scholarly journals The differential calibration of the HPA axis as a function of trauma versus adversity: A systematic review and p-curve meta-analyses

2021 ◽  
Author(s):  
Niki H. Kamkar ◽  
Cassandra J Lowe ◽  
J. Bruce Morton
Keyword(s):  
Hpa Axis ◽  
Early Life ◽  
Life Experiences ◽  
Curve Analysis ◽  
Early Life Adversity ◽  
Cortisol Reactivity ◽  
Evidential Value ◽  
Dsm 5 ◽  
Meta Analyses ◽  
The Relationship

Although there is an abundance of evidence linking the function of the hypothalamic-pituitary-adrenal (HPA) axis to adverse early-life experiences, the precise nature of the association remains unclear. Some evidence suggests early-life adversity leads to cortisol hyper-reactivity, while other evidence suggests adversity leads to cortisol hypo-reactivity. Here, we distinguish between trauma and adversity, and use p-curves to interrogate the conflicting literature. In Study 1, trauma was operationalized according to DSM-5 criteria; the p-curve analysis included 68 articles and revealed that the literature reporting associations between trauma and blunted cortisol reactivity contains evidential value. Study 2 examined the relationship between adversity and cortisol reactivity. Thirty articles were included in the analysis, and p-curve demonstrated that adversity is related to heightened cortisol reactivity. These results support an inverted U-shaped function relating severity of adversity and cortisol reactivity, and underscore the importance of distinguishing between “trauma” and “adversity”.

scholarly journals Gene regulation contributes to explain the impact of early life socioeconomic disadvantage on adult inflammatory levels in two cohort studies

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cristian Carmeli ◽  
Zoltán Kutalik ◽  
Pashupati P. Mishra ◽  
Eleonora Porcu ◽  
Cyrille Delpierre ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Gene Regulation ◽  
Cohort Studies ◽  
Early Life ◽  
Life Experiences ◽  
Socioeconomic Disadvantage ◽  
Mediating Role ◽  
The Impact ◽  
The Relationship

AbstractIndividuals experiencing socioeconomic disadvantage in childhood have a higher rate of inflammation-related diseases decades later. Little is known about the mechanisms linking early life experiences to the functioning of the immune system in adulthood. To address this, we explore the relationship across social-to-biological layers of early life social exposures on levels of adulthood inflammation and the mediating role of gene regulatory mechanisms, epigenetic and transcriptomic profiling from blood, in 2,329 individuals from two European cohort studies. Consistently across both studies, we find transcriptional activity explains a substantive proportion (78% and 26%) of the estimated effect of early life disadvantaged social exposures on levels of adulthood inflammation. Furthermore, we show that mechanisms other than cis DNA methylation may regulate those transcriptional fingerprints. These results further our understanding of social-to-biological transitions by pinpointing the role of gene regulation that cannot fully be explained by differential cis DNA methylation.

scholarly journals Early-life adversity programs long-term cytokine and microglia expression within the HPA axis in female Japanese quail

2019 ◽  
Vol 222 (6) ◽  
pp. jeb187039 ◽  
Author(s):  
David J. Walker ◽  
Cédric Zimmer ◽  
Maria Larriva ◽  
Susan D. Healy ◽  
Karen A. Spencer
Keyword(s):  
Hpa Axis ◽  
Japanese Quail ◽  
Early Life ◽  
Early Life Adversity

Inflammatory and Epigenetic Pathways for Perinatal Depression

2015 ◽  
Vol 18 (3) ◽  
pp. 331-343 ◽  
Author(s):  
Lindsey Garfield ◽  
Herbert L. Mathews ◽  
Linda Witek Janusek
Keyword(s):  
Early Life ◽  
Infant Health ◽  
Perinatal Depression ◽  
Life Experiences ◽  
Perinatal Period ◽  
Early Life Adversity ◽  
Targeted Interventions ◽  
Increased Risk ◽  
History Of ◽  
The Impact

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.

