Parenting mediates the impact of maternal depression on child internalizing symptoms

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141761/1/da22688.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141761/2/da22688_am.pd

Three Essays on Worldviews, Autonomy and the Family in Nepal.

This dissertation consists of three papers on the interrelatedness of beliefs about family behavior, beliefs about societal development, and variation in family behaviors in a rapidly changing social context. The first two essays address the beliefs of ordinary people concerning the relationship between family change and societal modernization. The last essay examines the ways in which individual, parental, and local community beliefs about spouse choice influence later spouse choice participation. My first two essays incorporate two prominent theories of social life—the modernization theory and W.I. Thomas’ theorem that people’s perceptions have real consequences—into an examination of the belief systems of people living in Nepal’s Chitwan Valley. In the first essay I document the extent to which survey respondents expect certain family types (late marriage, polygamy, small families) to be in certain types of societies (developed, poor, educated), and the extent to which they believe family change and societal change are causally connected. Survey results from this rural population in Nepal suggest that the majority of people strongly believe that behaviors related to fertility, marriage, and gender equality are causally related to societal development. Respondents provide similar answers whether a society changes via education, wealth, or development. The second essay extends previous work by examining subgroup variation in belief in developmental models. Results based on the Nepal survey data demonstrate that the most disadvantaged and geographically isolated groups are the most likely to reject aspects of the developmental model. Respondents with higher levels of education and mass media consumption are more supportive of developmental models. In the third essay I create a theoretical framework to explain how the individual, family and local community interrelate to determine spouse choice behavior. This framework pays particular attention to the role of education as an allocator of social status and influence. Analyses on a sample from Nepal show that the attitudes of both young adults and their fathers influence participation in spouse choice, and that young adults with higher levels of education are significantly more likely to get the level of participation they desire than do their counterparts with lower levels of education.Ph.D.SociologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/64614/1/cmsm_1.pd

Early Women, Late Men: Timing Attitudes and Gender Differences in Marriage

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138327/1/jomf12426_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138327/2/jomf12426.pd

Family structure instability, genetic sensitivity and child wellbeing

The association between family structure instability and children’s life chances is well documented, with children reared in stable, two-parent families experiencing more favorable outcomes than children in other family arrangements. This study examines father household entrances and exits, distinguishing between the entrance of a biological father and a social father and testing for interactions between family structure instability and children’s age, gender, and genetic characteristics. Using data from the Fragile Families and Child Wellbeing Study and focusing on changes in family structure by age (years 0–9), the authors show that father exits are associated with increases in children’s antisocial behavior, a strong predictor of health and well-being in adulthood. The pattern for father entrances is more complicated, with entrances for the biological father being associated with lower antisocial behavior among boys and social father entrances being associated with higher antisocial behavior. Child’s age does not moderate the association; however, genetic information in the models sharpens the findings substantially

Sensitive periods for the effect of child maltreatment on psychopathology symptoms in adolescence

Introduction: Child maltreatment is among the strongest risk factors for mental disorders. However, little is known about whether there are ages when children may be especially vulnerable to its effects. We sought to identify potential sensitive periods when exposure to the 2 most common types of maltreatment (neglect and harsh physical discipline) had a particularly detrimental effect on youth mental health. Methods: Data came from the Future of Families and Child Wellbeing Study (FFCWS), a birth cohort oversampled from “fragile families” (n=3,474). Maltreatment was assessed at 3, 5, and 9 years using an adapted version of the Parent-Child Conflict Tactics Scales (CTS-PC). Using least angle regression, we examined the relationship between repeated measures of exposure to maltreatment on psychopathology symptoms at age 15 (Child Behavior Checklist; CBCL/6-18). For comparison, we evaluated the strength of evidence to support the existence of sensitive periods in relation to an accumulation of risk model. Results: We identified sensitive periods for harsh physical discipline, whereby psychopathology symptom scores were highest among girls exposed at age 9 (r2=0.67 internalizing symptoms; r2=1% externalizing) and among boys exposed at age 5 (r2=0.41%). However, for neglect, the accumulation of risk model explained more variability in psychopathology symptoms for both boys and girls. Conclusion: Child maltreatment may have differential effects based on the child’s sex, type of exposure, and the age it occurs. These findings provide additional evidence for clinicians assessing the benefits and drawbacks of screening efforts and point towards mechanisms driving increased vulnerability to psychopathology

