Chronic stress can affect human health through a myriad of behavioral and biochemical pathways. Tauhis review focuses on some key hormonal and metabolic pathways that appear important today. In modern society, we are faced with excessive psychological stress, as well as an epidemic of overeating, and the two together appear to have synergistic effects. Chronic stress can lead to overeating, co-elevation of cortisol and insulin, and suppression of certain anabolic hormones. This state of metabolic stress in turn promotes abdominal adiposity.
The World Journal of Biological Psychiatry: The Official Journal of the World Federation of Societies of Biological Psychiatry
Stress is commonly associated with a variety of psychiatric conditions, including major depression, and with chronic medical conditions, including diabetes and insulin resistance. Whether stress causes these conditions is uncertain, but plausible mechanisms exist by which such effects might occur. To the extent stress-induced hormonal alterations (e.g., chronically elevated cortisol levels and lowered dehydroepiandrosterone [DHEA] levels) contribute to psychiatric and medical disease states, manipulations that normalize these hormonal aberrations should prove therapeutic.
Behavior is shaped by a variety of genetic and epigenetic mechanisms, including those underlying anxiety and fear. Neuropeptides are ideal candidates to be involved in the regulation of emotional facets as they are released within the brain and act as neuromodulators/neurotransmitters; furthermore, their large number is prone to direct changes by mutations.
Depression is a condition with a complex biologic pattern in etiology. Environmental stressors modulate subsequent vulnerability to depression. In particular, early adversity seems to induce heightened reactivity to stress through several possible mechanisms, both biologic and psychologic. This increased reactivity results in an enhancement of biologic stress-response mechanisms, especially the HPA axis.
BACKGROUND: Galanin (GAL) is a neuropeptide, which is expressed primarily in limbic nuclei in the brain and mediates miscellaneous physiological processes and behaviors. In animal studies, both the application of GAL and antagonism of its receptors have been shown to affect anxiety-like and depression-related behavior. In humans, intravenous administration of the neuropeptide galanin has been reported to have fast antidepressant efficacy.
Epidemiological evidence links exposure to stress hormones during fetal or early postnatal development with lifetime prevalence of cardiac, metabolic, auto-immune, neurological and psychiatric disorders. This has led to the concept of 'developmental programming through stress'. Importantly, these effects (specifically, hypertension, hyperglycaemia and neurodevelopmental and behavioural abnormalities) can be reproduced by exposure to high glucocorticoid levels, indicating a crucial role of glucocorticoids in their causation.
Early life stress (child and adolescent abuse, neglect and trauma) induces robust alterations in emotional and social functioning resulting in enhanced risk for the development of psychopathologies such as mood and aggressive disorders. Here, an overview is given on recent findings in primate and rodent models of early life stress, demonstrating that chronic deprivation of early maternal care as well as chronic deprivation of early physical interactions with peers are profound risk factors for the development of inappropriate aggressive behaviors.
Every individual experiences stressful life events. In some cases acute or chronic stress leads to depression and other psychiatric disorders, but most people are resilient to such effects. Recent research has begun to identify the environmental, genetic, epigenetic and neural mechanisms that underlie resilience, and has shown that resilience is mediated by adaptive changes in several neural circuits involving numerous neurotransmitter and molecular pathways.
Exposure to interpersonal violence or abuse affects the physical and emotional well-being of affected individuals. In particular, exposure to trauma during development increases the risk of psychiatric and other medical disorders beyond the risks associated with adult violence exposure. Alterations in the hypothalamic-pituitary-adrenal (HPA) axis, a major mediating pathway of the stress response, contribute to the long-standing effects of early life trauma.
The current status of glucocorticoid alterations in post-traumatic stress disorder (PTSD) will be described in this chapter. Emphasis will be placed on data that suggest that at least some glucocorticoid-related observations in PTSD reflect pretraumatic glucocorticoid status.