scholarly journals Paradoxical Associations Between Familial Affective Responsiveness, Stress, and Amygdala Reactivity

2017 ◽  
Author(s):  
Madeline J. Farber ◽  
Adrienne L. Romer ◽  
M. Justin Kim ◽  
Annchen R. Knodt ◽  
Nourhan M. Elsayed ◽  
...  
Keyword(s):  
Brain Function ◽  
Early Life ◽  
Emotional Behavior ◽  
Brain Circuits ◽  
Increased Risk ◽  
Abuse And Neglect ◽  
Interpersonal Threat ◽  
The Impact ◽  
Amygdala Reactivity ◽  
Affective Responsiveness

AbstractStudies of early life extremes such as trauma, abuse, and neglect highlight the critical importance of quality caregiving in the development of brain circuits supporting emotional behavior and mental health. The impact of normative variability in caregiving on such biobehavioral processes, however, is poorly understood. Here, we provide initial evidence that even subtle variability in normative caregiving shapes threat-related brain function and, potentially, associated psychopathology in adolescence. Specifically, we report that greater familial affective responsiveness is associated with heightened amygdala reactivity to interpersonal threat, particularly in adolescents having experienced relatively low recent stress. These findings extend the literature on the effects of caregiving extremes on brain function to subtle, normative variability, but suggest that presumably protective factors may be associated with increased risk-related amygdala reactivity. We consider these paradoxical associations with regard to studies of basic associative threat learning and further consider their relevance for understanding potential effects of caregiving on psychological development.

scholarly journals Effects of Early-Life Stress on the Brain and Behaviors: Implications of Early Maternal Separation in Rodents

2020 ◽  
Vol 21 (19) ◽  
pp. 7212
Author(s):  
Mayumi Nishi
Keyword(s):  
Child Abuse ◽  
Hpa Axis ◽  
Brain Function ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Emotional Behavior ◽  
Neural Basis ◽  
The Brain

Early-life stress during the prenatal and postnatal periods affects the formation of neural networks that influence brain function throughout life. Previous studies have indicated that maternal separation (MS), a typical rodent model equivalent to early-life stress and, more specifically, to child abuse and/or neglect in humans, can modulate the hypothalamic–pituitary–adrenal (HPA) axis, affecting subsequent neuronal function and emotional behavior. However, the neural basis of the long-lasting effects of early-life stress on brain function has not been clarified. In the present review, we describe the alterations in the HPA-axis activity—focusing on serum corticosterone (CORT)—and in the end products of the HPA axis as well as on the CORT receptor in rodents. We then introduce the brain regions activated during various patterns of MS, including repeated MS and single exposure to MS at various stages before weaning, via an investigation of c-Fos expression, which is a biological marker of neuronal activity. Furthermore, we discuss the alterations in behavior and gene expression in the brains of adult mice exposed to MS. Finally, we ask whether MS repeats itself and whether intergenerational transmission of child abuse and neglect is possible.

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.

scholarly journals Early life adversity, dispositional mindfulness, and longitudinal stress experience during the COVID-19 pandemic

2020 ◽  
Author(s):  
Annika Benz ◽  
Maria Meier ◽  
Ulrike U. Bentele ◽  
Stephanie J. Dimitroff ◽  
Bernadette Denk ◽  
...  
Keyword(s):  
Perceived Stress ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Dispositional Mindfulness ◽  
Early Life Adversity ◽  
Stress Buffering ◽  
Psychopathological Symptoms ◽  
Increased Risk ◽  
The Impact

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.

scholarly journals Dynamic Networks in the Emotional Brain

2016 ◽  
Vol 23 (4) ◽  
pp. 383-396 ◽  
Author(s):  
Luiz Pessoa ◽  
Brenton McMenamin
Keyword(s):  
Brain Function ◽  
Large Scale ◽  
Dynamic Networks ◽  
Brain Regions ◽  
Time Varying ◽  
Brain Circuits ◽  
Mental Faculty ◽  
Dynamic View ◽  
The Impact ◽  
Perception Action