Association between the timing of childhood adversity and epigenetic patterns across childhood and adolescence:findings from the Avon Longitudinal Study of Parents and Children (ALSPAC) prospective cohort

BACKGROUND: Childhood adversity is a potent determinant of health across development and is associated with altered DNA methylation signatures, which might be more common in children exposed during sensitive periods in development. However, it remains unclear whether adversity has persistent epigenetic associations across childhood and adolescence. We aimed to examine the relationship between time-varying adversity (defined through sensitive period, accumulation of risk, and recency life course hypotheses) and genome-wide DNA methylation, measured three times from birth to adolescence, using data from a prospective, longitudinal cohort study.METHODS: We first investigated the relationship between the timing of exposure to childhood adversity between birth and 11 years and blood DNA methylation at age 15 years in the Avon Longitudinal Study of Parents and Children (ALSPAC) prospective cohort study. Our analytic sample included ALSPAC participants with DNA methylation data and complete childhood adversity data between birth and 11 years. We analysed seven types of adversity (caregiver physical or emotional abuse, sexual or physical abuse [by anyone], maternal psychopathology, one-adult households, family instability, financial hardship, and neighbourhood disadvantage) reported by mothers five to eight times between birth and 11 years. We used the structured life course modelling approach (SLCMA) to identify time-varying associations between childhood adversity and adolescent DNA methylation. Top loci were identified using an R 2 threshold of 0·035 (ie, ≥3·5% of DNA methylation variance explained by adversity). We attempted to replicate these associations using data from the Raine Study and Future of Families and Child Wellbeing Study (FFCWS). We also assessed the persistence of adversity-DNA methylation associations we previously identified from age 7 blood DNA methylation into adolescence and the influence of adversity on DNA methylation trajectories from ages 0-15 years. FINDINGS: Of 13 988 children in the ALSPAC cohort, 609-665 children (311-337 [50-51%] boys and 298-332 [49-50%] girls) had complete data available for at least one of the seven childhood adversities and DNA methylation at 15 years. Exposure to adversity was associated with differences in DNA methylation at 15 years for 41 loci (R 2 ≥0·035). Sensitive periods were the most often selected life course hypothesis by the SLCMA. 20 (49%) of 41 loci were associated with adversities occurring between age 3 and 5 years. Exposure to one-adult households was associated with differences in DNA methylation at 20 [49%] of 41 loci, exposure to financial hardship was associated with changes at nine (22%) loci, and physical or sexual abuse was associated with changes at four (10%) loci. We replicated the direction of associations for 18 (90%) of 20 loci associated with exposure to one-adult household using adolescent blood DNA methylation from the Raine Study and 18 (64%) of 28 loci using saliva DNA methylation from the FFCWS. The directions of effects for 11 one-adult household loci were replicated in both cohorts. Differences in DNA methylation at 15 years were not present at 7 years and differences identified at 7 years were no longer apparent by 15 years. We also identified six distinct DNA methylation trajectories from these patterns of stability and persistence. INTERPRETATION: These findings highlight the time-varying effect of childhood adversity on DNA methylation profiles across development, which might link exposure to adversity to potential adverse health outcomes in children and adolescents. If replicated, these epigenetic signatures could ultimately serve as biological indicators or early warning signs of initiated disease processes, helping identify people at greater risk for the adverse health consequences of childhood adversity.FUNDING: Canadian Institutes of Health Research, Cohort and Longitudinal Studies Enhancement Resources, EU's Horizon 2020, US National Institute of Mental Health.</p

