scholarly journals Early-Life Adversity and Dysregulation of Adult Diurnal Cortisol Rhythm

2018 ◽  
Vol 74 (1) ◽  
pp. 160-169 ◽  
Author(s):  
Arun S Karlamangla ◽  
Sharon Stein Merkin ◽  
David M Almeida ◽  
Esther M Friedman ◽  
Jacqueline A Mogle ◽  
...  

Abstract Objectives Exposure to life stresses can lead to diminution in the capacity of stress response systems to mount a robust response to new challenges, with blunting of dynamic range—the spread between maximal attainable and minimal resting levels. We investigate the association between early-life adversity and the dynamic range of adult diurnal cortisol secretion. Method In 35- to 86-year-old adults, cortisol assayed from 16 saliva samples over 4 consecutive days was used to compute diurnal dynamic range and area under the curve (AUC). Economic adversity in childhood was indexed by recalled parental education, family welfare dependence, and perceived financial status; and childhood social adversity by parental separation, death, and abuse. Results Adjusted for age, gender, and race/ethnicity, both childhood adversities were strongly associated with smaller adult cortisol diurnal dynamic range, but not with AUC. The association with cortisol dynamic range was explained by adult social and economic variables. Discussion Early-life adversity appears to leave a long-term imprint on cortisol secretion dynamics, reducing diurnal dynamic range without increasing total secretion. This points to the importance of examining the adaptation capacity of physiological systems when studying the impact of early-life and chronic stresses on adult health.

2021 ◽  
pp. 1-16
Author(s):  
Courtenay L. Kessler ◽  
Suzanne Vrshek-Schallhorn ◽  
Susan Mineka ◽  
Richard E. Zinbarg ◽  
Michelle Craske ◽  
...  

Abstract Early life adversity influences the diurnal cortisol rhythm, yet the relative influence of different characteristics of adversity remains unknown. In this study, we examine how developmental timing (childhood vs. adolescence), severity (major vs. minor), and domain of early life adversity relate to diurnal cortisol rhythms in late adolescence. We assessed adversity retrospectively in early adulthood in a subsample of 236 participants from a longitudinal study of a diverse community sample of suburban adolescents oversampled for high neuroticism. We used multilevel modeling to assess associations between our adversity measures and the diurnal cortisol rhythm (waking and bedtime cortisol, awakening response, slope, and average cortisol). Major childhood adversities were associated with flatter daily slope, and minor adolescent adversities were associated with greater average daily cortisol. Examining domains of childhood adversities, major neglect and sexual abuse were associated with flatter slope and lower waking cortisol, with sexual abuse also associated with higher cortisol awakening response. Major physical abuse was associated with higher waking cortisol. Among adolescent adversities domains, minor neglect, emotional abuse, and witnessing violence were associated with greater average cortisol. These results suggest severity, developmental timing, and domain of adversity influence the association of early life adversity with stress response system functioning.


2019 ◽  
Vol 79 (1) ◽  
pp. 113-132 ◽  
Author(s):  
Marion Rincel ◽  
Muriel Darnaudéry

The developmental period constitutes a critical window of sensitivity to stress. Indeed, early-life adversity increases the risk to develop psychiatric diseases, but also gastrointestinal disorders such as the irritable bowel syndrome at adulthood. In the past decade, there has been huge interest in the gut–brain axis, especially as regards stress-related emotional behaviours. Animal models of early-life adversity, in particular, maternal separation (MS) in rodents, demonstrate lasting deleterious effects on both the gut and the brain. Here, we review the effects of MS on both systems with a focus on stress-related behaviours. In addition, we discuss more recent findings showing the impact of gut-directed interventions, including nutrition with pre- and probiotics, illustrating the role played by gut microbiota in mediating the long-term effects of MS. Overall, preclinical studies suggest that nutritional approaches with pro- and prebiotics may constitute safe and efficient strategies to attenuate the effects of early-life stress on the gut–brain axis. Further research is required to understand the complex mechanisms underlying gut–brain interaction dysfunctions after early-life stress as well as to determine the beneficial impact of gut-directed strategies in a context of early-life adversity in human subjects.


