Disease exposure in infancy affects women's reproductive outcomes and offspring health in southern Sweden 1905-2000.

Ample evidence demonstrates that early-life adversity negatively affects morbidity and survival in late life. We show that disease exposure in infancy also has a continuous impact on reproduction and health across the female life course and even affects early-life health of the next generation. Using Swedish administrative data, obstetric records, and local infant mortality rates as a measure of disease exposure, we follow women's reproductive careers and offspring health 1905-2000, examining a comprehensive set of outcomes. Women exposed to disease in infancy give birth to a lower proportion of boys, consistent with notions that male fetuses are more vulnerable to adverse conditions and are more often miscarried. Sons of exposed mothers are also more likely to be born preterm and have higher birthweight suggesting in utero out-selection. Exposed women have a greater risk of miscarriage and of male stillbirth, but their overall likelihood of giving birth is not affected.

Childhood neighborhoods and cause-specific adult mortality in Sweden 1939-2015.

The socioeconomic health gradient has widened in recent decades. We study how childhood socioeconomic neighborhood conditions influence gender- and cause-specific adult mortality. Using uniquely detailed geocoded longitudinal microdata for a Swedish town (1939-1967), with a follow-up in national registers (1968-2015), we apply Cox proportional hazards models and estimate individual neighborhoods at the address-level. We find that childhood neighborhood social class has a lasting influence on male adult mortality (ages 40-69), even when adjusting for class position, class origin, neighborhood physical attributes and school districts. This impact was particularly pronounced for preventable causes of death, pointing to lifestyle and behavioral factors as important mechanisms.

Increasing number of long-lived ancestors marks a decade of healthspan extension and healthier metabolomics profiles.

Globally, the lifespan of populations increases but the healthspan is lagging behind. Previous research showed that survival into extreme ages (longevity) clusters in families as illustrated by the increasing lifespan of study participants with each additional long-lived family member. Here we investigate whether the healthspan in such families follows a similar quantitative pattern using three-generational data from two databases, LLS (Netherlands), and SEDD (Sweden). We study healthspan in 2143 families containing index persons with 26 follow-up years and two ancestral generations, comprising 17,539 persons. Our results provide strong evidence that an increasing number of long-lived ancestors associates with up to a decade of healthspan extension. Further evidence indicates that members of long-lived families have a delayed onset of medication use, multimorbidity and, in mid-life, healthier metabolomic profiles than their partners. We conclude that both lifespan and healthspan are quantitatively linked to ancestral longevity, making family data invaluable to identify protective mechanisms of multimorbidity.

Short Lives: The Impact of Parental Death on Early-Life Mortality and Height in the Netherlands, 1850-1940.

We investigate how experiencing parental death in infancy, childhood, or adolescence affected individuals' health using two distinct measures: mortality before age 20 and young adult height. Using two complementary indicators of health enables us to gain more insights into processes of selection and the scarring of health. Employing nationally representative data for the Netherlands for the 1850-1940 period, we analyze the survival of roughly 36,000 boys and girls using Cox proportional hazard models, and the stature of more than 4,000 young adult men using linear regression models. Results show that losing a parent-particularly a mother-at an early age (0-1 or 1-5) was related to a strongly increased risk of mortality. We find no evidence that losing a parent at these ages affected stature in young adulthood. For boys, experiencing maternal death between ages five and 12 was strongly associated with a shorter young adult height; however, we did not find evidence for an association between experiencing paternal death and shorter stature. We conclude that stature may not be a particularly good measure of the effects of early-life adversity if the health shock greatly increases mortality, as these effects create potential issues of health selection.

Unequal excess mortality during the Spanish Flu pandemic in the Netherlands.

A century after the Spanish Flu, the COVID-19 pandemic has brought renewed attention to socioeconomic and occupational differences in mortality in the earlier pandemic. The magnitude of these differences and the pathways between occupation and increased mortality remain unclear, however. In this paper, we explore the relation between occupational characteristics and excess mortality among men during the Spanish Flu pandemic in the Netherlands. By creating a new occupational coding for exposure to disease at work, we separate social status and occupational conditions for viral transmission. We use a new data set based on men's death certificates to calculate excess mortality rates by region, age group, and occupational group. Using OLS regression models, we estimate whether social position, regular interaction in the workplace, and working in an enclosed space affected excess mortality among men in the Netherlands in the autumn of 1918. We find some evidence that men with occupations that featured high levels of social contact had higher mortality in this period. Above all, however, we find a strong socioeconomic gradient to excess mortality among men during the Spanish Flu pandemic, even after accounting for exposure in the workplace.

