Positive memory specificity reduces adolescent vulnerability to depression

Depression is the leading cause of ill health and disability worldwide1. A known risk factor of depression is exposure to early life stress2. Such early stress exposure has been proposed to sensitise the maturing psychophysiological stress system to later life stress3. Activating positive memories dampens acute stress responses with resultant lower cortisol response and improved mood in humans4 and reduced depression-like behaviour in mice5. It is unknown whether recalling positive memories similarly reduces adolescent vulnerability to depression. Here we used path modelling to examine the effects of positive autobiographical memory specificity on later morning cortisol and negative self-cognitions during low mood in adolescents at risk for depression due to early life stress (n = 427, age: 14 years)6. We found that experimentally assessed positive but not negative memory specificity was associated with lower morning cortisol and less negative self-cognitions during low mood one year later. Moderated mediation analyses demonstrated that positive memory specificity reduced later depressive symptoms through lowering negative self-cognitions in response to negative life events reported in the one-year interval. Positive memory specificity actively dampened the negative effect of stressors over time, thereby operating as a resilience factor reducing the risk of subsequent depression7. These findings suggest that developing methods to improve positive memory specificity in at-risk adolescents may counteract vulnerability to depression.

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Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation

Frontiers in Psychiatry ◽

10.3389/fpsyt.2019.00118 ◽

2019 ◽

Vol 10 ◽

Cited By ~ 51

Author(s):

Agorastos Agorastos ◽

Panagiota Pervanidou ◽

George P. Chrousos ◽

Dewleen G. Baker

Keyword(s):

Life Stress ◽

Early Life ◽

Developmental Trajectories ◽

Early Life Stress ◽

Narrative Review ◽

Stress System

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Early life stress and trauma: developmental neuroendocrine aspects of prolonged stress system dysregulation

HORMONES ◽

10.1007/s42000-018-0065-x ◽

2018 ◽

Vol 17 (4) ◽

pp. 507-520 ◽

Cited By ~ 20

Author(s):

Agorastos Agorastos ◽

Panagiota Pervanidou ◽

George P. Chrousos ◽

Gerasimos Kolaitis

Keyword(s):

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Stress System ◽

Prolonged Stress

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Early Life Stress and Pediatric Posttraumatic Stress Disorder

Brain Sciences ◽

10.3390/brainsci10030169 ◽

2020 ◽

Vol 10 (3) ◽

pp. 169 ◽

Cited By ~ 2

Author(s):

Panagiota Pervanidou ◽

Gerasimos Makris ◽

George Chrousos ◽

Agorastos Agorastos

Keyword(s):

Posttraumatic Stress Disorder ◽

Posttraumatic Stress ◽

Life Stress ◽

Early Life ◽

Stress Disorder ◽

Early Life Stress ◽

Traumatic Experiences ◽

Stress System ◽

Critical Periods ◽

Physical And Mental Health

Traumatic stress exposure during critical periods of development may have essential and long-lasting effects on the physical and mental health of individuals. Two thirds of youth are exposed to potentially traumatic experiences by the age of 17, and approximately 5% of adolescents meet lifetime criteria for posttraumatic stress disorder (PTSD). The role of the stress system is the maintenance of homeostasis in the presence of real/perceived and acute/chronic stressors. Early-life stress (ELS) has an impact on neuronal brain networks involved in stress reactions, and could exert a programming effect on glucocorticoid signaling. Studies on pediatric PTSD reveal diverse neuroendocrine responses to adverse events and related long-term neuroendocrine and epigenetic alterations. Neuroendocrine, neuroimaging, and genetic studies in children with PTSD and ELS experiences are crucial in understanding risk and resilience factors, and also the natural history of PTSD.

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Methylation of the glucocorticoid receptor promoter in children: Links with parents as teachers, early life stress, and behavior problems

Development and Psychopathology ◽

10.1017/s0954579420001984 ◽

2020 ◽

pp. 1-13

Author(s):

Elena Silvia Gardini ◽

Simone Schaub ◽

Alex Neuhauser ◽

Erich Ramseier ◽

Arna Villiger ◽

...

Keyword(s):

At Risk ◽

Behavior Problems ◽

Glucocorticoid Receptor ◽

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Parents As Teachers ◽

Cpg Site ◽

Glucocorticoid Receptor Gene ◽

And Behavior

Abstract The present study examined the effect of early life stress (ELS) on the glucocorticoid receptor gene (NR3C1) methylation, the associations between NR3C1 methylation and behavior problems, and the effect of the program Parents as Teachers (PAT) on NR3C1 methylation. Participants included 132 children, 72 assigned to the PAT intervention group and 60 to the PAT control group. Children were aged 3 years, and were living in psychosocially at-risk families. We assessed NR3C1 methylation of the NGFI-A binding regions of exon 1F via sodium bisulfite sequencing from saliva DNA. Results indicated that (a) children living in families receiving PAT had decreased methylation at one single cytosine–guanine dinucleotides (CpG) site; (b) current maternal depressive symptoms and parental disagreement were predictive of increased methylation of mean NGFI-A and three single CpG sites; and (c) increased methylation of mean NGFI-A and one single CpG site was significantly associated with increased internalizing and externalizing symptoms. In addition, mean NGFI-A was a mediator of the association between parental disagreement and a child's affective problems. These results suggest that PAT may contribute to preventing NR3C1 methylation in preschool children living in psychosocially at-risk situations, and confirm previous findings on the associations between ELS, NR3C1 methylation, and behavior problems.

