Introduction Childhood socioeconomic position (SEP) has been identified as a key determinant of health. However, earlier literature is largely from high-income countries and provides limited evidence on the prolonging impacts of childhood disadvantage on healthy ageing across diverse settings and populations. The aim of this study is to investigate the associations between childhood SEP and healthy ageing across multiple countries and the mediation effects of adult SEP, individual education and wealth, on these associations.

Methods Using the harmonised dataset of five cohort studies in the Ageing Trajectories of Health-Longitudinal Opportunities and Synergies (ATHLOS) project, this study was based on 57 956 people aged ≥50 years (women: 53.3%) living in China, Finland, UK, Poland, South Africa and Mexico. The associations between childhood SEP (parental education and occupation) and healthy ageing scores were examined using linear regression modelling. Causal mediation analysis was carried out to estimate the percentage of indirect effects via adult SEP (individual education and wealth).Results Higher levels of childhood SEP were associated with higher healthy ageing scores by up to five points and similar patterns were observed across populations from different countries. The associations were mediated by adult SEP and the range of mediation effects was between 21% and 78%.

Conclusions This study found childhood SEP was associated with poor health in later life across high-income, middle-income and low-income countries. Addressing socioeconomic disadvantage, such as improving education attainment, may moderate the impacts of adversity in early life and support health and functioning in later life.

Objectives: Polycystic ovary syndrome (PCOS) is an endocrine disorder in women of fertile age which may also affect the labor market attachment. We investigated labor market attachment trajectories among working age women diagnosed with PCOS.

Methods: A cohort of 157,356 women born in 1975–1977 were followed annually between the ages of 30 and 39, using data from Swedish administrative registers. Multinomial logistic regression was employed to assess associations between being diagnosed with PCOS (after the age of 15) and belonging to the identified clusters of labor market attachment trajectories.

Results: Women with PCOS spent less time in employment and were more dependent on sickness benefits during the follow-up time than those without PCOS. Five labor market attachment clusters were identified: stable employment, education into employment, labor market exclusion, continuously unstable position, long-term sickness. Compared to being in the stable employment cluster, women diagnosed with PCOS were more likely to experience long-term sickness [RRR (relative risk ratio): 1.97 (CI: 1.90–2.05)], and education into employment [RRR: 1.11 (CI: 1.07–1.15)].

Conclusion: PCOS can lead to disadvantaged labor market outcomes. Better strategies are needed to prevent economic exclusion among women diagnosed with PCOS.

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.

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.

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.

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.

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.

The ATHLOS cohort is composed of several harmonized datasets of international groups related to health and aging. As a result, the Healthy Aging index has been constructed based on a selection of variables from 16 individual studies. In this paper, we consider additional variables found in ATHLOS and investigate their utilization for predicting the Healthy Aging index. For this purpose, motivated by the volume and diversity of the dataset, we focus our attention upon data clustering, where unsupervised learning is utilized to enhance prediction power. Thus we show the predictive utility of exploiting hidden data structures. In addition, we demonstrate that imposed computation bottlenecks can be surpassed when using appropriate hierarchical clustering, within a clustering for ensemble classification scheme, while retaining prediction benefits. We propose a complete methodology that is evaluated against baseline methods and the original concept. The results are very encouraging suggesting further developments in this direction along with applications in tasks with similar characteristics. A straightforward open source implementation for the R project is also provided (https://github.com/Petros-Barmpas/HCEP).

Background: The study assessed socioeconomic position (SEP) over four time points and employed a latent class analysis (LCA) to explore the associations between longitudinal SEP trajectories and late-life mortality. Methods: We analyzed a cohort of 11 336 members born at the Uppsala University Hospital, Sweden during 1915–29 and followed up for mortality during 1980–2008. SEP was measured at birth, age 10, mid-adulthood and late adulthood. LCA was used to identify SEP trajectories, which were linked to all-cause and cause-specific mortality through Cox proportional hazard regression models. Results: The age and birth cohort adjusted hazard ratio (HR) of all-cause mortality among the upwardly mobile from middle vs. stable low SEP was 28% lower in men [HR: 0.72; 95% confidence interval (95% CI): 0.65, 0.81] and 30% lower in women (HR: 0.70; 95% CI: 0.62, 0.78). The corresponding HR of cardiovascular mortality was 30% lower in men (HR: 0.70; 95% CI: 0.60, 0.82) and 31% lower in women (HR: 0.69; 95% CI: 0.58, 0.83). Upward mobility was also associated with decreased HR of mortality from respiratory diseases and injuries among men and from cancer, respiratory diseases, injuries and mental disorders among women. The upwardly mobile were similar to the stable high group in terms of their HRs of mortality from all-causes and cardiovascular, cancer and mental diseases. Conclusions: Upward mobility appeared to be protective of mortality from a wide range of causes. Interventions aiming to prevent deaths can benefit from creating optimal conditions earlier in the life course, letting disadvantaged children maximize their socioeconomic and health potentials.