Early-Life Socioeconomic Status and the Prevalence of Breast Cancer in Later Life

Knowledge of mechanisms linking early-life social environment and breast cancer remains limited. We explore direct and indirect effects of early-life socioeconomic status (SES) on breast cancer prevalence in later life. Using 50-year data from the Wisconsin Longitudinal Study (N = 4,275) and structural equation modeling, we found a negative direct effect of early-life SES, indicating that women from higher-SES family background had lower breast cancer prevalence than women from lower-SES families. Additionally, early-life SES has a positive indirect effect on breast cancer via women's adult SES and age at first birth. Were it not for their higher SES in adulthood and delayed childbearing, women from higher-SES families of origin would have had lower breast cancer prevalence than women from lower-SES families. Yet, early-life SES is associated positively with adult SES and age at first birth, and women's higher adult SES and delayed childbearing are related to higher breast cancer prevalence.     

Socioeconomic status during childhood and health status in adulthood: the Wrocław growth study

It has been widely observed that socioeconomic status (SES) is associated with frequency of cardiovascular disease. Both men and women of low socioeconomic position have increased risk of cardiovascular disease morbidity and premature death. In this study the relationship between SES in childhood, and health status at the age of 50 years was examined. Socioeconomic status in childhood was measured using objective (father's educational level and number of children in the family) and subjective (self-assessed SES in childhood declared in early adulthood) indicators. Data from the Wroclaw Growth Study were completed when subjects were 50 years old, and information concerning health status was added. The results indicated that the objective, universally used measures of SES in childhood such as father's educational level and size of family did not show any essential relationships with health outcomes in adulthood, both for men and women. By contrast, retrospective, self-assessed SES (as better, average or worse as compared with peers) in childhood was significantly associated with the appearance of cardiovascular disease among women aged 50 years. Women who at the beginning of their adult life declared better socioeconomic condition in childhood were significantly healthier at the age of 50 years (OR=3.43; p=0.02). Moreover, this appeared to be independent of BMI, SES and life-style in adulthood. For men, retrospective self-assessed SES showed no relation to health status at the age of 50 years. The gender differences in the relationships between self-assessed SES in childhood and health status in adulthood are explained by possible selective premature mortality among men from lower childhood SES and/or sex differences in cognitive abilities.     

Life course pathways to adult-onset diabetes

Early life conditions, such as socioeconomic status (SES) and health, have the potential to set in motion multiple and reinforcing pathways that shape both the prevalence and onset of diabetes among older adults. Using data from the Health and Retirement Study (1998-2002) for persons age 51 years and older, we investigated the core mediating mechanisms linking early life conditions with diabetes prevalence in 1998 and onset over a 4-year follow-up period, focusing on adult achievement processes and obesity as key mechanisms. We found that father's education is negatively associated with diabetes prevalence for older men and women. However, no markers of early life SES are directly associated with older men's and women's onset of diabetes, and the negative effects of adult SES on diabetes onset pertain only to women. Early life health affects the onset of diabetes among women--but not the prevalence--and no evidence of this association was found for men. We found no evidence that obesity is an important mechanism connecting either early life or adult SES with diabetes development in men or women. We speculate that early life SES may accelerate the development of diabetes at younger ages, and that the pathways linking life course SES, early life health, and diabetes are partly gender-specific and biological in nature.     

Colloquium on the role and behavior of sex chromosomes in mammalian development and reproduction: Basel,May 6–8, 1965

Abstract

There are significant mortality disparities across racial and socioeconomic (SES) groups. Although the mechanisms behind these disparities remain vague, there is a clear connection between the mortality disparities across racial and SES groups. It is less clear, though, if the relationship between SES and racial mortality disparities varies across the life course. Prior research indicates that both racial and SES mortality disparities decline over the life course. These results suggest that if we standardize mortality rates for age‐variation in the SES‐mortality relationship, then the age‐pattern of racial mortality disparities will be attenuated. Using data from the National Longitudinal Mortality Study, I analyze the relationship between SES and racial disparities in age‐specific mortality among adults aged 25 and over. The results suggest that racial differences in SES are most important early in the adult life, and are minimally related to the convergence in racial mortality disparities at the oldest ages.     

