3.6.2 Stress response
Stress: Physiological and Psychological aspects
Hans Selye in 1936 first used the term ‘stress’ when he described “the non-specific response of the body to any demand placed upon it” (Selye, 1936). Selye described positive and negative stress as ‘eustress and ‘distress’ respectively. This balanced an individual’s psychological equilibrium. Another term commonly used in the 21st century is ‘resilience’ which refers to the ‘psychological process developed in response to intent life stressor that facilitates healthy functioning’ or generically bouncing back from a stressor. (Johnson, 2009).
The mammalian stress response is a physiological and psychological response to real or perceived hardship.
At several levels, the concept of stress pervades our culture. In everyday language, it denotes a difficult, sometimes overpowering mood accompanied by bad emotions. Many scientists equate the term stress with Selye’s description of a “fight-or-flight” response to a threat, that is, an acute, adaptive response to environmental stimuli. This is via a route that involves:
- the amygdala,
- the hypothalamus,
- and the medulla of the adrenal gland.
However, science in general, and neuroscience in particular, have advanced these notions along many dimensions during the previous 50 years. We think of biological reactions to stress not as causing a bad condition, but as a typically positive, adaptive collection of mechanisms that improve survival.
A slower looped response is the hypothalamic-pituitary-adrenal (HPA) axis which engages when there is persistent or chronic stress. Resulting in the release of cortisol, a hormone that induces metabolic changes aiming to sustain the fight-or-flight response.
This perspective on stress biology has given rise to the concepts of allostasis and allostatic load/overload. Allostasis is the active process of adjusting and maintaining stability (or homeostasis) by the creation of mediators that encourage adaptation, such as cortisol. However, if the environmental disturbances remain constant, the equilibrium set point must be changed to a “new normal,” which can be costly to the organism. “The price the body pays for being compelled to adjust to undesirable psychosocial or physical settings is referred to as allostatic stress” (McEwen, 2000). These ideas emphasise the protective effects of many, nonlinear adaptation mediators, as well as the harm that happens when the same mediators are overused or dysregulated.
The below disorders can all be attributed to psychosomatic disorders:
| Physical effects resulting from psychological stress: | Examples: |
| Gastrointestinal | IBS, peptic ulcer, heartburn |
| Cardiovascular | Hypertension, coronary artery disease |
| Respiratory | Asthma |
| Dermatology | Atopic dermatitis, psoriasis |
Stress Response Effect of Glucocorticoids
Glucocorticoids play a key role in this response, functioning to allocate energy resources in order to optimise survival in the face of a challenge and to restore homeostasis after the immediate threat has passed.
The hypothalamus sends signals to the adrenal glands, which release glucocorticoids, hormones that have a number of consequences when under stress. In response to stress, the paraventricular nucleus (PVN) of the hypothalamus releases corticotrophin-releasing factor (CRF), the primary regulator of the HPA axis, which triggers the release of adrenocorticotropic hormone (ACTH) into the bloodstream. The adrenal cortex then secretes glucocorticoids (cortisol in humans and corticosterone in rodents) as a result of the action of ACTH. The release of glucocorticoids causes the binding of glucocorticoids to the glucocorticoid receptors (GR) located in stress-responsive brain areas via transcriptional regulation, causing feedback inhibition (Herman et al., 2012).
Acute Stress Reaction
Clinical features: An acute stress reaction is a transient disorder of significant severity which develops with any prior psychiatric disorder. It is in response to exceptional physical and/or mental stress. Usually, it subsides within hours/days. A clear relationship between the emotional stressor and the onset of symptoms must be described.
Personality structure and the utilization of suitable coping mechanisms are apparent key factors.
Treatment: An acute stress reaction is self-limiting and only supportive treatment is required.
References:
(1) Selye, H. (1936). A Syndrome produced by Diverse Nocuous Agents. Nature, 138(3479), pp.32–32. doi:10.1038/138032a0
(2) Johnson, D.C. (2009). Key Facts On Reslilience And Response To Stress For Navy And USMC Leaders. Journal of Special Operations Medicine, 09(4), p.110. doi:10.55460/wnun-ehdm.
(3) McEwen BS (2000). Allostasis and allostatic load: implications for neuropsychopharmacology. Neuropsychopharmacology 22:108–124. doi:10.1016/S0893-133X(99)00129-3 pmid:10649824
(4) McEwen, B.S. and Akil, H. (2020). Revisiting the Stress Concept: Implications for Affective Disorders. The Journal of Neuroscience, 40(1), pp.12–21. doi:10.1523/jneurosci.0733-19.2019.
(5) Herman, J., McKlveen, J., Solomon, M., Carvalho-Netto, E., & Myers, B. (2012). Neural regulation of the stress response: glucocorticoid feedback mechanisms. Brazilian journal of medical and biological research, 45, 292-298.
(6) Harvard Health Publishing (2020). Understanding the Stress Response. [online] Harvard Health. Available at: https://www.health.harvard.edu/staying-healthy/understanding-the-stress-response.