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Perturbations to the gut microbiome are implicated in altered neurodevelopmental trajectories that may shape life span risk for emotion dysregulation and affective disorders. However, the sensitive periods during which the microbiome may influence neurodevelopment remain understudied. We investigated relationships between gut microbiome composition across infancy and temperament at 12 months of age. In 67 infants, we examined if gut microbiome composition assessed at 1–3 weeks, 2, 6, and 12 months of age was associated with temperament at age 12 months. Stool samples were sequenced using the 16S Illumina MiSeq platform. Temperament was assessed using the Infant Behavior Questionnaire-Revised (IBQ-R). Beta diversity at age 1–3 weeks was associated with surgency/extraversion at age 12 months. Bifidobacterium and Lachnospiraceae abundance at 1–3 weeks of age was positively associated with surgency/extraversion at age 12 months. Klebsiella abundance at 1–3 weeks was negatively associated with surgency/extraversion at 12 months. Concurrent composition was associated with negative affectivity at 12 months, including a positive association with Ruminococcus-1 and a negative association with Lactobacillus. Our findings support a relationship between gut microbiome composition and infant temperament. While exploratory due to the small sample size, these results point to early and late infancy as sensitive periods during which the gut microbiome may exert effects on neurodevelopment.

The fetal phase of life has long been recognized as a sensitive period of development. Here we posit that pregnancy represents a simultaneous sensitive period for the adult female with broad and persisting consequences for her health and development, including risk for psychopathology. In this review, we examine the transition to motherhood through the lens of developmental psychopathology. Specifically, we summarize the typical and atypical changes in brain and behavior that characterize the perinatal period. We highlight how the exceptional neuroplasticity exhibited by women during this life phase may account for increased vulnerability for psychopathology. Further, we discuss several modes of signaling that are available to the fetus to affect maternal phenotypes (hormones, motor activity, and gene transfer) and also illustrate how evolutionary perspectives can help explain how and why fetal functions may contribute to maternal psychopathology. The developmental psychopathology perspective has spurred advances in understanding risk and resilience for mental health in many domains. As such, it is surprising that this major epoch in the female life span has yet to benefit fully from similar applications.

Acculturation represents an important construct for elucidating the determinants and consequences of health disparities in minority populations. However, the processes and mechanisms underlying acculturation's effects on health are largely undetermined and warrant further study. We integrate concepts from anthropology and statistics to describe the role of sociocultural context as a putative modifier of the relationship between acculturation and health. Sociocultural context may influence the extent to which exposure to host culture leads to internalization of host cultural orientation, and may influence the extent to which acculturation leads to stress and adoption of unhealthy behaviors. We focus on specific aspects of sociocultural context: (1) neighborhood ethno-cultural composition; (2) discrimination; (3) discrepancy between origin and host environments; (4) discrepancy between heritage and host cultures; (5) origin group, host group, and individual attitudes towards assimilation; (6) variation in targets of assimilation within host community; (7) public policy and resources; (8) migration selection bias. We review and synthesize evidence for these moderation effects among first- and later-generation immigrants, refugees, and indigenous populations. Furthermore, we propose best-practices data-collection and statistical-analysis methods for this purpose, in order to improve our understanding of the complex, multilevel aspects of the relationship between acculturation and health.

Evolution by natural selection eliminates maladaptive traits from a species, and yet Alzheimer’s Disease (AD) persists with rapidly increasing prevalence globally. This apparent paradox begs an explanation within the framework of evolutionary sciences. Here, I summarize and critique previously proposed theories to explain human susceptibility to AD, grouped into 8 distinct hypotheses based on the concepts of novel extension of the lifespan; lack of selective pressure during the post-reproductive phase; antagonistic pleiotropy; rapid brain evolution; delayed neuropathy by selection for grandmothering; novel alleles selected to delay neuropathy; by-product of selection against cardiovascular disease; and thrifty genotype. Subsequently, I describe a new hypothesis inspired by the concept of mismatched environments. Many of the factors that enhance AD risk today may have been absent or functioned differently before the modern era, potentially making AD a less common affliction for age-matched individuals before industrialization and for the majority of human history. Future research is needed to further explore whether changes in environments and lifestyles across human history moderate risk factors and susceptibility to AD.

