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The human body has biological mechanisms which are adaptive in times of acute stress. However, these mechanisms become maladaptive in situations of chronic stress. This article will discuss adaptive and maladaptive stress with relation to existing theories of psychological stress. From a biological perspective, Seyle (1975) argues that stress is both adaptive and maladaptive. He recognises different types of stress: sustress (also called neustress), eustress and distress. Sustress may be defined as a state of no or inadequate levels of stress. Sustress may exert a negative impact on health as there are no opportunities to build resilience or be motivated. In long term situations of sustress, homeostatic buffering capabilities may be challenged, resulting in reduced ability to adapt and cope with stress (Lu, Wei & Li, 2021). Eustress is associated with achievement and involves adapting to present conditions resiliently. Eustress has the long-term effect of enhancing homeostasis and therefore promoting health and resilience to stress (Selye, 1975). Examples of eustress include physical exercise that is moderate and strenuous, but not excessive (Sanchis-Gomar et al., 2012). 

Selye (1975) hypothesised that distress causes “diseases of adaptation” to occur. Biologically, this is due to the disruption of biological systems, because in situations of chronic stress blood glucose levels may become dysregulated and insulin sensitivity decreased via Hypothalmic Pituatury Adrenal, or HPA, axis activation. Moreover, chronic stress increases the metabolic needs of the body, resulting in an increased uptake in, and excretion of, vital nutrients (Yau & Potenza, 2013). These factors combined may increase risk of obesity and developing chronic disease, including type II diabetes (Siervo, Wells & Cizza, 2009; Tomiyama, 2014).  Distress has been defined as chronic stress induced by high levels of negative stressors, which exerts maladaptive effects via initiating structural changes to the brain (Lu, Wei & Li, 2021; Selye, 1975).

Chronic stress and resulting burnout are prevalent in modern 21st century life. Contributing stressors may be lifestyle factors, such as educational, professional, relationship, financial and health-related stressors and concerns. The human body has biological mechanisms which are supportive in times of short-term stress, but not suited to long term, chronic stress. Over a prolonged period, chronic stress may exert serious effects on the body, and increase the risk for developing mental health conditions and chronic diseases.

HPA Axis and The Stress Response

The HPA axis plays a key role in the stress response and mediates the effects of the stress response in the body. The HPA axis is regulated by neurotransmitters, such as GABA which exerts a calming effect, and noradrenaline and serotonin, which exert neuro-excitatory effects.  Therefore, the central nervous system and endocrine systems work closely to regulate the stress response via this mechanism (Stephens, 2012). In periods of stress, hypothalamic neurons from the paraventricular nucleus release corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) into the hypophysial portal blood, which connects the hypothalamus and pituitary gland. CRH and AVP produce adrenocorticotropic hormone (ACTH) and this is then secreted into the circulation. ACTH has the function of inducing the synthesis of glucocorticoids and signalling cortisol release from the adrenal glands (Stephens, 2012).  As the HPA axis also increases the availability of glucose in times of stress, this mechanism may additionally cause blood glucose (sugar) levels to become imbalanced and cause weight gain (Tryon et al., 2015).

Impact of Chronic Stress on Health Span

Chronic stress and related disruptions to biological mechanisms, such as glucose homeostasis, as well as lifestyle factors such as alcohol consumption and smoking, which are often coping mechanisms for stress have been indicated to increase levels of reactive oxygen species (ROS), resulting in elevated levels of oxidative stress (Astuti, Wardhana, Watkins, 2017;  Kovacic and Somanathan, 2006; Valdes et al., 2005; Wu et al., 2016).

Oxidative stress may impact mitochondrial functioning, as ROS disrupts the Shelterin complex in neurovascular cells, which impairs the functioning of the genes human telomerase reverse transcriptase (hTERT) and human telomerase RNA component (hTERC). These genes are involved in modulating telomerase activity, which regulates telomere length. When hTERT and hTERC functioning becomes impaired due to excessive levels of oxidative stress, telomerase is inhibited and this causes telomere length to shorten. Telomere shortening results in the activation of p53, a gene which downregulates PGC-1α and PGC-1β. The downregulation of PGC-1α and PGC-1β results in reduced mitochondrial biogenesis and causes mitochondrial dysfunction, resulting in dysfunctional oxidative phosphorylation, which in turn causes defective generation of ATP, impacting on energy production (Epel et al, 2004; Sahin et al., 2011). 

Blood glucose levels may become imbalanced and insulin sensitivity decreased due to downregulation of PGC1 α and β, as they coordinate insulin-sensitising gene expression, (Epel et al, 2004; Ristow et al., 2009).  Additionally, downregulated PGC1 α and PGC1 β results in decreased detoxification of ROS, due to reduced availability of superoxide dismutase 2 and glutathione peroxidase 1 (Ristow et al., 2009; St-Pierre et al., 2009). Furthermore, PGC1- α is essential for the transcription of SIRT1, and therefore downregulation results in increased cell senescence. Reduced expression of SIRT1 may reduce the stimulation of essential antioxidant enzymes (Brunt et al., 2004; Xiong et al., 2011).  Telomere length shortening – or telomere attrition – due to chronic stress has been associated with accelerated ageing, increased risk of developing chronic diseases and shortened lifespan.

