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Women who bear twins may possess a robust phenotype compared to non-twinning mothers. We examine mortality patterns for the singleton offspring of mothers of twins compared to the offspring of non-twinning mothers to determine whether they share the hypothesized robust phenotype of their mothers. Using data from the Utah Population Database, we show that both male and female singleton offspring of twinning mothers experience a survival disadvantage prior to age 5, no survival benefit or penalty between ages 5 and 49, and - for males only - a statistically significant survival advantage after age 50. We further examine the survival effects on singletons born before and after a twinset. We observe a survival disadvantage in early life for singleton offspring of twinning mothers born after the twinset for both sexes. In addition, we find a significant survival advantage at older ages in certain categories of male singleton offspring - a likely reflection of mortality selection. The findings suggest that while bearing twins may reflect a robust maternal phenotype, the toll of bearing twins may disadvantage subsequent offspring, especially during infancy.

The timings of historical fertility transitions in different regions are well understood by demographers, but much less is known regarding their specific features and causes. In the study reported in this paper, we used longitudinal micro-level data for five local populations in Europe and North America to analyse the relationship between socio-economic status and fertility during the fertility transition. Using comparable analytical models and class schemes for each population, we examined the changing socio-economic differences in marital fertility and related these to common theories on fertility behaviour. Our results do not provide support for the hypothesis of universally high fertility among the upper classes in pre-transitional society, but do support the idea that the upper classes acted as forerunners by reducing their fertility before other groups. Farmers and unskilled workers were the latest to start limiting their fertility. Apart from these similarities, patterns of class differences in fertility varied significantly between populations.

Only a portion of those individuals exposed to parental death in early life (PDE) develop behavioral health disorders. We utilized demographic pedigree data from the Utah Population Database to test for differential vulnerability to PDE by creating a risk score of familial susceptibility to suicide (FS) at the population level. Using logistic panel regression models, we tested for multiplicative interactions between PDE and FS on the risks of major depressive disorder (MDD) and substance abuse (SA), measured using Medicare claims, after age 65. The final sample included 155,983 individuals (born 1886-1944), yielding 1,431,060 person-years at risk (1992-2009). Net of several potential confounders, including probability of survival to age 65, we found an FS × PDE interaction for females, in which PDE and FS as main effects had no impact but jointly increased MDD risk. No statistically significant main or interactive effects were found for SA among females or for either phenotype among males. Our findings are consistent with a differential vulnerability model for MDD in females, in which early-life stress increases the risk for poor behavioral health only among the vulnerable. Furthermore, we demonstrate how demographic and pedigree data might serve as tools for investigating differential vulnerability hypotheses.

We used age-period-cohort (APC) analyses to describe the simultaneous effects of age, period, and cohort on cancer incidence rates in an attempt to understand the population dynamics underlying their patterns among those aged 85+. Data from the Utah Cancer Registry (UCR), the US Census, the National Center for Health Statistics (NCHS), and the National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) programme were used to generate age-specific estimates of cancer incidence at ages 65-99 from 1973 to 2002 for Utah. Our results showed increasing cancer incidence rates up to the 85-89 age group followed by declines at ages 90-99 when not confounded by the separate influences of period and cohort effects. We found significant period and cohort effects, suggesting the role of environmental mechanisms in cancer incidence trends between the ages of 85 and 100.