Author(s): Fox, Molly; Sandman, Curt A; Davis, Elysia Poggi; Glynn, Laura M | Abstract: BACKGROUND:An issue of critical importance for psychiatry and women's health is whether postpartum depression (PPD) represents a unique condition. The Diagnostic and Statistical Manual of Mental Disorders asserts that major depressive disorder (MDD) may present with peripartum onset, without suggesting any other differences between MDD and PPD. The absence of any distinct features calls into question the nosologic validity of PPD as a diagnostic category. The present study investigates whether symptom profiles differ between PPD and depression occurring outside the postpartum phase. METHODS:In a prospective, longitudinal study of parturient women (Nn=n239), we examine the manifestation of depression symptoms. We assess factor structure of symptom profiles, and whether factors are differentially pronounced during and after the postpartum period. RESULTS:Factors were revealed representing: Worry, Emotional/Circadian/Energetic Dysregulation, Somatic/Cognitive, Appetite, Distress Display, and Anger symptoms. The factor structure was validated at postpartum and after-postpartum timepoints. Interestingly, the Worry factor, comprising anxiety and guilt, was significantly more pronounced during the postpartum timepoint, and the Emotional/Circadian/Energetic Dysregulation factor, which contained sadness and anhedonia, was significantly less pronounced during the postpartum period. CONCLUSIONS:These results suggest that PPD may be a unique syndrome, necessitating research, diagnosis, and treatment strategies distinct from those for MDD. Results indicate the possibility that Worry is an enhanced feature of PPD compared to depression outside the postpartum period, and the crucial role of sadness/anhedonia in MDD diagnosis may be less applicable to PPD diagnosis.

The effect of estrogen on Alzheimer's Disease (AD) risk has received substantial research and media attention, especially in terms of hormone replacement therapy. But reproductive history is also an important modifier of estrogenic exposure, and deserves further investigation. Importantly, there is wide variation in reproductive patterns that modifies estrogen exposure during the reproductive span, which previous AD studies have not incorporated into their calculations. We measured degree of Alzheimer's-type dementia in a cohort of elderly British women, and collected detailed reproductive and medical history information, which we used to estimate number of months with estrogen exposure and number of months with menstrual cycles. Using Cox proportional-hazards models, we find that longer duration of estrogen exposure may have a protective effect against AD risk, such that for every additional month with estrogen, women experienced on average a 0.5% decrease in AD risk (N=89, p=0.02). More menstrual cycles may also have a protective effect against AD risk, although this result was of borderline statistical significance (p0.10). These results build upon previous methodologies by taking into account a variety of parameters including oral contraceptive use, breastfeeding, post-partum anovulation, abortions, and miscarriages. Additionally, Cox models revealed that longer reproductive span, age21 at first birth, and more months in lifetime spent pregnant had protective effects against AD risk.

Acculturation represents an important construct in the context of health disparities. Although several studies have reported relationships between various aspects of acculturation and health in minority populations, crucial inconsistencies remain. One likely reason for these inconsistencies may relate to limitations in the conceptualization and operationalization of acculturation, particularly in the context of health research. The acculturation construct underwent major conceptual and operational change when it was adapted from anthropology to psychology, and we argue another major shift is now required for use of this construct in health research. Issues include determining whether acculturation measures should focus on an individual's internal attitudes or overt behaviors; whether they should characterize cultural orientation status at a given point in time or change over time; whether measures should be culture-specific or more global in nature; how the issue of multiculturalism should be addressed; how measures can optimally incorporate multiple dimensions of acculturation; and whether proxy measures should be used. These issues are important in the context of health research because of their implications for determining the direct and indirect effects of cultural change on health-related biological and behavioral processes. We elaborate on and address each of these issues from a perspective that spans multiple disciplines across the biological and social sciences, and offer concrete recommendations with the ultimate goal of achieving a better understanding of the role of acculturation in minority health and health disparities.

We propose a transdisciplinary, life span framework for examining the underlying cause of the observed intergenerational decline in health among Hispanic Americans. We focus on acculturation, and we posit that acculturation-related processes in first-generation Hispanic immigrant mothers may affect the intrauterine development of an unborn child, via the process of fetal programming, to produce phenotypic effects that may alter the susceptibility for noncommunicable chronic diseases. In this manner, an intergenerational cascade of perpetuation may become established. Our framework may shed light on the biological, behavioral, and social causes of intergenerational cycles of vulnerability among immigrant minority groups, with public health and policy implications for primary prevention and intervention.

The role of serotonin in depression and antidepressant treatment remains unresolved despite decades of research. In this paper, we make three major claims. First, serotonin transmission is elevated in multiple depressive phenotypes, including melancholia, a subtype associated with sustained cognition. The primary challenge to this first claim is that the direct pharmacological effect of most symptom-reducing medications, such as the selective serotonin reuptake inhibitors (SSRIs), is to increase synaptic serotonin. The second claim, which is crucial to resolving this paradox, is that the serotonergic system evolved to regulate energy. By increasing extracellular serotonin, SSRIs disrupt energy homeostasis and often worsen symptoms during acute treatment. Our third claim is that symptom reduction is not achieved by the direct pharmacological properties of SSRIs, but by the brain's compensatory responses that attempt to restore energy homeostasis. These responses take several weeks to develop, which explains why SSRIs have a therapeutic delay. We demonstrate the utility of our claims by examining what happens in animal models of melancholia and during acute and chronic SSRI treatment.