Objectives

Alterations in adult hypothalamic-pituitary-adrenal (HPA) axis activity have increasingly been linked with early life stress and adult depression, but a limited number of studies have used longitudinal data to explore HPA axis dysregulation as an underlying mechanism driving the long-term depressive impacts of early stressors. Here we address potential long-term impacts of early life, family-based stress on depressive symptoms among young adults in a longitudinal birth cohort study begun in 1983 in the Philippines.

Materials and methods

We relate a composite measure of family-based stressors experienced between birth and adolescence to circadian dynamics in adult salivary cortisol and depressive risk measured at 21-22 years of age. Multiple regression analyses were conducted to examine the relationship between early life stress levels and risk of adult depressive symptoms, as well as the role of adult diurnal cortisol activity in this relationship.

Results

Greater levels of early life familial stress predicted more severe depressive symptomatology at age 21-22 in a dose-response fashion (p < .0001) independent of adult diurnal cortisol patterns. Flatter diurnal cortisol slopes are directly associated with higher adult depressive symptoms, an effect mostly driven by evening cortisol levels (p = .004). When considering the cumulative effects of early life stress measures, however, exposure to more of these stressors during development is associated with even higher depressive symptoms.

Discussion

The long-term depressive effects of early life familial stress extend to this large sample of Cebuano young adults, and early life stress and HPA axis function may shape adult depressive symptoms through independent pathways in this sample. Our findings provide further evidence that HPA axis activity is shaped by early life conditions and is associated with depressive symptoms.

Chronic inflammation is a potentially important physiological mechanism linking early life environments and health in adulthood. Elevated concentrations of C-reactive protein (CRP)--a key biomarker of inflammation--predict increased cardiovascular and metabolic disease risk in adulthood, but the developmental factors that shape the regulation of inflammation are not known. We investigated birth weight and breastfeeding duration in infancy as predictors of CRP in young adulthood in a large representative cohort study (n = 6951). Birth weight was significantly associated with CRP in young adulthood, with a negative association for birth weights 2.8 kg and higher. Compared with individuals not breastfed, CRP concentrations were 20.1%, 26.7%, 29.6% and 29.8% lower among individuals breastfed for less than three months, three to six months, 6-12 months and greater than 12 months, respectively. In sibling comparison models, higher birth weight was associated with lower CRP for birth weights above 2.5 kg, and breastfeeding greater than or equal to three months was significantly associated with lower CRP. Efforts to promote breastfeeding and improve birth outcomes may have clinically relevant effects on reducing chronic inflammation and lowering risk for cardiovascular and metabolic diseases in adulthood.

Individuals' social experiences are associated with their mental health, physical health, and even mortality. Over the last 30 years, researchers have examined the ways in which these social experiences might be associated with chronic inflammation - a component underlying many of the chronic diseases of aging. Little research, however, has examined the role of adults' attachment style as a specific social component that might be associated with inflammation. In the present study, we utilized data from a sample of 59 African-American adults from the Maryland Adolescent Development in Context Study (MADICS) to examine the links between attachment avoidance and attachment anxiety and C-reactive protein (CRP) and interleukin (IL)-6. After controlling for demographic characteristics, body mass index, and depressive symptoms, attachment avoidance and anxiety were associated with IL-6 but not CRP. This study adds to the growing body of research identifying the wide range of social experiences associated with inflammation and further suggests that attachment relationship experiences may have implications for biological processes relevant to many chronic diseases of aging.

Background and objective

Rates of paternal depression range from 5% to 10% with a growing body of literature describing the harm to fathers, children, and families. Changes in depression symptoms over the life course, and the role of social factors, are not well known. This study examines associations with changes in depression symptoms during the transition to fatherhood for young fathers and whether this association differed by key social factors.

Methods

We combined all 4 waves of the National Longitudinal Study of Adolescent Health to support a 23-year longitudinal analysis of 10 623 men and then created a "fatherhood-year" data set, regressing age-adjusted standardized depressive symptoms scores on fatherhood status (nonresidence/residence), fatherhood-years, and covariates to determine associations between Center for Epidemiologic Studies Depression Scale scores and fatherhood life course intervals.