Life Events Shape Us

2018 ◽  
Author(s):  
Jack M. Gorman
Keyword(s):  
Life Events ◽  
Brain Function ◽  
Early Life ◽  
Life Experiences ◽  
Regulation Of Gene Expression ◽  
Laboratory Animals ◽  
Early Life Adversity ◽  
Psychiatric Conditions ◽  
The 1960S ◽  
The Brain

Psychiatry downplayed the importance of life events in causing mental illness from the 1960s on, favoring a view that all disorders except one are the result of abnormal genes affecting chemical processes in the brain. Studying the exception, posttraumatic stress disorder (PTSD), when it was defined in 1980 helped lead to renewed recognition that early life adversity is central to all psychiatric conditions. At the same time, neuroscientists showed that early life experiences are capable of changing life-long behavior and brain function in laboratory animals. One mechanism by which this occurs is through the epigenetic regulation of gene expression. Epigenetics is the way that the expression levels of genes are controlled without changing the underlying genetic code. Epigenetics is an attractive way of understanding how individual life experiences are translated in the brain into each person’s unique set of emotions, behaviors, abilities, and risks for psychiatric abnormalities.

scholarly journals Repeated Three-Hour Maternal Separation Induces Depression-Like Behavior and Affects the Expression of Hippocampal Plasticity-Related Proteins in C57BL/6N Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Yaoyao Bian ◽  
Lili Yang ◽  
Zhongli Wang ◽  
Qing Wang ◽  
Li Zeng ◽  
...  
Keyword(s):  
Early Life ◽  
Maternal Separation ◽  
Forced Swimming Test ◽  
Life Experiences ◽  
Tail Suspension Test ◽  
Early Life Stages ◽  
Early Life Adversity ◽  
Swimming Test ◽  
Related Proteins ◽  
The Brain

Adverse early life experiences can negatively affect behaviors later in life. Maternal separation (MS) has been extensively investigated in animal models in the adult phase of MS. The study aimed to explore the mechanism by which MS negatively affects C57BL/6N mice, especially the effects caused by MS in the early phase. Early life adversity especially can alter plasticity functions. To determine whether adverse early life experiences induce changes in plasticity in the brain hippocampus, we established an MS paradigm. In this research, the mice were treated with mild (15 min, MS15) or prolonged (180 min, MS180) maternal separation from postnatal day 2 to postnatal day 21. The mice underwent a forced swimming test, a tail suspension test, and an open field test, respectively. Afterward, the mice were sacrificed on postnatal day 31 to determine the effects of MS on early life stages. Results implied that MS induces depression-like behavior and the effects may be mediated partly by interfering with the hippocampal GSK-3β-CREB signaling pathway and by reducing the levels of some plasticity-related proteins.

The relationship of early life experiences to later life leisure involvement

1987 ◽  
Vol 9 (4) ◽  
pp. 251-257 ◽  
Author(s):  
Francis A. McGuire ◽  
F. Dominic Dotta Vio ◽  
Joseph T. O'leary
Keyword(s):  
Early Life ◽  
Life Experiences ◽  
Later Life ◽  
Leisure Involvement ◽  
Relationship Of ◽  
The Relationship

scholarly journals Hair glucocorticoids are associated with childhood adversity, depressive symptoms and reduced global and lobar grey matter in Generation Scotland

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Claire Green ◽  
Aleks Stolicyn ◽  
Mathew A. Harris ◽  
Xueyi Shen ◽  
Liana Romaniuk ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Life Stress ◽  
Early Life ◽  
Childhood Adversity ◽  
Later Life ◽  
Early Life Adversity ◽  
Brain Volumes ◽  
Stable Measure ◽  
Regional Brain ◽  
Generation Scotland