Early life socioeconomic factors and genomic DNA methylation in mid-life

Epigenetic modifications may be one mechanism linking early life factors, including parental socioeconomic status (SES), to adult onset disease risk. However, SES influences on DNA methylation patterns remain largely unknown. In a US birth cohort of women, we examined whether indicators of early life and adult SES were associated with white blood cell methylation of repetitive elements (Sat2, Alu and LINE-1) in adulthood. Low family income at birth was associated with higher Sat2 methylation (β = 19.7, 95% CI: 0.4, 39.0 for lowest vs. highest income quartile) and single parent family was associated with higher Alu methylation (β = 23.5, 95% CI: 2.6, 44.4), after adjusting for other early life factors. Lower adult education was associated with lower Sat2 methylation (β = -16.7, 95% CI: -29.0, -4.5). There were no associations between early life SES and LINE-1 methylation. Overall, our preliminary results suggest possible influences of SES across the life-course on genomic DNA methylation in adult women. However, these preliminary associations need to be replicated in larger prospective studies.     

Investing in early human development: Timing and economic efficiency

Policy discussions to ameliorate socioeconomic (SES) inequalities are increasingly focused on investments in early childhood. Yet such interventions are costly to implement, and clear evidence on the optimal time to intervene to yield a high economic and social return in the future is meagre. The majority of successful early childhood interventions start in the preschool years. However socioeconomic gradients in cognitive skills, socio-emotional functioning and health can be observed by age three, suggesting that preventative programmes starting earlier in childhood may be even more effective. We discuss the optimal timing of early childhood intervention with reference to recent research in developmental neuroscience. We motivate the need for early intervention by providing an overview of the impact of adverse risk factors during the antenatal and early childhood periods on outcomes later in life. We provide a brief review of the economic rationale for investing early in life and propose the “antenatal investment hypothesis”. We conclude by discussing a suite of new European interventions that will inform this optimal timing debate.     

Polygenic and socioeconomic risk for high body mass index: 69 years of follow-up across life

Genetic influences on body mass index (BMI) appear to markedly differ across life, yet existing research is equivocal and limited by a paucity of life course data. We thus used a birth cohort study to investigate differences in association and explained variance in polygenic risk for high BMI across infancy to old age (2–69 years). A secondary aim was to investigate how the association between BMI and a key purported environmental determinant (childhood socioeconomic position) differed across life, and whether this operated independently and/or multiplicatively of genetic influences. Data were from up to 2677 participants in the MRC National Survey of Health and Development, with measured BMI at 12 timepoints from 2–69 years. We used multiple polygenic indices from GWAS of adult and childhood BMI, and investigated their associations with BMI at each age. For polygenic liability to higher adult BMI, the trajectories of effect size (β) and explained variance (R²) diverged: explained variance peaked in early adulthood and plateaued thereafter, while absolute effect sizes increased throughout adulthood. For polygenic liability to higher childhood BMI, explained variance was largest in adolescence and early adulthood; effect sizes were marginally smaller in absolute terms from adolescence to adulthood. All polygenic indices were related to higher variation in BMI; quantile regression analyses showed that effect sizes were sizably larger at the upper end of the BMI distribution. Socioeconomic and polygenic risk for higher BMI across life appear to operate additively; we found little evidence of interaction. Our findings highlight the likely independent influences of polygenic and socioeconomic factors on BMI across life. Despite sizable associations, the BMI variance explained by each plateaued or declined across adulthood while BMI variance itself increased. This is suggestive of the increasing importance of chance (‘non-shared’) environmental influences on BMI across life.     

Early socioeconomic status,social mobility and cognitive trajectories in later life: A life course perspective

Using the Chinese Longitudinal Healthy Longevity Survey (CLHLS) from 2008 to 2018 accompanied by the growth curve model, we examined the association between early socioeconomic status, social mobility, and divergent cognitive trajectories in later life within a society undergoing significant transformation. The study confirmed a positive relationship between socioeconomic status in early life and cognitive ability in later life. However, socioeconomic status in adulthood is associated with better cognitive ability in old age compared to that in childhood. Meanwhile, upward social mobility mitigates the negative correlation between socioeconomic disadvantage in early life and cognitive ability in later life. In addition, the inequality in socioeconomic status at earlier stages resulted in heterogeneous cognitive trajectories, with the double cumulative disadvantage effect resulting from education being particularly noteworthy. Thus, Chinese health policy should focus on the earlier stages of life, actively promoting inclusive family policies and improving the family's role in protecting childhood from an adverse environment. Simultaneously, education and employment fairness should be strengthened to accelerate social mobility and enhance the “Health Repair Mechanism” of the second life course.     

