scholarly journals Stress Response and Perinatal Reprogramming: Unraveling (Mal)adaptive Strategies

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Laura Musazzi ◽  
Jordan Marrocco
Keyword(s):  
Stress Response ◽  
Early Life ◽  
Neuropsychiatric Disorders ◽  
Brain Morphology ◽  
Postnatal Life ◽  
Behavioral Stress ◽  
Corticosteroid Hormones ◽  
Excitatory Neurotransmission ◽  
Early Life Events

Environmental stressors induce coping strategies in the majority of individuals. The stress response, involving the activation of the hypothalamic-pituitary-adrenocortical axis and the consequent release of corticosteroid hormones, is indeed aimed at promoting metabolic, functional, and behavioral adaptations. However, behavioral stress is also associated with fast and long-lasting neurochemical, structural, and behavioral changes, leading to long-term remodeling of glutamate transmission, and increased susceptibility to neuropsychiatric disorders. Of note, early-life events, bothin uteroand during the early postnatal life, trigger reprogramming of the stress response, which is often associated with loss of stress resilience and ensuing neurobehavioral (mal)adaptations. Indeed, adverse experiences in early life are known to induce long-term stress-related neuropsychiatric disorders in vulnerable individuals. Here, we discuss recent findings about stress remodeling of excitatory neurotransmission and brain morphology in animal models of behavioral stress. These changes are likely driven by epigenetic factors that lie at the core of the stress-response reprogramming in individuals with a history of perinatal stress. We propose that reprogramming mechanisms may underlie the reorganization of excitatory neurotransmission in the short- and long-term response to stressful stimuli.

scholarly journals Stress and Growth in children and adolescents

2021 ◽  
Author(s):  
Maria Mousikou ◽  
Andreas Kyriakou ◽  
Nicos Skordis
Keyword(s):  
Growth Hormone ◽  
Stress Response ◽  
Chronic Stress ◽  
Early Life ◽  
Stress System ◽  
Childhood And Adolescence ◽  
Conservation Of Energy ◽  
Targeted Interventions ◽  
The Impact

The infantile, childhood, and adolescent periods of growth and development represent times of increased vulnerability to stressors. The rate of growth in each period depends on the interplay of genetic, environmental, dietary, socioeconomic, developmental, behavioral, nutritional, metabolic, biochemical, and hormonal factors. A stressor may have an impact on growth directly through modulation of the growth hormone axis or indirectly through modulation of other factors. The adaptive response to stressors culminates in behavioral, physiological, and biochemical responses, which together support survival and conservation of energy. The process begins within seconds and involves activation of sympathetic nervous system and Hypothalamic-Pituitary-Adrenal axis. The time-limited stress response is at once anti-growth, anti-reproductive and catabolic with no lasting adverse consequences. However, chronic activation of the stress system and hypercortisolism have consequential negative impacts on growth, thyroid function, reproduction-puberty, and metabolism. They suppress Growth Hormone-Insulin like growth factor 1, Hypothalamic-Pituitary-Gonadal and Thyroid axes and can be responsible for an increase in visceral adiposity, a decrease in lean mass, suppression of osteoblastic activity with risk of osteoporosis, and induction of insulin resistance. Early life adversities, emotional or physical, have been associated with long-term negative physical and mental health outcomes. There are many models of chronic stress that corroborate that early life adversities affect optimal growth and have consequences throughout the lifespan. Targeted interventions to reduce stress during infancy, childhood and adolescence can have far reaching benefits to long-term health as well as attaining adequate growth. In this review we describe the neuroendocrinology of the stress response, the factors influencing growth, and the impact of chronic stress on growth during critical periods of infancy, childhood, and puberty with reference to each of growth, thyroid, and gonadal axis.

scholarly journals Sustained TNF signaling is required for the synaptic and behavioral response to acute stress

2021 ◽  
Author(s):  
Gina M Kemp ◽  
Haider F Altimimi ◽  
Yoonmi Nho ◽  
Renu Heir ◽  
David Stellwagen
Keyword(s):  
Stress Response ◽  
Acute Stress ◽  
Ventral Hippocampus ◽  
Behavioral Changes ◽  
Stress Disorders ◽  
Behavioral Stress ◽  
Factor Α ◽  
Necrosis Factor

