Intergenerational transmission of health inequalities: research agenda for a life course approach to socioeconomic inequalities in health.

Explanations for socioeconomic inequalities in adult health are usually sought in behaviours and environments in adulthood. Yet, there is compelling evidence that the first two decades of life contribute substantially to both adult socioeconomic position (SEP) and adult health. This has implications for explanatory health inequalities research.We propose an analytical framework to advance research on the intergenerational transmission of health inequalities, that is, on intergenerational transmission of socioeconomic and associated health (dis)advantages at the family level, and its contribution to health inequalities at the population level. The framework distinguishes three transmission pathways: (1) intergenerational transmission of SEP, with effects on offspring health fully mediated by offspring SEP; (2) intergenerational transmission of health problems affecting SEP and (3) intergenerational transmission of both SEP and health, without a causal relationship between offspring adult SEP and health. We describe areas for future research along this framework and discuss the challenges and opportunities to advance this field.

Intergenerational transmission of health inequalities: towards a life course approach to socioeconomic inequalities in health - a review.

Adult health inequalities are a persistent public health problem. Explanations are usually sought in behaviours and environments in adulthood, despite evidence on the importance of early life conditions for life course outcomes. We review evidence from a broad range of fields to unravel to what extent, and how, socioeconomic health inequalities are intergenerationally transmitted.We find that transmission of socioeconomic and associated health (dis)advantages from parents to offspring, and its underlying structural determinants, contributes substantially to socioeconomic inequalities in adult health. In the first two decades of life-from conception to early adulthood-parental socioeconomic position (SEP) and parental health strongly influence offspring adult SEP and health. Socioeconomic and health (dis)advantages are largely transmitted through the same broad mechanisms. Socioeconomic inequalities in the fetal environment contribute to inequalities in fetal development and birth outcomes, with lifelong socioeconomic and health consequences. Inequalities in the postnatal environment-especially the psychosocial and learning environment, physical exposures and socialisation-result in inequalities in child and adolescent health, development and behavioural habits, with health and socioeconomic consequences tracking into adulthood. Structural factors shape these mechanisms in a socioeconomically patterned and time-specific and place-specific way, leading to distinct birth-cohort patterns in health inequality.Adult health inequalities are for an important part intergenerationally transmitted. Effective health inequality reduction requires addressing intergenerational transmission of (dis)advantage by creating societal circumstances that allow all children to develop to their full potential.

Comorbidities in women with polycystic ovary syndrome: a sibling study.

BACKGROUND: Polycystic ovary syndrome (PCOS) has previously been associated with several comorbidities that may have shared genetic, epigenetic, developmental or environmental origins. PCOS may be influenced by prenatal androgen excess, poor intrauterine or childhood environmental factors, childhood obesity and learned health risk behaviors. We analyzed the association between PCOS and several relevant comorbidities while adjusting for early-life biological and socioeconomic conditions, also investigating the extent to which the association is affected by familial risk factors. METHODS: This total-population register-based cohort study included 333,999 full sisters, born between 1962 and 1980. PCOS and comorbidity diagnoses were measured at age 17-45 years through national hospital register data from 1997 to 2011, and complemented with information on the study subjects´ early-life and social characteristics. In the main analysis, sister fixed effects (FE) models were used to control for all time-invariant factors that are shared among sisters, thereby testing whether the association between PCOS and examined comorbidities is influenced by unobserved familial environmental, social or genetic factors. RESULTS: Three thousand five hundred seventy women in the Sister sample were diagnosed with PCOS, of whom 14% had obesity, 8% had depression, 7% had anxiety and 4% experienced sleeping, sexual and eating disorders (SSE). Having PCOS increased the odds of obesity nearly 6-fold (adjusted OR (aOR): 5.9 [95% CI:5.4-6.5]). This association was attenuated in models accounting for unobserved characteristics shared between full sisters, but remained considerable in size (Sister FE: aOR: 4.5 [95% CI: 3.6-5.6]). For depression (Sister FE: aOR: 1.4 [95% CI: 1.2-1.8]) and anxiety (Sister FE: aOR: 1.5 [95% CI: 1.2-1.8), there was a small decrease in the aORs when controlling for factors shared between sisters. Being diagnosed with SSE disorders yielded a 2.4 aOR (95% CI:2.0-2.6) when controlling for a comprehensive set of individual-level confounders, which only decreased slightly when controlling for factors at the family level such as shared genes or parenting style. Accounting for differences between sisters in observed early-life circumstances influenced the estimated associations marginally. CONCLUSION: Having been diagnosed with PCOS is associated with a markedly increased risk of obesity and sleeping, sexual and eating disorders, also after accounting for factors shared between sisters and early-life conditions.

Early Life Factors and Polycystic Ovary Syndrome in a Swedish Birth Cohort.

Polycystic ovary syndrome (PCOS) is a medical condition with important consequences for women's well-being and reproductive outcomes. Although the etiology of PCOS is not fully understood, there is increasing evidence of both genetic and environmental determinants, including development in early life. We studied a population of 977,637 singleton women born in in Sweden between 1973 and 1995, followed sometime between the age 15 and 40. The incidence of PCOS was measured using hospital register data during 2001-2012, complemented with information about the women's, parents' and sisters' health and social characteristics from population and health care registers. Cox regression was used to study how PCOS is associated with intergenerational factors, and a range of early life characteristics. 11,594 women in the study sample were diagnosed with PCOS during the follow-up period. The hazard rate for PCOS was increased 3-fold (HR 2.98, 95% CI 2.43-3.64) if the index woman's mother had been diagnosed with PCOS, and with 1.5-fold (HR 1.51, 95% CI 1.39-1.63) if their mother had diabetes mellitus. We found associations of PCOS with lower (<7) one-minute Apgar score (HR 1.19, 95% CI 1.09-1.29) and with post-term birth (HR 1.19, 95% CI 1.13-1.26). Furthermore, heavy (10+ cigarettes/day) maternal smoking (HR 1.30, 95% CI 1.18-1.44) and maternal obesity (HR 1.90, 95% CI 1.62-2.36) were strongly associated with PCOS. This study finds support for the heritability and fetal origins of PCOS. Risk of PCOS could be reduced by further emphasizing the importance of maternal and early life health.