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The Impact of Covid-19 on Future Higher-Age Mortality

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Covid-19 has predominantly affected mortality at high ages. It kills by inflaming and clogging the air sacs in the lungs, depriving the body of oxygen-inducing hypoxia-which closes down essential organs, in particular the heart, kidneys and liver, and causes blood clots (which can lead to stroke or pulmonary embolism) and neurological malfunction. Evidence from different countries points to the fact that people who die from Covid-19 are often, but not always, much less healthy than the average for their age group. This is true for England & Wales-the two countries we focus on in this study. The implication is that the years of life lost through early death are less than the average for each age group, with how much less being a source of considerable debate. We argue that many of those who die from coronavirus would have died anyway in the relatively near future due to their existing frailties or co-morbidities. We demonstrate how to capture this link to poorer-than-average health using a model in which individual deaths are 'accelerated' ahead of schedule due to Covid-19. The model structure and its parameterization build on the observation that Covid-19 mortality by age is approximately proportional to all-cause mortality. This, in combination with current predictions of total deaths, results in the important conclusion that, everything else being equal, the impact of Covid-19 on the mortality rates of the surviving population will be very modest. Specifically, the degree of anti-selection is likely to be very small, since the life expectancy of survivors does not increase by a significant amount over pre-pandemic levels. We also analyze the degree to which Covid-19 mortality varies with socio-economic status. Headline statistics suggest that the most deprived groups have been disproportionately affected by Covid-19. However, once we control for regional differences in mortality rates, Covid-19 deaths in both the most and least deprived groups are also proportional to the all-cause mortality of these groups. However, the groups in between have approximately 10-15% lower Covid-19 deaths compared with their all-cause mortality. We argue that useful lessons about the potential pattern of accelerated deaths from Covid-19 can be drawn from examining deaths from respiratory diseases, especially at different age ranges. We also argue that it is possible to draw useful lessons about volatility spikes in Covid-19 deaths from examining past seasonal flu epidemics. However, there is an important difference. Whereas the spikes in seasonal flu increase with age, our finding that Covid-19 death rates are approximately proportional to all-cause mortality suggests that any spike in Covid-19 mortality in percentage terms would be similar across all age ranges. Finally, we discuss some of the indirect consequences for future mortality of the pandemic and the ‘lockdown’ measures governments have imposed to contain it. For example, there is evidence that some surviving patients at all ages who needed intensive care could end up with a new impairment, such as organ damage, which will reduce their life expectancy. There is also evidence that many people in lockdown did not seek a timely medical assessment for a potential new illness, such as cancer, or deferred seeking treatment for an existing serious illness, with the consequence that non-Covid-19-related mortality rates could increase in future. Self-isolation during lockdown has contributed to an increase in alcohol and drug consumption by some people which might, in turn, reduce their life expectancy. If another consequence of the pandemic is a recession and/or an acceleration in job automation, resulting in long-term unemployment, then this could lead to so-called ‘deaths of despair’ in future. Other people, by contrast, might permanently change their social behaviour or seek treatments that delay the impact or onset of age-related diseases, one of the primary factors that make people more susceptible to the virus – both of which could have the effect of increasing their life expectancy. It is, however, too early to quantify these possibilities, although it is conceivable that these indirect consequences could have a bigger impact on future average life expectancy than the direct consequences measured by the accelerated deaths model.
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Although the respiratory and immune systems are the major targets of Coronavirus Disease 2019 (COVID-19), acute kidney injury and proteinuria have also been observed. Currently, detailed pathologic examination of kidney damage in critically ill patients with COVID-19 has been lacking. To help define this we analyzed kidney abnormalities in 26 autopsies of patients with COVID-19 by light microscopy, ultrastructural observation and immunostaining. Patients were on average 69 years (19 male and 7 female) with respiratory failure associated with multiple organ dysfunction syndrome as the cause of death. Nine of the 26 showed clinical signs of kidney injury that included increased serum creatinine and/or new-onset proteinuria. By light microscopy, diffuse proximal tubule injury with the loss of brush border, non-isometric vacuolar degeneration, and even frank necrosis was observed. Occasional hemosiderin granules and pigmented casts were identified. There were prominent erythrocyte aggregates obstructing the lumen of capillaries without platelet or fibrinoid material. Evidence of vasculitis, interstitial inflammation or hemorrhage was absent. Electron microscopic examination showed clusters of coronavirus particles with distinctive spikes in the tubular epithelium and podocytes. Furthermore, the receptor of SARS-CoV-2, ACE2 was found to be upregulated in patients with COVID-19, and immunostaining with SARS-CoV nucleoprotein antibody was positive in tubules. In addition to the direct virulence of SARS-CoV-2, factors contributing to acute kidney injury included systemic hypoxia, abnormal coagulation, and possible drug or hyperventilation-relevant rhabdomyolysis. Thus, our studies provide direct evidence of the invasion of SARSCoV-2 into kidney tissue. These findings will greatly add to the current understanding of SARS-CoV-2 infection.