Research on the emotional brain has often focused on a few structures thought to be central to this type of processing—hypothalamus, amygdala, insula, and so on. Conceptual thinking about emotion has viewed this mental faculty as linked to broader brain circuits, too, including early ideas by Papez and others. In this article, we discuss research that embraces a distributed view of emotion circuits and efforts to unravel the impact on emotional manipulations on the processing of several large-scale brain networks that are chiefly important for mental operations traditionally labeled with terms such as “perception,” “action,” and “cognition.” Furthermore, we describe networks as dynamic processes and how emotion-laden stimuli strongly affect network structure. As networks are not static entities, their organization unfolds temporally, such that specific brain regions affiliate with them in a time-varying fashion. Thus, at a specific moment, brain regions participate more strongly in some networks than others. In this dynamic view of brain function, emotion has broad, distributed effects on processing in a manner that transcends traditional boundaries and inflexible labels, such as “emotion” and “cognition.” What matters is the coordinated action that supports behaviors.

scholarly journals Long-Term Burden of Increased Body Mass Index from Childhood on Adult Dyslipidemia: The i3C Consortium Study

2019 ◽  
Vol 8 (10) ◽  
pp. 1725 ◽  
Author(s):  
Yinkun Yan ◽  
Lydia A. Bazzano ◽  
Markus Juonala ◽  
Olli T. Raitakari ◽  
Jorma S. A. Viikari ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Early Life ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Lipid Levels ◽  
Increased Risk ◽  
The Impact

Background: Data are limited regarding the association of cumulative burden and trajectory of body mass index (BMI) from early life with adult lipid disorders. Methods: The study cohort consisted of 5195 adults who had BMI repeatedly measured 4 to 21 times from childhood and had blood lipid measurements of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) and information on lipid-lowering medications in the last adult survey. The area under the curve (AUC) was calculated as a measure of long-term burden (total AUC) and trends (incremental AUC) of BMI. Results: Participants with dyslipidemia, high LDL-C, low HDL-C and high TG had consistently and significantly higher BMI levels from childhood to adulthood compared to those with normal lipid levels. After adjusting for age, race, sex, and cohort, increased risk of adult dyslipidemia was significantly associated with higher values of childhood BMI, adulthood BMI, total AUC and incremental AUC, with odds ratio (95% confidence interval) = 1.22 (1.15–1.29), 1.85 (1.74–1.97), 1.61 (1.52–1.71), and 1.59 (1.50–1.69), respectively, and p < 0.001 for all. The association patterns were similar in most race–sex subgroups. Conclusions: Adults with dyslipidemia versus normal lipid levels have consistently higher levels and distinct life-course trajectories of BMI, suggesting that the impact of excessive body weight on dyslipidemia originates in early life.

Early life environment: does it have implications for predisposition to disease?

2002 ◽  
Vol 14 (6) ◽  
pp. 292-302 ◽  
Author(s):  
Nola Shanks
Keyword(s):  
Environmental Factors ◽  
Immune Function ◽  
Hpa Axis ◽  
Early Life ◽  
Inflammatory Responses ◽  
Psychiatric Disease ◽  
Disease Etiology ◽  
Increased Risk ◽  
The Impact ◽  
Postnatal Factors

Early life environmental factors have been associated with altered predisposition to a variety of pathologies. A considerable literature examines pre- and postnatal factors associated with increased risk of cardiovascular, metabolic (i.e. insulin resistance, hyperlipidemia) and psychiatric disease, and the importance of hormonal programming. The brain is exquisitely sensitive to environmental inputs during development and the stress responsiveness of the hypothalamic–pituitary–adrenal (HPA) axis has been shown to be both up- and down-regulated by early life exposure to limited nutrition, stress, altered maternal behaviors, synthetic steroids and inflammation. It has been suggested that peri-natal programming of HPA axis regulation might therefore contribute to metabolic and psychiatric disease etiology. In addition, glucocorticoids play modulatory roles regulating many aspects of immune function, notably controlling both acute and chronic inflammatory responses. Neuroendocrine–immune communication is bidirectional, and therefore it is expected that environmental factors altering HPA regulation have implications for stress effects on immune function and predisposition to inflammation. The impact of pre- and postnatal factors altering immune function, stress responsivity and predisposition to inflammatory disease are reviewed. It is also examined whether the early ‘immune environment’ might similarly influence predisposition to disease and alter neuroendocrine function. Evidence indicating a role for early life inflammation and infection as an important factor programming the neuroendocrine–immune axis and altering predisposition to disease is considered.