2015 ◽  
Vol 18 (3) ◽  
pp. 331-343 ◽  
Author(s):  
Lindsey Garfield ◽  
Herbert L. Mathews ◽  
Linda Witek Janusek

Depression during the perinatal period is common and can have adverse consequences for women and their children. Yet, the biobehavioral mechanisms underlying perinatal depression are not known. Adverse early life experiences increase the risk for adult depression. One potential mechanism by which this increased risk occurs is epigenetic embedding of inflammatory pathways. The purpose of this article is to propose a conceptual model that explicates the linkage between early life adversity and the risk for maternal depression. The model posits that early life adversity embeds a proinflammatory epigenetic signature (altered DNA methylation) that predisposes vulnerable women to depression during pregnancy and the postpartum period. As proposed, women with a history of early life adversity are more likely to exhibit higher levels of proinflammatory cytokines and lower levels of oxytocin in response to the demands of pregnancy and new motherhood, both of which are associated with the risk for perinatal depression. The model is designed to guide investigations into the biobehavioral basis for perinatal depression, with emphasis upon the impact of early life adversity. Testing this model will provide a better understanding of maternal depressive risk and improve identification of vulnerable women who would benefit from targeted interventions that can reduce the impact of perinatal depression on maternal–infant health.


2016 ◽  
Vol 28 (4pt2) ◽  
pp. 1259-1272 ◽  
Author(s):  
Renaud Massart ◽  
Zsofia Nemoda ◽  
Matthew J. Suderman ◽  
Sheila Sutti ◽  
Angela M. Ruggiero ◽  
...  

AbstractStudies in rodents, nonhuman primates, and humans suggest that epigenetic processes mediate between early life experiences and adult phenotype. However, the normal evolution of epigenetic programs during child development, the effect of sex, and the impact of early life adversity on these trajectories are not well understood. This study mapped the genome-wide DNA methylation changes in CD3+ T lymphocytes from rhesus monkeys from postnatal day 14 through 2 years of age in both males and females and determined the impact of maternal deprivation on the DNA methylation profile. We show here that DNA methylation profiles evolve from birth to adolescence and are sex dependent. DNA methylation changes accompany imposed weaning, attenuating the difference between males and females. Maternal separation at birth alters the normal evolution of DNA methylation profiles and targets genes that are also affected by a later stage maternal separation, that is, weaning. Our results suggest that early life events dynamically interfere with the normal developmental evolution of the DNA methylation profile and that these changes are highly effected by sex.


2020 ◽  
Author(s):  
Cédric Girard-Buttoz ◽  
Patrick J. Tkaczynski ◽  
Liran Samuni ◽  
Pawel Fedurek ◽  
Cristina Gomes ◽  
...  

AbstractIn mammals, early life adversity negatively affects survival and reproductive success. A key causal mechanism is proposed by the biological embedding model which posits that adversity experienced early in life has deleterious consequences on individual physiology across the lifespan. In particular, early life adversity is expected to be a severe stressor leading to long-term alteration of the hypothalamic pituitary adrenal (HPA) axis activity. Here we tested this idea by assessing whether, as in humans, maternal loss had short and long-term impacts on orphan chimpanzee urinary cortisol levels and diurnal urinary cortisol slopes, as an indicator of the HPA axis functioning. We used 18 years of data on 50 immature and 28 mature male wild chimpanzees belonging to four communities in Taï National Park, Ivory Coast. Immature orphans who experienced early maternal loss had diurnal cortisol slopes characterised by higher early morning and late afternoon cortisol levels indicative of high activation of the HPA axis. Recently orphaned immatures had higher cortisol levels than other immatures, possibly reflecting social and nutritional stress. However, unlike in humans, we did not find significantly different cortisol profiles in orphan and non-orphan adult male chimpanzees. Our study highlights that long-term alteration of stress physiology related to early life adversity may not be viable in some wild animal populations and/or that chimpanzees, as humans, may have access to mechanisms that buffer this physiological stress, such as adoption. Our results suggest that biological embedding of altered HPA axis function is unlikely to be a mechanism contributing to the demonstrated long-term fitness consequences of maternal loss, such as reduced reproductive success, in wild long-lived mammals.


2021 ◽  
Vol 15 ◽  
Author(s):  
Aashita Batra ◽  
Lawrence M. Chen ◽  
Zihan Wang ◽  
Carine Parent ◽  
Irina Pokhvisneva ◽  
...  

