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Since its conceptualization, there has been a lack of consensus on the best way to operationalize allostatic load (AL). As a marker of the cumulative, physiological wear and tear on the body resulting from chronic exposure to stressors, it follows that AL should be higher among people who have faced more stressful life experiences. Thus, the purpose of this study was to construct AL scores using different operationalizations and, as a measure of construct validity, compare whether each construction produced expected disparities in AL by race and a composite socioeconomic status (SES) variable which accounts for measures over the life course; we also explored differences by sex. We conducted the study in a sample of 45-52-year-old offspring from the Child Health and Development Studies, a longitudinal birth cohort established in the early 1960s. AL scores were constructed in 6 different ways and included 10 biomarkers from inflammatory, neuroendocrine, cardiovascular, and metabolic systems. Our main approach to constructing AL was to sum across high-risk biomarker quartiles, correct for medication use, and use sex-specific high-risk quartiles for specific biomarkers. Alternative constructions did not use sex-specific quartiles and/or weighted biomarkers within subsystems and/or did not correct for medication use. We estimated differences in AL scores by race, SES, sex and their pairwise interactions. All constructions of AL, including the main approach, produced expected disparities by race (higher scores for Black vs. non-Black participants) and life course SES (higher scores for low vs. high SES participants). However, disparities by sex only emerged when the AL score was constructed via approaches that did not use sex-specific high-risk quartiles; for these alternative constructions, overall, female participants had higher AL scores than male participants and Black female participants had the highest AL scores in the sample. For most constructions, the pairwise interaction between sex and SES, showed a stronger disparity in AL scores between low and high-SES female compared with low- and high-SES male participants; this suggests that, in terms of lowering AL, high life course SES may be more important for female than male participants. In conclusion, our results suggest that the basic AL concept is consistently expressed in different operationalizations, making it an especially useful and robust tool for understanding disparities by race and SES.

Little research has investigated the long-term relationship between low wages and memory decline, despite the growing share of low-wage workers in the US labor market. Here, we examined whether cumulative exposure to low wages over 12 years in midlife is associated with memory decline in later life. Using 1992–2016 data from the Health and Retirement Study, we analyzed data from 2,879 individuals born in 1936–1941 using confounder-adjusted linear mixed-effects models. Low-wage work was defined as an hourly wage lower than two-thirds of the federal median wage for the corresponding year and was categorized into “never,” “intermittent,” and “sustained” based on wages earned from 1992 to 2004. Memory function was measured at each study visit from 2004 to 2016 via a memory composite score. The confounder-adjusted annual rate of memory decline among “never” low-wage earners was −0.12 standard units (95% confidence interval: −0.13, −0.10). Compared with this, memory decline among workers with sustained earning of low midlife wages was significantly faster (βtime×sustained = −0.014, 95% confidence interval: −0.02, −0.01), corresponding to an annual rate of −0.13 standard units for this group. Sustained low-wage earning in midlife was significantly associated with a downward trajectory of memory performance in older age. Enhancing social policies to protect low-wage workers may be especially beneficial for their cognitive health.

ImportanceEarning a low wage is an increasingly recognized public health concern, yet little research exists on the long-term health consequences of sustained low-wage earning.ObjectiveTo examine the association of sustained low-wage earning and mortality in a sample of workers with hourly wage reported biennially during peak midlife earning years.Design, Setting, and ParticipantsThis longitudinal study included 4002 US participants, aged 50 years or older, from 2 subcohorts of the Health and Retirement Study (1992-2018) who worked for pay and reported earning hourly wages at 3 or more time points during a 12-year period during their midlife (1992-2004 or 1998-2010). Outcome follow-up occurred from the end of the respective exposure periods until 2018.ExposuresLow-wage—less than the hourly wage for full-time, full-year work at the federal poverty line—earning history was categorized as never earning a low wage, intermittently earning a low wage, and sustained earning a low wage.Main Outcomes and MeasuresCox proportional hazards and additive hazards regression models sequentially adjusted for sociodemographics, and economic and health covariates were used to estimate associations between low-wage history and all-cause mortality. We examined interaction with sex or employment stability on multiplicative and additive scales.ResultsOf the 4002 workers (aged 50-57 years at the beginning of exposure period and 61-69 years at the end), 1854 (46.3%) were female; 718 (17.9%) experienced employment instability; 366 (9.1%) had a history of sustained low-wage earning; 1288 (32.2%) had intermittent low-wage earning periods; and 2348 (58.7%) had never earned a low wage. In unadjusted analyses, those who had never earned low wages experienced 199 deaths per 10 000 person-years, those with intermittent low wages, 208 deaths per 10 000 person-years, and those with sustained low wages, 275 deaths per 10 000 person-years. In models adjusted for key sociodemographic variables, sustained low-wage earning was associated with mortality (hazard ratio [HR], 1.35; 95% CI, 1.07-1.71) and excess deaths (66; 95% CI, 6.6-125); these findings were attenuated with additional adjustments for economic and health covariates. Significant excess death and elevated mortality risk were observed for workers with sustained low-wage exposure and employment fluctuations (eg, for sustained low-wage × employment fluctuated, HR, 2.18; 95% CI, 1.35-3.53; for sustained low-wage × stable employment, HR, 1.17; 95% CI, 0.89,-1.54; P for interaction = .003).Conclusions and RelevanceSustained low-wage earning may be associated with elevated mortality risk and excess deaths, especially when experienced alongside unstable employment. If causal, our findings suggest that social and economic policies that improve the financial standing of low-wage workers (eg, minimum wage laws) could improve mortality outcomes.