Results

Depressive symptom scores reported at the entry into fatherhood are higher for nonresident fathers than nonfathers, which in turn are higher than those of resident fathers. Resident fathers have a significant decrease in scores during late adolescence (β = -0.035, P = .023), but a significant increase in scores during early fatherhood (β = 0.023, P = .041). From entrance into fatherhood to the end of early fatherhood (+5 years), the depressive symptoms score for resident fathers increases on average by 68%.

Conclusions

In our longitudinal, population-based study, resident fathers show increasing depressive symptom scores during children's key attachment years of 0-5. Identifying at-risk fathers based on social factors and designing effective interventions may ultimately improve health outcomes for the entire family.

Childhood and adolescent adversity is of great interest in relation to risk for psychopathology, and interview measures of adversity are thought to be more reliable and valid than their questionnaire counterparts. One interview measure, the Childhood Trauma Interview (CTI; Fink et al., 1995), has been positively evaluated relative to similar measures, but there are some psychometric limitations to an existing scoring approach that limit the full potential of this measure. We propose several new summary indices for the CTI that permit examination of different types of adversity and different developmental periods. Our approach creates several summary indices: one sums the severity scores of adversities endorsed; another utilizes the number of minor and major (moderate to severe) adversities. The new indices were examined in association with first onsets of major depressive disorder (MDD) and anxiety disorders across a 5-year period using annual clinical diagnostic interviews (Structured Clinical Interview for DSM-IV-TR). Summary scores derived with the previously used approach were also examined for comparison. Data on 332 participants came from the Youth Emotion Project, a longitudinal study of risk for emotional disorders. Results support the predictive validity of the proposed summary scoring methods and indicate that several forms of major (but typically not minor) adversity are significantly associated with first onsets of MDD and anxiety disorders. Finally, multivariate regression models show that, in many instances, the new indices contributed significant unique variance predicting disorder onsets over and above the previously used summary indices.

Meta-analytic evidence supports a gene-environment (G×E) interaction between life stress and the serotonin transporter polymorphism (5-HTTLPR) on depression, but few studies have examined factors that influence detection of this effect, despite years of inconsistent results. We propose that the "candidate environment" (akin to a candidate gene) is key. Theory and evidence implicate major stressful life events (SLEs)-particularly major interpersonal SLEs-as well as chronic family stress. Participants (N = 400) from the Youth Emotion Project (which began with 627 high school juniors oversampled for high neuroticism) completed up to five annual diagnostic and life stress interviews and provided DNA samples. A significant G×E effect for major SLEs and S-carrier genotype was accounted for significantly by major interpersonal SLEs but not significantly by major non-interpersonal SLEs. S-carrier genotype and chronic family stress also significantly interacted. Identifying such candidate environments may facilitate future G×E research in depression and psychopathology more broadly.

Despite a growing understanding that the social determinants of health have an impact on body mass index (BMI), the role of fatherhood on young men's BMI is understudied. This longitudinal study examines BMI in young men over time as they transition from adolescence into fatherhood in a nationally representative sample. Data from all four waves of the National Longitudinal Study of Adolescent Health supported a 20-year longitudinal analysis of 10,253 men beginning in 1994. A "fatherhood-year" data set was created and changes in BMI were examined based on fatherhood status (nonfather, nonresident father, resident father), fatherhood years, and covariates. Though age is positively associated with BMI over all years for all men, comparing nonresident and resident fathers with nonfathers reveals different trajectories based on fatherhood status. Entrance into fatherhood is associated with an increase in BMI trajectory for both nonresident and resident fathers, while nonfathers exhibit a decrease over the same period. In this longitudinal, population-based study, fatherhood and residence status play a role in men's BMI. Designing obesity prevention interventions for young men that begin in adolescence and carry through young adulthood should target the distinctive needs of these populations, potentially improving their health outcomes.

