Early Adversity, Symptoms of Depression and Breastfeeding

2017 ◽  
Vol 41 (S1) ◽  
pp. S30-S30
Author(s):  
W. Jonas ◽  
A. Fleming ◽  
M. Steiner ◽  
M.J. Meaney ◽  
L. Atkinson ◽  
...  

BackroundThere is considerable variation in the prevalence of breastfeeding, which allows for investigation of factors that influence the initiation and duration of breastfeeding and its association with well being of the mother infant dyad.AimsTo better understand factors that influence (1) maternal breastfeeding status and (2) the “effects” of breastfeeding on mothers and infants.MethodsParticipants (n = 170) derive from a longitudinal Canadian study “Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN)”, a project designed to understand the pre- and postnatal influences on maternal health and child social-emotional development. Mothers provided data on breastfeeding status, early life adversity, oxytocin gene and oxytocin gene receptor polymorphisms, depression/anxiety, infant temperament and maternal sensitivity.ResultsEarly life adversity associated with a shorter breastfeeding duration and higher maternal depression levels. The relation between mothers’ early adversity and the duration of breastfeeding was mediated by mothers’ depression level, but only in women carrying one variant of the oxytocin rs2740210 gene marker (CC genotype). Mothers who breastfeed at 3 months acted more sensitively towards their infants when they were 6 months old and they in turn had infants who at 18 months showed reduced negative affectivity.ConclusionWomen who have been exposed to early adversity are “living with the past” and they are, to certain extent, protected or more vulnerable to depression, depending on their genotype. Breastfeeding associated with higher maternal sensitivity, which associated with decreased negative emotionality in the infant at 18 months. Our results help to clarify associations between early life experiences, breastfeeding, and the mother-infant relationship.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Author(s):  
Anne Rifkin-Graboi ◽  
Shaun Kok-Yew Goh ◽  
Hui Jun Chong ◽  
Stella Tsotsi ◽  
Lit Wee Sim ◽  
...  

Abstract From a conditional adaptation vantage point, early life caregiving adversity likely enhances aspects of cognition needed to manage interpersonal threats. Yet, research examining early life care and offspring cognition predominantly relies upon experiments including affectively neutral stimuli, with findings generally interpreted as “early-life caregiving adversity is, de facto, ‘bad’ for cognitive performance.” Here, in a Southeast Asian sample, we examined observed maternal sensitivity in infancy and cognitive performance 3 years later as preschoolers took part in three tasks, each involving both a socioemotional (SE) and non-socioemotional (NSE) version: relational memory (n = 236), cognitive flexibility (n = 203), and inhibitory control (n = 255). Results indicate the relation between early life caregiving adversity and memory performance significantly differs (Wald test = 7.67, (1), P = 0.006) depending on the SE versus NSE context, with maternal sensitivity in infancy highly predictive of worse memory for SE stimuli, and amongst girls, also predictive of better memory when NSE stimuli are used. Results concerning inhibitory control, as well as cognitive flexibility in girls, also tentatively suggest the importance of considering the SE nature of stimuli when assessing relations between the caregiving environment and cognitive performance. As not all approaches to missing data yielded similar results, implications for statistical approaches are elaborated. We conclude by considering how an adaptation-to-context framework approach may aid in designing pedagogical strategies and well-being interventions that harness pre-existing cognitive strengths.


2019 ◽  
Vol 28 (3) ◽  
pp. 241-246 ◽  
Author(s):  
Jay Belsky

Most developmental work regards adverse developmental experiences as forces that undermine well-being. Here, I present an alternative—or complementary—view, summarizing recent evidence on puberty, endocrinology, cellular aging, and brain connectivity that collectively reveals developmental acceleration in response to contextual adversity. Findings are cast in evolutionary-developmental terms, highlighting the trade-off between accelerated aging and (a) increased morbidity and (b) premature mortality.