AbstractHypothalamic–pituitary–adrenal (HPA) axis dysregulation has been commonly reported in major depressive disorder (MDD), but with considerable heterogeneity of results; potentially due to the predominant use of acute measures of an inherently variable/phasic system. Chronic longer-term measures of HPA-axis activity have yet to be systematically examined in MDD, particularly in relation to brain phenotypes, and in the context of early-life/contemporaneous stress. Here, we utilise a temporally stable measure of cumulative HPA-axis function (hair glucocorticoids) to investigate associations between cortisol, cortisone and total glucocorticoids with concurrent measures of (i) lifetime-MDD case/control status and current symptom severity, (ii) early/current-life stress and (iii) structural neuroimaging phenotypes, in N = 993 individuals from Generation Scotland (mean age = 59.1 yrs). Increased levels of hair cortisol were significantly associated with reduced global and lobar brain volumes with reductions in the frontal, temporal and cingulate regions (βrange = −0.057 to −0.104, all PFDR < 0.05). Increased levels of hair cortisone were significantly associated with MDD (lifetime-MDD status, current symptoms, and severity; βrange = 0.071 to 0.115, all PFDR = < 0.05), with early-life adversity (β = 0.083, P = 0.017), and with reduced global and regional brain volumes (global: β = −0.059, P = 0.043; nucleus accumbens: β = −0.075, PFDR = 0.044). Associations with total glucocorticoids followed a similar pattern to the cortisol findings. In this large community-based sample, elevated glucocorticoids were significantly associated with MDD, with early, but not later-life stress, and with reduced global and regional brain phenotypes. These findings provide important foundations for future mechanistic studies to formally explore causal relationships between early adversity, chronic rather than acute measures of glucocorticoids, and neurobiological associations relevant to the aetiology of MDD.

scholarly journals Early maternal loss affects diurnal cortisol slopes in immature but not mature wild chimpanzees

2020 ◽  
Author(s):  
Cédric Girard-Buttoz ◽  
Patrick J. Tkaczynski ◽  
Liran Samuni ◽  
Pawel Fedurek ◽  
Cristina Gomes ◽  
...  
Keyword(s):  
Reproductive Success ◽  
Hpa Axis ◽  
Early Life ◽  
Urinary Cortisol ◽  
Maternal Loss ◽  
Early Life Adversity ◽  
Diurnal Cortisol ◽  
Animal Populations ◽  
Cortisol Levels

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.

scholarly journals The ‘Jekyll and Hyde’ of Gluconeogenesis: Early-Life Adversity, Later Life Stress, and Metabolic Disturbances

2021 ◽  
Author(s):  
Snehaa V. Seal ◽  
Jonathan D. Turner
Keyword(s):  
Type 2 Diabetes ◽  
Energy Metabolism ◽  
Hpa Axis ◽  
Physiological Response ◽  
Early Life ◽  
Energy Homeostasis ◽  
Early Life Adversity ◽  
The Metabolic Syndrome ◽  
Psychological Stressor

The physiological response to a psychological stressor broadly impacts energy metabolism. Inversely, changes in energy availability affect the physiological response to the stressor in terms of hypothalamus, pituitary adrenal gland axis and sympathetic nervous system activation upon exposure to a stressor. Glucocorticoids, the endpoint of the HPA axis, are critical checkpoints in endocrine control of energy homeostasis. Glucocorticoid actions have been linked to many severe metabolic diseases including obesity, insulin resistance and type 2 diabetes. Glucocorticoids, through the glucocorticoid receptor, activate transcription of many genes associated with glucose and lipid regulatory pathways and thereby intricately control both physiological and pathophysiological systemic energy homeostasis. Here, we summarize the current knowledge of glucocorticoid functions in energy metabolism and systemic metabolic dysfunction, particularly focusing on glucose and lipid metabolism. There are many elements in the external environment that induce lifelong changes in the HPA axis stress response and glucocorticoid levels, the most prominent are early-life adversity, or exposure to traumatic stress. We hypothesise that when the HPA axis is so disturbed after early-life adversity, it will fundamentally alter hepatic gluconeogenesis, inducing hyperglycaemia, and hence crystalise the significant lifelong risk of developing either the metabolic syndrome, or type 2 diabetes. This gives a &ldquo;Jekyll and Hyde&rdquo; role to gluconeogenesis, providing the necessary energy in situations of acute stress, but driving towards pathophysiological consequences when the HPA axis has been altered.

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