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Demographers have emphasized the importance of age in explaining the spread of COVID-19 and its impact on mortality. However, the relationship between COVID-19 mortality and age should be contextualized in relation to other causes of death. To compare the age pattern of COVID-19 mortality with other causes of death and across countries, and to use these regularities to impute age-specific death counts in countries with limited data. The COVID-19 mortality doubling time in a Gompertz context was compared with 65 major causes of death using US vital statistics. COVID-19 fatality doubling time was similarly compared across 27 countries and used for estimating death counts by age in Israel as a case in point. First, COVID-19 mortality increases exponentially with age at a Gompertz rate near the median of aging-related causes of death, as well as pneumonia and influenza. Second, COVID-19 mortality levels are 2.8 to 8.2 times higher than pneumonia and influenza across the adult age range. Third, the relationship between both COVID-19 mortality and fatality and age varies considerably across countries. The increase in COVID-19 mortality with age resembles the population rate of aging. Country differences in the age pattern of COVID-19 mortality and fatality may point to differences in underlying population health, standards of clinical care, or data quality.

Life expectancy at birth in the United States will likely surpass 80 years in the coming decade. Yet recent studies suggest that longevity gains are unevenly shared across age and socioeconomic groups. First, mortality in midlife has risen among non-Hispanic whites. Second, low-educated whites have suffered stalls (men) or declines (women) in adult life expectancy, which is significantly lower than among their college-educated counterparts. Estimating the number of life years lost or gained by age and cause of death, broken down by educational attainment, is crucial in identifying vulnerable populations. Using U.S. vital statistics data from 1990 to 2010, this study decomposes the change in life expectancy at age 25 by age and cause of death across educational attainment groups, broken down by race and gender. The findings reveal that mortality in midlife increased for white women (and to a lesser extent men) with 12 or fewer years of schooling, accounting for most of the stalls or declines in adult life expectancy observed in those groups. Among blacks, mortality declined in nearly all age and educational attainment groups. Although an educational gradient was found across multiple causes of death, between 60 and 80 percent of the gap in adult life expectancy was explained by cardiovascular diseases, smoking-related diseases, and external causes of death. Furthermore, the number of life years lost to smoking-related, external, and other causes of death increased among low- and high school-educated whites, explaining recent stalls or declines in longevity. Large segments of the American population-particularly low- and high school-educated whites under age 55-are diverging from their college-educated counterparts and losing additional years of life to smoking-related diseases and external causes of death. If this trend continues, old-age mortality may also increase for these birth cohorts in the coming decades.

In August 2014, the so-called Islamic State of Iraq and Syria (ISIS) attacked the Yazidi religious minority living in the area of Mount Sinjar in Nineveh governorate, Iraq. We conducted a retrospective household survey to estimate the number and demographic profile of Yazidis killed and kidnapped. The survey covered the displaced Yazidi population from Sinjar residing in camps in the Kurdistan Region of Iraq. Fieldwork took place between 4 November and 25 December, 2015. A systematic random sample of 1,300 in-camp households were interviewed about the current household composition and any killings and kidnappings of household members by ISIS. Of the 1,300 interviewed households, 988 were Yazidi from Sinjar. Yazidi households contained 6,572 living residents at the time of the survey; 43 killings and 83 kidnappings of household members were reported. We calculated the probability of being killed and kidnapped by dividing the number of reported killings and kidnappings by the number of sampled Yazidis at risk, adjusting for sampling design. To obtain the overall toll of killings and kidnappings, those probabilities were multiplied by the total Yazidi population living in Sinjar at the time of the ISIS attack, estimated at roughly 400,000 by the United Nations and Kurdish officials. The demographic profile of those killed and kidnapped was examined, distinguishing between children and adults and females and males. We estimated that 2.5% of the Yazidi population was either killed or kidnapped over the course of a few days in August 2014, amounting to 9,900 (95% CI 7,000-13,900) people in total. An estimated 3,100 (95% CI 2,100-4,400) Yazidis were killed, with nearly half of them executed-either shot, beheaded, or burned alive-while the rest died on Mount Sinjar from starvation, dehydration, or injuries during the ISIS siege. The estimated number kidnapped is 6,800 (95% CI 4,200-10,800). Escapees recounted the abuses they had suffered, including forced religious conversion, torture, and sex slavery. Over one-third of those reported kidnapped were still missing at the time of the survey. All Yazidis were targeted regardless of age and sex, but children were disproportionately affected. They were as likely as adults to be executed but constituted 93.0% (95% CI 71.9-98.6) of those who died on Mount Sinjar. Moreover, children only accounted for 18.8% (95% CI 8.4-36.9) of those who managed to escape captivity. A sensitivity analysis suggests that the actual toll of killings and kidnappings may be underestimated in our data because of survival bias. The uncertainty associated with inference from a small sample of in-camp households and the reliance on a rough figure of 400,000 for extrapolation to the total Yazidi population of Sinjar at the time of the ISIS attack are the main limitations of this study. Consistent with other existing evidence, our data provide a clear indication of the severity of the ISIS attack against the Yazidis in terms of both the number and demographic profile of those targeted.