Early menarche is associated with adverse health outcomes during adolescence as well as breast and other reproductive cancers later in adulthood. However, the causes of early menarche and the pathways through which they operate are not fully understood. Though maternal thyroid function during pregnancy affects child growth, and rapid childhood growth is associated with a decreased age at menarche, the relationship between prenatal maternal thyroid function and daughters’ age at menarche has not been examined. We conducted a mediation analysis in a historical cohort of 260 mother-child pairs to estimate the total and indirect effects of maternal prenatal thyroid function on daughters’ age at menarche. No association was observed between thyroid stimulating hormone (TSH) or anti-thyroid peroxidase antibodies (ATPO) and daughters’ age at menarche. Using a sample-specific, a-priori cutoff at the 10th percentile, low levels of maternal free thyroxine (FT4) were associated with earlier daughter age at menarche, with a hazard ratio (95 % CI) of 1.70 (1.02, 2.84) comparing the bottom 10th percentile with the top 90th percentile of exposure levels. Higher maternal FT4 was associated with rapid child weight gain from ages 5–9, and rapid child weight gain from ages 5–9 was associated with earlier age at menarche; the estimated indirect effect of this pathway was null. While maternal FT4 is associated with earlier age at menarche in daughters, this is not mediated by rapid weight gain in our study population, suggesting that maternal FT4 is operating through a different pathway.

Objective Epidemiologic and clinical research papers often describe the study sample in the first table. If well-executed, this “Table 1” can illuminate potential threats to internal and external validity. However, little guidance exists on best practices for designing a Table 1, especially for complex study designs and analyses. We aimed to summarize and extend the literature related to reporting descriptive statistics. Study Design and Setting In consultation with existing guidelines, we synthesized and developed reporting recommendations driven by study design and focused on transparency related to potential threats to internal and external validity. Results We describe a basic structure for Table 1 and discuss simple modifications in terms of columns, rows, and cells to enhance a reader's ability to judge both internal and external validity. We further highlight several analytic complexities common in epidemiologic research (missing data, sample weights, clustered data, and interaction) and describe possible variations to Table 1 to maintain and add clarity about study validity in light of these issues. We discuss considerations and tradeoffs in Table 1 related to breadth and comprehensiveness vs. parsimony and reader-friendliness. Conclusion We anticipate that our work will guide authors considering layouts for Table 1, with attention to the reader's perspective.

Purpose The purpose of this study was to assess when in the life-course race-by-sex disparities in body mass index (BMI) emerge. Methods Child Health and Development Studies participants, from whom height and weight data were collected at ages 5, 9–11, and 15–17 years, were followed up at the age of 50 years for anthropometric outcomes. Follow-up was completed for 605 subjects, 460 of whom were assessed for height and weight at the age of 50 years, had at least one available childhood BMI measure, and self-identified as either non-Hispanic black or non-Hispanic white. Linear regression analyses were conducted to determine whether interactions existed between race (black vs. white) and sex for predicting BMI at ages 5, 9–11, 15–17, and 50 years. Results At age 5 years, BMI was independent of sex for both blacks and whites, but by the age of 9–11 years, BMI was sex-dependent in blacks, with higher BMI observed among black females. This sex dependence for BMI among blacks persisted at ages 15–17 years and age 50 years. The race-by-sex interaction was significant at ages 9–11, 15–17, and 50 years (P for interaction = 0.001, 0.002, and 0.01, respectively). Conclusions Race-by-sex disparities in body size were observed by the age of 9–11 years and persisted until the age of 50 years.