Unequal chances for reaching 'a good old age'. Socio-economic health differences among older adults from a life course perspective

This article provides an overview of the socioeconomic inequality in physical and psychological health of older adults between 55 and 85 years of age, with a focus on the older adults whose socioeconomic status (SES) remains at a low level all their life. Data are derived from 1471 men and 1568 women, participating in the Longitudinal Aging Study Amsterdam (LASA) in 1992/1993. Based on the parental and own level of education, respondents are divided in four categories: those with a life time low level of SES, those with downward or upward mobility in SES, and those with a life time high level of SES. Logistic regression analyses showed that older adults with upward SES mobility and life time high SES, had a lower risk for functional limitations, chronic diseases (men only), 6-year mortality, depression and loneliness, compared with the older adults with life time low SES. The disadvantaged position of the low SES persons with regard to age, health and psychosocial conditions explained the SES differences in depression, but SES differences in mortality (for men) and in functional disability (for men and women) are not explained by the risk factors under study. SES differences in loneliness were attributed to differences in psychosocial conditions. Lifestyle did not add to the explanation of any of the SES differences. There were only small differences between those with a life time low SES and those with downward mobility in SES. It is concluded that a low level of education (regardless of the parental level) contributes to restricted psychosocial conditions, health problems and low well-being in old age, thereby decreasing the chances for a 'good old age' considerably.     

Early-life adversity and long-term neurobehavioral outcomes: epigenome as a bridge?

Accumulating evidence suggests that adversities at critical periods in early life, both pre- and postnatal, can lead to neuroendocrine perturbations, including hypothalamic-pituitary-adrenal axis dysregulation and inflammation persisting up to adulthood. This process, commonly referred to as biological embedding, may cause abnormal cognitive and behavioral functioning, including impaired learning, memory, and depressive- and anxiety-like behaviors, as well as neuropsychiatric outcomes in later life. Currently, the regulation of gene activity by epigenetic mechanisms is suggested to be a key player in mediating the link between adverse early-life events and adult neurobehavioral outcomes. Role of particular genes, including those encoding glucocorticoid receptor, brain-derived neurotrophic factor, as well as arginine vasopressin and corticotropin-releasing factor, has been demonstrated in triggering early adversity-associated pathological conditions. This review is focused on the results from human studies highlighting the causal role of epigenetic mechanisms in mediating the link between the adversity during early development, from prenatal stages through infancy, and adult neuropsychiatric outcomes. The modulation of epigenetic pathways involved in biological embedding may provide promising direction toward novel therapeutic strategies against neurological and cognitive dysfunctions in adult life.     

Programming of adipose tissue miR-483-3p and GDF-3 expression by maternal diet in type 2 diabetes

Nutrition during early mammalian development permanently influences health of the adult, including increasing the risk of type 2 diabetes and coronary heart disease. However, the molecular mechanisms underlying such programming are poorly defined. Here we demonstrate that programmed changes in miRNA expression link early-life nutrition to long-term health. Specifically, we show that miR-483-3p is upregulated in adipose tissue from low-birth-weight adult humans and prediabetic adult rats exposed to suboptimal nutrition in early life. We demonstrate that manipulation of miR-483-3p levels in vitro substantially modulates the capacity of adipocytes to differentiate and store lipids. We show that some of these effects are mediated by translational repression of growth/differentiation factor-3, a target of miR-483-3p. We propose that increased miR-483-3p expression in vivo, programmed by early-life nutrition, limits storage of lipids in adipose tissue, causing lipotoxicity and insulin resistance and thus increasing susceptibility to metabolic disease.     

Socioeconomic position at different stages of the life course and its influence on body weight and weight gain in adulthood: a longitudinal study with 13-year follow-up

Socioeconomic inequalities in body weight have been demonstrated in numerous cross-sectional studies; however, little research has investigated these inequalities from a life course and longitudinal perspective. We examined the association between child- and adulthood socioeconomic position (SEP) and BMI and overweight/obesity in 1991 (baseline) and changes in BMI and the prevalence of overweight and obesity between 1991 and 2004. Data from the 1991 and 2004 waves of the longitudinal Dutch GLOBE study were used. Participants (n = 1,465) were aged 40-60 years at baseline. BMI was calculated from self-reported height and weight collected by postal questionnaire. Retrospective recall of father's occupation was used as childhood socioeconomic indicator, and adulthood SEP was measured by the occupation of the main income earner of the household. The findings showed that among women, childhood SEP exerted a greater influence on body weight than SEP in adulthood: at baseline, women from disadvantaged backgrounds in childhood had a higher BMI and were more likely to be overweight or obese, and they gained significantly more weight between baseline and follow-up. In contrast, adult SEP had a greater impact than childhood circumstances on men's body weight: those from disadvantaged households had a higher mean BMI and were more likely to be overweight or obese at baseline, and they gained significantly more weight between 1991 and 2004. The findings suggest that exposure to disadvantaged circumstances at critically important periods of the life course is associated with body weight and weight gain in adulthood. Importantly, these etiologically relevant periods differ for men and women, suggesting gender-specific pathways to socioeconomic inequalities in body weight in adulthood.     

