Simply, stated, stress is a stimulus perceived by the body that elicits a response and dependent upon numerous contextual factors, the outcome of the stimulus-response exchange may be beneficial or detrimental.
For example, exercise is considered a “positive” form of stress. As force is applied to the body, it demands an increase in the body’s normal physiological and mechanical output. If this is introduced gradually, with a safe and proper approach, muscular strength, cardiovascular functioning and flexibility is improved.
“Task” challenges undertaken may also yield positive results. The practice required to play a musical instrument or the intellectual agility associated with puzzles and brain teasers develop physical and mental acuity. The instinctual desire for an infant to walk and a child’s love of play promotes a solid sense of self’ both physically and mentally.
However, the common use of stress carries a negative connotation. The difference between a positive and a negative outcome is primarily dependent upon the intensity, duration and/or the frequency of the stressors involved.
How does the body respond?
Under normal conditions, the body functions in a highly complex, integrated conglomeration of rhythms: heartbeats, seasonal changes, monthly cycles, hunger, sleep, work and play. Although these are the most familiar patterns, there is a diurnal (daily) rhythm highly critical for the maintenance of our well being: the production of cortisol and DHEA. This daily production, via the adrenal glands, acts as the body’s primary modulator to stress.
In a relatively healthy individual, these steroids have a predictable, measurable pattern. In response to stress, the balance to these hormones will shift accordingly. The resulting change in their ratio will reflect the severity and chronicity of the individual’s stress response. When the body perceives stress, (whether it is physical, chemical or emotional), it requires glucose to assist in its’ response.
A series of chemical reactions involving a part of the brain known as the hypothalamus, the pituitary gland and the adrenals occur to allocate the necessary quantity of glucose to match the demand. First, the hypothalamus sends the chemical messenger CRF (corticotrophin releasing factor) to the pituitary, located on the underside of the brain. Upon receiving this input, the pituitary then transmits its chemical messenger, ACTH (adrenocorticotrophic hormone) to the adrenal glands, perched on top of the kidneys. Specialized glands in the adrenals receive this input. One type of cell produces cortisol, primarily known for its’ anti-inflammatory properties, i.e. cortisone is a pharmaceutical facsimile, and the other cell manufactures DHEA, the precursor to the sex hormones testosterone and estrogen.
Cortisol released in response to a stress stimulus initiates the needed glucose production via the liver, and if necessary, will convert protein from muscle tissue or triglycerides from adipose stores into glucose. For cortisol to be fully effective, the body’s physiological hierarchy is temporarily shifted to direct its attention towards its’ immediate needs at the expense of other biological activities including hunger, the immune system, sleep and reproductive capacities. As the stressors subside, cortisol returns to its’ previous levels and normal functioning is resumed. This biochemical adaptation evolved to handle short-term stress.
If the stressful condition(s) persist and prevents the body from returning to its’ previous levels, the stress response will accumulate and lay the groundwork for eventual health dysfunctions.
What happens next?
The body will move through three basic stages of stress. The first phase is the alarm stage. This is comparable to the aforementioned description of short-term stress, Initially, cortisol increases, accompanied by the increase in DHEA levels If the stimulus persists, DHEA output gradually declines and shifts the body into the next phase called the resistance stage, characterized by physical alterations in organ tissue structure and invariably, adaptive compromises in function.
Within the resistance phase (stage 2) the variable range of cortisol/DHEA imbalances is sp far reaching it is beyond the scope of this article. However, the effects are easily demonstrated in asthma, bowel dysfunctions, hypoglycemia, fatigue, thyroid impairment, and recurring infections.
Stage 3 is adrenal fatigue. The cortisol producing cells are replaced by fat and hemmorhagic blood vessels are visibly noticeable. Daily cortisol output is below normal, creating serious fatigue, chronic blood sugar instability and impaired mental functioning i.e. memory, learning and Alzheimers disease. Verification of this stage, concurrent with the precipitous drop in cortisol, is denoted by an increase in the HEA levels.
The original groundbreaking groundwork in this field, by Dr. Hans Selye, revealed that regardless of the illness, three changes always occur; adrenal gland hypertrophy, atrophy of the thymus gland and lymphatic structures (immune system related) and gastric ulcerations.
As research progressed and the mechanism by which cortisol produced these changes became clearly understood, missing pieces to numerous illnesses started to fall into place.
The implications of stress, termed the “neuroendocrine response”, are one of the major cornerstones to be considered when evaluating any health condition. According to a laboratory having conducted more than 200,00 salivary cortisol and DHEA tests, approximately 45-55% of the population tested displayed adrenal hyperfunction (stage 2 stress), referred to as hypercortisolemia. Another 15 % suffered from overproduction for such a prolonged period of time, adrenal fatigue set in and cortisol production became debilitated and inadequate (stage 3). In basic terms, approximately 70% of the population contends with a level of stress capable of setting the stage for serious illnesses.