The feelings that we experience when we are stressed are due to the physiological changes in our bodies that occur in response to a stressor. When there is a threat from our environment, our body immediately begins to prepare itself for either fighting the threat - or running away from it - what is called the fight or flight response.  The body does this before we are even consciously aware of the threat.

The response is triggered by the hypothalamus which activates the sympathetic nervous system and the adrenal-cortical system. The sympathetic nervous system "speeds up" the body's systems and increases a sense of alertness.  The adrenal glands release epinephrine (adrenaline) and norepinephrine (noradrenaline) into the bloodstream.

• An increase in heart rate and blood pressure
• Pupils dilate to take in as much light as possible
• Increased circulation to the major muscle groups
• Increased breathing rate
• Digestion, the reproductive system, and the immune system are suppressed to allow more energy for emergency functions

At the same time, the hypothalamus activates the adrenal-cortical system. As a result, over 30 hormones are released into the bloodstream, including cortisol.  Glucose is released into the blood to provide energy quickly and efficiently.

The goal of the Fight or Flight response is to get us ready to deal with a stressor.  It is supposed to be a "short-term response." In Robert Sapolsky's classic book Why Zebras Don't Get Ulcers, he argues that the problem of modern-day stress is that our fight or flight responses are activated too often for situations that do not threaten our lives.  When a zebra's sympathetic nervous system kicks in, it is to flee a lion that is about to attack the herd.  What is the rationale for getting so stressed in a traffic jam?  Or at the check-out counter at the grocery store?  For humans, this theory alone does not explain stress, because our long-term stress is due to the perception of the triggers.  But regardless, the effects on our bodies are the same.

General Adaptation Syndrome

Hans Selye (1956) took our understanding of the effects of stress on our physiological systems a step further with his General Adaptation Syndrome model.

Selye's findings were accidental.  As a young endocrinologist, he was trying to discover a new hormone.  In order to do this, he was injecting rats with ovarian extract. Over time, the rats developed symptoms such as swollen lymph nodes, bleeding ulcers, and enlarged adrenal glands. Some of them died. Although he thought that he was onto something, he found that the control group, which was being injected with a simple saline solution, also had these symptoms.

It appeared that the stress of the repeated injections - and not the substance being injected - was the reason for the physiological response. Stress was the culprit.

According to Selye, there are three stages of the G.A.S.  During the alarm stage the hypothalamus responds to the stressor by activating the fight or flight response.

In the resistance stage, the adrenal cortex continues to release glucocorticoids to help the body react to the stressor until the stress is resolved or the body can no longer resist. Because one of the results of the activation of the sympathetic nervous system is the suppression of the immune system, the body is not able to fight off colds and flu during this time.

What follows is one of two stages. The negative outcome is the exhaustion stage. During this phase, the stress has been persistent for a longer period. The body's ability to cope with the stressor is depleted and the body is not able to maintain normal function. The immune system is depleted. It is in this stage that major health effects may be seen.

The positive outcome is the recovery stage. This happens when the stressor is gone or coping has been successful. Homeostasis of the physiological systems is restored.

Researchers are interested in how stress is related to health problems. They are now aware that long-term stress causes an increase in cortisol, which can lead to depression or memory problems. Cortisol also affects the immune system, thereby making the individual more susceptible to infection, because of a decrease in the number of T-cells.

Cohen (1993) carried out a study to see if stress leads to colds. In his study, he gave 276 healthy participants a series of tests to determine their overall general health and their recent exposure to stress. He then exposed 276 healthy participants to either a cold virus or to a simple saline solution, which served as the placebo. Participants were then quarantined for five days. They checked daily for any sign of illness. The researchers found that the duration and nature of stress that an individual experiences are strong predictors of who gets a cold. Those who had high levels of stress for a month or more were over twice as likely to get ill as those who had no such stress. The type of stress also seems to matter. Participants who were unemployed were three times more likely to develop colds than those who didn’t have work-related problems. And those who reported serious problems in their close relationships were 2.5 times more likely to contract viruses than those without such problems.

This study is an interesting one, but it doesn't look at how stress actually leads to a decrease in our body's ability to fight off disease. To get more information on that, we need to turn to a classic study in psychology carried out by Kiecolt-Glaser et al (1984).