scholarly journals Perfluorooctanoic Acid (PFOA) Exposure in Early Life Increases Risk of Childhood Adiposity: A Meta-Analysis of Prospective Cohort Studies

2018 ◽  
Vol 15 (10) ◽  
pp. 2070 ◽  
Author(s):  
Pingping Liu ◽  
Fang Yang ◽  
Yongbo Wang ◽  
Zhanpeng Yuan
Keyword(s):  
Cohort Studies ◽  
Prospective Cohort ◽  
Early Life ◽  
Meta Analysis ◽  
Perfluorooctanoic Acid ◽  
Analysis Model ◽  
Prospective Cohort Studies ◽  
Childhood Adiposity ◽  
Increased Risk ◽  
The Impact

Some articles have examined perfluorooctanoic acid (PFOA) exposure in early life in relation to risk of childhood adiposity. Nevertheless, the results from epidemiological studies exploring the associations remain inconsistent and contradictory. We thus conducted an analysis of data currently available to examine the association between PFOA exposure in early life and risk of childhood adiposity. The PubMed, EMBASE, and Web of Science databases were searched to identify studies that examined the impact of PFOA exposure in early life on childhood adiposity. A random-effects meta-analysis model was used to pool the statistical estimates. We identified ten prospective cohort studies comprising 6076 participants with PFOA exposure. The overall effect size (relative risk or odds ratio) for childhood overweight was 1.25 (95% confidence interval (CI): 1.04, 1.50; I2 = 40.5%). In addition, exposure to PFOA in early life increased the z-score of childhood body mass index (β = 0.10, 95% CI: 0.03, 0.17; I2 = 27.9%). Accordingly, exposure to PFOA in early life is associated with an increased risk for childhood adiposity. Further research is needed to verify these findings and to shed light on the molecular mechanism of PFOA in adiposity.

scholarly journals Effects of Chronic Exposure to Low-Dose delta-9-Tetrahydrocannabinol in Adolescence and Adulthood on Serotonin/Norepinephrine Neurotransmission and Emotional Behavior

2020 ◽  
Vol 23 (11) ◽  
pp. 751-761
Author(s):  
Danilo De Gregorio ◽  
Joshua Dean Conway ◽  
Martha-Lopez Canul ◽  
Luca Posa ◽  
Francis Rodriguez Bambico ◽  
...  
Keyword(s):  
Neural Activity ◽  
Chronic Exposure ◽  
Low Dose ◽  
Forced Swim Test ◽  
Emotional Behavior ◽  
Long Term Effects ◽  
Adult Rats ◽  
Increased Risk ◽  
Adult Exposure ◽  
The Impact

Abstract Background Chronic exposure to D9-tetrahydrocannabinol (THC), the main pharmacological component of cannabis, during adolescence has been shown to be associated with an increased risk of depression and suicidality in humans. Little is known about the impact of the long-term effects of chronic exposure to low doses of THC in adolescent compared with adult rodents. Methods THC (1 mg/kg i.p., once per day) or vehicle was administered for 20 days in both adolescent (post-natal day 30–50) and young adult rats (post-natal day 50–70). After a long washout period (20 days), behavioral tests and electrophysiological recordings of serotonin and norepinephrine neurons were carried out. Results Adolescent THC exposure resulted in depressive behaviors: decreased latency to first immobility in the forced swim test and increased anhedonia in the sucrose preference test. Decreased entries in the open arms were observed in the elevated plus maze after adolescent and adult exposure, indicating an anxious phenotype. A significant reduction in dorsal raphe serotonergic neural activity without a change in locus coeruleus noradrenergic neural activity was found after adolescent and adult exposure. Conclusions Altogether, these findings suggest that chronic low-dose THC exposure during the critical developmental period of adolescence and during adulthood could result in increased vulnerability of the serotonin system accompanied by anxiety symptoms. However, depressive phenotypes occur only after adolescent exposure but not after adult exposure, underscoring the greater vulnerability of young ages to the mental effects of cannabis.

