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STRESS SPECIFICITY; WHY DOES STRESS NOT CAUSE ILLNESS IN EVERYONE?


Human beings are a uniquely varied specie. No two persons are remotely the same not even homozygote twins. Genetic makeup and the environment in which each man finds himself, predominantly goes a long way to shape one’s physique, personality, and interactions with other and the environment. Thus it comes as no surprise that we all respond to stressful life events in varied ways.


Cohen et al. (1995) define stress as a process in which environmental demands strain an organism’s adaptive capacity resulting in both psychological demands as well as biological changes that could place it at risk for illness. Being not a respecter of persons, stress affects all people — man or woman, young or old, rich or poor. Stress is an ever-present fact of life that we must all deal with. Life in and of itself is full of stress. It comes in all shapes, sizes and conundrums; to the extent that even one’s own thoughts can cause predominant discomfort and strain, making the body more susceptible to illness.

The relationship between stress and illness is an intricately complex one. Susceptibility to stress varies from person to person. An event that causes a stress-induced illness in a person may not necessarily cause illness in another person. Stressors must interact with a wide variety of background factors to manifest as an illness. Key among the factors that influence the susceptibility to stress are genetic vulnerability, coping skills, personality type and social support. When confronted with a challenge, we tend to assess the seriousness of the problem and determine whether or not we have the resources necessary to cope with  the said problem. If we believe that the problem is serious and do not have the resources necessary to cope with the problem, we will perceive ourselves as being under stress (Lazarus, 1966).

The physiological stress responses, which are designed to produce stress adaptation and maintain homeostasis, are mediated through the ‘fight-or-flight’ mode via the sympathetic arm of the autonomic nervous system (ANS), output of stress hormones, primarily cortisol via the hypothalamic-pituitary-adrenal (HPA) axis and interaction with mediators of immune and metabolic systems (Ewen et al., 2015).




While normally protective, these response mechanisms can woefully fail when dysregulated thereby
 failing to cease after exposure to the offending stressor is terminated. According to Ewen et al. (2015), the dysregulation of the stress-response mechanism can be attributed at least in part to alterations in genes (mutations) that code for distinct neural pathways involved in the regulation and limitation of the neuroendocrine stress axis. Research from animal studies have shown that stress-susceptible rodents display  reduced stress-inhibitory function in corticolimbic areas ( the part of the brain that processes a broad range of behavioral and cognitive functions including emotional regulation) such as the hippocampus (Yang et al., 2015). Collectively, these alterations contribute to a maladaptive stress response including a constantly turned-on HPA axis activity through an impairment of negative feedback and increased pituitary excitability which are key altered parameters of patients with stress-related disorders.
Therefore in layman terms, the individual differences in how we deal with daily life stressors, stem primarily from how we are wired up genetically. Congenital and acquired mutations that undermine the synchrony of our genetic imprints are reflected in the malfunctioning of our body’s internal response to stressors, thereby leading to increased susceptibility to stress-induced illnesses.


However it is not all gloom and doom though. Simple remedies such as adopting techniques  that promote relaxation (breathing exercises, meditating on a soothing word, visualization of tranquil scenes, prayer and spiritual devotion, yoga, and tai chi), increasing physical activity and deepening  ones social support base go a long way to boost an individual’s stress-response readiness.
These modalities ameliorate stress via enhancing the body’s realizsation of what is referred to as the ‘relaxation response’. In contrast to the stress response, the relaxation response, occurs when the body is no longer in perceived danger mode, and thus the autonomic nervous system (ANS) functioning ‘returns to normal’. In that the parasympathetic arm of the ANS predominates in controlling autonomic body functioning. Thus simply put, the relaxation response is the opposite of the body's stress response — the body’s “off-switch” to its tendency toward fight-or-flight. Do not be too quick to dismiss these techniques as ‘new age medicine hogwash’ because there is relevant evidence to support the fact that these relaxation therapies actually do have positive genetic impacts.

A recent study (Bhasin et al., 2013) found that achieving a relaxation state through activities like meditation, yoga, prayer, and breathing exercises actually alter your genes! The results of the study indicated that elicitation of the response rate, particularly after long-term practice, may evoke its downstream health benefits by improving mitochondrial energy production and utilization and thus enhancing mitochondrial resiliency through upregulation of ATPase and insulin function. Mitochondrial resiliency might also be strengthened by relaxation response-induced downregulation of NF-kB-associated upstream and downstream transcription factors that mitigate stress. So you will agree with me that, it is a better idea to pull  out your yoga mat instead when you feel like worrying to death about tomorrow. Trust me it will save you from your next cold!


  
Author: Kwame Panyin Essuman



REFERENCES
1.      Cohen S, Kessler RC, Gordon LU. Strategies for measuring stress in studies of psychiatric and physical disorders. In: Cohen S, Kessler RC, Gordon LU, editors. Measuring stress: A guide for Health and Social Scientists. Oxford: Oxford University Press; 1995. [Google Scholar]
2.      Lazarus RS. Psychological stress and the coping process. New York: McGraw-Hill; 1966. [Google Scholar]
3.      B.S. McEwen, N.P. Bowles, J.D. Gray, M.N. Hill, R.G. Hunter, I.N. Karatsoreos, C. Nasca Mechanisms of stress in the brain Nat Neurosci, 18 (2015), pp. 1353-1363
4.      C. Yang, Y. Shirayama, J.C. Zhang, Q. Ren, K. Hashimoto Regional differences in brain-derived neurotrophic factor levels and dendritic spine density confer resilience to inescapable stress. Int J Neuropsychopharmacol, 18 (2015), p. pyu121 [Google Scholar]
5.     Bhasin MK, Dusek JA, Chang B-H, Joseph MG, Denninger JW, et al. (2013) Relaxation Response Induces Temporal Transcriptome Changes in Energy Metabolism, Insulin Secretion and Inflammatory Pathways. PLoS ONE 8(5): e62817. doi:10.1371/journal.pone.0062817

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