What Is a Representative Brain? Neuroscience Meets Population Science

The last decades of neuroscience research have produced immense progress in the methods available to understand brain structure and function. Social, cognitive, clinical, affective, economic, communication, and developmental neurosciences have begun to map the relationships between neuro-psychological processes and behavioral outcomes, yielding a new understanding of human behavior and promising interventions. However, a limitation of this fast moving research is that most findings are based on small samples of convenience. Furthermore, our understanding of individual differences may be distorted by unrepresentative samples, undermining findings regarding brain–behavior mechanisms. These limitations are issues that social demographers, epidemiologists, and other population scientists have tackled, with solutions that can be applied to neuroscience. By contrast, nearly all social science disciplines, including social demography, sociology, political science, economics, communication science, and psychology, make assumptions about processes that involve the brain, but have incorporated neural measures to differing, and often limited, degrees; many still treat the brain as a black box. In this article, we describe and promote a perspective—population neuroscience—that leverages interdisciplinary expertise to (i) emphasize the importance of sampling to more clearly define the relevant populations and sampling strategies needed when using neuroscience methods to address such questions; and (ii) deepen understanding of mechanisms within population science by providing insight regarding underlying neural mechanisms. Doing so will increase our confidence in the generalizability of the findings. We provide examples to illustrate the population neuroscience approach for specific types of research questions and discuss the potential for theoretical and applied advances from this approach across areas

Genomewide association studies of suicide attempts in US soldiers

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/139960/1/ajmgb32594.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/139960/2/ajmgb32594_am.pd

DEVELOPMENTAL EFFECTS OF DIETARY N-3 FATTY ACIDS ON ACTIVITY AND RESPONSE TO NOVELTY

Insufficient availability of n-3 polyunsaturated fatty acids (PUFA) during pre- and neonatal development decreases accretion of docosahexaenoic acid (DHA, 22:6n-3) in the developing brain. Low tissue levels of DHA are associated with neurodevelopmental disorders including attention deficit hyperactivity disorder (ADHD). In this study, 1st-and 2nd-litter male Long-Evans rats were raised from conception on a Control diet containing α-linolenic acid (4.20 g/kg diet), the dietarily essential fatty acid precursor of DHA, or a diet Deficient in α-linolenic acid (0.38 g/kg diet). The Deficient diet resulted in a decrease in brain phospholipid DHA of 48% in 1st-litter pups and 65% in 2nd-litter pups. Activity, habituation, and response to spatial change in a familiar environment were assessed in a single-session behavioral paradigm at postnatal days 28 and 70, inclusive. Activity and habituation varied by age with younger rats exhibiting higher activity, less habituation, and less stimulation of activity induced by spatial novelty. During the first and second exposures to the test chamber, 2nd-litter Deficient pups exhibited higher levels of activity than Control rats or 1st-litter Deficient pups and less habituation during the first exposure, but were not more active after introduction of a novel spatial stimulus. The higher level of activity in a familiar environment, but not after introduction of a novel stimulus is consistent with clinical observations in ADHD. The observation of this effect only in 2nd-litter rats fed the Deficient diet suggests that brain DHA content, rather than dietary n-3 PUFA content, likely underlies these effects

Investigating the genetic architecture of noncognitive skills using GWAS-by-subtraction

Little is known about the genetic architecture of traits affecting educational attainment other than cognitive ability. We used genomic structural equation modeling and prior genome-wide association studies (GWASs) of educational attainment (n = 1,131,881) and cognitive test performance (n = 257,841) to estimate SNP associations with educational attainment variation that is independent of cognitive ability. We identified 157 genome-wide-significant loci and a polygenic architecture accounting for 57% of genetic variance in educational attainment. Noncognitive genetics were enriched in the same brain tissues and cell types as cognitive performance, but showed different associations with gray-matter brain volumes. Noncognitive genetics were further distinguished by associations with personality traits, less risky behavior and increased risk for certain psychiatric disorders. For socioeconomic success and longevity, noncognitive and cognitive-performance genetics demonstrated associations of similar magnitude. By conducting a GWAS of a phenotype that was not directly measured, we offer a view of genetic architecture of noncognitive skills influencing educational success