Explore the vast range of titles available.

Background Individuals with low socioeconomic status (SES) experience a higher risk of mortality, in general, and alcohol-attributable mortality in particular. However, a knowledge gap exists concerning the dose-response relationships between the level of socioeconomic deprivation and the alcohol-attributable mortality risk. Methods We conducted a systematic literature search in August of 2020 to update a previous systematic review that included studies published up until February of 2013. Quantitative studies reporting on socioeconomic inequality in alcohol-attributable mortality among the general adult population were included. We used random-effects dose-response meta-analyses to investigate the relationship between the level of socioeconomic deprivation and the relative alcohol-attributable risk (RR), by sex and indicator of SES (education, income, and occupation). Results We identified 25 eligible studies, comprising about 241 million women and 230 million men, among whom there were about 75,200 and 308,400 alcohol-attributable deaths, respectively. A dose-response relationship between the level of socioeconomic deprivation and the RR was found for all indicators of SES. The sharpest and non-linear increase in the RR of dying from an alcohol-attributable cause of death with increasing levels of socioeconomic deprivation was observed for education, where, compared to the most educated individuals, individuals at percentiles with decreasing education had the following RR of dying: women: 25th: 2.09 [95% CI 1.70–2.59], 50th: 3.43 [2.67–4.49], 75th: 4.43 [3.62–5.50], 100th: 4.50 [3.26–6.40]; men: 25th: 2.34 [1.98–2.76], 50th: 4.22 [3.38–5.24], 75th: 5.87 [4.75–7.10], 100th: 6.28 [4.89–8.07]. Conclusions The findings of this study show that individuals along the entire continuum of SES are exposed to increased alcohol-attributable mortality risk. Differences in the dose-response relationship can guide priorities in targeting public health initiatives.

Bird bills possess an important thermoregulatory function as they are a site for environmental heat exchange. Previous studies have demonstrated that birds in warmer climates have larger bills than those living in colder climates, as larger bills can dissipate more heat. Because this dry heat transfer does not incur water loss, it may be additionally advantageous in water‐restricted habitats. Here, we examine the influence of climate on bill morphology in Toxostoma thrashers, a group of 10 North American species that varied in bill morphology and occupied climate niche, with several species inhabiting arid climates. Past examinations of thrasher bill morphology have only considered foraging, leaving unanswered the role of climate in morphological divergence within this group. We photographed 476 Toxostoma museum specimens encompassing all 10 species and calculated bill measurements from the photos using a MATLAB‐based program. For each species, we calculated occupied climate niche using data from WorldClim describing temperature and precipitation. We found no reliable significant relationships between climate variables and bill morphology across species, suggesting that other factors such as foraging behavior may be more important in shaping bill morphology in this genus. Within species, we found three Toxostoma species have significant relationships between bill morphology and climate that follow Allen's rule. However, we also found the relationships between climate and bill morphology varied in strength and direction across species. Notably, we found a negative relationship between maximum temperature of the hottest month and bill surface area in LeConte's thrasher, which occupies the hottest and most arid climates of the thrashers. This adds to the evidence that Allen's rule may reverse in extremely hot climates when the bill may become a heat sink instead of a heat radiator. These results demonstrate the importance of considering the generality of ecogeographical rules across lineages that occupy extreme climates.

Probst and Rehm examine the core drivers of the development in life expectancy in Canada. In Canada, alcohol and drug use were identified as the most important risk factors among younger adults, accounting for less than 20% in 1990 and 25% of the total deaths in 2016, respectively. \"Deaths of despair\" are also prevalent in Canada. Deaths from opioid overdoses have risen to record levels for each of the past few years; current estimates suggest close to or more than 4000 such deaths for 2017.7 Deaths and hospital admissions attributable to alcohol have also increased markedly, paralleling the increases in the US. However, Canada's mortality rates are still substantially lower for both opioid-related deaths and for the most important alcohol-attributable death, alcoholic liver cirrhosis. Furthermore, while suicide rates have decreased in Canada since 2000, there has been a steady increase in suicide deaths in the US.

