Sarah K. G. Jensen

Prenatal maternal depression symptoms and nutrition, and child cognitive function

BACKGROUND Little is currently known about how maternal depression symptoms and unhealthy nutrition during pregnancy may developmentally interrelate to negatively affect child cognitive function. AIMS To test whether prenatal maternal depression symptoms predict poor prenatal nutrition, and whether this in turn prospectively associates with reduced postnatal child cognitive function. METHOD In 6979 mother-offspring pairs participating in the Avon Longitudinal Study of Parents and Children (ALSPAC) in the UK, maternal depression symptoms were assessed five times between 18 weeks gestation and 33 months old. Maternal reports of the nutritional environment were assessed at 32 weeks gestation and 47 months old, and child cognitive function was assessed at age 8 years. RESULTS During gestation, higher depressive symptoms were related to lower levels of healthy nutrition and higher levels of unhealthy nutrition, each of which in turn was prospectively associated with reduced cognitive function. These results were robust to postnatal depression symptoms and nutrition, as well as a range of potential prenatal and postnatal confounds (i.e. poverty, teenage mother, low maternal education, parity, birth complications, substance use, criminal lifestyle, partner cruelty towards mother). CONCLUSIONS Prenatal interventions aimed at the well-being of children of parents with depression should consider targeting the nutritional environment.

Biological embedding of childhood adversity: from physiological mechanisms to clinical implications

BackgroundAdverse psychosocial exposures in early life, namely experiences such as child maltreatment, caregiver stress or depression, and domestic or community violence, have been associated in epidemiological studies with increased lifetime risk of adverse outcomes, including diabetes, heart disease, cancers, and psychiatric illnesses. Additional work has shed light on the potential molecular mechanisms by which early adversity becomes “biologically embedded” in altered physiology across body systems. This review surveys evidence on such mechanisms and calls on researchers, clinicians, policymakers, and other practitioners to act upon evidence.ObservationsChildhood psychosocial adversity has wide-ranging effects on neural, endocrine, immune, and metabolic physiology. Molecular mechanisms broadly implicate disruption of central neural networks, neuroendocrine stress dysregulation, and chronic inflammation, among other changes. Physiological disruption predisposes individuals to common diseases across the life course.ConclusionsReviewed evidence has important implications for clinical practice, biomedical research, and work across other sectors relevant to public health and child wellbeing. Warranted changes include increased clinical screening for exposures among children and adults, scale-up of effective interventions, policy advocacy, and ongoing research to develop new evidence-based response strategies.

DEVELOPMENTAL INTER‐RELATIONS BETWEEN EARLY MATERNAL DEPRESSION, CONTEXTUAL RISKS, AND INTERPERSONAL STRESS, AND THEIR EFFECT ON LATER CHILD COGNITIVE FUNCTIONING

Maternal depression and contextual risks (e.g. poverty) are known to impact childrens cognitive and social functioning. However, few published studies have examined how stress in the social environment (i.e. interpersonal stress) might developmentally inter‐relate with maternal depression and contextual risks to negatively affect a child in these domains. This was the purpose of the current study.

Effect of Early Adversity and Childhood Internalizing Symptoms on Brain Structure in Young Men

IMPORTANCE Early adversity is an important risk factor that relates to internalizing symptoms and altered brain structure. OBJECTIVE To assess the direct effects of early adversity and child internalizing symptoms (ie, depression, anxiety) on cortical gray matter (GM) volume, as well as the extent to which early adversity associates with variation in cortical GM volume indirectly via increased levels of internalizing symptoms. DESIGN, SETTING, AND PARTICIPANTS A prospective investigation of associations between adversity within the first 6 years of life, internalizing symptoms during childhood and early adolescence, and altered brain structure in late adolescence (age, 18-21 years) was conducted in a community-based birth cohort in England (Avon Longitudinal Study of Parents and Children). Participants from the cohort included 494 mother-son pairs monitored since the mothers were pregnant (estimated date of delivery between April 1, 1991, and December 31, 1992). Data collection for the present study was conducted between April 1, 1991, and November 30, 2010; the neuroimaging data were collected between September 1, 2010, and November 30, 2012, and data analyses for the present study occurred between January 25, 2013, and February 15, 2015. Risk factors were adversity within the first 6 years of the childs life (including prenatal exposure) and the childs internalizing symptoms between age 7 and 13 years. EXPOSURES Early childhood adversity. MAIN OUTCOMES AND MEASURES The main outcome was GM volume of cortical regions previously associated with major depression measured through T1-weighted magnetic resonance images collected in late adolescence. RESULTS Among 494 young men included in this analysis, early adversity was directly associated with lower GM volumes in the anterior cingulate cortex (β = -.18; P = .01) and higher GM volume in the precuneus (β = .18; P = .009). Childhood internalizing symptoms were associated with lower GM volume in the right superior frontal gyrus (β = -.20; P = .002). Early adversity was also associated with higher levels of internalizing symptoms (β = .37; P < .001), which, in turn, were associated with lower superior frontal gyrus volume (ie, an indirect effect) (β = -.08; 95% CI, -0.14 to -0.01; P = .02). CONCLUSIONS AND RELEVANCE Adversity early in life was associated with higher levels of internalizing symptoms as well as with altered brain structure. Early adversity was related to variation in brain structure both directly and via increased levels of internalizing symptoms. These findings may suggest that some of the structural variation often attributed to depression might be associated with early adversity in addition to the effect of depression.

Enhancing the child survival agenda to promote protect and support early child development.