2019 ◽  
Author(s):  
Matthew N. Zipple ◽  
Elizabeth A. Archie ◽  
Jenny Tung ◽  
Jeanne Altmann ◽  
Susan C. Alberts

AbstractIn humans and nonhuman animals, early life adversity can affect an individual’s health, survival, and fertility for many years after the adverse experience. However, whether early life adversity also imposes intergenerational effects on the exposed individual’s offspring is not well understood. Here, we fill this gap by leveraging prospective, longitudinal data on a wild, long-lived primate. We find that juveniles whose mothers experienced early life adversity exhibit high mortality before age 4, and this effect is independent of the juvenile’s own experience of early adversity. Furthermore, our results point towards a strong role for classic parental effects in driving these effects: mothers that experienced early life adversity displayed reduced viability in adulthood, which in turn led to reductions in offspring survival. Importantly, these mothers’ juvenile offspring often preceded them in death by 1 to 2 years, indicating that, for high adversity mothers, the quality of maternal care declines near the end of life. While we cannot exclude direct effects of a parent’s environment on offspring quality (e.g., transgenerational epigenetic changes), our results are most consistent with a classic parental effect, in which the environment experienced by a parent affects its future phenotype and therefore its offspring’s phenotype. Together, our findings demonstrate that adversity experienced by individuals in one generation can have strong effects on the survival of offspring in the next generation, even if those offspring did not themselves experience early adversity.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 924-924
Author(s):  
Janae Briggs ◽  
Stephanie Child

Abstract Early life adversity (ELA) is associated with poor health through social and economic pathways. ELA also shapes cognitive and emotional development, including self-perception, social attachment and mental well-being. As such, ELA may shape later life health through social relationships, yet few studies have examined these associations. Data from the UC Berkeley Social Network Study were used to examine ELA measured retrospectively and current personal network characteristics among young (21-30 years) and older adults (50-70 years). ELA was operationalized as a summary of six experiences occurring before age 18 (e.g., parents’ divorce/separation, violence/drug use in the home, etc.). Personal network characteristics included objective measures, such as the number of ties who provide or receive various types of support, and subjective assessments about the adequacy of support received. Multivariate regression models adjusted for gender, race/ethnicity, and level of education. Among young adults, ELA was associated with more ties who rely upon the ego for support (b=0.15, 95% CI: 0.02, 0.28, p=0.02). Among older adults, ELA was associated with more ties named as either an advisor (b=0.14, 95% CI: 0.04, 0.21, p=0.02) or difficult/demanding (b=0.12, 95% CI: 0.04, 0.21, p<0.01). Furthermore, ELA was associated with less confidence in family support available (b= -0.09, 95% CI: -0.16, -0.03, p<0.01) and fewer emotionally close family members (b= -0.18, 95% CI: -0.32, -0.03, p=0.02) among older adults. In conclusion, clear differences emerged in network characteristics by exposure to ELA, particularly among older adults. The findings highlight potential pathways through which ELA patterns later life health.


2016 ◽  
Vol 42 (1) ◽  
pp. 143-147 ◽  
Author(s):  
Patrick L. Hill ◽  
Nicholas A. Turiano ◽  
Anthony L. Burrow

Feeling a sense of purpose in life appears to hold consistent benefits for positive aging and well-being. As such, it is important to consider the potential factors that promote or hinder the development of purposefulness over the lifespan. For instance, it remains unclear whether early life experiences, particularly adverse ones, may hold lasting influences on whether one feels purposeful into adulthood. The current study examined whether early life adversity predicted a diminished sense of purpose in adulthood using data from participants ( N = 3835) in the Midlife in the United States (MIDUS) study. Reports of early life adversity were associated with lower levels of purpose in adulthood, and chronological age failed to moderate this relationship.


2020 ◽  
Vol 117 (33) ◽  
pp. 20052-20062 ◽  
Author(s):  
Stacy Rosenbaum ◽  
Shuxi Zeng ◽  
Fernando A. Campos ◽  
Laurence R. Gesquiere ◽  
Jeanne Altmann ◽  
...  

