Physical Health Effects of Stress and Why They Occur

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The brain is the key organ of the stress response, determining what is upsetting and the behavioral and physiological reactions to prospective and actual stresses. The brain is also a stress recipient, undergoing structural and biochemical changes reacting to acute and chronic stresses. Glucocorticoids mediate these changes, but there are other intermediates.

What are the physical health effects of stress, and why do they occur?

Although glucocorticoids and catecholamine are the two significant hormones of the “fight or flight” stress reaction, several other mediators, including pro-and anti-inflammatory cytokines and the parasympathetic nervous system, are also engaged in the modification of stressors, as well as the adverse effect of chronic stress, which is referred to in ordinary speech as being “stressed out.” Indeed, there are significant disparities in the effects of acute and chronic stress and discrepancies in the outcomes of acute and chronic glucocorticoid treatments.


“Stress” is an imprecise phrase with implications that make it less than beneficial in comprehending how the body may adapt or fail to adjust appropriately to daily life experiences, such as little inconveniences and significant life events like abuses or trauma. Awareness of biological and behavioral processes can contribute to a greater understanding of how to intervene. This narrative has two sides (McEwen, 1998): On the one hand, the body reacts to practically any rapid, unexpected incident by producing chemical mediators – such as catecholamine, which elevate blood pressure and heart rate pressure – to help the person cope.

Elevated heartbeat and blood pressure

Chronically elevated heartbeat and blood pressure, for example, cause chronic wear and tear on the cardiovascular system, which can lead to illnesses such as stroke and heart attacks with time. As a result, Sterling and Eyer (1988) coined the word “allostasis” to allude to the interactive way by which the body adapts to everyday events and keeps homeostasis (allostasis means precisely “establishing stability via change” and is not meant to displace “homeostasis”). Because persistently elevated or disrupted allostasis can cause illness, “allostatic load or overload” is coined to describe the wear and tear caused by either excessively intense stress or inadequate allostasis regulation.

Activate an appropriate response

Other types of allostatic overload include failing to activate an appropriate response in the very first place or failing to habituate to the repetition of the same stressor, which dampens the allostatic reaction. The advantage of using the wording “allostatic load/overload” over aspects such as “the strain of chronic stress” is that there are behavioral changes (poor sleep, excessive eating, smoking, drinking, and lack of exercise) that are components of the allostatic load/overload notion that are not as noticeable when the word “stress” is used. (McEwen, 2008).

Chronic stress

Chronic stress, on the other hand, has far-reaching consequences because sometimes life-saving reactions to stress influence other systems. For example, when the body is subjected to prolonged stress, its immune system function is compromised, and the gastrointestinal, excretory, and reproductive systems no longer work properly. These symptoms usually go away as our bodies realize the threat has passed, but if the cause of stress is chronic, various physical and mental health concerns might arise.

Check the following reference articles to learn more about the Physical Health effects of stress and why they occur.

McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338(3), 171-179.

Sterling, P. (1988). Allostasis: a new paradigm to explain arousal pathology. Handbook of life stress, cognition, and health.

McEwen, B. S. (2008). Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators. European journal of pharmacology, 583 (2-3), 174-185.

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