ADAPTATION, COPING, AND ILLNESS
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Although much has been learned about the dynamic biological systems and human/environmental interactions involved, stress is personal in that individual stress responses change with time and circumstances. Indeed, the effects of stress on each individual are influenced by genet- ics, SES, environmental context, perception, developmental history, prior susceptibilities, preexisting health status, and individual coping abilities. Clearly, the maintenance of homeostasis requires the human organism to routinely initiate allostatic responses to the stressors of daily life, as well as to the less frequent severe assaults on the integrity of the body and the mind, responsible for allostatic load. Systemically, allostasis may be seen as beginning with some degree of the alarm stage (fight-or-flight activation), and ideally moving to an effective resolution through adaptation, ultimately culminating in a return to homeostasis. The prolonged effects of allostatic overload—the long- term wear-and-tear costs of adaptation efforts—provide a conceptual foundation for examining the long-term consequences of stress on health. What Selye called “diseases of adaptation” are the outcomes of allostatic overload.
Adaptation, Coping, and Resilience Adaptation broadly refers to the biopsychosocial process of adjusting physiology, morphology, and behavior in response to new or altered circumstances, internal and external in origin, in the physical and social environment. Related to adaptation is the term resilience. Resilience is the ability to withstand threats to stability and is a measure of the capacity to adapt to challenges. It has been described as the “ability to
KEY POINTS • Modern views of allostatic maintenance of homeostasis in the face of stress
are primarily derived from an understanding of negative feedback, as well as the roles of the sympathetic nervous system catecholamines and the glucocorticoid cortisol.
• The primary role of the sympathetic nervous system (SNS) is appraisal of a stressful stimulus and release of norepinephrine. Norepinephrine released from sympathetic nerve endings increases heart rate and contractility, constricts blood vessels to decrease blood flow to less essential tissues and organs and raise blood pressure, reduces gastrointestinal motility and gastric acid secretion, dilates the pupils, and inhibits insulin secretion.
• Stress stimulates sympathetic activation of the adrenal medulla to release epinephrine. Epinephrine’s actions are similar to norepinephrine and are particularly important for increasing cardiac performance (increased heart rate, contractility, and cardiac output), promoting the release of glucose from the liver, and enhancing bronchodilation.
• Cortisol, from the adrenal cortex, has widespread effects on numerous tissues that are both synergistic and antagonistic with catecholamines and has an antiinflammatory role.
• Aldosterone promotes fluid volume expansion and increases blood pressure.
• Endorphins and enkephalins are released by the CNS in response to painful stressors, leading to decreased perception of pain and increased sedation and euphoria. Immune cells in the periphery also contribute to pain modulation.
• Immune cells respond to the hormones released by the HPA axis and sympathetic nervous system. They also release cytokines that in turn affect the functioning of these stress systems.
• Sex hormones and differential release of growth hormone, prolactin, and oxytocin produce effects on the stress response that may differ between genders.
CHAPTER 2 Homeostasis, Allostasis, and Adaptive Responses to Stressors 21
pathologies. Not only do catecholamines contribute to the development of atherosclerosis and hypertension, they also increase the risk of developing cardiac dysrhythmias and sudden cardiac death, and even stress-induced cardiomyopathy. They increase platelet activity, resulting in clot formation, and elevate serum lipid levels, significant factors in the pathogenesis of myocardial infarction. A growing body of evidence further suggests that inflammation may mediate a link between stress and cardiovascular disease. Stress has been associated with the production of proinflammatory cytokines such as IL-1, IL-6, and tumor necrosis factor (TNF). These cytokines can trigger the production of C-reactive protein (CRP), a cytokine associated with cardiovascular disease.