Stress and Impact on HPG Axis 

The aforementioned HPA axis interacts with another integrative system known as the HPG axis, or hypothalamic-pituitary-gonadal), in a reciprocal, bi-directional relationship.  

In response to chronic stress, the balance of hormones can therefore be disrupted via this mechanism (Toufexis et al., 2014). Stress can affect three key sex hormones: oestrogen, progesterone and testosterone. 

Oestrogen

Oestrogen has a modulating role on brain processes that are involved in changes related to the stress response, cognition and also emotional regulation, as oestrogen increases amygdala and hippocampus sensitivity (Albert and Newhouse, 2019). Oestrogen additionally has a modulatory effect on the HPA axis, and in periods of chronic stress, oestrogen secretion is decreased (Toufexis et al., 2014). 

Progesterone

Chronic stress inhibits ovarian secretion of progesterone, whilst also causing noradrenaline to be released into the ovary (Toufexis et al., 2014). Progesterone has the function of modulating GABA, which has a calming effect on the brain (Guennoun, 2020).  

Testosterone  

There may be some variation on the effects of stress on testosterone levels (Albert and Newhouse, 2019), as differences have been observed depending on the variables of extroversion vs introversion, openness to challenges, and control and expression of emotion, as well as obvious sex-specific differences (Afrisham et al., 2016). However, in periods of chronic stress testosterone secretion is generally decreased (Toufexis et al., 2014).

Key Nutrients for Stress

Nutrition can be used as a means of supporting the body during times of stress, increasing resilience, building strength and re-equipping the body with nutrients which may become depleted during periods of chronic stress. 

Blood Glucose Balance

To support blood glucose balance:

  •  eliminate refined sugars and processed foods
  •  consume vegetables and fruit with protein (i.e. apple with handful of nuts; vegetables with beans/legumes or chicken/fish)
  • Avoid caffeine and other stimulants

Magnesium and Vitamin B6

Research has indicated that magnesium and Vitamin B6 may be supportive to individuals experiencing stress. A recent study indicated that combined these nutrients helped to alleviate stress levels in subjects who were experiencing chronic, long-term stress (Pouteau, et al., 2018). 

Increasing magnesium

To increase magnesium levels, increase consumption of green leafy vegetables, nuts and also cacao. Epsom salt baths are an additional way to increase magnesium levels, and when enjoyed with essential oils, can be a wonderful way of relaxing and rejuvenating in times of stress.

Increasing Vitamin B6

To increase Vitamin B6, consume turkey, chickpeas and also fish, such as salmon.

Omega 3

A recent study indicated that individuals who were administered omega 3 demonstrated reduced markers of psychological and physiological burnout, including decreased cortisol levels, compared with controls (Jangharad et al., 2019).

Increasing Omega 3 Fatty Acids: Salmon, mackerel, herring and sardines, chia, flaxseeds and walnuts are all a great way to increase omega 3.

References

Afrisham, R et al., 2016. Salivary Testosterone Levels Under Psychological Stress and Its Relationship with Rumination and Five Personality Traits in Medical Students. Psychiatry Investigation13(6), pp 637–643. Available at: <https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5128352/>

Albert KM, Newhouse PA. Estrogen, Stress, and Depression: Cognitive and Biological Interactions. Annu Rev Clin Psychol. 2019 May 7;15:399-423. doi: 10.1146/annurev-clinpsy-050718-095557. Epub 2019 Feb 20. PMID: 30786242.

Astuti, Y, Wardhana, A, Watkins, J, 2017. Cigarette smoking and telomere length: A systematic review of 84 studies and meta-analysis. EnvironRes158, pp480 -489. Av

Brunet, A, Sweeney, L, Sturgill, J, Chua, K, Greer, P, Lin, Y, 2004. Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 Deacetylase. Science, 303 (5666), pp 2011-2015. Available at:<http://science.sciencemag.org/content/303/5666/2011ijkey=9dec7ffa528186638ab60d3f63a42bb89c437fac&keytype2=tf_ipsecsha>

Epel, E, Blackburn, E, Lin, J, Dhabhar, F, Adler, N, Morrow, J, Cawthon, 2004. Accelerated telomere shortening in response to life stress. Proceedings of the National Academy of Sciences of the United States of America, 101 (49), pp17312 –17315. Available at <http://www.pnas.org/content/101/49/17312.long> 

Guennoun, R.,  2020. Progesterone in the Brain: Hormone, Neurosteroid and Neuroprotectant. Int J Mol Sci21(15), p 5271. Available at: <https://pubmed.ncbi.nlm.nih.gov/32722286/>