The educational gradient in life expectancy is well documented in the United States and in other low-mortality countries. Highly educated Americans, on average, live longer than their low-educated counterparts, who have recently seen declines in adult life expectancy. However, limiting the discussion on lifespan inequality to mean differences alone overlooks other dimensions of inequality and particularly disparities in lifespan variation. The latter represents a unique form of inequality, with higher variation translating into greater uncertainty in the time of death from an individual standpoint, and higher group heterogeneity from a population perspective. Using data from the National Vital Statistics System from 1990 to 2010, this is the first study to document trends in both life expectancy and S25—the standard deviation of age at death above 25—by educational attainment. Among low-educated whites, adult life expectancy declined by 3.1 years for women and by 0.6 years for men. At the same time, S25 increased by about 1.5 years among high school–educated whites of both genders, becoming an increasingly important component of total lifespan inequality. By contrast, college-educated whites benefited from rising life expectancy and record low variation in age at death, consistent with the shifting mortality scenario. Among blacks, adult life expectancy increased, and S25 plateaued or declined in nearly all educational attainment groups, although blacks generally lagged behind whites of the same gender on both measures. Documenting trends in lifespan variation can therefore improve our understanding of lifespan inequality and point to diverging trajectories in adult mortality across socioeconomic strata.

Exposure to endocrine disruptors is associated with developmental defects. One compound of concern, to which humans are widely exposed, is bisphenol A (BPA). In model organisms, BPA exposure is linked to metabolic disorders, infertility, cancer, and behavior anomalies. Recently, BPA exposure has been linked to DNA methylation changes, indicating that epigenetic mechanisms may be relevant. We investigated effects of exposure on genomic imprinting in the mouse as imprinted genes are regulated by differential DNA methylation and aberrant imprinting disrupts fetal, placental, and postnatal development. Through allele-specific and quantitative real-time PCR analysis, we demonstrated that maternal BPA exposure during late stages of oocyte development and early stages of embryonic development significantly disrupted imprinted gene expression in embryonic day (E) 9.5 and 12.5 embryos and placentas. The affected genes included Snrpn, Ube3a, Igf2, Kcnq1ot1, Cdkn1c, and Ascl2; mutations and aberrant regulation of these genes are associated with imprinting disorders in humans. Furthermore, the majority of affected genes were expressed abnormally in the placenta. DNA methylation studies showed that BPA exposure significantly altered the methylation levels of differentially methylated regions (DMRs) including the Snrpn imprinting control region (ICR) and Igf2 DMR1. Moreover, exposure significantly reduced genome-wide methylation levels in the placenta, but not the embryo. Histological and immunohistochemical examinations revealed that these epigenetic defects were associated with abnormal placental development. In contrast to this early exposure paradigm, exposure outside of the epigenetic reprogramming window did not cause significant imprinting perturbations. Our data suggest that early exposure to common environmental compounds has the potential to disrupt fetal and postnatal health through epigenetic changes in the embryo and abnormal development of the placenta.