While the co-morbidity between metabolic and psychiatric behaviors is well-established, the mechanisms are poorly understood, and exposure to early life adversity (ELA) is a common developmental risk factor. ELA is associated with altered insulin sensitivity and poor behavioral inhibition throughout life, which seems to contribute to the development of metabolic and psychiatric disturbances in the long term. We hypothesize that a genetic background associated with higher fasting insulin interacts with ELA to influence the development of executive functions (e.g., impulsivity in young children). We calculated the polygenic risk scores (PRSs) from the genome-wide association study (GWAS) of fasting insulin at different thresholds and identified the subset of single nucleotide polymorphisms (SNPs) that best predicted peripheral insulin levels in children from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort [N = 467; pt– initial = 0.24 (10,296 SNPs), pt– refined = 0.05 (57 SNPs)]. We then calculated the refined PRS (rPRS) for fasting insulin at this specific threshold in the children from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) cohort and investigated its interaction effect with adversity on an impulsivity task applied at 36 months. We found a significant effect of interaction between fasting insulin rPRS and adversity exposure predicting impulsivity measured by the Snack Delay Task at 36 months [β = −0.329, p = 0.024], such that higher PRS [β = −0.551, p = 0.009] was linked to more impulsivity in individuals exposed to more adversity. Enrichment analysis (MetaCoreTM) of the SNPs that compose the fasting insulin rPRS at this threshold was significant for certain nervous system development processes including dopamine D2 receptor signaling. Additional enrichment analysis (FUMA) of the genes mapped from the SNPs in the fasting insulin rPRS showed enrichment with the accelerated cognitive decline GWAS. Therefore, the genetic background associated with risk for adult higher fasting insulin moderates the impact of early adversity on childhood impulsivity.


2020 ◽  
Author(s):  
Annika Benz ◽  
Maria Meier ◽  
Ulrike U. Bentele ◽  
Stephanie J. Dimitroff ◽  
Bernadette Denk ◽  
...  

Experiencing severe or prolonged stressors in early life is associated with increased risk for mental and physical disorders in adulthood. Further, individuals who experienced early life stress (ELS) may use dysfunctional coping strategies like stress-related eating, in contrast to more beneficial stress buffering mechanisms e.g. based on mindfulness. Whether these mechanisms contribute to increased levels of perceived stress and symptoms of mental disorders in individuals with ELS in times of crisis is yet unclear. As part of a larger project, we assessed changes in perceived stress and psychopathological symptoms in a sample of N=102 participants (81% female; meanage=23.49, SDage= 7.11, range 18–62) from October/December 2019 (prior to the Covid-19 pandemic) to April/June 2020 (after the German government introduced Covid-19 related restrictions). Additionally, we assessed ELS and dispositional mindfulness.Perceived stress and depression significantly increased while anxiety levels decreased. No significant change was observed for somatization. ELS and dispositional mindfulness were not associated with change scores, but with perceived stress and psychopathological symptoms at both assessments. The increase in perceived stress during the pandemic in a majority of participants demonstrates the impact of the pandemic in the general population.


Author(s):  
Jenny Svanberg

This chapter examines the impact of health inequalities on addiction and how the recommendations of the Marmot Review could influence recovery from addiction. The Marmot Review was tasked with devising strategies to reduce health inequalities in England, and rightly recognised that health equality requires a debate about what kind of society we want to live in. When considering societies as a whole, there is a clearer relationship between poor health outcomes and societal inequality; rich countries with a steep social gradient do worse than poorer, but more equal, countries. The chapter first provides an overview of factors that cause substance use and addiction before discussing the role of early life adversity in addiction and the link between inequality and addiction. More specifically, it explains how unequal societies lead to addiction and goes on to consider how society can support recovery from addiction.


2019 ◽  
Vol 100 ◽  
pp. S21
Author(s):  
Arun S. Karlamangla ◽  
Sharon Stein Merkin ◽  
David M. Almeida ◽  
Esther M. Friedman ◽  
Jacqueline A. Mogle ◽  
...  

2020 ◽  
Author(s):  
Joao F Guassi Moreira ◽  
Adriana Sofia Méndez Leal ◽  
Yael Haya Waizman ◽  
Natalie Marie Saragosa-Harris ◽  
Emilia Ninova ◽  
...  

Cognitive systems that track, update, and utilize information about reward (consequences) and risk (uncertainty) are critical for adaptive decision-making as well as everyday functioning and wellbeing. However, little is known about what shapes individual differences in reward and risk sensitivity, independent of each other, during decision-making. Here, we investigate the impact of early life experience—a potent sculptor of development—on behavioral sensitivity to reward and risk. We administered a widely used decision-making paradigm to 62 adolescents and young adults exposed to early life adversity in the form of institutional orphanage care and 81 comparison individuals. Leveraging random coefficient regression and computational modeling, we observed that previously institutionalized individuals displayed general reward hyposensitivity, contributing to a decreased propensity for adaptive decision-making relative to comparison individuals (e.g., when prospective rewards are high). By contrast, group differences in risk sensitivity were selectively observed on loss, but not gain, trials. These results are the first to independently and explicitly link early experiences to reward and risk sensitivity during decision-making. As such, they lay the groundwork for therapeutic efforts to identify and treat adversity-exposed individuals at risk for psychiatric disorders characterized by aberrant decision-making processes.


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