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.
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!
REFERENCES
1.
Cohen S, Kessler RC, Gordon LU.
Strategies for measuring stress in studies of psychiatric and physical
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guide for Health and Social Scientists. Oxford: Oxford University Press; 1995.
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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
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C. Yang, Y. Shirayama, J.C. Zhang, Q.
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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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