeconomic inequalities related to it

Can lifestyle factors explain racial and ethnic inequalities in all-cause mortality among US adults?

Background Racial and ethnic inequalities in all-cause mortality exist, and individual-level lifestyle factors have been proposed to contribute to these inequalities. In this study, we evaluate the extent to which the association between race and ethnicity and all-cause mortality can be explained by differences in the exposure and vulnerability to harmful effects of different lifestyle factors. Methods The 1997–2014 cross-sectional, annual US National Health Interview Survey (NHIS) linked to the 2015 National Death Index was used. NHIS reported on race and ethnicity (non-Hispanic White, non-Hispanic Black, and Hispanic/Latinx), lifestyle factors (alcohol use, smoking, body mass index, physical activity), and covariates (sex, age, education, marital status, survey year). Causal mediation using an additive hazard and marginal structural approach was used. Results 465,073 adults (18–85 years) were followed 8.9 years (SD: 5.3); 49,804 deaths were observed. Relative to White adults, Black adults experienced 21.7 (men; 95%CI: 19.9, 23.5) and 11.5 (women; 95%CI: 10.1, 12.9) additional deaths per 10,000 person-years whereas Hispanic/Latinx women experienced 9.3 (95%CI: 8.1, 10.5) fewer deaths per 10,000 person-years; no statistically significant differences were identified between White and Hispanic/Latinx men. Notably, these differences in mortality were partially explained by both differential exposure and differential vulnerability to the lifestyle factors among Black women, while different effects of individual lifestyle factors canceled each other out among Black men and Hispanic/Latinx women. Conclusions Lifestyle factors provide some explanation for racial and ethnic inequalities in all-cause mortality. Greater attention to structural, life course, healthcare, and other factors is needed to understand determinants of inequalities in mortality and to advance health equity

Simulation of alcohol control policies for health equity (SIMAH) project: study design and first results

Since about 2010, life expectancy at birth in the United States has stagnated and begun to decline, with concurrent increases in the socioeconomic divide in life expectancy. The Simulation of Alcohol Control Policies for Health Equity (SIMAH) Project uses a novel microsimulation approach to investigate the extent to which alcohol use, socioeconomic status (SES), and race/ethnicity contribute to unequal developments in US life expectancy and how alcohol control interventions could reduce such inequalities. Representative, secondary data from several sources will be integrated into one coherent, dynamic microsimulation to model life-course changes in SES and alcohol use and cause-specific mortality attributable to alcohol use by SES, race/ethnicity, age, and sex. Markov models will be used to inform transition intensities between levels of SES and drinking patterns. The model will be used to compare a baseline scenario with multiple counterfactual intervention scenarios. The preliminary results indicate that the crucial microsimulation component provides a good fit to observed demographic changes in the population, providing a robust baseline model for further simulation work. By demonstrating the feasibility of this novel approach, the SIMAH Project promises to offer superior integration of relevant empirical evidence to inform public health policy for a more equitable future

Sex-specific association between alcohol consumption and liver cirrhosis: an updated systematic review and meta-analysis

Different studies have shown that females develop liver diseases at lower levels of alcohol consumption than males. Our aim was to quantify the dose-response relationship between alcohol consumption and the risk of liver cirrhosis by sex and identify the differences between females and males. A systematic review was conducted using PubMed/Medline and Embase to identify longitudinal and case-control studies that analyzed the relationship between the level of alcohol use and liver cirrhosis (LC) incidence, and mortality (ICD-8 and ICD-9 codes 571 and ICD-10 codes K70, K73, K74). Pooled relative risks (RR) were calculated by random effects models. Restricted cubic splines were used to model the dose-response relationship. A total of 24 studies were included in the analysis. There were collectively 2,112,476 females and 924,853 males, and a total of 4,301 and 4,231 cases of LC for females and males, respectively. We identified a non-linear dose-response relationship. Females showed a higher risk for LC compared to males with the same amount of alcohol consumed daily. For instance, drinking 40 g/day showed RRs of 9.35 (95% CI 7.64-11.45) in females and 2.82 (95% CI 2.53-3.14) in males, while drinking 80 g/day presented RRs of 23.32 (95% CI 18.24-29.82) in females and 7.93 (95% CI 7.12-8.83) in males. Additional analyses showed that a higher risk for females was found for morbidity and for mortality. Understanding the influence of sex on the association of alcohol consumption and the risk of LC is needed to develop recommendations and clinical guidelines for prevention and treatment

Beyond the 'Grid-Lock' in Electricity Interconnectors: The Case of Germany and Poland

The common European electricity market requires both market integration and transmission grid expansion, including trans-border interconnectors. Although the benefits of increased interconnectivity are widely acknowledged, expansion of interconnectors is often very slow. This paper gathers insights on the reasons behind this grid-lock drawing on the study of the German-Polish border. Although two interconnectors already exist, the trade is blocked by unplanned electricity loop flows. A third interconnector has been discussed for years, but saw little progress in spite of declarations of support on both sides. Drawing on the existing literature on the topic of grid expansion we identify four hypotheses for the grid-lock: inadequate financing; diverging interests; governance and administration problems; and different actors' motivations, trust and security perceptions. We evaluate them using the empirical material gathered through document analysis and stakeholder interviews conducted in Germany and Poland. None of the hypotheses on its own can explain the gridlock. However, while financing has not been a major obstacle, divergent interests had an impact on the project delay, administrative and governance problems are a great hindrance on the technical level, while motivations influence interstate political relations and policy shaping. EU support and closer bilateral cooperation provide opportunities to address these challenges

Effect of Hypoxia on Expression of Selected Proteins Involved in Regulation of Apoptotic Activity in Striatum of Newborn Piglets

The levels of selected neuroregulatory proteins that inhibit or promote apoptotic cell death were measured in the striatum of piglets subjected to precisely controlled 1 h hypoxic insult followed by 0, 2 and 4 h recovery and compared to sham operated animals. The anti-apoptotic proteins: there were increases in Survivin at 0 (157%, P = 0.031) and 4 h (171%, P = 0.033), in Bcl-XL at 0 (138%, P = 0.028) and 4 h (143%, P = 0.007), in VEGF at 4 h (185%, P = 0.019) and Hsp27 at 2 h (144%, P = 0.05) and 4 h (143%, P = 0.05). The pro-apoptotic proteins: caspases-1 and 7 increased at 4 h (135%, P = 0.05) and (129%, P = 0.038), respectively. Bim increased after 4 h (115%, P = 0.028), Apoptosis Inducing Factor after 2 h (127%, P = 0.048) and Calpain after 4 h (143% of control, P = 0.04). Hypoxia causes increase in levels of both anti- and pro-apoptotic proteins. Their relative activity determines the outcome in terms of cell damage and neuronal deficit