Acute stress triggers plasticity of forebrain synapses as well as behavioral changes. Here we reveal that Tumor Necrosis Factor α (TNF) is a required downstream mediator of the stress response in mice, necessary for stress-induced synaptic potentiation in the ventral hippocampus and for an increase in anxiety-like behaviour. Acute stress is sufficient to activate microglia, triggering the long-term release TNF. Critically, on-going TNF signaling in the ventral hippocampus is necessary to sustain both the stress-induced synaptic and behavioral changes, as these could be reversed hours after induction by antagonizing TNF signaling. This demonstrates that TNF maintains the synaptic and behavioral stress response in vivo, making TNF a potential novel therapeutic target for stress disorders.

scholarly journals Nutritional adversity, sex and reproduction: 30 years of DOHaD and what have we learned?

2019 ◽  
Vol 242 (1) ◽  
pp. T51-T68 ◽  
Author(s):  
Patrycja A Jazwiec ◽  
Deborah M Sloboda
Keyword(s):  
Germ Cells ◽  
Early Life ◽  
Disease Risk ◽  
Primordial Germ Cells ◽  
Reproductive Function ◽  
Postnatal Life ◽  
Early Life Adversity ◽  
Increased Risk ◽  
Health And Disease

It is well established that early life environmental signals, including nutrition, set the stage for long-term health and disease risk – effects that span multiple generations. This relationship begins early, in the periconceptional period and extends into embryonic, fetal and early infant phases of life. Now known as the Developmental Origins of Health and Disease (DOHaD), this concept describes the adaptations that a developing organism makes in response to early life cues, resulting in adjustments in homeostatic systems that may prove maladaptive in postnatal life, leading to an increased risk of chronic disease and/or the inheritance of risk factors across generations. Reproductive maturation and function is similarly influenced by early life events. This should not be surprising, since primordial germ cells are established early in life and thus vulnerable to early life adversity. A multitude of ‘modifying’ cues inducing developmental adaptations have been identified that result in changes in reproductive development and impairments in reproductive function. Many types of nutritional challenges including caloric restriction, macronutrient excess and micronutrient insufficiencies have been shown to induce early life adaptations that produce long-term reproductive dysfunction. Many pathways have been suggested to underpin these associations, including epigenetic reprogramming of germ cells. While the mechanisms still remain to be fully investigated, it is clear that a lifecourse approach to understanding lifetime reproductive function is necessary. Furthermore, investigations of the impacts of early life adversity must be extended to include the paternal environment, especially in epidemiological and clinical studies of offspring reproductive function.

scholarly journals Bronchopulmonary dysplasia: what are its links to COPD?

2019 ◽  
Vol 13 ◽  
pp. 175346661989249 ◽  
Author(s):  
Sharon A. McGrath-Morrow ◽  
Joseph M. Collaco
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Lung Development ◽  
Early Life ◽  
Airflow Obstruction ◽  
Adult Life ◽  
Normal Lung ◽  
Chronic Obstructive ◽  
Postnatal Life ◽  
Small Airways

Emerging evidence suggests that adverse early life events can affect long-term health trajectories throughout life. Preterm birth, in particular, is a significant early life event that affects approximately 10% of live births. Worldwide, prematurity is the number one cause of death in children less than 5 years of age and has been shown to disrupt normal lung development with lasting effects into adult life. Along with impaired lung development, interventions used to support gas exchange and other sequelae of prematurity can lead to the development of bronchopulmonary dysplasia (BPD). BPD is a chronic respiratory disease of infancy characterized by alveolar simplification, small airways disease, and pulmonary vascular changes. Although many survivors of BPD improve with age, survivors of BPD often have chronic lung disease characterized by airflow obstruction and intermittent pulmonary exacerbations. Long-term lung function trajectories as measured by FEV1 can be lower in children and adults with a history BPD. In this review, we discuss the epidemiology and manifestations of BPD and its long-term consequences throughout childhood and into adulthood. Available evidence suggests that disrupted lung development, genetic susceptibility and subsequent environment and infectious events that occur in prenatal and postnatal life likely increase the predisposition of children with BPD to develop early onset chronic obstructive pulmonary disease (COPD). The reviews of this paper are available via the supplemental material section.

scholarly journals Early life epigenetic regulation of CRH expression pattern in the PVN affects long-term stress response