In humans and other animals, harsh conditions in early life can have profound effects on adult physiology, including the stress response. This relationship may be mediated by a lack of supportive relationships in adulthood. That is, early life adversity may inhibit the formation of supportive social ties, and weak social support is itself often linked to dysregulated stress responses. Here, we use prospective, longitudinal data from wild baboons in Kenya to test the links between early adversity, adult social bonds, and adult fecal glucocorticoid hormone concentrations (a measure of hypothalamic–pituitary–adrenal [HPA] axis activation and the stress response). Using a causal inference framework, we found that experiencing one or more sources of early adversity led to a 9 to 14% increase in females’ glucocorticoid concentrations across adulthood. However, these effects were not mediated by weak social bonds: The direct effects of early adversity on adult glucocorticoid concentrations were 11 times stronger than the effects mediated by social bonds. This pattern occurred, in part, because the effect of social bonds on glucocorticoids was weak compared to the powerful effects of early adversity on glucocorticoid levels in adulthood. Hence, in female baboons, weak social bonds in adulthood are not enough to explain the effects of early adversity on glucocorticoid concentrations. Together, our results support the well-established notions that early adversity and weak social bonds both predict poor adult health. However, the magnitudes of these two effects differ considerably, and they may act independently of one another.


2020 ◽  
Vol 117 (40) ◽  
pp. 24909-24919 ◽  
Author(s):  
Chelsea J. Weibel ◽  
Jenny Tung ◽  
Susan C. Alberts ◽  
Elizabeth A. Archie

In humans and other long-lived species, harsh conditions in early life often lead to profound differences in adult life expectancy. In response, natural selection is expected to accelerate the timing and pace of reproduction in individuals who experience some forms of early-life adversity. However, the adaptive benefits of reproductive acceleration following early adversity remain untested. Here, we test a recent version of this theory, the internal predictive adaptive response (iPAR) model, by assessing whether accelerating reproduction following early-life adversity leads to higher lifetime reproductive success. We do so by leveraging 48 y of continuous, individual-based data from wild female baboons in the Amboseli ecosystem in Kenya, including prospective, longitudinal data on multiple sources of nutritional and psychosocial adversity in early life; reproductive pace; and lifetime reproductive success. We find that while early-life adversity led to dramatically shorter lifespans, individuals who experienced early adversity did not accelerate their reproduction compared with those who did not experience early adversity. Further, while accelerated reproduction predicted increased lifetime reproductive success overall, these benefits were not specific to females who experienced early-life adversity. Instead, females only benefited from reproductive acceleration if they also led long lives. Our results call into question the theory that accelerated reproduction is an adaptive response to both nutritional and psychosocial sources of early-life adversity in baboons and other long-lived species.


2016 ◽  
Vol 28 (4pt2) ◽  
pp. 1273-1283 ◽  
Author(s):  
Katherine B. Ehrlich ◽  
Kharah M. Ross ◽  
Edith Chen ◽  
Gregory E. Miller

AbstractAccumulating evidence suggests that the experience of early life adversity is a risk factor for a range of poor outcomes across development, including poor physical health in adulthood. The biological embedding model of early adversity (Miller, Chen, & Parker, 2011) suggests that early adversity might become embedded within immune cells known as monocytes/macrophages, programming them to be overly aggressive to environmental stimuli and insensitive to inhibitory signals, creating a “proinflammatory phenotype” that increases vulnerability to chronic diseases across the life span. We tested this hypothesis in the present study. Adolescent girls (n = 147) had blood drawn every 6 months across a 2.5-year period. To assess inflammatory responses to challenge, their monocytes were stimulated in vitro with a bacterial product, and production of the cytokine interleukin-6 was quantified. Hydrocortisone was added to cultures to assess the cells’ sensitivity to glucocorticoids’ anti-inflammatory signal. Using cluster analyses, we found that early life adversity was associated with greater odds of displaying a proinflammatory phenotype characterized by relatively larger interleukin-6 responses and relatively less sensitivity to glucocorticoids. In contrast, ongoing social stress was not associated with increasing odds of being categorized in the proinflammatory cluster. These findings suggest that early life adversity increases the probability of developing a proinflammatory phenotype, which, if sustained, could forecast risk for health problems later in life.


2017 ◽  
Vol 41 (S1) ◽  
pp. S19-S20 ◽  
Author(s):  
T. Frodl ◽  
L. Tozzi ◽  
C. Farrell ◽  
K. Doolin ◽  
V. O’Keane ◽  
...  

