Parental and family determinants of the Flynn effect.

Research about the Flynn effect, the secular rise in IQ, is heavily based on conscript data from successive male birth cohorts. This inevitably means that two distinct phenomena are mixed: fertility differences by IQ group ('compositional Flynn effect'), and any difference between parents and children ('within-family Flynn effect'). Both will influence trends in cognitive ability. We focused on the latter phenomenon, exploring changes in cognitive abilities during adolescence within one generation, and between two successive generations within the same family. We identified determinants and outcomes in three linked generations in the Stockholm Multigenerational Study. School and conscript data covered logical/numerical and verbal scores for mothers at age 13, fathers at 13 and 18, and their sons at 18. Raw scores, and change in raw scores, were used as outcomes in linear regressions. Both parents' abilities at 13 were equally important for sons' abilities at 18. Boys from disadvantaged backgrounds caught up with other boys during adolescence. Comparing fathers with sons, there appeared to be a positive Flynn effect in logical/numeric and verbal abilities. This was larger if the father had a working-class background or many siblings. A Flynn effect was only visible in families where the father had low general cognitive ability at 18. We conclude that there is a general improvement in logical/numeric and verbal skills from one generation to the next, primarily based on improvement in disadvantaged families. The Flynn effect in Sweden during the later 20th century appears to represent a narrowing between social categories.

Food abundance in men before puberty predicts a range of cancers in grandsons.

Nutritional conditions early in human life may influence phenotypic characteristics in later generations. A male-line transgenerational pathway, triggered by the early environment, has been postulated with support from animal and a small number of human studies. Here we analyse individuals born in Uppsala Sweden 1915-29 with linked data from their children and parents, which enables us to explore the hypothesis that pre-pubertal food abundance may trigger a transgenerational effect on cancer events. We used cancer registry and cause-of-death data to analyse 3422 cancer events in grandchildren (G2) by grandparental (G0) food access. We show that variation in harvests and food access in G0 predicts cancer occurrence in G2 in a specific way: abundance among paternal grandfathers, but not any other grandparent, predicts cancer occurrence in grandsons but not in granddaughters. This male-line response is observed for several groups of cancers, suggesting a general susceptibility, possibly acquired in early embryonic development. We observed no transgenerational influence in the middle generation.

Stress resilience in young men mediates the effect of childhood trauma on their offspring's birth weight - An analysis of 250,000 families.

Experiencing the death of a parent during childhood is a severe trauma that seems to affect the next generation's birth weight. We studied the consequences of parental loss during childhood for men's psychological and physiological characteristics at age 18, and whether these were important for their first-born offspring's birth outcomes. We used a structured life-course approach and four-way decomposition analysis to analyse data for 250,427 three-generation families retrieved from nationwide Swedish registers and found that psychological resilience was impaired and body mass index was higher in men who had experienced parental death. Both characteristics were linked to offspring birth weight. This was lower by 18.0 g (95% confidence interval: 5.7, 30.3) for men who lost a parent at ages 8-17 compared to other ages. Resilience mediated 40% of this influence. Mediation by body mass index, systolic and diastolic blood pressure was negligible, as was the effect of parental loss on length of gestation. There was no mediation by the education of the men's future spouse. Previous literature has indicated that the period before puberty, the "slow growth period", is sensitive. Our evidence suggests that this may be too narrow a restriction: boys aged 8-17 appear to be particularly likely to respond to parental loss in a way which affects their future offspring's birth weight. We conclude that the observed transgenerational influence on birth weight is mediated by the father's psychological resilience but not by his body mass index or blood pressure.

Paternal grandfather's access to food predicts all-cause and cancer mortality in grandsons.

Studies of animals and plants suggest that nutritional conditions in one generation may affect phenotypic characteristics in subsequent generations. A small number of human studies claim to show that pre-pubertal nutritional experience trigger a sex-specific transgenerational response along the male line. A single historical dataset, the Överkalix cohorts in northern Sweden, is often quoted as evidence. To test this hypothesis on an almost 40 times larger dataset we collect harvest data during the pre-pubertal period of grandparents (G0, n = 9,039) to examine its potential association with mortality in children (G1, n = 7,280) and grandchildren (G2, n = 11,561) in the Uppsala Multigeneration Study. We find support for the main Överkalix finding: paternal grandfather's food access in pre-puberty predicts his male, but not female, grandchildren's all-cause mortality. In our study, cancer mortality contributes strongly to this pattern. We are unable to reproduce previous results for diabetes and cardiovascular mortality.

Why is parental lifespan linked to children's chances of reaching a high age? A transgenerational hypothesis.