Racial/Ethnic Differences in Early-Life Mortality in the United States

U.S. early-life (ages 1–24) deaths are tragic, far too common, and largely preventable. Yet demographers have focused scant attention on U.S. early-life mortality patterns, particularly as they vary across racial and ethnic groups. We employed the restricted-use 1999–2011 National Health Interview Survey–Linked Mortality Files and hazard models to examine racial/ethnic differences in early-life mortality. Our results reveal that these disparities are large, strongly related to differences in parental socioeconomic status, and expressed through different causes of death. Compared to non-Hispanic whites, non-Hispanic blacks experience 60 percent and Mexican Americans 32 percent higher risk of death over the follow-up period, with demographic controls. Our finding that Mexican Americans experience higher early-life mortality risk than non-Hispanic whites differs from much of the literature on adult mortality. We also show that these racial/ethnic differences attenuate with controls for family structure and especially with measures of socioeconomic status. For example, higher mortality risk among Mexican Americans than among non-Hispanic whites is no longer significant once we controlled for mother’s education or family income. Our results strongly suggest that eliminating socioeconomic gaps across groups is the key to enhanced survival for children and adolescents in racial/ethnic minority groups.     

Variation in the relationship between BMI and survival by socioeconomic status in Great Britain

We investigate the relationship between obesity and survival, and the extent to which this relationship varies by socioeconomic status (SES). The underlying model is based on the “Pathways to health” framework in which SES affects health by modifying the relationship between lifestyles and health. We use data from the British Health and Lifestyle Survey (1984–1985) and the longitudinal follow-up in June 2009, and run parametric Gompertz survival models to investigate the association between obesity and survival, also accounting for interactions between obesity and both age and SES. Generally we find that obesity is negatively associated with survival, and that SES is positively associated with survival, in both men and women. The interactions between obesity and SES predict survival among women but not among men. Obesity compared with normal weight is associated with a reduction in survival of 3.3, 3.2 and 2.8 years in men aged 40, 50 and 60 years, respectively. Corresponding numbers among women in the lowest SES group are 13.1, 9.7 and 6.1 years, respectively; in the highest SES group they are 6.2, 3.1 and 0.1 years, respectively, a difference of approximately 6 years between the highest and lowest SES groups.     

Using the life history model to set the stage(s) of growth and senescence in bioarchaeology and paleodemography

Paleodemography, the study of demographic parameters of past human populations, relies on assumptions including biological uniformitarianism, stationary populations, and the ability to determine point age estimates from skeletal material. These assumptions have been widely criticized in the literature and various solutions have been proposed. The majority of these solutions rely on statistical modeling, and have not seen widespread application. Most bioarchaeologists recognize that our ability to assess chronological age is inherently limited, and have instead resorted to large, qualitative, age categories. However, there has been little attempt in the literature to systematize and define the stages of development and ageing used in bioarchaeology. We propose that stages should be based in the human life history pattern, and their skeletal markers should have easily defined and clear endpoints. In addition to a standard five-stage developmental model based on the human life history pattern, current among human biologists, we suggest divisions within the adult stage that recognize the specific nature of skeletal samples. We therefore propose the following eight stages recognizable in human skeletal development and senescence: infancy, early childhood, late childhood, adolescence, young adulthood, full adulthood, mature adulthood, and senile adulthood. Striving toward a better prediction of chronological ages will remain important and could eventually help us understand to what extent past societies differed in the timing of these life stages. Furthermore, paleodemographers should try to develop methods that rely on the type of age information accessible from the skeletal material, which uses life stages, rather than point age estimates.     