In any research study, there is an underlying process that should begin with a clear articulation of the study’s goal. The study’s goal drives this process; it determines many study features, including the estimand of interest, the analytic approaches that can be used to estimate it, and which coefficients, if any, should be interpreted. Misalignment can occur in this process when analytic approaches and/or interpretations do not match the study’s goal; misalignment is potentially more likely to arise when study goals are ambiguously framed. In this study, misalignment in the observational epidemiologic literature was documented and how the framing of study goals contributes to misalignment was explored. The following 2 misalignments were examined: use of an inappropriate variable selection approach for the goal (a “goal–methods” misalignment) and interpretation of coefficients of variables for which causal considerations were not made (e.g., Table 2 Fallacy, a “goal–interpretation” misalignment). A random sample of 100 articles published 2014–2018 in the top 5 general epidemiology journals were reviewed. Most reviewed studies were causal, with either explicitly stated (n = 13; 13%) or associational-framed (n = 71; 69%) aims. Full alignment of goal–methods–interpretations was infrequent (n = 9; 9%), although clearly causal studies (n = 5 of 13; 38%) were more often fully aligned than were seemingly causal ones (n = 3 of 71; 4%). Goal–methods misalignments were common (n = 34 of 103; 33%), but most frequently, methods were insufficiently reported to draw conclusions (n = 47; 46%). Goal–interpretations misalignments occurred in 31% (n = 32) of the studies and occurred less often when the methods were aligned (n = 2; 2%) compared with when the methods were misaligned (n = 13; 13%).

Lifecourse epidemiology is hampered by the absence of studies with exposures and outcomes measured at different life stages. We describe when the effect of an exposure (A) on an outcome (Y) in a target population is identifiable in a combined (“synthetic”) cohort created by pooling an early-life cohort including exposure measures with a late-life cohort including outcome measures. We enumerate the causal assumptions needed for unbiased effect estimation in the synthetic cohort and illustrate by simulating target populations under four causal models. From each population, we drew hypothetical early- and late-life cohorts and created a synthetic cohort by matching individuals from the two cohorts based on mediators and/or confounders. We compared bias when estimating the effect of A on Y in the synthetic cohort, varying which matching variables were available, the match ratio, and the distance matching criterion. When the set of matching variables includes all variables d-connecting exposure and outcome (i.e., variables blocking all back and front door pathways), the synthetic cohort yields unbiased effect estimates. Methods based on merging cohorts provide opportunities to hasten the evaluation of early- and mid-life determinants of late life health, but rely on available measures of both confounders and mediators.

Background: Obesity is present in 17% of US youth, age 2–19 years, but the extent to which obesity in childhood is associated with higher BMI and fat mass in middle age is unclear. In this study, links between childhood body size and BMI and body composition at age ∼50 were assessed. Methods: Child Health and Development Studies participants, born between 1960 and 1963 in Alameda County, and still living in California, from whom anthropometric data were collected at age 5, 9–11, and/or 15–17 years were followed-up at age ∼50 for anthropometric outcomes (251 women; 249 men). Linear regression analyses assessed whether overweight (85th to

We strongly support efforts to generate, rigorously test, and falsify hypotheses derived from the Environmental Affordances (EA) Model of Health Disparities, as originated by the late Dr. James S. Jackson (1940–2020). Such efforts are critical to establishing robust, theoretically grounded scientific frameworks that explain the fundamental causes of racial disparities in health and wellbeing. Pamplin et al. (2021) fundamentally misrepresents the EA Model as a framework that (falsely) reifies the role of race as a determinant of health behaviors and health outcomes. Further, both their study design and analytic approach are inappropriate for testing predictions of this framework. We address these issues with the goal of recentering the scholarly conversation about how stress contributes to health, and disparities in health, over the life course.

