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Theories of Stress

Thursday, Jan 10 2008


There are several theoretical positions devised for examining and understanding stress and stress-related disorders. Brantley and Thomason (1995) categorized them into three groups: response theories, stimulus theories, and interaction (or transaction) theories. Given the distinction made earlier between stress as a stimulus and as a response, this system serves as a useful way to present the various theories and associated research.

Response Theories and Research

Because chronic stress responses involve actual physiological changes to body systems and organs, a good bit of attention has been paid to acute physiological stress responses and how they might possibly lead to subsequent chronic stress responses (McEwen and Stellar, 1993).

Historically, both Walter Cannon (1929) and Hans Selye (1956) provided the foundation for the current interest in this physiological process.

The Work of Walter Cannon
Cannon was a physiologist at Harvard University who was the first to use the term ‘homeostasis.’ According to Cannon (1929), the body possesses an internal mechanism to maintain stable bodily functioning or equilibrium. As the environment presents the organism with various challenges, the body must respond to each new situation by adjusting various physiological systems to compensate for the resources being taxed. A classic example of this type of compensation involves fluid regulation.

When an organism ingests a large amount of water, the kidney releases more waste fluid into the bladder for eventual disposal in an effort to maintain bodily equilibrium. Many of the feedback mechanisms that regulate blood pressure presented in Chapter 1 share similar characteristics with bodily systems that maintain homeostasis. According to Cannon (1935), failure of the body to respond to environmental challenges by maintaining bodily homeostasis results in damage to target organs and eventually death.

Translating his work with physical challenges associated with eating, drinking, and physical activity into those of a psychological nature, Cannon hypothesized that common homeostatic mechanisms were involved. Accordingly, if an organism’s response to threat involves significant sympathetic nervous system arousal so that respiration and heart rate increase significantly, the body’s compensatory response should involve either reducing sympathetic nervous system activity or increasing parasympathetic nervous system counter-activity.

If the compensatory response is inadequate, tissue damage can result, placing the organism at a greater risk for subsequent medical problems associated with the damaged tissue.

In brief, the concept of homeostasis introduced by Cannon has proved to be very valuable in explaining how acute physiological stress responses to threats of survival lead toward chronic stress responses.

The Work of Hans Selye
Selye (1956) was the first investigator to use the term ‘stress’ to describe the problems associated with homeostasis identified by Cannon decades earlier. Although he borrowed the term from physics, he used it to describe the effects on the organism rather than the environmental stressors he examined in his empirical work.

According to Selye, the ‘stress’ response of the organism represented a common set of generalized physiological responses that were experienced by all organisms exposed to a variety of environmental challenges like temperature change or exposure to noise. From his perspective, the stress response was nonspecific; that is, the type of stressor experienced did not affect the pattern of response. In other words, a wide variety of stressors elicited an identical or general stress response. He termed this nonspecific response the General Adaptation Syndrome, which consisted of three stages: Alarm Reaction, Resistance, and Exhaustion.

Selye reasoned that the first stage, Alarm Reaction, involved the classic ‘fight-flight’ response described above. As a result, the body’s physiological system dropped below optimal functioning. As the body attempted to compensate for the physiological reactions observed in the Alarm Reaction stage, the organism entered the Resistance stage. Physiological compensatory systems began working at peak capacity to resist the challenges the entire system was confronting, and according to Selye, actually raised the body’s resistance to stress above homeostatic levels.

However, because this response consumed so much energy, a body could not sustain it forever. Once energy had been depleted, the organism entered the stage of Exhaustion. In this stage, resistance to environmental stressors broke down and the body became susceptible to tissue damage and perhaps even death. In Selye’s terminology, the Alarm Reaction Stage was comparable to the acute stress response described above and the Exhaustion Stage was comparable to a chronic stress response.

The Work of Bruce McEwen
More recently, the historic works of Cannon and Selye that have attempted to explain how acute physiological stress responses evolved into chronic stress responses have been revisited by Bruce McEwen and colleagues (McEwen and Stellar, 1993; McEwen, 1998) at Rockefeller University. In contrast to the state of physiological equilibrium of homeostasis essential for survival that Cannon discussed, McEwen used the term ‘allostasis,’ referring to the body’s ability to adapt to a changing environment in situations that did not challenge survival.

From his perspective, an organism that maintained a perfectly stable physiological equilibrium during a stressful encounter (a nonresponse) might be just as problematic as an organism that exhibited an exaggerated physiological response. Allostasis referred to the body’s ability to adjust to a ‘new steady state’ in response to the environmental challenge (McEwen and Stellar, 1993).

To clarify the distinction between homeostasis and allostasis, consider two physiological parameters: body temperature and heart rate. For an organism to survive in a changing environment, there exists a very narrow window of acceptable body temperatures. Even though the temperature of the environment can change 50 degrees over the course of a single day, body temperature remains constant.

