What are physiological responses to stress?

Introduction

Although the term
stress
is commonly used by the general population to refer to various responses to events that individuals find taxing, the concept involves much more. For centuries, scientific thinkers and philosophers have been interested in learning more about the interactions between the environment (stressful events), emotions, and the body. Much is now known about this interaction, although there is still much left to discover. In the late twentieth century and beyond, much was learned about how stressful events affect the activity of the body (or physiology); for example, it has been established that these physiological responses to stressors sometimes increase the risk of development or exacerbate a number of diseases. To best understand the body’s response to stressful events (or stressors), the general sequence of events and the specific responses of various organ systems must be considered.

Almost all bodily responses are mediated at least partially by the central nervous system: the brain and spinal cord. The brain takes in and analyzes information from the external environment as well as from the internal environment (the rest of the body), and it acts to regulate the activities of the body to optimize adaptation or survival. When the brain detects a threat, a sequence of events occurs to prepare the body to fight or to flee the threat. Walter Bradford Cannon, in the early twentieth century, was the first to describe this fight-or-flight response
of the body. It is characterized by generalized physiological activation. Heart rate, blood pressure, and respiration increase to enhance the amount of oxygen available to the tissues. The distribution of blood flow changes to optimize efficiency of the tissues most needed to fight or flee: blood flow to the muscles, brain, and skin increases, while it decreases in the stomach and other organs less important for immediate survival. Increased sweating and muscle tension help regulate the body’s temperature and enhance movement if action is needed. Levels of blood glucose and insulin also increase to provide added energy sources, and immune function is depressed. Brain activity increases, resulting in enhanced sensitivity to incoming information and faster reactions to this information.

Taken together, these physiological changes serve to protect the organism and to prepare it to take action to survive threat. They occur quite rapidly and are controlled by the brain through a series of neurological and hormonal events. When the brain detects a threat (or stressor), it sends its activating message to the rest of the body through two primary channels, the sympathetic nervous system(SNS) and the pituitary-adrenal axis. The sympathetic nervous system is a branch of the nervous system that has multiple, diffuse neural connections to the rest of the body. It relays activating messages to the heart, liver, muscles, and other organs that produce the physiological changes already described. The sympathetic nervous system also stimulates the adrenal gland to secrete two hormones, epinephrine and norepinephrine (also known as adrenaline and noradrenaline), into the bloodstream. Epinephrine and norepinephrine further activate the heart, blood vessels, lungs, sweat glands, and other tissues.

Also, the brain sends an activating message through its hypothalamus to the pituitary gland, at the base of the brain. This message causes the pituitary to release hormones into the bloodstream that circulate to the peripheral tissues and activate them. The primary stress hormone that the pituitary gland releases is adrenocorticotropic hormone (ACTH), which in turn acts on the adrenal gland to cause the release of the hormone cortisol. The actions of cortisol on other organs cause increases in blood glucose and insulin, among many other reactions.

In addition to isolating these primary stress mechanisms, research has demonstrated that the body secretes naturally occurring opiates—endorphins and enkephalins—in response to stress. Receptors for these opiates are found throughout the body and brain. Although their function is not entirely clear, some research suggests that they serve to buffer the effects of stressful events by counteracting the effects of the sympathetic nervous system and stress hormones.

General Adaptation Syndrome

The human body contains a very sophisticated series of mechanisms that have evolved to enhance survival. When stressors and the subsequent physiological changes that are adaptive in the short run are chronic, however, they may produce long-term health risks. This idea was first discussed in detail in the mid-twentieth century by physiologist Hans Selye, who coined the term
general adaptation syndrome

to describe the body’s physiological responses to stressors and the mechanisms by which these responses might result in disease.

Selye’s general adaptation syndrome involves three stages of physiological response: alarm, resistance, and exhaustion. During the alarm stage, the organism detects a stressor and responds with sympathetic nervous system and hormonal activation. The second stage, resistance, is characterized by the body’s efforts to neutralize the effects of the stressor. Such attempts are meant to return the body to a state of homeostasis, or balance. (The concept of homeostasis, or the tendency of the body to seek to achieve an optimal, adaptive level of activity, was developed earlier by Cannon.) Finally, if the resistance stage is prolonged, exhaustion occurs, which can result in illness. Selye referred to such illnesses as diseases of adaptation. In this category of diseases, he included hypertension, cardiovascular disease, kidney disease, peptic ulcer, hyperthyroidism, and asthma.

Selye’s general adaptation syndrome has received considerable attention as a useful framework within which to study the effects of stressors on health, but there are several problems with his theory. First, it assumes that all stressors produce characteristic, widespread physiological changes that differ only in intensity and duration. There is compelling evidence, however, that different types of stressors can produce very different patterns of neural and hormonal responses. For example, some stressors produce increases in heart rate, while others can actually cause heart rate deceleration. Thus, Selye’s assumption of a nonspecific stress response must be questioned.

Also, Selye’s theory does not take into account individual differences in the pattern of response to threat. Research during the later twentieth century demonstrated that individuals vary widely in their physiological responses to identical stressors. Such differences may result from genetic or environmental influences. For example, some studies have demonstrated that normotensive offspring of hypertensive parents are more cardiovascularly responsive to brief stressors than individuals with normotensive parents. Although the genes responsible for hypertension might have been passed on from the hypertensive parents, these children might also have different socialization or learning histories that contribute to their exaggerated cardiovascular reactivity to stressors. Whatever the mechanism, this research highlights the fact that individuals and organ systems vary in the degree to which they respond to stress.