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Background: During the 2007-11 recessions in Europe, suicide increases were concentrated in men. Substantial differences across countries and over time remain unexplained. We investigated whether increases in unaffordable housing, household indebtedness or job loss can account for these population differences, as well as potential mitigating effects of alternative forms of social protection. Methods: Multivariate statistical models were used to evaluate changes in suicide rates in 20 EU countries from 1981-2011. Models adjusted for pre-existing time trends and country-fixed effects. Interaction terms were used to evaluate modifying effects. Results: Changes in levels of unaffordable housing had no effect on suicide rates (P = 0.32); in contrast, male suicide increases were significantly associated with each percentage point rise in male unemployment, by 0.94% (95% CI: 0.51-1.36%), and indebtedness, by 0.54% (95% CI: 0.02-1.06%). Spending on active labour market programmes (ALMP) (-0.26%, 95% CI: -0.08 to -0.45%) and high levels of social capital (-0.048%, 95% CI: -0.0096 to -0.087) moderated the unemployment-suicide association. There was no interaction of the volume of anti-depressant prescriptions (P = 0.51), monetary benefits to unemployed persons (P = 0.77) or total social protection spending per capita (P = 0.37). Active labour market programmes and social capital were estimated to have prevented ∼ 540 and ∼ 210 male suicides, respectively, arising from unemployment in the countries studied. Conclusion: Job losses were a critical determinant of variations in male suicide risks in Europe's recessions. Greater spending on ALMP and levels of social capital appeared to mitigate suicide risks.
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Suicide mortality is high among the unemployed, but the role of causation and selection models in producing employment status differences remains to be understood. This study analyses the association between unemployment and suicide during different levels of national unemployment adjusting for several factors that might explain or mediate the relationship. The data comprised annual population-register and death-register information on 25-64-year-old Finns at the beginning of each year in the period 1988-2003; thus, forming 16 separate follow-up cohorts. Experience of unemployment was measured at baseline and during the previous year for each cohort. Suicide was followed for 12 months after each baseline giving a total of 7388 suicides. Overall, age-adjusted suicide mortality was two to three times higher among the unstably employed and almost fourfold among the long-term unemployed. Adjustment for social class and living arrangements had small effect on the HRs, but adjustment for household income per consumption unit decreased the differences by 13% and 31% among the long-term unemployed women and men, respectively. When the national unemployment level was high, excess suicide mortality among the unstably employed was lower than during low unemployment when those becoming unemployed might be more selected. No such differences were found among the long-term unemployed. Long-term unemployment seems to have causal effects on suicide, which may be partly mediated by low income. As the effect of unstable employment is lower during the recessionary stage of the economic cycle some part of the excess suicide among the unstably employed is likely to be attributable to selection into unemployment.
The U.S. labor force participation rate has declined since 2007, primarily because of population aging and ongoing trends that preceded the Great Recession. The labor force participation rate has evolved differently, and for different reasons, across demographic groups. A rise in school enrollment has largely offset declining labor force participation for young workers since the 1990s. Labor force participation has been declining for prime age men for decades, and about half of prime age men who are not in the labor force may have a serious health condition that is a barrier to working. Nearly half of prime age men who are not in the labor force take pain medication on any given day; and in nearly two-thirds of these cases, they take prescription pain medication. Labor force participation has fallen more in U.S. counties where relatively more opioid pain medication is prescribed, causing the problem of depressed labor force participation and the opioid crisis to become intertwined. The labor force participation rate has stopped rising for cohorts of women born after 1960. Prime age men who are out of the labor force report that they experience notably low levels of emotional well-being throughout their days, and that they derive relatively little meaning from their daily activities. Employed women and women not in the labor force, by contrast, report similar levels of subjective well-being; but women not in the labor force who cite a reason other than “home responsibilities” as their main reason report notably low levels of emotional well-being. During the past decade, retirements have increased by about the same amount as aggregate labor force participation has declined, and the retirement rate is expected to continue to rise. A meaningful rise in labor force participation will require a reversal in the secular trends affecting various demographic groups, and perhaps immigration reform.