IntroductionMajor depressive disorder (MDD) is a common psychiatric condition, affecting up to 350 million people worldwide. Its pathogenesis seems to involve dysregulation of the hypothalamic-pituitary (HPA) axis and inflammation as key elements of the condition. Stressful life events and in particular early life adversity seem to play an important role as risk factors for MDD. Epigenetic, which has been found to impact in the transcription of genes, seem to be associated with brain structure and function. Aim of the research was to provide an overview about neuroimaging (epi)-genetics in MDD.MethodsFunctional MRI, epigenetic and genetic information was obtained in a cohort of patients with MDD and healthy controls. Associations between, early life adversity, methylation of FKBP5 and SLC6A4, genetic variants and brain function and connectivity have been analysed.ResultsHigher methylation of SLC6A4 gene was associated with higher BOLD response during emotion processing and lower BOLD response during higher order cognitive processes. Healthy participants with higher SLC6A4 methylation involved prefrontal cortical regions to a greater extent than the participants with lower SLC6A4 methylation, when trying to switch attention away from negative emotional stimuli (Frodl et al., 2015). Moreover, FKBP5 methylation was association with HPA axis functioning and amygdala brain function in patients with MDD. FKBP5 methylation also was related to grey matter volume.ConclusionsOur study provides further support to the hypothesis that DNA methylation plays a role. Particular peripheral DNA methylation states of MDD candidate genes are associated with brain function during emotion processing in patients with MDD.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Danusa Mar Arcego ◽  
Nick O’Toole ◽  
Jan-Paul Buschdorf ◽  
Nirmala Arul Rayan ◽  
Barbara Barth ◽  
...  

Abstract Exposure to stress during the life-course has consistently been associated with neuropsychological disorders, but the precise role of stress released glucocorticoids remains unclear in this context. We aimed at using hippocampal gene expression data from macaques to identify clusters of genes sensible to glucocorticoid exposure and create a biologically relevant polygenic score to investigate emotional disorders in a child and adult humans exposed to early adversity. RNA-sequencing data from the posterior dentate gyrus (pDG) of adult Macaca fascicularis females treated with Betamethasone (glucocorticoid) or saline injections for 8 consecutive days were analyzed from two cohorts: Singapore (reference) and Vietnam (replication) with N=12/each. Weighted gene co-expression network analysis (WGCNA) was used to identify clusters (modules) of co-expressed genes associated with betamethasone. In Singaporean animals, genes were clustered in 52 modules, in which 5 were associated with betamethasone. Two modules were preserved in a replication dataset (Vietnam) and in data from female rats treated with corticosterone for 6 weeks, being the black module (557 genes, P=0.01, r=0.7) the one having the highest correlation with glucocorticoid exposure. Gene ontology analysis (FDR<0.05, Metacore®) revealed that this module is associated with transcription processes. The SNPs derived from genes within the module were used to calculate an expression-based polygenic risk score (ePRS) in the human samples, weighing each SNP by the slope of the association between genotype and gene expression (GTex). Linear regression analysis showed a significant interaction between ePRS and early adversity on the Dominique - major depressive disorder domain (β=1304; P=0.003; N=65) in girls aged 6 years (MAVAN), in which a higher ePRS was associated with more symptoms as the adversity scores increases (simple slope analysis,P=0.004). A comparable interaction between the ePRS and postnatal adversity was also observed in adult women (UK Biobank), in which there was an increased risk for early depression onset (β= -424.3, P=0.04; N=13899). In the adult cohort, whole brain gray matter volume was also associated with differences in the expression of the genes that composed the ePRS-black network (main ePRS effect, β=1865776, P=0.03, N=10902). Glucocorticoid exposure affects a specific group of genes in pDG of adult female macaques and rats, influencing transcriptional processes. Variations in the expression of this gene network sensible to glucocorticoids were associated with susceptibility for the development of depression in girls and adult women exposed to early life adversity. These show the importance of glucocorticoids on the development of depressive symptoms. The gene network affected by glucocorticoids can guide future pharmacological or mechanistic studies in other samples or species.


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