PURPOSE: Transgenerational determinants of longevity are poorly understood. We used data from four linked generations (G0, G1, G2 and G3) of the Uppsala Birth Cohort Multigeneration Study to address this issue. METHODS: Mortality in G1 (N = 9565) was followed from 1961-2015 and analysed in relation to tertiles of their parents' (G0) age-at-death using Cox regression. Parental social class and marital status were adjusted for in the analyses, as was G1's birth order and adult social class. For an almost entirely deceased segment of G1 (n = 1149), born 1915-1917, we compared exact age-at-death with G0 parents' age-at-death. Finally, we explored 'resilience' as a potentially important mechanism for intergenerational transmission of longevity, using conscript information from psychological interviews of G2 and G3 men. RESULTS: G0 men's and women's ages-at-death were independently associated with G1 midlife and old age mortality. This association was robust and minimally reduced when G0 and G1 social class were adjusted for. We observed an increased lifespan in all social groups. Median difference in age-at-death for sons compared to fathers was + 3.9 years, and + 6.9 years for daughters compared to mothers.Parents' and maternal grandmother's longevity were associated with resilience in subsequent generations. Resilience scores of G2 men were also associated with those of their G3 sons and with their own mortality in midlife. CONCLUSIONS: The chance of reaching a high age is transmitted from parents to children in a modest, but robust way. Longevity inheritance is paralleled by the inheritance of individual resilience. Individual resilience, we propose, develops in the first part of life as a response to adversity and early experience in general. This gives rise to a transgenerational pathway, distinct from social class trajectories. A theory of longevity inheritance should bring together previous thinking around general susceptibility, frailty and resilience with new insights from epigenetics and social epidemiology.

Does childhood trauma influence offspring's birth characteristics?

Background: : A recent epigenetic hypothesis postulates that 'a sex-specific male-line transgenerational effect exists in humans', which can be triggered by childhood trauma during 'the slow growth period' just before puberty. The evidence is based on a few rather small epidemiological studies. We examine what response childhood trauma predicts, if any, in the birth size and prematurity risk of almost 800 000 offspring. Methods: Children of parity 1, 2 or 3, born 1976-2002 in Sweden, for whom we could trace both parents and all four grandparents, constituted generation 3 (G3, n = 764 569). Around 5% of their parents, G2, suffered parental (G1) death during their own childhood. The association of such trauma in G2 with G3 prematurity and birthweight was analysed, while controlling for confounders in G1 and G2. We examined whether the slow growth period was extra sensitive to parental loss. Results: Parental (G1) death during (G2) childhood predicts premature birth and lower birthweight in the offspring generation (G3). This response is dependent on G2 gender, G2 age at exposure and G3 parity, but not G3 gender. Conclusions: The results are compatible with the Pembrey-Bygren hypothesis that trauma exposure during boys' slow growth period may trigger a transgenerational response; age at trauma exposure among girls seems less important, suggesting a different set of pathways for any transgenerational response. Finally, parental death during childhood was not important for the reproduction of social inequalities in birthweight and premature birth.

Does unemployment cause long-term mortality? Selection and causation after the 1992-96 deep Swedish recession.

BACKGROUND: Mass unemployment in Europe is endemic, especially among the young. Does it cause mortality? METHODS: We analyzed long-term effects of unemployment occurring during the deep Swedish recession 1992-96. Mortality from all and selected causes was examined in the 6-year period after the recession among those employed in 1990 (3.4 million). Direct health selection was analyzed as risk of unemployment by prior medical history based on all hospitalizations 1981-91. Unemployment effects on mortality were estimated with and without adjustment for prior social characteristics and for prior medical history. RESULTS: A prior circulatory disease history did not predict unemployment; a history of alcohol-related disease or suicide attempts did, in men and women. Unemployment predicted excess male, but not female, mortality from circulatory disease, both ischemic heart disease and stroke, and from all causes combined, after full adjustment. Adjustment for prior social characteristics reduced estimates considerably; additional adjustment for prior medical history did not. Mortality from external and alcohol-related causes was raised in men and women experiencing unemployment, after adjustment for social characteristics and medical history. For the youngest birth cohorts fully adjusted alcohol mortality HRs were substantial (male HR = 4.44; female HR = 5.73). The effect of unemployment on mortality was not uniform across the population; men, those with a low education, low income, unmarried or in urban employment were more vulnerable. CONCLUSIONS: Direct selection by medical history explains a modest fraction of any increased mortality risk following unemployment. Mass unemployment imposes long-term mortality risk on a sizeable segment of the population.

Small for gestational age and adulthood risk of disability pension: the contribution of childhood and adulthood conditions.