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Stress-system activation in children with chronic pain: A focus for clinical intervention

Clinical Child Psychology and Psychiatry ◽

10.1177/1359104519864994 ◽

2019 ◽

Vol 25 (1) ◽

pp. 78-97 ◽

Cited By ~ 1

Author(s):

Peter M McInnis ◽

Taylor A Braund ◽

Zhi Kai Chua ◽

Kasia Kozlowska

Keyword(s):

Heart Rate ◽

Chronic Pain ◽

Psychological Distress ◽

Life Stress ◽

Early Life ◽

Early Life Stress ◽

Stress System ◽

Identification Task ◽

System Activation ◽

Elevated Heart Rate

Accumulating evidence indicates that psychological and neurophysiological processes interconnect and interact to activate the body’s stress system and to trigger and maintain functional somatic symptoms. This study used the Early Life Stress Questionnaire, Depression Anxiety Stress Scales and biological markers (heart rate, heart rate variability, skin conductance, C-reactive protein (CRP) titre, respiratory rate, and accuracy and reaction time in an emotion-face identification task), to examine childhood adversity, psychological distress and stress-system activation in 35 children and adolescents (23 girls and 12 boys, 9–17 years old) disabled by chronic pain (vs two groups of age- and sex-matched healthy controls). Patients reported more early-life stress ( U = 798.5, p = .026) and more psychological distress ( U = 978, p < .001). They showed activation of the autonomic system: elevated heart rate ( U = 862.5, p = .003), elevated electrodermal activity ( U = 804.5, p = .024) and lower heart rate variability in the time domain ( U = 380.5, p = .007) and frequency domain ( U = 409.5, p = .017). The group showed an upward shift of CRP titres (with 75th and 90th CRP percentiles of 4.5 and 10.5 mg/L, respectively), suggesting the activation of the immune–inflammatory system. Elevated CRP titres were associated with elevated heart rate ( p = .028). There were no differences in respiratory rate or in accuracy and reaction time in the emotion-face identification task. The results indicate that interventions for children and adolescents with chronic pain need a multidisciplinary mind–body approach that concurrently addresses psychological distress, physical impairment and stress-system dysregulation.

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Histamine-dependent interactions between mast cells, glia, and neurons are altered following early-life adversity in mice and humans

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00041.2020 ◽

2020 ◽

Vol 319 (6) ◽

pp. G655-G668

Author(s):

Jonathon L. McClain ◽

Elvio A. Mazzotta ◽

Nidia Maradiaga ◽

Natalia Duque-Wilckens ◽

Iveta Grants ◽

...

Keyword(s):

At Risk ◽

Mast Cell ◽

Mast Cells ◽

Life Stress ◽

Early Life ◽

Functional Gastrointestinal Disorders ◽

Early Life Stress ◽

Gastrointestinal Disorders ◽

Early Life Adversity ◽

Potential Mediator

Early-life adversity places an individual at risk for developing functional gastrointestinal disorders later in life through unknown mechanisms. Here, we show that interactions between mast cells and glia are disrupted by early-life stress in mice and that histamine is a potential mediator of mast cell-glial interactions.

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Mindfulness interventions for offsetting health risk following early life stress: Promising directions

10.31231/osf.io/r6z4v ◽

2021 ◽

Author(s):

Emily K Lindsay

Keyword(s):

At Risk ◽

Health Risk ◽

Health Outcomes ◽

Physical Health ◽

Life Stress ◽

Early Life ◽

Disease Risk ◽

Early Life Stress ◽

Present Moment ◽

At Risk Populations

Early life stress (ELS), common to childhood maltreatment, socioeconomic disadvantage, and racial discrimination, is thought to create a proinflammatory phenotype that increases risk for poor health in adulthood. Systemic change is needed to address the root causes of ELS, but a substantial number of adults are already at increased health risk by virtue of ELS exposure. Interventions that target stress pathways have the potential to interrupt the trajectory from ELS to inflammatory disease risk in adulthood. Mindfulness-based interventions (MBIs), which train acceptance toward present-moment experience, have shown promise for reducing stress and improving a variety of stress-sensitive health outcomes. Although MBIs have primarily been conducted in more advantaged populations, evidence suggests that they may be uniquely effective for improving mental health and health-related quality of life among those with a history of ELS. Whether these effects extend to physical health remains unknown. To shed light on this question, I review evidence that MBIs influence inflammatory markers in at-risk samples, explore the promise of MBIs for improving stress-related health outcomes in diverse at-risk populations, and describe adaptations to MBIs that may increase their acceptability and efficacy in populations exposed to ELS. This prior work sets the stage for well-controlled RCTs to evaluate whether MBIs influence stress and inflammatory pathways among those exposed to ELS and for pragmatic and implementation trials focused on disseminating MBIs to reach these at-risk populations. Overall, the evidence assembled here shows the potential of MBIs for offsetting physical health risk related to ELS.

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