Stress and Illness

Coinciding with the scientific community’s growing acknowledgment that stressful events have direct physiological effects, much interest has developed in understanding the relations between these events and the development or maintenance of specific diseases. Probably the greatest amount of research has focused on the link between stress and heart disease, the primary cause of death in the United States. Much empirical work also has focused on gastrointestinal disorders, diabetes, and pain (for example, headache and arthritis). Researchers are beginning to develop an understanding of the links between stress and immune function. Such work has implications for the study of infectious disease (such as flu and mononucleosis), cancer, and acquired immunodeficiency syndrome (AIDS).

A number of types of research paradigms have been employed to study the effects of stressors on health and illness. Longitudinal studies have identified a number of
environmental stressors that contribute to the development or exacerbation of disease. For example, one study of more than four thousand residents of Alameda County, California, spanning two decades, showed that a number of environmental stressors such as social isolation were significant predictors of mortality from all causes. Other longitudinal investigations have linked stressful contexts such as loud noise, crowding, and low socioeconomic status with the onset or exacerbation of disease.

A major drawback of such longitudinal research is that no clear conclusions can be made about the exact mechanism or mechanisms by which the stressor affected health. Although it is possible, in the Alameda County study, that the relationship between social isolation and disease was mediated by the sympathetic nervous system/hormonal mechanisms already discussed, individuals who are isolated also may be less likely to engage in health care behaviors such as eating healthy diets, exercising, and maintaining preventive health care. Thus, other research paradigms have been used to try to clarify the causal mechanisms by which stressors may influence particular diseases. For example, many scientists use laboratory stress procedures to investigate the influence of brief, standardized stressors on physiology. This type of research has the advantage of being more easily controlled. That is, the researcher can manipulate one or a small number of variables (for example, noise) in the laboratory and measure the physiological effects. These effects are then thought to mimic the physiological effects of such a variable in the natural environment.

This research primarily is conducted to ask basic questions about the relations between stressors, physiology, and subsequent health. The findings also have implications, however, for prevention and intervention. If a particular stressor is identified that increases risk of a particular disease, prevention efforts could be developed to target the populations exposed to this stressor. Prevention strategies might involve either modifying the stressor, teaching people ways to manage more effectively their responses to it, or both.

During the last two or three decades, applied researchers have attempted to develop intervention strategies aimed at controlling the body’s physiological responses to stress. This work has suggested that a number of stress management strategies can actually attenuate physiological responsivity. Most strategies teach the individual some form of relaxation (such as deep muscle relaxation, biofeedback, hypnosis, or meditation), and most of this work has focused on populations already diagnosed with a stress-related disease, such as hypertension, diabetes, or ulcer. The techniques are thought to produce their effects by two possible mechanisms: lowering basal physiological activation (or changing the level at which homeostasis is achieved) and providing a strategy for more effectively responding to acute stressors to attenuate their physiological effects. Research has not proceeded far enough to make any statements about the relative importance of these mechanisms. Indeed, it is not clear whether either mechanism is active in many of the successful intervention studies. Although research does indicate that relaxation strategies often improve symptoms of stress-related illnesses, the causal mechanisms of such techniques remain to be clarified.

The Mind-Body Connection

The notion that the mind and body are connected has been considered since the writings of ancient Greece. Hippocrates described four bodily humors (fluids) that he associated with differing behavioral and psychological characteristics. Thus, the road was paved for scientific thinkers to consider the interrelations between environment, psychological state, and physiological state (that is, health and illness). Such considerations developed most rapidly in the twentieth century, when advancements in scientific methodology permitted a more rigorous examination of the relationships among these variables.

In the early twentieth century, Cannon was the first to document and discuss the fight-or-flight response to threatening events. He also reasoned that the response was adaptive, unless prolonged or repeated. In the 1940s, two physicians published observations consistent with Cannon’s of an ulcer patient who had a gastric fistula, enabling the doctors to observe directly the contents of the stomach. They reported that stomach acids and bleeding increased when the patient was anxious or angry, thus documenting the relations between stress, emotion, and physiology. Shortly after this work was published, Selye began reporting his experiments on the effects of cold and fatigue on the physiology of rats. These physical stressors produced enlarged adrenal glands and small thymus and lymph glands (involved in immune system functioning) as well as increasing ulcer formation.

Psychiatrists took this information, along with the writings of Sigmund Freud, to mean that certain disease states might be associated with particular personality types. Efforts to demonstrate the relationship between specific personality types and physical disease endpoints culminated in the development of a field known as psychosomatic medicine. Research, however, does not support the basic tenet of this field, that a given disease is linked with specific personality traits; thus, psychosomatic medicine has not received much support from the scientific community. The work of clinicians and researchers in psychosomatic medicine paved the way for late twentieth-century conceptualizations of the relations between stress and physiology. Most important, biopsychosocial models that view people’s health status in the context of the interaction between their biological vulnerability, psychological characteristics, and socio-occupational environment have been developed for a number of physical diseases.

Future research into individual differences in stress responses will further clarify the mechanisms by which stress exerts its effects on physiology. Once these mechanisms are identified, intervention strategies for use with patients or for prevention programs for at-risk individuals can be identified and implemented. Clarification of the role of the endogenous opiates in the stress response, for example, represents an important dimension in developing new strategies to enhance individual coping with stressors. Further investigation of the influence of stressors on immune function should also open new doors for prevention and intervention.

Much remains to be learned about why individuals differ in their responses to stress. Research in this area will seek to determine the influence of genes, environment, and behavior on the individual, elucidating the important differences between stress-tolerant and stress-intolerant individuals. Such work will provide a better understanding of the basic mechanisms by which stressors have their effects, and should lead to exciting new prevention and intervention strategies that will enhance health and improve the quality of life.

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