Introduction
The journey to understanding psychological response to stress started with Hans Seyle letter. Seyle published a 595-word letter back in 1936, titled A Syndrome Produced by Diverse Nocuous Agents (Fink, 2017). It gave a detailed description of the syndrome, which later became known as General Adaptation Syndrome – it became the most discussed issue in the early Annual Review of Medicine Paper (Fink, 2017).
The main argument, as elucidated by Fink (2017), was that anything that causes stress puts an individual’s life at risk unless it is addressed urgently by an adequate adaptive response. It, therefore, follows that adaptability and response to stress are two fundamental components of life and require the participation of all vital organs and functions (Ellis and Del Giudice, 2019). Seyle’s letter made it necessary for scientists to focus more on understanding not only a person’s psychobiological response to acute and chronic stress but also the way it affects brain function and health.
Psychobiological Response
For the purpose of clarity, psychobiology describes the existing relationship between psychological and behavioral processes. It is important to note that psychobiology does not depend only on brain functions but also the interaction between different body activities, including behavior and cognition (O’Connor et al., 2021). Zapater-Fajarí et al. (2021) noted in their study that people face and handle stressful situations differently, which essentially determine their psychobiological response and, “therefore, their risk of stress-related diseases” (p. 133).
As explicated further by the authors, the differences in stress response depend largely on an individual’s awareness of the situation and the availability of resources to manage it (Zapater-Fajarí et al., 2021). According to the theory of positive emotions, having an understanding of the situation by experiencing multiple positive emotions even in different situations broadens one’s thought action repertoire (Stifter et al., 2020). This helps improve personal resources including social and physical ones. However, this might not work the same way when a person is subjected to continued acute and chronic stress.
From the onset, two systems are activated when a person experiences acute and chronic stress. Sympathetic adrenal medullary (SAM) systems easily get activated as a result of acute stress (Turner et al., 2020). The second system is referred to as hypothalamic-pituitary-adrenal (HPA) axis (Turner et al., 2020). When an individual suddenly experiences an acute stress, such as being frightened, the brain, hypothalamus, activates the autonomic nervous system ANS. It, in turn, sends a message to the adrenal glands which stimulates the release of noradrenaline – it further activates the internal organs (Christensen et al., 2020). This is basically how ANS sympathetic response to acute stress works.
However, as a person continues experiencing this type of stress, the adrenal medulla may end up releasing adrenaline, which gets transported through the bloodstream – this aims at preparing the body for additional response (Christensen et al., 2020). The system involved in this kind of response is referred to as SAM. It initiates a fight or flight response once the adrenaline and noradrenaline have been activated. Consequently, “breathing quickens, the heart beats faster and powerfully, the eyes dilate, and the activity of the digestive system decreases to permit more blood to the muscle” (Christensen et al., 2020, p. 231).
This effect is even more intense when one experiences chronic stress. Similarly, SAM may end up triggering corticotropin releasing factor (CRF), a peptide hormone, when an individual encounters an unpleasant event within their environment.
CRF, once released, is transported in the blood supply to the pituitary gland where it activates the release of adrenocorticotropic hormone (ACTH). ACTH, as explained further by Turner et al. (2020), travels to the adrenal cortex where it stimulates the release of stress hormone, glucocorticoid cortisol. Cortisol is largely responsible for a number of functions: it increases access to energy, protein and fat utilization as well as decreasing inflammation. In essence, Cortisol’s role is to “trigger excess energy stored in the muscle and liver as glycogen to be liberated and broken down into glucose ready for utilization by the muscles’ ‘ (Degroote et al., 2020, p. 90).
However, chronic stress causes a long-term activation of the stress response system and the overexposure to cortisol, in the end, disrupts almost all the body’s processes (Lehrer et al., 2020). This puts an individual at a high risk of health problems such as anxiety, depression, weight gain, heart disease and memory impairment.
Impact of Chronic Stress Responses on a Person’s Health
Repeated and long term exposure to stress causes the body to experience allostatic load – wear and tear of the body due to chronic stress responses. Yaribeygi et al. (2017) described allostatic load in terms of the “inefficient switching on and turning off of what he called “stress mediators” (p. 22). However, these mediators may fail to provide the necessary response. Keynejad et al. (2019), in their study, observed that long-term exposure to chronic stress affects the body at multiple levels: cardiovascular, metabolic, neural, behavioral and cellular.
It also increases the risk of developing health-related conditions such as high blood pressure because the systems may stop functioning effectively. Kivimäki and Steptoe, 2018) in discussing the issue of allostatic overload, focused more on the harmful effects of chronic stress on biological systems, especially when several mediators are released to help with adaptability. At a basic level, allostatic load emphasizes the idea that stress affects multiple biological systems and that they (systems) must interact in order to adapt and respond to any changes.
Cortisol Responses to Stress and Future Health Risk
Several studies have been carried out to determine whether individuals who exhibit prolonged cortisol responses to chronic stress are at a high risk of future ill health. Some of these researchers, including Bunea et al. (2017) and Zorn et al., 2017, based their studies on the reactivity hypothesis. It argues that people who experience an increase in blood pressure or heat rate in response to acute and chronic stress are at a high risk of future health diseases. These studies, further informed by cortisol reactivity, found evidence linking high cortisol reactivity to stress with negative health outcomes.