2019 ◽  
Vol 24 (7) ◽  
pp. 935-935
Author(s):  
Tomer Cramer ◽  
Tali Rosenberg ◽  
Tatiana Kisliouk ◽  
Noam Meiri
Keyword(s):  
Stress Response ◽  
Expression Pattern ◽  
Epigenetic Regulation ◽  
Early Life

Primate Infancies

2017 ◽  
Author(s):  
Kristen Hawkes ◽  
James S. Chisholm ◽  
Lynn A. Fairbanks ◽  
Johannes Johow ◽  
Elfriede Kalcher-Sommersguter ◽  
...  
Keyword(s):  
Life Events ◽  
Early Life ◽  
Recent Experience ◽  
Social Forces ◽  
Evolutionary Perspective ◽  
Long Term Effects ◽  
Human Infants ◽  
Early Life Events ◽  
Mothering Style

Bowlby recognized that studying other primates could help identify the needs of human infants; his evolutionary perspective has had a wide impact on understanding of human development. Much more is now known about evolutionary processes and variation, within and between species. This chapter reviews aspects of evolutionary theory and primatology relevant to Bowlby’s theory of attachment. Beginning with primate phylogeny, ecological and social forces that contribute to the varieties of primate sociality are considered and some reasons canvassed that explain why primatologists do not all agree on the choice of words to describe the relationships between animals, including use of the term “attachment.” Variations and commonalities are identified and used to explore how development in human infants can be understood in terms of social relationships and maturational state at birth and weaning compared to other primates. Infant experience has long-term effects in primates other than humans. Some of that evidence is summarized and special attention is given to interactions between particular chimpanzee mothers and infants in an unusual setting, where trusting relationships between mothers and human researchers reveal variations in mothering style that appear to result from early life events, recent experience, and social context.

scholarly journals Early nutrition programming of long-term health

2012 ◽  
Vol 71 (3) ◽  
pp. 371-378 ◽  
Author(s):  
Berthold Koletzko ◽  
Brigitte Brands ◽  
Lucilla Poston ◽  
Keith Godfrey ◽  
Hans Demmelmair
Keyword(s):  
Weight Gain ◽  
Early Life ◽  
Adverse Outcomes ◽  
Postnatal Life ◽  
Long Term Effects ◽  
Public Health Importance ◽  
Rapid Weight Gain ◽  
Early Nutrition ◽  
Increased Risk

Increasing evidence from the EU Project EARNEST and many other investigators demonstrates that early nutrition and lifestyle have long-term effects on later health and the risk of common non-communicable diseases (known as ‘developmental programming’). Because of the increasing public health importance and the transgenerational nature of the problem, obesity and associated disorders are the focus of the new EU funded project ‘EarlyNutrition’. Currently, three key hypotheses have been defined: the fuel mediated ‘in utero’ hypothesis suggests that intrauterine exposure to an excess of fuels, most notably glucose, causes permanent changes of the fetus that lead to obesity in postnatal life; the accelerated postnatal weight gain hypothesis proposes an association between rapid weight gain in infancy and an increased risk of later obesity and adverse outcomes; and the mismatch hypothesis suggests that experiencing a developmental ‘mismatch’ between a sub-optimal perinatal and an obesogenic childhood environment is related to a particular predisposition to obesity and corresponding co-morbidities. Using existing cohort studies, ongoing and novel intervention studies and a basic science programme to investigate those key hypotheses, project EarlyNutrition will provide the scientific foundations for evidence-based recommendations for optimal nutrition considering long-term health outcomes, with a focus on obesity and related disorders. Scientific and technical expertise in placental biology, epigenetics and metabolomics will provide understanding at the cellular and molecular level of the relationships between early life nutritional status and the risk of later adiposity. This will help refine strategies for intervention in early life to prevent obesity.

Long-Term Impact of Early Life Events on Physiology and Behaviour

2014 ◽  
Vol 26 (9) ◽  
pp. 587-602 ◽  
Author(s):  
G. J. Boersma ◽  
T. L. Bale ◽  
P. Casanello ◽  
H. E. Lara ◽  
A. B. Lucion ◽  
...  
Keyword(s):  
Life Events ◽  
Early Life ◽  
Long Term Impact ◽  
Early Life Events
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