Building on our earlier research (Case and Deaton 2015), we find that mortality and morbidity among white non-Hispanic Americans in midlife since the turn of the century continued to climb through 2015. Additional increases in drug overdoses, suicides, and alcohol-related liver mortality- particularly among those with a high school degree or less-are responsible for an overall increase in all-cause mortality among whites. We find marked differences in mortality by race and education, with mortality among white non- Hispanics (males and females) rising for those without a college degree, and falling for those with a college degree. In contrast, mortality rates among blacks and Hispanics have continued to fall, irrespective of educational attainment. Mortality rates in comparably rich countries have continued their premillennial fall at the rates that used to characterize the United States. Contemporaneous levels of resources-particularly slowly growing, stagnant, and even declining incomes-cannot provide a comprehensive explanation for poor mortality outcomes. We propose a preliminary but plausible story in which cumulative disadvantage from one birth cohort to the next-in the labor market, in marriage and child outcomes, and in health-is triggered by progressively worsening labor market opportunities at the time of entry for whites with low levels of education. This account, which fits much of the data, has the profoundly negative implication that policies-even ones that successfully improve earnings and jobs, or redistribute income-will take many years to reverse the increase in mortality and morbidity, and that those in midlife now are likely to do worse in old age than the current elderly. This is in contrast to accounts in which resources affect health contemporaneously, so that those in midlife now can expect to do better in old age as they receive Social Security and Medicare. None of this, however, implies that there are no policy levers to be pulled. For instance, reducing the overprescription of opioids should be an obvious target for policymakers.
Significance Midlife increases in suicides and drug poisonings have been previously noted. However, that these upward trends were persistent and large enough to drive up all-cause midlife mortality has, to our knowledge, been overlooked. If the white mortality rate for ages 45−54 had held at their 1998 value, 96,000 deaths would have been avoided from 1999–2013, 7,000 in 2013 alone. If it had continued to decline at its previous (1979‒1998) rate, half a million deaths would have been avoided in the period 1999‒2013, comparable to lives lost in the US AIDS epidemic through mid-2015. Concurrent declines in self-reported health, mental health, and ability to work, increased reports of pain, and deteriorating measures of liver function all point to increasing midlife distress.
There is widespread concern that the present economic crisis, particularly its effect on unemployment, will adversely affect population health. We investigated how economic changes have affected mortality rates over the past three decades and identified how governments might reduce adverse effects. We used multivariate regression, correcting for population ageing, past mortality and employment trends, and country-specific differences in health-care infrastructure, to examine associations between changes in employment and mortality, and how associations were modified by different types of government expenditure for 26 European Union (EU) countries between 1970 and 2007. We noted that every 1% increase in unemployment was associated with a 0.79% rise in suicides at ages younger than 65 years (95% CI 0.16-1.42; 60-550 potential excess deaths [mean 310] EU-wide), although the effect size was non-significant at all ages (0.49%, -0.04 to 1.02), and with a 0.79% rise in homicides (95% CI 0.06-1.52; 3-80 potential excess deaths [mean 40] EU-wide). By contrast, road-traffic deaths decreased by 1.39% (0.64-2.14; 290-980 potential fewer deaths [mean 630] EU-wide). A more than 3% increase in unemployment had a greater effect on suicides at ages younger than 65 years (4.45%, 95% CI 0.65-8.24; 250-3220 potential excess deaths [mean 1740] EU-wide) and deaths from alcohol abuse (28.0%, 12.30-43.70; 1550-5490 potential excess deaths [mean 3500] EU-wide). We noted no consistent evidence across the EU that all-cause mortality rates increased when unemployment rose, although populations varied substantially in how sensitive mortality was to economic crises, depending partly on differences in social protection. Every US$10 per person increased investment in active labour market programmes reduced the effect of unemployment on suicides by 0.038% (95% CI -0.004 to -0.071). Rises in unemployment are associated with significant short-term increases in premature deaths from intentional violence, while reducing traffic fatalities. Active labour market programmes that keep and reintegrate workers in jobs could mitigate some adverse health effects of economic downturns. Centre for Crime and Justice Studies, King's College, London, UK; and Wates Foundation (UK).
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