Families in comparison: An individual-level comparison of life-course and family reconstructions between population and vital event registers.

It remains unknown how different types of sources affect the reconstruction of life courses and families in large-scale databases increasingly common in demographic research. Here, we compare family and life-course reconstructions for 495 individuals simultaneously present in two well-known Dutch data sets: LINKS, based on the Zeeland province's full-population vital event registration data (passive registration), and the Historical Sample of the Netherlands (HSN), based on a national sample of birth certificates, with follow-up of individuals in population registers (active registration). We compare indicators of fertility, marriage, mortality, and occupational status, and conclude that reconstructions in the HSN and LINKS reflect each other well: LINKS provides more complete information on siblings and parents, whereas the HSN provides more complete life-course information. We conclude that life-course and family reconstructions based on linked passive registration of individuals constitute a reliable alternative to reconstructions based on active registration, if case selection is carefully considered.

The Long Harm of Childhood: Childhood Exposure to Mortality and Subsequent Risk of Adult Mortality in Utah and The Netherlands.

How do early-life conditions affect adult mortality? Research has yielded mixed evidence about the influence of infant and child mortality in birth cohorts on adult health and mortality. Studies rarely consider the specific role of mortality within the family. We estimated how individuals' exposure to mortality as a child is related to their adult mortality risk between ages 18 and 85 in two historical populations, Utah (USA) 1874-2015 and Zeeland (The Netherlands) 1812-1957. We examined these associations for early community-level exposure to infant and early (before sixth birthday) and late (before eighteenth birthday) childhood mortality as well as exposure during these ages to sibling deaths. We find that that exposure in childhood to community mortality and sibling deaths increases adult mortality rates. Effects of sibling mortality on adult all-cause mortality risk were stronger in Utah, where sibling deaths were less common in relation to Zeeland. Exposure to sibling death due to infection was related to the surviving siblings' risk of adult mortality due to cardiovascular disease (relative risk: 1.06) and metabolic disease (relative risk: 1.42), primarily diabetes mellitus, a result consistent with an inflammatory immune response mechanism. We conclude that early-life conditions and exposure to mortality in early life, especially within families of origin, contribute to adult mortality.

Longevity defined as top 10% survivors and beyond is transmitted as a quantitative genetic trait.

Survival to extreme ages clusters within families. However, identifying genetic loci conferring longevity and low morbidity in such longevous families is challenging. There is debate concerning the survival percentile that best isolates the genetic component in longevity. Here, we use three-generational mortality data from two large datasets, UPDB (US) and LINKS (Netherlands). We study 20,360 unselected families containing index persons, their parents, siblings, spouses, and children, comprising 314,819 individuals. Our analyses provide strong evidence that longevity is transmitted as a quantitative genetic trait among survivors up to the top 10% of their birth cohort. We subsequently show a survival advantage, mounting to 31%, for individuals with top 10% surviving first and second-degree relatives in both databases and across generations, even in the presence of non-longevous parents. To guide future genetic studies, we suggest to base case selection on top 10% survivors of their birth cohort with equally long-lived family members.

Early-life mortality clustering in families: A literature review.

Research on early-life mortality in contemporary and historical populations has shown that infant and child mortality tend to cluster in a limited number of high-mortality families, a phenomenon known as 'mortality clustering'. This paper is the first to review the literature on the role of the family in early-life mortality. Contemporary results, methodological and theoretical shortfalls, recent developments, and opportunities for future research are all discussed in this review. Four methodological approaches are distinguished: those based on sibling deaths, mother heterogeneity, thresholds, and excess deaths in populations. It has become clear from research to date that the death of an older child harms the survival chances of younger children in that family, and that fertility behaviour, earlier stillbirths, remarriages, and socio-economic status all explain mortality clustering to some extent.