Early exiting from the labor force and into disability pension (DP) represents a major social problem in Sweden and elsewhere. We examined how being asymmetric (A-SGA) or symmetric (S-SGA) small for gestational age predicts transitioning into DP. We analyzed a longitudinal sample of 8125 men and women from the Stockholm Birth Cohort (SBC), born in 1953 and not on DP in 1990. The SBC consists of data from various sources, including self-reported information and data from administrative registers. The follow-up period was from 1991 to 2009. Yearly information on the receipt of DP benefits from register data was operationalized as a dichotomous variable. 13 percent of the sample moved into DP during follow-up. Cox proportional hazards regression was used to examine whether disadvantageous fetal growth--A-SGA and S-SGA--predicted DP. Men and women born A-SGA had a substantially increased hazard of DP. The full model suggested a hazard ratio of 1.68 (CI: 1.11-2.54), only being affected slightly by adulthood conditions. Several childhood conditions were also associated with DP. Such factors, however, mainly affected DP risk through adulthood conditions. The effect of SGA on DP appeared particularly strong among individuals from socioeconomically disadvantaged backgrounds. The evidence presented suggests that being A-SGA influences the risk of DP, independent of childhood and adulthood conditions, and similarly for men and women. Due to A-SGA being rather infrequent, reducing the occurrence of A-SGA would, however, only have a marginal impact on the stock of DP pensioners. For the individual affected, the elevation in the risk of DP was nevertheless substantial. Other childhood conditions exercised a larger influence on the stock of DP recipients, but they mostly operated through adulthood attainment. The importance of socioeconomic resources in childhood for the long term health consequences of SGA is interesting from a policy perspective and warrants further research.

Cold ambient temperature in utero and birth outcomes in Uppsala, Sweden, 1915-1929.

PURPOSE: Although the literature reports adverse birth outcomes following ambient heat, less work focuses on cold. We, moreover, know of no studies of cold that examine stillbirth. We tested the relation between cold ambient temperature during pregnancy in Sweden and four outcomes: stillbirth, preterm, birth weight for gestational age, and birth length. We examined births from 1915 to 1929 in Uppsala, Sweden, which-unlike most societies today-experienced substandard indoor-heating and fewer amenities to provide shelter from cold. METHODS: We retrieved data on almost 14,000 deliveries from the Uppsala Birth Cohort Study. We linked a validated, daily ambient temperature series to all pregnancies and applied Cox proportional hazards (stillbirth and preterm) and linear regression models (birth weight and length). We tested for nonlinearity using quadratic splines. RESULTS: The risk of stillbirth rose as ambient temperature during pregnancy fell (hazard ratio for a 1°C decrease in temperature, 1.08; 95% confidence interval, 1.00 to 1.17). Cold extremes adversely affected preterm and birth length, whereas warm extremes increased preterm risk. We observed no relation between cold and birth weight for gestational age. CONCLUSION: In historical Sweden, cold temperatures during pregnancy increased stillbirth and preterm risk and reduced birth length among live births.

Unemployment and suicide during and after a deep recession: a longitudinal study of 3.4 million Swedish men and women.

OBJECTIVES: We tested 2 hypotheses found in studies of the relationship between suicide and unemployment: causal (stress and adversity) and selective interpretation (previous poor health). METHODS: We estimated Cox models for adults (n = 3,424,550) born between 1931 and 1965. We examined mortality during the recession (1993-1996), postrecession (1997-2002), and a combined follow-up. Models controlled for previous medical problems, and social, family, and employer characteristics. RESULTS: During the recession there was no excess hazard of mortality from suicide or events of undetermined intent. Postrecession, there was an excess hazard of suicide mortality for unemployed men but not unemployed women. However, for unemployed women with no health-problem history there was a modest hazard of suicide. Finally, there was elevated mortality from events of undetermined intent for unemployed men and women postrecession. CONCLUSIONS: A small part of the relationship may be related to health selection, more so during the recession. However, postrecessionary period findings suggest that much of the association could be causal. A narrow focus on suicide mortality may understate the mortality effects of unemployment in Sweden.

Cohort profile: The Stockholm Public Health Cohort.

The Stockholm Public Health Cohort was set up within the Stockholm County Council public health surveys to inform on determinants and consequences of significant contributors to the current burden of disease. Participants are 89 268 randomly selected individuals from the adult population of Stockholm County. Baseline surveys took place in 2002, 2006 and 2010 via self-administered questionnaires. So far, participants recruited in 2002 were re-surveyed twice, in 2007 and 2010, and those enrolled in 2006 were re-surveyed once, in 2010. Self-reported data are regularly supplemented by information from national and regional health data and administrative registers, for study participants and their relatives (including their offspring). Available data are extensive and include a wide array of health, lifestyle, perinatal, demographic, socio-economic and familial factors. The cohort is an international resource for epidemiological research, and the data available to the research community for specific studies obtained approval from the Stockholm Public Health Cohort Steering Committee and the Stockholm Regional Ethical Review Board.