In a sample of 442 births from the Child Health and Development Studies cohort, we examined associations between maternal prenatal exposure to hydroxylated polychlorinated biphenyl metabolites (OH-PCBs) and pregnancy outcomes, and whether associations were mediated by maternal thyroid hormone levels and/or modified by maternal smoking. Compared to nonsmokers, smokers had twice the mean concentration of 4-OH-CB107 (p

The authors examined the relationship of prepregnancy body mass index (BMI) and gestational weight gain (GWG) with child neurodevelopment. Mother-child dyads were a subgroup (n = 2,084) of the Child Health and Development Studies from the Oakland, California, area enrolled during pregnancy from 1959 to 1966 and followed at child age 9 years. Linear regression was used to examine associations between prepregnancy BMI, GWG, and standardized Peabody Picture Vocabulary Test and Raven Progressive Matrices scores and to evaluate effect modification of GWG by prepregnancy BMI. Before pregnancy, 77% of women were normal weight, 8% were underweight, 11% were overweight, and 3% were obese. Associations between GWG and child outcomes did not vary by prepregnancy BMI, suggesting no evidence for interaction. In multivariable models, compared to normal prepregnancy BMI, prepregnancy overweight and obesity were associated with lower Peabody scores (b: -1.29; 95% CI [-2.6, -0.04] and b: -2.7; 95% CI [-5.0, -0.32], respectively). GWG was not associated with child Peabody score [b: -0.03 (95% CI: -0.13, 0.07)]. Maternal BMI and GWG were not associated with child Raven score (all P >0.05). Maternal prepregnancy overweight and obesity were associated with lower scores for verbal recognition in mid-childhood. These results contribute to evidence linking maternal BMI with child neurodevelopment. Future research should examine the role of higher prepregnancy BMI values and the pattern of pregnancy weight gain in child cognitive outcomes.

Extensive evidence leads us to expect that health disparities by race and socioeconomic status found in one generation might be reproduced in the next. To the extent that this occurs it is important to assess life course processes responsible for the reproduction. Prospective evidence concerning such life course processes is hard to come by as it requires long-term follow-up of individuals from childhood through adult life. We present data from the Child Health and Development Disparities study that provides evidence relevant to this issue with respect to self-rated health. Mothers and offspring recruited in California's Bay Area between 1959 and 1967 were assessed during pregnancy with follow-up exams of offspring along with in-person interviews with mothers (at offspring ages 5, 9-11, 15-17) and offspring (at ages 15-17, ∼50). Available data allow us to assess the importance of three potential life course pathways in the reproduction of inequalities in self-rated health - socioeconomic pathways, cognitive pathways and pathways involving emerging health itself. As expected we found that race and SES disparities in SRH are reproduced across generations. They are evident in mothers, not strong or significant in offspring at 15-17, but present once again in offspring at age ∼50. Concerning potential pathways, we found that indicators of child health were related to adult SRH and played some role in accounting for race but not SES disparities in adult SRH. Cognitive abilities were unrelated to adult SRH with childhood SES controlled. Childhood SES was associated with adult SRH independent of other childhood factors and is reduced to non-significance only when offspring college attainment is controlled. Race and SES disparities in self-reported health in one generation are re-expressed in the next with strongest support for SES pathways in this transmission.

Purpose Cognitive development during adolescence affects health long term. We investigated whether level of and change in language-based cognition during adolescence are associated with cognitive performance in midlife. Methods Participants were enrolled in the Child Health and Development Study and followed during midlife (47–52 years). Adolescent cognition was measured with the Peabody Picture Vocabulary Test at ages 9–11 years (PPVT-9) and 15–17 years (PPVT-15). We examined PPVT-9, as well as a PPVT change score (derived using the standardized regression-based method) in relation to midlife cognition measures of Wechsler Test of Adult Reading, Verbal Fluency, and Digit Symbol tests. Linear regression models were adjusted for childhood socioeconomic status, age, sex, race, and midlife marital status, education, and occupational score. Results In 357 participants (52.1% female, 25.6% African American), both PPVT-9 (β [95% confidence interval [CI] = 0.26 [0.18, 0.34]) and PPVT change score (β [95% CI] = 2.03 [1.27, 2.80]) were associated with Wechsler Test of Adult Reading at midlife. PPVT-9 was associated with midlife Verbal Fluency (β [95% CI] = 0.18 [0.10, 0.25]), whereas PPVT change score was not (β [95% CI] = −0.01 [−0.68, 0.67]). Neither PPVT-9 nor PPVT change score was associated with midlife Digit Symbol. Conclusions Both level of and change in language-based cognition during adolescence were associated with midlife vocabulary and language function, even after controlling for midlife occupation and education.