Cigarette smoking and alcohol consumption during pregnancy can have detrimental effects on the developing fetus, including fetal alcohol syndrome and low birth weight. Surprisingly little is known about the association of personality traits with smoking and alcohol consumption in the specific subpopulation of pregnant women. This study analyzed data from a geographically diverse sample of 603 pregnant women, aged 18 years and older, who provided information regarding their smoking and drinking habits before and during pregnancy. We compared women who consumed alcohol or smoked cigarettes before pregnancy with women who quit or continued smoking or drinking during pregnancy. Associations between personality and maladaptive behaviors prior to and during pregnancy were modeled using logistic regression. The study revealed that women who scored high on openness to experience were significantly more likely to continue alcohol consumption during pregnancy (OR = 1.07, 95% CI 1.01, 1.14, p = .02). This association was maintained after adjusting for potential confounds. This study demonstrated a significant relationship between personality traits and women's likelihood of continued alcohol consumption prior to and during pregnancy. Understanding personality-based determinants of health-detrimental behavior is important in order to design interventions that aim at decreasing rates of maladaptive health behaviors among pregnant women.

Purpose

With a growing focus on the importance of men's reproductive health, including preconception health, the ways in which young men's knowledge, attitudes, and beliefs (KAB) predict their reproductive paths are understudied. To determine if reproductive KAB predicts fatherhood status, timing and residency (living with child or not).

Methods

Reproductive KAB and fatherhood outcomes were analyzed from the National Longitudinal Study of Adolescent Health, a 20-year, nationally representative study of individuals from adolescence into adulthood. Four measures of reproductive KAB were assessed during adolescence in waves I and II. A generalized linear latent and mixed model predicted future fatherhood status (nonfather, resident/nonresident father, adolescent father) and timing while controlling for other socio-demographic variables.

Results

Of the 10,253 men, 3,425 were fathers (686 nonresident/2,739 resident) by wave IV. Higher risky sexual behavior scores significantly increased the odds of becoming nonresident father (odds ratio [OR], 1.30; p < .0001), resident father (OR, 1.07; p = .007), and adolescent father (OR, 1.71; p < .0001); higher pregnancy attitudes scores significantly increased the odds of becoming a nonresident father (OR, 1.20; p < .0001) and resident father (OR, 1.11; p < .0001); higher birth control self-efficacy scores significantly decreased the odds of becoming a nonresident father (OR, .72; p < .0001) and adolescent father (OR, .56; p = .01).

Conclusions

Young men's KAB in adolescence predicts their future fatherhood and residency status. Strategies that address adolescent males' reproductive KAB are needed in the prevention of unintended reproductive consequences such as early and nonresident fatherhood.

The current study investigates whether prepregnancy maternal posttraumatic stress disorder (PTSD) symptoms, depressive symptoms, and stress predict children's cortisol diurnal slopes and cortisol awakening responses (CARs) adjusting for relevant variables. Mothers were enrolled after delivering a baby and followed through their subsequent pregnancy with 5 years of longitudinal data on their subsequent child. This prospective design allowed assessment of PTSD symptoms, depressive symptoms, and perceived stress prior to pregnancy. Children provided three saliva samples per day on three consecutive days at two timepoints in early childhood (M age = 3.7 years, SD = 0.38; M age = 5.04 years, SD = 0.43). Mothers' PTSD symptoms prior to pregnancy were significantly associated with flatter child diurnal cortisol slopes at 4 and 5 years, but not with child CAR. Findings at the age of 4 years, but not 5 years, remained statistically significant after adjustment for maternal socioeconomic status, race/ethnicity, child age, and other covariates. In contrast, maternal prepregnancy depressive symptoms and perceived stress did not significantly predict cortisol slopes or CAR. Results suggest that maternal prepregnancy PTSD symptoms may contribute to variation in early childhood physiology. This study extends earlier work demonstrating risk of adverse outcomes among children whose mothers experienced trauma but associations cannot be disentangled from effects of prenatal mental health of mothers on children's early childhood.