The field of psychoneuroimmunology has provided substantive evidence of the roles of the stress hormones in the brain. In the central nervous system, specifically the brain, the mediators of adaptation facilitate learning, memory, and neuroendocrine and autonomic regula- tion. This heightened memory, at least in the short term, allows the individual to be more aware of the potential stressor in the future. Chronic overactivity or underactivity, however, may result in atrophy of some nerve cells (especially in the hippocampus), impairing memory, whereas others have been found to hypertrophy (especially in the amygdala) and undergo remodeling, resulting in an increase in fear, anxiety, and other mood disorders. In essence, allostatic overload results in altered and impaired cognitive function. Some evidence suggests that inflammation associated with allostatic overload may play a role in learning and memory impairment. For instance, elevated levels of proinflammatory cytokines, such as IL-1 and IL-6, markers of
a point at which they barely notice the noise of airplanes flying over their homes. They become habituated to the stressor (loud noise). One important way to habituate to a stressor is to manipulate, or “train,” the hypothalamus to react less forcefully to a perceived threat or stressor. Repeatedly ignoring a specific stressor prevents the inappropriate trig- gering of the GAS. The result is a more acceptable level of stress response. Techniques that accomplish this desensitization change the predominant brain waves of the individual from beta to alpha waves, which are slower and more normal. Biofeedback, visualization, and meditation are examples of therapies that use this principle. Practicing these techniques for 20 to 30 minutes daily can enhance the ability to alter how a stressor is perceived and modulate the stress response. These techniques have documented efficacy in enhancing immune function. Desensitization methods have been found to be beneficial for common stress-related conditions, such as migraine headache, chronic back pain, and hypertension.
Allostatic Overload and Illness When adaptation mechanisms are inadequate or the total amount of allostatic load is excessive, overwhelming allostasis capacities, the result is allostatic overload. There are several ways in which allostatic load can accumulate in an individual: (1) repeated exposures to multiple stressors, (2) inability to habituate or adapt to the stressor, (3) unneces- sarily prolonged stress response or stress response that continues after the stressor is removed, and (4) inadequate response to the stressor that causes other stress response mediators to attempt to compensate. Homeostasis, the steady-state that previously existed, cannot be attained. Instead, allostatic overload occurs, and the resulting maladaptation can be reflected in a range of pathophysiologic states that span the traditional boundaries of health care, from psychiatric and endocrine disorders to inflammatory disease.
Hair loss, emotional tension, burnout, mouth sores, insomnia, asthma, heart palpitations, neuromuscular movement disorders (tics), tension headaches, muscle contraction backaches, digestive disorders, and irritable bladder are just a few of the common disorders that can be caused by or worsened by stress. Reproductive disorders such as menstrual irregularity in women and male impotence also have been linked with the effects of allostatic overload. Box 2.2 summarizes some of the physiologic and psychological effects of excessive stress. Fig. 2.3 depicts the multiple body organs and systems in which the effects of insufficient or overactive stress responses may be seen.
The chemical mediators of stress have a strong physiologic basis for the role they play in contributing to illness. Cortisol being released from the adrenal cortex supports Selye’s stage of resistance or adaptation, but may also be accountable for pathologic changes. The same can be said of the catecholamines and the other chemical mediators (e.g., immune cytokines). Because these bloodborne chemicals have such broad effects systemically, the impact of excessive or inadequate amounts is understandably wide reaching. In some cases, the relationships have been well substantiated by research; in others, they are hypothesized based upon knowledge of the effects of these chemicals.
The relationship between excessive catecholamine levels and what historically have been called “stress-related” illnesses has often been associated with cardiovascular pathologies such as hypertension, stroke, and myocardial infarction. Abdominal fat cells are well supplied with cortisol receptors, and excessive secretion of cortisol results in the collection of fat in this area. When this fat is released into the bloodstream, the resulting increase in the levels of circulating free fatty acids plays a role in cardiovascular risk. Additionally, repeated or prolonged elevation of blood pressure, especially in combination with the metabolic effects of elevated cortisol and catecholamine levels, promotes the development of atherosclerosis and, ultimately, many cardiovascular
Physical Indicators Elevated blood pressure Increased muscle tension Elevated pulse rate Increased respiration Sweaty palms Cold extremities (hands and feet) Fatigue Tension headache Upset stomach: nausea, vomiting, diarrhea Change in appetite Change in weight Increased blood catecholamine level Hyperglycemia Restlessness Insomnia
Behavioral and Emotional Indicators Anxiety (nonspecific fears) Depression Increased use of mind-altering substances (e.g., alcohol, chemical substances) Change in eating, sleeping, or activity pattern Mental exhaustion Feelings of inadequacy; loss of self-esteem Increased irritability Loss of motivation Decreased productivity Inability to make good judgments Inability to concentrate Increased absenteeism and illness Increased proneness to accidents