In utero and childhood exposure to alcohol and old age mortality: Evidence from the temperance movement in the US

Previous research suggests the relevance of in-utero insults and early-life circumstances for a wide array of life cycle outcomes. This research note joins this strand of studies by exploring the long-run mortality effects of in-utero and early-life exposure to alcohol accessibility. In so doing, we take advantage of the prohibition movement during the early part of the twentieth century that generated quasi-natural reductions in alcohol consumption. We use Social Security Administration Death Master Files linked to the full-count 1940 census and compare the longevity of male individuals exposed to the prohibition during in-utero and early childhood (1900–1930) as a result of statewide and federal alcohol ban to those wet counties after the law change to before. The results suggest an intent-to-treat effect of 0.17 years higher longevity as a result of prohibition. A back-of-an-envelope calculation suggests a minimum treatment-on-treated effect of 1.7 years impact. Furthermore, we show that these effects are not driven by other county-level demographic and socioeconomic changes, endogenous selection of births, and preexisting trends in the outcome. Our findings contribute to the growing body of research that explores the in-utero and childhood circumstances on long-term health outcomes.     

Family Member Deaths in Childhood Predict Systemic Inflammation in Late Life

Biological and epidemiological evidence has linked early-life psychosocial stress with late-life health, with inflammation as a potential mechanism. We report here the association between familial death in childhood and adulthood and increased levels of high-sensitivity C-reactive protein (CRP), a marker of systemic inflammation. The Cache County Memory Study is a prospective study of persons initially aged 65 and older in 1995. In 2002, there were 1,955 persons in the study with data on CRP (42.3 percent male, mean [SD] age = 81.2 [5.8] years), linked with objective data on family member deaths. Using logistic regression, high (> 10 mg/L) versus low (≤ 10 mg/L) CRP was regressed on cumulative parental, sibling, spouse, and offspring deaths during childhood and during early adulthood, adjusted for family size in each period (percentage family depletion; PFD). Findings revealed PFD during childhood to be significantly associated with CRP (OR = 1.02, 95% CI [1.01, 1.04]). Individuals with two or more family deaths were 79 percent more likely to have elevated CRP than those with zero family deaths (OR = 1.79, 95% CI [1.07, 2.99]). Early adulthood PFD was not related to CRP. This study demonstrates a link between significant psychosocial stress in early life and immune-inflammatory functioning in late life, and suggests a mechanism explaining the link between early-life adversity and late-life health.     

Socioeconomic inequalities in prevalence and development of multimorbidity across adulthood: A longitudinal analysis of the MRC 1946 National Survey of Health and Development in the UK

BackgroundWe aimed to estimate multimorbidity trajectories and quantify socioeconomic inequalities based on childhood and adulthood socioeconomic position (SEP) in the risks and rates of multimorbidity accumulation across adulthood.Methods and findingsParticipants from the UK 1946 National Survey of Health and Development (NSHD) birth cohort study who attended the age 36 years assessment in 1982 and any one of the follow-up assessments at ages 43, 53, 63, and 69 years (N = 3,723, 51% males). Information on 18 health conditions was based on a combination of self-report, biomarkers, health records, and prescribed medications. We estimated multimorbidity trajectories and delineated socioeconomic inequalities (based on childhood and adulthood social class and highest education) in multimorbidity at each age and in longitudinal trajectories.Multimorbidity increased with age (0.7 conditions at 36 years to 3.7 at 69 years). Multimorbidity accumulation was nonlinear, accelerating with age at the rate of 0.08 conditions/year (95% CI 0.07 to 0.09, p < 0.001) at 36 to 43 years to 0.19 conditions/year (95% CI 0.18 to 0.20, p < 0.001) at 63 to 69 years. At all ages, the most socioeconomically disadvantaged had 1.2 to 1.4 times greater number of conditions on average compared to the most advantaged. The most disadvantaged by each socioeconomic indicator experienced an additional 0.39 conditions (childhood social class), 0.83 (adult social class), and 1.08 conditions (adult education) at age 69 years, independent of all other socioeconomic indicators. Adverse adulthood SEP was associated with more rapid accumulation of multimorbidity, resulting in 0.49 excess conditions in partly/unskilled compared to professional/intermediate individuals between 63 and 69 years. Disadvantaged childhood social class, independently of adulthood SEP, was associated with accelerated multimorbidity trajectories from age 53 years onwards.Study limitations include that the NSHD cohort is composed of individuals of white European heritage only, and findings may not be generalizable to the non-white British population of the same generation and did not account for other important dimensions of SEP such as income and wealth.ConclusionsIn this study, we found that socioeconomically disadvantaged individuals have earlier onset and more rapid accumulation of multimorbidity resulting in widening inequalities into old age, with independent contributions from both childhood and adulthood SEP.

Amal Khanolkar and co-workers study associations between multimorbidity and socioeconomic position in the UK.