Aims/hypothesis Maternal obesity is associated with an increased risk of obesity and impaired glucose homeostasis in offspring. However, it is not known whether a gestational or pre-gestational exposure confers similar risks, and if so, what the underlying mechanisms are. Methods We used reciprocal two-cell embryo transfers between mice fed either a control or high-fat diet (HFD) starting at the time of weaning. Gene expression in placenta was assessed by microarray analyses. Results A pre-gestational exposure to a maternal HFD (HFD/control) impaired fetal and placental growth despite a normal gestational milieu. Expression of imprinted genes and genes regulating vasculogenesis and lipid metabolism was markedly altered in placenta of HFD/control. An exposure to an HFD (control/HFD) only during gestation also resulted in fetal growth restriction and decreased placental weight. Interestingly, only a gestational exposure to an HFD (control/HFD) resulted in obesity and impaired glucose tolerance in adulthood. Conclusions/interpretation An HFD during pregnancy has profound consequences for the offspring later in life. Our data demonstrate that the mechanism underlying this phenomenon is not related to placental dysfunction, intrauterine growth restriction or postnatal weight gain, but rather an inability of the progeny to adapt to the abnormal gestational milieu of an HFD. Thus, the ability to adapt to an adverse intrauterine environment is conferred prior to pregnancy and it is possible that the effects of a maternal HFD may be transmitted to subsequent generations.

Background In accordance with the global trend, over the past decades, countries in the Western Pacific Region (WPR) have also experienced substantial improvement in life expectancy. However, this accomplishment was coupled with the differences between countries. Methods Using the latest data from the Global Burden of Disease study, we explored the underlying reasons for changes in life expectancy among observed WPR countries. Results Compared with observed high-income countries, lower-middle-income countries remain disadvantaged with respect to life expectancy, despite their substantial growth over time. The patterns of contribution varied considerably across countries. From 1990 to 2019, in lower-middle-income countries such as Cambodia and Laos, the gains in life expectancy could be mainly explained by reductions in under-5, 5–24, 25–44 mortality from communicable diseases and maternal-neonatal disorders, as well as reductions in mortality from communicable diseases and cardiovascular diseases at 45–84 years. In high-income countries, declines in middle and old-age mortality from cardiovascular diseases and neoplasms were mainly responsible for their life expectancy gains. After 2019, COVID-19 and related outcomes contributed to different magnitude of declines in life expectancy in lower-middle-income countries and Malaysia. In high-income countries, the impact of the pandemic resulted in a stagnation of life expectancy in Singapore and slight decline in life expectancy in South Korea. Conclusions Despite the efforts from the government and WHO in the WPR, the gaps between lower-middle-income and high-income countries remain substantial and further enlarged because of the COVID-19 pandemic. Long-term reductions in mortality and gains in life expectancy in all observed countries in the Region require the further modification of the profile of the underlying risks.

Maternal obesity during pregnancy increases the risk for offspring obesity, in part through effects on the developing brain. Previous research has shown that perinatal consumption of highly palatable foods by the mother can influence the development of offspring taste preferences and alter gene expression within the central nervous system (CNS) reward system. Opioids stimulate consumption of both fats and carbohydrates, and overconsumption of these energy dense foods increases the risk for obesity. What has remained unclear is whether this risk can be transmitted to the offspring before gestation or if it is wholly the gestational exposure that affects offspring brain development. Utilizing an embryo transfer experimental design, 2-cell embryos were obtained from obese or control dams, and transferred to obese or control gestational carriers. Expression of the mu-opioid receptor (MOR), preproenkephalin (PENK), and the dopamine transporter was evaluated in the hypothalamus and reward circuitry (ventral tegmental area, prefrontal cortex, and nucleus accumbens) in adult and late embryonic brains. Obesity before pregnancy altered expression levels of both MOR and PENK, with males relatively more affected than females. These data are the first to demonstrate that obesity at conception, in addition to during gestation, can program the brain reward system.

Sasson comments on Arun S. Hendi's article Trends in Education-Specific Life Expectancy, Data Quality, and Shifting Education Distributions: A Note on Recent Research (same journal issue).