Ischemic heart disease (IHD) is a major cause of death in the United States (US), with marked mortality inequalities. Previous studies have reported inconsistent findings regarding the contributions of behavioral risk factors (BRFs) to socioeconomic inequalities in IHD mortality. To our knowledge, no nationwide study has been conducted on this topic in the US. In this cohort study, we obtained data from the 1997 to 2018 National Health Interview Survey with mortality follow-up until December 31, 2019 from the National Death Index. A total of 524,035 people aged 25 years and older were followed up for 10.3 years on average (SD: 6.1 years), during which 13,256 IHD deaths occurred. Counterfactual-based causal mediation analyses with Cox proportional hazards models were performed to quantify the contributions of 4 BRFs (smoking, alcohol use, physical inactivity, and BMI) to socioeconomic inequalities in IHD mortality. Education was used as the primary indicator for socioeconomic status (SES). Analyses were performed stratified by sex and adjusted for marital status, race and ethnicity, and survey year. In both males and females, clear socioeconomic gradients in IHD mortality were observed, with low- and middle-education people bearing statistically significantly higher risks compared to high-education people. We found statistically significant natural direct effects of SES (HR = 1.16, 95% CI: 1.06, 1.27 in males; HR = 1.28, 95% CI: 1.10, 1.49 in females) on IHD mortality and natural indirect effects through the causal pathways of smoking (HR = 1.18, 95% CI: 1.15, 1.20 in males; HR = 1.11, 95% CI: 1.08, 1.13 in females), physical inactivity (HR = 1.16, 95% CI: 1.14, 1.19 in males; HR = 1.18, 95% CI: 1.15, 1.20 in females), alcohol use (HR = 1.07, 95% CI: 1.06, 1.09 in males; HR = 1.09, 95% CI: 1.08, 1.11 in females), and BMI (HR = 1.03, 95% CI: 1.02, 1.04 in males; HR = 1.03, 95% CI: 1.02, 1.04 in females). Smoking, physical inactivity, alcohol use, and BMI mediated 29% (95% CI, 24%, 35%), 27% (95% CI, 22%, 33%), 12% (95% CI, 10%, 16%), and 5% (95% CI, 4%, 7%) of the inequalities in IHD mortality between low- and high-education males, respectively; the corresponding proportions mediated were 16% (95% CI, 11%, 23%), 26% (95% CI, 20%, 34%), 14% (95% CI, 11%, 19%), and 5% (95% CI, 3%, 7%) in females. Proportions mediated were slightly lower with family income used as the secondary indicator for SES. The main limitation of the methodology is that we could not rule out residual exposure-mediator, exposure-outcome, and mediator-outcome confounding. In this study, BRFs explained more than half of the educational differences in IHD mortality, with some variations by sex. Public health interventions to reduce intermediate risk factors are crucial to reduce the socioeconomic disparities and burden of IHD mortality in the general US population.

Objectives(1) A comprehensive mortality assessment of alcoholic cardiomyopathy (ACM) and (2) examination of under-reporting using vital statistics data.MethodsA modelling study estimated sex-specific mortality rates for each country, which were subsequently aggregated by region and globally. Input data on ACM mortality were obtained from death registries for n=91 countries. For n=99 countries, mortality estimates were predicted using aggregate alcohol data from WHO publications. Descriptive additional analyses illustrated the scope of under-reporting.ResultsIn 2015, there were an estimated 25 997 (95% CI 17 385 to 49 096) global deaths from ACM. This translates into 6.3% (95% CI 4.2% to 11.9%) of all global deaths from cardiomyopathy being caused by alcohol. There were large regional variations with regard to mortality burden. While the majority of ACM deaths were found in Russia (19 749 deaths, 76.0% of all ACM deaths), for about one-third of countries (n=57) less than one ACM death was found. Under-reporting was identified for nearly every second country with civil registration data. Overall, two out of three global ACM deaths might be misclassified.ConclusionsThe variation of ACM mortality burden is greater than for other alcohol-attributable diseases, and partly may be the result of stigma and lack of detection. Misclassification of ACM fatalities is a systematic phenomenon, which may be caused by low resources, lacking standards and stigma associated with alcohol-use disorders. Clinical management may be improved by including routine alcohol assessments. This could contribute to decrease misclassifications and to provide the best available treatment for affected patients.