Jangharad, L, 2019. Omega-3-polyunsatured fatty acids (O3PUFAs), compared to placebo, reduced symptoms of occupational burnout and lowered morning cortisol secretion. Psychoneuroendocrinology. Available at: <https://pubmed.ncbi.nlm.nih.gov/31382171/>

Kovacic, P., Somanathan, R., 2006. Mechanism of teratogenesis: electron transfer, reactive oxygen species, and antioxidants. Birth Defects Research. Part C, Embryo Today: Reviews, 78 (4), pp 308 – 325. Available at:<https://www.ncbi.nlm.nih.gov/pubmed/17315244>

Lu, S., Wei, F., & Li, G. (2021). The evolution of the concept of stress and the framework of the stress system. Cell stress, 5(6), 76–85. https://doi.org/10.15698/cst2021.06.250

Pouteau, E, et al., 2018. Superiority of magnesium and vitamin B6 over magnesium alone on severe stress in healthy adults with low magnesemia: A randomized, single-blind clinical trial. PLoS One13

(12). Available at: <https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC6298677/>

Ristow, M, Zarse, K, Oberbach, A, Kloting, N, Birringer, M, Kiehntopf, M, Stumvoll, M, Kahn, C, Bluher, M, 2009. Antioxidants prevent health-promoting effects of physical exercise in humans. Proceedings of the National Academy of Sciences of the United States of America, 106(21), pp 8665 – 8670. Available at: <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680430>

Sahin, E., Colla, S., Liesa, M., Moslehi, J., Müller, F. L., Guo, M., Cooper, M., Kotton, D, Fabian, A., Walkey, C., Maser, R., Tonon, G., Foerster, F., Xiong, R., Wang, A., Shukla, S., Jaskeliff, M., Martin, E., Heffernan, T., Protopopov, A., Ivanova, E., Mahoney, J., Kost-Alimova, M., Perry, S., Bronson, R., Liao, Ronglih, Mulligan, R., Shirhai, O., Chin, L., DePinho, R., 2011. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature, 470(7334), pp 359–365. Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741661/

Sanchis-Gomar, F., Garcia-Gimenez, J. L., Perez-Quilis, C., Gomez-Cabrera, M. C., Pallardo, F. V., & Lippi, G. (2012). Physical exercise as an epigenetic modulator: Eustress, the “positive stress” as an effector of gene expression. Journal of strength and conditioning research, 26(12), 3469–3472. https://doi.org/10.1519/JSC.0b013e31825bb594

Selye, H. (1975). Implications of stress concept. New York State Journal of Medicine, 75(12), 2139–2145.

Siervo, M., Wells, J. C., & Cizza, G. (2009). The contribution of psychosocial stress to the obesity epidemic: an evolutionary approach. Hormone and metabolic research = Hormon- und

Stoffwechselforschung = Hormones et metabolisme, 41(4), 261–270. https://doi.org/10.1055/s-0028-1119377

Stephens, MA, 2012. Stress and the HPA Axis: Role of Glucocorticoids in Alcohol Dependence.  Alcohol Research Current Reviews, 34 (4), pp 468 – 483. Available at:  <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860380/>

St-Pierre, J, Drori, S, Uldry, M, Silvaggi, J, Rhee, J, Jager, S, Handschin, C, Zheng, K, Lin, J, Yang, W, Simon, D, Bachoo, R, Spiegelman, B, 2006.  Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. Cell127 (2), pp397 – 408. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/17055439>

Tomiyama A. J. (2014). Weight stigma is stressful. A review of evidence for the Cyclic Obesity/Weight-Based Stigma model. Appetite, 82, 8–15. https://doi.org/10.1016/j.appet.2014.06.108

Toufexis D, Rivarola MA, Lara H, Viau V. Stress and the reproductive axis. J Neuroendocrinol. 2014 Sep;26(9):573-86. doi: 10.1111/jne.12179. PMID: 25040027; PMCID: PMC4166402.

Tryon, M, Stanhope, K, Epel, E, Mason, A, Brown, R, Medici, V, Harvel, P, Laugero, K, 2015. Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body. The Journal of Clinical Endocrinology & Metabolism100 (6), pp 2239 – 2247. Available at:

<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4454811/>

Valdes, A, Andrew, T, Gardner, J, Kimura, M, 2005. Obesity, cigarette smoking, and telomere length in women. Lancet, 366 (9486), pp 662-664. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/16112303> 

Wu, N, Shen, H, Liu, H, Wang, Y, 2016. Acute blood glucose fluctuation enhances rat aorta endothelial cell apoptosis, oxidative stress and pro-inflammatory cytokine expression in vivo. Cardiovasc Diabetol, 15 (109). Available at:< https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4974767/> [Accessed 16 September 2018] 

Xiong, S, Salazar, G, Pastrushev, N, Alexander, R, 2011. FoxO1 mediates an autofeedback loop regulating SIRT1 expression. J Biol Chem, 286 (7), pp 5289-5299. Available at: <https://www.ncbi.nlm.nih.gov/pubmed/21149440/>