On one hand, Bunea et al. ‘s (2017) evidence of heightened HPA activity to chronic stressor was directly linked to hypertension. On the other hand, Zorn et al.’s (2017) investigation found enhanced reactivity to a stressor to be directly associated with coronary artery calcification. This is often described as a marker of subclinical coronary atherosclerosis.
In line with the above, many scholars in the recent past have carried out different studies to establish a link between chronic stress and health. In Lateef et al. ‘s (2020) cohort study, the findings showed a 59 percent increase in probability of incident hypertension per standard deviation in response to chronic stressors. Additional analysis further indicated that enhanced cortisol reactivity to stress was directly related to progression of coronary artery calcification after three years (Lateef et al., 2020). It is clear from this that cortisol responsibility is one of the main mediators of the relationship between psychological chronic stress and cellular aging.
Overall, the evidence above seems to suggest that enhanced and blunted cortisol response to chronic stress is directly linked to high risk for health-related diseases. Carroll et al. (2017) proposed a model of blunted stress reactivity that strives to “integrate the evidence linking exaggerated and blunted stress responses into a single unifying framework” (p. 74). The authors argued that the risks associated with heightened reactivity to chronic stress are well-established, especially with regard to cardiovascular pathology (Carroll et al. (2017). However, additional research is needed to develop a clear understanding of the effects of low or blunted reactivity.
Impact of Chronic Stress Responses on Brain
Brain is the central organ of stress and adaptation– it is capable of perceiving and determining the kind of threat. Similarly, the brain also determines the behavioral and physiological responses to the stressor, which helps with adaptation. However, Bourdon et al. (2020) noted that chronic stress may lead to pathophysiology, also referred to as allostatic load. The authors observed that the brain has the ability to show both structural and functional elasticity in responding to stress-related activities such as neural replacement and synapse turnover (Bourdon et al., 2020). Chronic stress is regarded as one of the triggers of an imbalance of neural circuitry subserving cognition (Lupien et al., 2018). It also contributes to anxiety and mood which, in turn, increase or decrease expression of those behaviors and behavioral states’ ‘ (Lupien et al., 2018, p. 91).
This imbalance, as explicated by Bourdon et al. (2020), affects systemic physiology through several mediators such as metabolic and neuroendocrine. While these changes tend to be adaptive for acute stress, they become a threat if the behavioral state persists, combined with changes in neural circuitry. In such a situation, healthcare providers recommend one to seek treatment in the form of pharmacological and behavioral therapies.
Moreover, repeated stress is regarded as one of the main triggers of persistent inflammation in the body. From the onset, chronic inflammation is associated with several health conditions such as heart disease and diabetes. Although the brain is protected against circulating molecules by a blood-brain barrier, chronic stress causes the barrier to become leaky (Goodman et al., 2017). Circulating inflammatory proteins can easily end up in the brain. Chen et al. (2019), in their study, identified hippocampus as an essential brain region responsible for learning and memory. However, this region, as argued by the authors, is particularly vulnerable to stress – chronic stress can cause long term damage. “Hippocampus tends to shrink in size in people suffering from an ongoing HPA axis stress response” (Chen et al., 2019, p. 7). As a matter of fact, prolonged cortisol levels resulting from chronic stress affects the hippocampus by causing a significant loss of long-term memory.
Studies further show that inflammation can have a major impact on brain systems associated with motivation behavior and mental agility. It is imperative to note that the mesolimbic dopamine system plays an important role in controlling motivated behavior. Klein et al. (2019) carried out a study in which they examined multiple forms of motivated behavior through protracted stress manipulations. Their findings showed that midbrain dopamine neurons play contradictory roles when subjected to different types of stressors (Klein et al., 2019). It is clear that chronic stress has the ability to alter behavior through modulation of mesolimbic dopamine system activity.
Chronic stress also changes the chemicals in the brain linked to cognition and mood. For example, stress affects serotonin which is critical mood regulation and well-being. Under chronic stress, “the capacity for increase in serotonin transporter has reached its limit due to the chronically elevated blood cortisol level” (Goodman et al., 2017, p. 26). In other words, cortisol damages the receptor sites which explain why it easily depletes serotonin levels. Lack of enough serotonin is directly linked to depression, mania, and other health conditions.
Conclusion
As evidenced above, anything that causes stress puts an individual at a high risk unless it is addressed with an adequate adaptive response. Scientists have been interested in understanding psychobiological responses to stress with an emphasis on adaptability function. It is clear that people experience stress differently which essentially determines their psychobiological response and, therefore, their risk of stress-related diseases.
Two systems play an important role in the psychobiological response; Sympathetic adrenal medullary (SAM) and autonomic nervous system ANS. However, chronic stress causes a long-term activation of the stress response system and the overexposure to cortisol, in the end disrupts almost all the body’s processes. Furthermore, chronic stress, as evidenced above, has a major impact on a person’s health and brain functionality. For instance, long term exposure to stress causes the body to experience allostatic load – wear and tear of the body. It also increases the risk of developing health-related conditions such as high blood pressure because the systems may stop functioning effectively.
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