Figure 1 – HPA Axis Stress response (Tortora & Derrickson, 2012: 715)
The second system which forms part of the stress response is the Hypothalamic-Pituitary-Adrenal (HPA) Axis. The Paraventricular Nucleus (PVN) located in the Hypothalamus releases a peptide hormone called Corticotrophin-Releasing Hormone (CRH) which targets the Anterior Pituitary lobe to synthesise and release Adrenocorticotrophic Hormone ACTH (Tortora & Derrickson, 2012: 715). ACTH then stimulates a reaction of biochemical events which results in the release of the stress hormone Cortisol. There are two types of Corticosteroids (Cortisol) which are involved in the stress response, and these are Glucocorticoids and Mineralocorticoids (aldosterone). Glucocorticoids are primarily responsible for regulating metabolism by raising blood glucose levels; this inhibits the production of insulin and ensures an immediate supply of energy to working muscles (Sherwood, 2010: 700). Mineralocorticoids on the other hand stimulate the uptake of Sodium (Na+) and excretion of Potassium (K+) resulting in salt and water retention which induces a temporary state of hypertension due to increase in blood pressure and blood volume. These systems all work together through a negative feedback loop to ensure that the body returns to homeostasis once the threat or temporary state of stress subsides (Waugh & Grant, 2011: 210-219). Whilst all these built in mechanisms play an important role in helping our body to mobilize during times of acute stress, research has shown that chronic on-going stress can wreak havoc with our Cardiovascular and Immune systems and subsequently cause the body to break down (Ogden, 2004: 257-266).
From a physiological perspective, the effects of chronic stress can leave the sympathetic nervous system in a constant state of ‘fight or flight’, causing elevated levels of cortisol to surge throughout the body. Whilst cortisol does play a pivotal role in metabolism and balancing blood glucose levels, research has also shown that prolonged exposure to high levels of cortisol can produce multiple symptoms associated with risk factors for cardiovascular disease and metabolic syndrome (Walker, 2012). Cortisol has a direct effect on cardiac health firstly by reducing the secretion of Human Growth Hormones (HGH). Deficiencies in HGH negatively affect the heart by weakening cardiac muscle; this subsequently results in decreased cardiac contractility, thus threatening vital transportation of oxygenated blood to organs and tissues throughout the body. Furthermore, research also shows that chronic elevated levels of cortisol also promotes hypertension, and as a consequence, accelerates the development of Atherosclerosis (Tortora & Derrickson, 2012: 319). Atherosclerosis is one of the leading causes of coronary heart disease in the world, and is characterised by a build-up of fibro fatty plaque on the inner walls of the arteries. As a result, the build-up of plaque causes restrictions in blood flow, thus increasing the risk of formation of blood clots and potentially, a heart attack (myocardial infarction) or a stroke if left untreated (Farris & Marin, 2008).
Figure 2 – Progression of Atherosclerosis (Tortora & Derrickson, 2012, p. 319)
Chronic stress also plays a major role in the development of cardiovascular related conditions such as metabolic syndrome. Metabolic syndrome presents with a cluster of symptoms such as diabetes, high blood pressure and obesity, and is a well-known precursor for cardiovascular diseases. Prior research suggests that metabolic syndrome occurs as a result of nutritional deficiencies and sedentary lifestyle (Sharma & P.K.Majumdar, 2009: 109-112). However, on-going research has also implicated excessive amounts of adrenaline and the stress hormone cortisol to be contributing factors in the development of these disorders. During times of acute stress or physical activity, cortisol assists metabolism by simulating various fuel sources such as glucose, fats and amino acids, whilst adrenaline speeds up the fat burning process. However, in situations where stress is on-going and relentless, the body eventually builds up a tolerance to adrenaline and cortisol; as a consequence, this prevents energy sources from being utilised and subsequently causes an excess of blood glucose, insulin resistance and the storage of excess fat (Farris & Marin, 2008). If left untreated, excess glucose in the blood, which can result in diabetes, along with excess fat storage, can both have serious implications for health, namely an increased risk of heart disease, kidney disease and other complications (Walker, 2012; Evans-Martin, 2007: 76).
Figure 3 – Metabolic Syndrome (Farris & Marin, 2008)
An equally significant health risk caused by chronic stress and elevated levels of cortisol is the physiological changes that occur in immune functions. In times of acute stress, cortisol undoubtedly plays an important role in supressing immune and inflammatory responses, however, when stress is severe and chronic, this can induce a state of hyper-cortisolism, which subsequently overwhelms the immune system and inhibits the body’s ability to fight infection and disease (Tortora & Derrickson, 2012: 713-714). One of the ways in which cortisol can devastate the immune system is by causing shrinkage to the thymus gland and lymph tissues. The Thymus gland plays an essential role in the maturation of T-cells (Lymphocytes/White Blood Cells) which are one of the key players of the immune system (Talbott, 2007). T Cell’s work to protect the body against invading pathogens, such as viruses, bacteria, fungi, helminths (worms) and parasitic protozoa, and do so by directly killing infected cells or instructing other killer cells to destroy invading pathogens. Research has shown that chronic stress often presents with a significant reduction in T-Cell lymphocytes, partly due to the fact that elevated cortisol levels affect the T-Cell’s ability to proliferate and work effectively (Ogden, 2004: 257-261). Moreover, when immune cells become compromised, this weakens their ability to differentiate between the body’s own healthy tissues and infected tissues, and as a result may even contribute to the development of autoimmune disorders (Johnson, 2013) such as multiple sclerosis (MS), or the acceleration of cancer (McKenna, 2011: 211).
Figure 3 – Autoimmune Triggers (Johnson, 2013)
To conclude, we can see that psychological stressors most definitely have a far reaching impact on the physiological wellbeing of the human body, with evidence of the stress hormone cortisol being implicated in coronary heart disease, metabolic syndrome and other disorders resulting from immunodeficiency. Furthermore, whilst the Nervous, Endocrine and Cardiovascular systems have a very sophisticated network in place to ensure that the body reacts and responds effectively and with precision to acute stressors, research literature shows that chronic stress is most definitely a serious problem, and by causing these systems to become perturbed, it could undoubtedly mean the difference between life and death.
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Grade : 73.00 out of 100
A great essay.Your interpretation is largely convincing and there is evidence of critical thinking. Your discussion is appropriate and you have clearly identified the issues involved. There is clear evidence of a comprehensive grasp of all of the main concepts. You have a wide range of relevant reading which is very well referenced. The essay develops logically and language used is appropriate and concise. You have drawn relevant conclusions that are well argued. Well done.