BACKGROUND AND OBJECTIVE: In adults, leukocyte telomere length (LTL) is variable, familial, and longer in women and in offspring conceived by older fathers. Although short LTL is associated with atherosclerotic cardiovascular disease, long LTL is associated with major cancers. The prevailing notion is that LTL is a “telomeric clock,” whose movement (expressed in LTL attrition) reflects the pace of aging. Accordingly, individuals with short LTL are considered to be biologically older than their peers. Recent studies suggest that LTL is largely determined before adulthood. We examined whether factors that largely characterize LTL in adults also influence LTL in newborns. METHODS: LTL was measured in blood samples from 490 newborns and their parents. RESULTS: LTL (mean ± SD) was longer (9.50 ± 0.70 kb) in newborns than in their mothers (7.92 ± 0.67 kb) and fathers (7.70 ± 0.71 kb) (both P < .0001); there was no difference in the variance of LTL among the 3 groups. Newborn LTL correlated more strongly with age-adjusted LTL in mothers (r = 0.47; P < .01) than in fathers (r = 0.36; P < .01) (P for interaction = .02). Newborn LTL was longer by 0.144 kb in girls than in boys (P = .02), and LTL was longer by 0.175 kb in mothers than in fathers (P < .0001). For each 1-year increase in father’s age, newborn LTL increased by 0.016 kb (95% confidence interval: 0.04 to 0.28) (P = .0086). CONCLUSIONS: The large LTL variation across newborns challenges the telomeric clock model. Having inherently short or long LTL may be largely determined at birth, anteceding by decades disease manifestation in adults.

Introduction Previous research suggests that prenatal exposure to chlorinated compounds, such as polychlorinated biphenyls (PCBs) may be associated with adverse birth outcomes. However, there are n...

Organochlorine pesticides (OCPs) are persistent endocrine disruptors. OCPs cross the placenta; this prenatal exposure has been associated with adverse pregnancy outcomes. We investigated associations between prenatal exposure to OCPs and gestational age and birth weight in 600 infants born between 1960 and 1963. The primary OCP was 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (p,p′-DDT), its primary metabolite, 1,1′-dichloro-2,2'-bis(p-chlorophenyl)ethylene(p,p′-DDE) and the contaminant, 1,1,1-trichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl)-ethane (o,p′-DDT). Regression analysis indicated that for each natural log unit increase in p,p′-DDT, birth weight increased by 274 grams (95% CI 122, 425) when controlling for p,p′-DDE and o,p′-DDT. At a given level of p,p′-DDT exposure, o,p′-DDT and p,p′-DDE were associated with decreased birth weight. p,p′-DDE was negatively associated with length of gestation, controlling for p,p′-DDT and o,p′-DDT. These findings suggest opposing associations between exposure to p,p′-DDT and p,p′-DDE and birth weight. We did not find evidence to support mediation by maternal thyroid hormone status nor that the association differed by sex.

Background Polychlorinated biphenyls (PCBs), known endocrine disruptors, were banned in 1979 but persist in the environment. Previous studies are inconsistent regarding prenatal exposure to PCBs and pregnancy outcomes. We investigated associations between prenatal exposure to PCBs and gestational length and birth weight. Methods In a sample of 600 infants (born between 1960 and 1963) randomly selected from Child Health and Development Studies participants followed through adolescence we measured 11 PCB congeners in maternal post partum sera (within three days of delivery). Length of gestation was computed from the reported first day of the last menstrual period (LMP) and delivery date. Linear regression was used to estimate associations between PCB exposure and gestational age and birth weight, adjusting for potential confounders. PCBs were grouped according to hypothesized biological action (1b (sum of weak phenobarbital inducers), 2b (sum of limited dioxin activity), and 3 (sum of CYP1A and CYP2b inducers)) or degree of ortho- substitution (mono, di, tri). Secondary analyses examined associations between total PCB exposure and exposure to individual congeners. Results Each unit increase in mono-ortho substituted PCBs was associated with a 0.30 week decrease (95% confidence interval (CI) -0.59, -0.016), corresponding to a 2.1 (95% CI −4.13, -0.11) day decrease in length of gestation. Similar associations were estimated for di-ortho substituted PCBs, (1.4 day decrease; (95% CI −2.9, 0.1)) and group 3 PCBs (0.84 day decrease; (95% CI −1.8, 0.11). We found similar associations in congener specific analyses and for the sum of congeners. Conclusions Our study provides new evidence that PCB exposure shortens length of gestation in humans. This may have public health implications for population exposures.