Kiecolt-Glaser et al. (1984) analyzed blood samples from volunteer medical students one month before and after students had completed the first two examinations. The participants were given the Social Readjustment Rating Scale to account for life changes that occurred within the last year that would raise their level of stress. As a result of this test, the participants were divided into two groups: a high-stress and a low-stress group. Levels of loneliness were also measured and the participants were also divided into two groups: high loneliness and low loneliness.

Natural Killer cell (NK) activity was measured in the students' blood samples. NK cells are lymphocytes that provide rapid responses to viral-infected cells. A low level of NK activity indicates a poorly functioning immune system.

There was a significant decrease in NK cell activity between the first blood test and the second blood test - which was given during the stress of examinations. Those participants in the "high-stress" group were more likely to have lower levels of NK than those in the "low-stress" group. This means that stress experienced previous to the exams played a role in their immune systems' ability to cope with the stress of examinations. In addition, those participants in the "high loneliness" group had lower levels of NK than those in the "low loneliness" group. This confirms the role of social support as a protective factor for better health.

The research seems to support the General Adaptation Model that is proposed by Selye. As our body continues to cope with stressors, it eventually becomes "exhausted." In this exhausted stage, this is when we are most likely to become ill. Up until Kiecolt-Glaser carried out this study, much of the research carried out on stress's role on the immune system had been carried out on animals.

Unlike Cohen's study, Kiecolt-Glaser actually used biological markers to determine the effect of stress, rather than simply observing whether someone gets ill or not. But even with this, the cause-and-effect relationship is still rather difficult to fully establish. As it was a natural experiment, the controls over the experiment were not as good as would be in a laboratory experiment. For example, it is not known how the participants cope with stress. Some of the participants may have better coping strategies that would better regulate their stress response. This may have affected the results. However, the study is naturalistic and has high ecological validity. It also seems to reflect the personal experience that many students experience with regard to illness during and immediately following exam experiences.

The link between cognitive factors - that is, coping with the problem - and the recovery stage is not clear. Selye's model may be an oversimplification - in reality, the process is more complex.

The effects of stress on memory

As if the effects on heart disease and your immune system are not enough, stress also has a negative effect on memory - specifically, on the hippocampus. Sustained increased levels of cortisol lead to hippocampal cell death, which in turn leads to memory impairment.  Research on veterans with PTSD and victims of child abuse shows hippocampal atrophy - that is, they have smaller hippocampi than average.

Newcomer et al (1999) carried out an experiment to test whether high levels of the stress hormone cortisol interfere with verbal declarative memory.

All participants were employees or students at the Washington University Medical Center. All participants were asked to listen to and recall parts of a prose paragraph. This tested their verbal declarative memory. It is known that verbal declarative memory is often affected during long-term stress and the researchers knew from previous studies that cortisol could be involved in memory impairment.

In order to investigate a possible link between cortisol and memory the researchers designed an experiment with three experimental conditions:

• Condition 1 – high level of cortisol: The participants in the high-level cortisol group were given a tablet containing 160 mg of cortisol on each day of the four-day experiment. This dose of cortisol is similar to what is seen in people experiencing a major stress event.

• Condition 2 – low level of cortisol: The participants in the low-level of cortisol group were given a tablet containing 40 mg of cortisol per day. This dose is similar to the amount of cortisol circulating in the bloodstream of people undergoing a minor stress event.

• Condition 3 – placebo group: The participants in this condition were given placebo tablets - that is, a tablet that looked like the other tablets but with no active ingredient. This was done in order to have a control group.

The experiment was done under a double-blind control.

The results indicated that high cortisol levels impaired performance in the memory task since the participants who received the highest level of cortisol also showed the worst performance in verbal declarative memory. The effect was not permanent, however. The performance of participants in the high cortisol condition returned to normal after they stopped taking the hormone tablet.

It appears that cortisol interferes with the transfer of short-term memory to long-term memory that takes place in the hippocampus. This makes sense as there are several cortisol receptor sites in the hippocampus.

Since this study was experimental, the researchers could establish a clear cause-and-effect relationship between the IV and the DV. The experiment ran over several days and the participants were not in the lab the whole time, so the researchers did not have full control over extraneous variables.  In spite of this, there was a clear relationship between the amount of cortisol ingested and the performance on the memory test.

Checking for understanding