In a Perspective, Jürgen Rehm and Charlotte Probst examine the links between socioeconomic status, alcohol use, and cardiovascular mortality and discuss implications for policy.In a Perspective, Jürgen Rehm and Charlotte Probst examine the links between socioeconomic status, alcohol use, and cardiovascular mortality and discuss implications for policy.

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.

Background Alcohol consumption is the most important risk factor responsible for the disease burden of liver cirrhosis (LC). Estimates of risk relationships available usually neither distinguish between different causes such as alcohol-related LC or hepatitis-related LC, nor differentiate between morbidity and mortality as outcome. We aimed to address this research gap and identify dose–response relationships between alcohol consumption and LC, by cause and outcome. Methods A systematic review using PubMed/Medline and Embase was conducted, identifying studies that reported an association between level of alcohol use and LC. Meta-regression models were used to estimate the dose–response relationships and control for heterogeneity. Results Totally, 44 studies, and 1 secondary data source, with a total of 5,122,534 participants and 15,150 cases were included. Non-linear dose–response relationships were identified, attenuated for higher levels of consumption. For morbidity, drinking 25 g/day was associated with a RR of 1.81 (95% CI 1.68–1.94) compared to lifetime abstention; 50 g/day and 100 g/day corresponded to 3.54 (95% CI 3.29–3.81) and 8.15 (95% CI 7.46–8.91), respectively. For mortality, for 25 g/day, a RR of 2.65 (95% CI 2.22–3.16); for 50 g/day, a RR of 6.83 (95% CI 5.84–7.97); for 100 g/day, a RR of 16.38 (95% CI 13.81–19.42) were identified. A higher risk for alcohol-related and all-cause LC as compared to hepatitis C-related LC was found. Conclusion Our results demonstrated higher acceleration for mortality compared to morbidity. The current findings will inform the way we quantify the burden due to LC attributable to alcohol use. Graphical abstract

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.

Background As several regulatory and environmental changes have occurred in North America, trends in overdose deaths were examined in the United States (US), Ontario and British Columbia (BC), including changes in consumption levels of prescription opioids (PO) and overdose deaths, changes in correlations between consumption levels of PO and overdose deaths and modeled differences between observed and predicted overdose deaths if no changes had occurred. Methods Consumption levels of PO included defined daily doses for statistical purposes per million inhabitants per day for the US and Canada (2001–2015). Overdose deaths included opioid overdose deaths for the US (2001–2017) and Ontario (2003–2017) and illicit drug overdose deaths for BC (2001–2017). The analytic techniques included structural break point analyses, Pearson product-moment correlations and multivariate Gaussian state space modeling. Results Consumption levels of PO changed in the US in 2010 and in Canada in 2012. Overdose deaths changed in the US in 2014 and in Ontario and BC in 2015. Prior to the observed changes in consumption levels of PO, there were positive correlations between consumption levels of PO and overdose deaths in the US ( r  = 0.99, p  < 0.001) and Ontario ( r  = 0.92, p  = 0.003). After the observed changes in consumption levels of PO, there was a negative correlation between consumption levels of PO and overdose deaths in the US ( r  = − 0.99, p  = 0.002). Observed overdose deaths exceeded predicted overdose deaths by 5.7 (95% Confidence Interval [CI]: 4.8–6.6), 3.5 (95% CI: 3.2–3.8) and 21.8 (95% CI: 18.6–24.9) deaths per 100,000 people in the US, Ontario and BC, respectively in 2017. These excess deaths corresponded to 37.7% (95% CI: 31.9–43.6), 39.2% (95% CI: 36.3–42.1) and 72.2% (95% CI: 61.8–82.6) of observed overdose deaths in the US, Ontario and BC, respectively in 2017. Conclusions The opioid crisis has evolved in North America, as a sizeable proportion of overdose deaths are now attributable to the several regulatory and environmental changes. These findings necessitate substance use policies to be conceptualized more broadly as well as the continued expansion of harm reduction services and types of pharmacotherapy interventions.