scholarly journals Pregnancy, obesity and insulin resistance: maternal overnutrition and the target windows of fetal development

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Beverly S. Muhlhausler ◽  
Jessica R. Gugusheff ◽  
Zhi Yi Ong ◽  
Mini A. Vithayathil
Keyword(s):  
Insulin Resistance ◽  
Early Life ◽  
Maternal Obesity ◽  
Nutrient Supply ◽  
Personal Perspective ◽  
Human Populations ◽  
Maternal Undernutrition ◽  
Increased Risk ◽  
Maternal Overnutrition ◽  
The Impact

AbstractA substantial body of literature has demonstrated that the nutritional environment an individual experiences before birth or in early infancy is a key determinant of their health outcomes across the life course. This concept, the developmental origins of health and disease (DOHaD) hypothesis, was initially focused on the adverse consequences of exposure to a suboptimal nutrient supply and provided evidence that maternal undernutrition, fetal growth restriction, and low birth weight were associated with heightened risk of central adiposity, insulin resistance, and cardiovascular disease. More recently, the epidemic rise in the incidence of maternal obesity has seen the attention of the DOHaD field turn toward identifying the impact on the offspring of exposure to an excess nutrient supply in early life. The association between maternal obesity and increased risk of obesity in the offspring has been documented in human populations worldwide, and animal models have provided critical insights into the biological mechanisms that drive this relationship. This review will discuss the important roles that programming of the adipocyte and programming of the central neural networks which control appetite and reward play in the early life programming of metabolic disease by maternal overnutrition. It will also highlight the important research gaps and challenges that remain to be addressed and provide a personal perspective on where the field should be heading in the coming 5–10 years.

The impact of early life gut colonization on metabolic and obesogenic outcomes: what have animal models shown us?

2015 ◽  
Vol 7 (1) ◽  
pp. 15-24 ◽  
Author(s):  
J. G. Wallace ◽  
W. Gohir ◽  
D. M. Sloboda
Keyword(s):  
Animal Models ◽  
Gut Microbiota ◽  
Early Life ◽  
Maternal Obesity ◽  
Communicable Disease ◽  
Critical Periods ◽  
Early Life Adversity ◽  
Gut Colonization ◽  
Increased Risk ◽  
The Impact

The rise in the occurrence of obesity to epidemic proportions has made it a global concern. Great difficulty has been experienced in efforts to control this growing problem with lifestyle interventions. Thus, attention has been directed to understanding the events of one of the most critical periods of development, perinatal life. Early life adversity driven by maternal obesity has been associated with an increased risk of metabolic disease and obesity in the offspring later in life. Although a mechanistic link explaining the relationship between maternal and offspring obesity is still under investigation, the gut microbiota has come forth as a new factor that may play a role modulating metabolic function of both the mother and the offspring. Emerging evidence suggests that the gut microbiota plays a much larger role in mediating the risk of developing non-communicable disease, including obesity and metabolic dysfunction in adulthood. With the observation that the early life colonization of the neonatal and postnatal gut is mediated by the perinatal environment, the number of studies investigating early life gut microbial establishment continues to grow. This paper will review early life gut colonization in experimental animal models, concentrating on the role of the early life environment in offspring gut colonization and the ability of the gut microbiota to dictate risk of disease later in life.

Sign in / Sign up

Export Citation Format

Share Document