High rates of child mortality and lost developmental potential in children under 5 years of age remain important challenges and drivers of inequity in the developing world. Substantive progress has been made toward Millennium Development Goal (MDG) 4 to improve child survival, but as we move into the post-2015 sustainable development agenda, much more work is needed to ensure that all children can realize their full and holistic physical, cognitive, psychological, and socio-emotional development potential. This article presents child survival and development as a continuous and multifaceted process and suggests that a life-course perspective of child development should be at the core of future policy making, programming, and research. We suggest that increased attention to child development, beyond child survival, is key to operationalize the sustainable development goals (SDGs), address inequities, build on the demographic dividend, and maximize gains in human potential. An important step toward implementation will be to increase integration of existing interventions for child survival and child development. Integrated interventions have numerous potential benefits, including optimization of resource use, potential additive impacts across multiple domains of health and development, and opportunity to realize a more holistic approach to client-centered care. However, a notable challenge to integration is the continued division between the health sector and other sectors that support child development. Despite these barriers, empirical evidence is available to suggest that successful multisectoral coordination is feasible and leads to improved short- and long-term outcomes in human, social, and economic development.

Preliminary investigation of the influence of dopamine regulating genes on social working memory

Working memory (WM) refers to mental processes that enable temporary retention and manipulation of information, including information about other people (“social working memory”). Previous studies have demonstrated that nonsocial WM is supported by dopamine neurotransmission. Here, we investigated in 131 healthy adults whether dopamine is similarly involved in social WM by testing whether social and nonsocial WM are influenced by genetic variants in three genes coding for molecules regulating the availability of dopamine in the brain: catechol-O-methyltransferase (COMT), dopamine active transporter (DAT), and monoamine-oxidase A (MAOA). An advantage for the Met allele of COMT was observed in the two standard WM tasks and in the social WM task. However, the influence of COMT on social WM performance was not accounted for by its influence on either standard WM paradigms. There was no main effect of DAT1 or MAOA, but a significant COMT x DAT1 interaction on social WM performance. This study provides novel preliminary evidence of effects of genetic variants of the dopamine neurotransmitter system on social cognition. The results further suggest that the effects observed on standard WM do not explain the genetic effects on effortful social cognition.

Associations between prenatal, childhood, and adolescent stress and variations in white-matter properties in young men

Objective Previous studies have shown that both pre‐ and post‐natal adversities, the latter including exposures to stress during childhood and adolescence, explain variation in structural properties of white matter (WM) in the brain. While previous studies have examined effects of independent stress exposures within one developmental period, such as childhood, we examine effects of stress across development using data from a prospective longitudinal study. More specifically, we ask how stressful events during prenatal development, childhood, and adolescence relate to variation in WM properties in early adulthood in young men recruited from a birth cohort. Method Using data from 393 mother‐son pairs from a community‐based birth cohort from England (Avon Longitudinal Study of Parents and Children), we examined how stressful life events relate to variation in different structural properties of WM in the corpus callosum and across the whole brain in early adulthood in men aged 18–21 years. We distinguish between stress occurring during three developmental periods: a) prenatal maternal stress, b) postnatal stress within the first four years of life, c) stress during adolescence (age 12–16 years). To obtain a comprehensive quantification of variation in WM, we assess structural properties of WM using four different measures, namely fractional anisotropy (FA), mean diffusivity (MD), magnetization transfer ratio (MTR) and myelin water fraction (MWF). Results The developmental model shows that prenatal stress is associated with lower MTR and MWF in the genu and/or splenium of the corpus callosum, and with lower MTR in global (lobar) WM. Stress during early childhood is associated with higher MTR in the splenium, and stress during adolescence is associated with higher MTR in the genu and lower MD in the splenium. We see no associations between postnatal stress and variation in global (lobar) WM. Conclusions The current study found evidence for independent effects of stress on WM properties during distinct neurodevelopmental periods. We speculate that these independent effects are due to differences in the developmental processes unfolding at different developmental time points. We suggest that associations between prenatal stress and WM properties may relate to abnormalities in neurogenesis, affecting the number and density of axons, while postnatal stress may interfere with processes related to myelination or radial growth of axons. Potential consequences of prenatal glucocorticoid exposure should be considered in obstetric care. HighlightsPre‐ and post‐natal adversities may explain variation in structural properties of white matter.Multimodal characterization of structural properties of the corpus callosum was carried out in ˜400 male members of a birth cohort in early adulthood (mean age ≈20 years).Prenatal stress is associated with lower magnetization transfer ratio (MTR) and myelin water fraction.Stress during early childhood is associated with higher values of MTR.

Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence

In 785 mother-child (50% male) pairs from a longitudinal epidemiological birth cohort, we investigated associations between inflammation-related epigenetic polygenic risk scores (i-ePGS), environmental exposures, cognitive function, and child and adolescent internalizing and externalizing problems. We examined prenatal and postnatal effects. For externalizing problems, one prenatal effect was found: i-ePGS at birth associated with higher externalizing problems (ages 7-15) indirectly through lower cognitive function (age 7). For internalizing problems, we identified two effects. For a prenatal effect, i-ePGS at birth associated with higher internalizing symptoms via continuity in i-ePGS at age 7. For a postnatal effect, higher postnatal adversity exposure (birth through age 7) associated with higher internalizing problems (ages 7-15) via higher i-ePGS (age 7). Hence, externalizing problems were related mainly to prenatal effects involving lower cognitive function, whereas internalizing problems appeared related to both prenatal and postnatal effects. The present study supports a link between i-ePGS and child and adolescent mental health.