Social origin, schooling and individual change in intelligence during childhood influence long-term mortality: a 68-year follow-up study.

BACKGROUND: Intelligence at a single time-point has been linked to health outcomes. An individual's IQ increases with longer schooling, but the validity of such increase is unclear. In this study, we assess the hypothesis that individual change in the performance on IQ tests between ages 10 and 20 years is associated with mortality later in life. METHODS: The analyses are based on a cohort of Swedish boys born in 1928 (n = 610) for whom social background data were collected in 1937, IQ tests were carried out in 1938 and 1948 and own education and mortality were recorded up to 2006. Structural equation models were used to estimate the extent to which two latent intelligence scores, at ages 10 and 20 years, manifested by results on the IQ tests, are related to paternal and own education, and how all these variables are linked to all-cause mortality. RESULTS: Intelligence at the age of 20 years was associated with lower mortality in adulthood, after controlling for intelligence at the age of 10 years. The increases in intelligence partly mediated the link between longer schooling and lower mortality. Social background differences in adult intelligence (and consequently in mortality) were partly explained by the tendency for sons of more educated fathers to receive longer schooling, even when initial intelligence levels had been accounted for. CONCLUSIONS: The results are consistent with a causal link from change in intelligence to mortality, and further, that schooling-induced changes in IQ scores are true and bring about lasting changes in intelligence. In addition, if both these interpretations are correct, social differences in access to longer schooling have consequences for social differences in both adult intelligence and adult health.

The length of unemployment predicts mortality, differently in men and women, and by cause of death: a six year mortality follow-up of the Swedish 1992-1996 recession.

This study examines the relationship between the total amount of accumulated unemployment during the deep Swedish recession of 1992-1996 and mortality in the following 6 years. Nearly 3.4 million Swedish men and women, born between 1931 and 1965 who were gainfully employed at the time of the 1990 census were included. Almost 23% of these individuals were unemployed at some point during the recession. We conduct a prospective cohort study utilizing Cox proportional hazard regression with a mortality follow-up from January 1997 to December 2002. We adjust for health status (1982-1991), baseline (1991) social, family, and employer characteristics of individuals before the recession. The findings suggest that long-term unemployment is related to elevated all-cause mortality for men and women. The excess mortality effects were small for women and attributable to a positive, linear increase in the hazard of alcohol disease-related mortality and external causes-of-death not classified as suicides or transport accidents. For men, the excess hazard of all-cause mortality was best represented by a cubic, non-linear shape. The predicted hazard increases rapidly with the shortest and longest accumulated levels of unemployment. However, the underlying pattern differed by cause-of-death. The cancer, circulatory, and alcohol disease-related analyses suggest that mortality peaks with mid-levels of accumulated unemployment and then declines with longer duration unemployment. For men, we observed a positive, linear increase in the hazard ratios associated with transport and suicide mortality, and a very steep non-linear increase in the excess hazard ratio associated with other external causes of death that were not classified as suicide or transport accidents. In conclusion, mortality risk increases with the duration of unemployment among men and women. This was best described by a cubic function for men and a linear function for women. Behind this pattern, different causes-of-death varied in their relation to the accumulation of unemployment.

Social determinants of cardiac disease biomarkers: investigating a Swedish male cohort at ages 50 and 70.

BACKGROUND: Social status is associated with cardiovascular disease (CVD) prevalence and incidence. AIMS: to investigate relationships between socioeconomic position (SEP) and common CVD biomarkers including adiponectin not previously investigated in a Swedish-population sample, and to assess if these associations changed with age. DESIGN: Population-based longitudinal cohort study of men born 1920-24 with clinical measurements, blood samples, questionnaire data, and register-based information on SEP and cause of death. METHODS: A total of 2322 men attended an investigation at age 50 of which 1221 attended a reinvestigation at age 70. Association between SEP and CVD biomarkers [cholesterol, low-density lipoprotein/high-density lipoprotein (LDL/HDL), apolipoprotein (Apo) ApoB/ApoA1, and adiponectin] were analysed by linear regression (adjusted for age, body mass index, and physical activity). SEP was measured as occupational class and educational level. CVD mortality over 36 years of follow-up was analysed by Cox regression. RESULTS: At age 50, we found a significant inverse association of education with cholesterol level, LDL/HDL ratio and ApoB/ApoA1 ratio. Cholesterol was also associated with occupational class, statistically significant after adjustment for all covariates. At age 70, no significant associations were found between either measurement of SEP and any of the biomarkers studied. Highest educated men had decreased risk for CVD mortality during follow-up. CONCLUSIONS: Associations of SEP with cholesterol levels and LDL/HDL ratio that exist at age 50 are no longer apparent in the same group of men at age 70. We found no significant association between SEP and adiponectin levels at age 70.