Deviations from a normal temperature are met with a range of symptoms (sweating, chills) that occur as part of our body’s attempt to regain homeostasis. For body temperature, homeostasis is a very important mechanism of survival. Now, let’s consider heart rate. In contrast to body temperature, our body can tolerate a wide range of heart rates. When we are asleep, our heart rate drops to basal levels. When we are awake, heart rates increase substantially, and when we are engaged in aerobic exercise, heart rates climb even higher.

Rather than maintaining stability in the face of a changing environment, as body temperature does, heart rate adjusts to a changing environment to optimize functioning. In this case, the ability of the body to adjust to aerobic exercise by resetting heart rate at a higher level is called allostasis, not homeostasis. McEwen argues that most acute stress responses represent challenges to the body’s allostasis, not challenges to its homeostasis.

According to the work of McEwen and colleagues, ‘allostatic load’ is a term that refers to the price the body pays for being challenged repeatedly by a variety of environmental stressors. Increased allostatic load, or what McEwen and Wingfield (2003) called ‘allostatic overload,’ occurs with increased frequency of exposure to stressors, increased intensities of these stressors, or decreased efficiency in coordinating the onset and termination of the physiological response.

McEwen (1998) outlined four distinct types of allostatic overload (see Figure 3.1). In the first type, the organism is exposed to multiple environmental stressors during a short period of time. image Figure 3.1. The various types of allostatic overload. Reprinted from B. S. McEwen (1998), Protective and damaging effects of stress mediators, The New England Journal of Medicine, 338, 171??“179.

For example, imagine chasing a pesky salesperson off your front porch, running to get the phone only to realize it is a telemarketer, then finding your three-year-old coloring on the kitchen wall with permanent markers, and the family dog urinating on the floor. In a case like this, the physiological response associated with the first stressor was just starting to lessen when the second stressor hit, and likewise, recovery from the second stressor was interrupted by the onset of the third stressor. In this type of allostatic overload, the problem is associated with the frequency of the stressors encountered.

In the second form of allostatic overload, repeated stressors elicit responses that fail to habituate. Consider an example in which you are dealing with five consecutive irate customers who are demanding their money back for a defective product that you sold them. Normally, one’s physiological response to this series of encounters would decrease, or habituate, with each subsequent encounter. When the body fails to exhibit the normal habituation response, this type of allostatic overload occurs.

A third form of allostatic overload involves delayed physiological recovery from a given environmental stressor. In this case, the frequency or magnitude of the physiological response may be entirely normal; however, it is the length of time that the response is sustained that leads to allostatic overload.

For example, imagine having an argument with a family member and experiencing some physiological arousal associated with the argument. Rather than the arousal gradually declining after the argument, in this type of allostatic overload the physiological recovery is delayed and the arousal is still apparent hours or days later.

The final form of allostatic overload involves an inadequate physiological response. In this case, the organism encounters a stressful circumstance or environmental change, but the physiological response is either very weak or entirely absent. Imagine walking through the woods and encountering a black bear, only to find that your body’s fight-flight response failed to occur and therefore did not provide the necessary energy and altered blood flow to run away from the threat.

According to McEwen and Stellar (1993), allostatic overload, whatever its source, is the mechanism through which acute physiological responses result in permanent tissue damage. Research using animals documents not only changes in peripheral tissues associated with increased allostatic load, but also altered functioning in the cerebral cortex (McEwen, 1998).

This altered brain functioning has included atrophy of dendrites on neurons, suppression of neurogenesis (creation and proliferation of new neurons), and permanent loss of pyramidal neurons. Obviously, McEwen and other contemporary stress researchers have extended the theories and empirical work of Cannon and Selye to further our understanding of how stress results in actual tissue damage in the brain and peripheral body systems.

Selye’s (1956) General Adaptation Syndrome described above is a classic representation of a theoretical perspective that focuses upon stress as a response. In fact, Selye went so far as to state that the nature of the stimulus was irrelevant to the stress response. To support his view, he subjected animals to a wide variety of experimental conditions that elicited very similar physiologic stress responses including temperature change, pain stimulation, and exposure to infection.

Likewise, although acknowledging the importance of the stress stimulus in their theoretical models, McEwen and colleagues have also focused on the physiological stress response, paying less attention to the type or nature of the eliciting stimulus (McEwen and Stellar, 1993; McEwen, 1998).

Although response theories have contributed greatly to our understanding of the physiological response systems that mediate the relation between environmental stressors and chronic stress responses, they have typically neglected a detailed exploration of types of environmental stressors and how they might influence the disease process.

Provided by Armina Hypertension Association

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