A common theme I have noticed in practice is stress. This response is programmed as a general life saving mechanism, helping us deal with potential threats on a more short term basis.
Stress response basics.
To understand the effects of the stress reaction it is good to have an appreciation of the physiological processes involved.
Stressor signals such as oncoming cars or fire alarms are sent from our eyes and ears to the amygdala of the brain where they are emotionally processed. If a threat or danger is perceived a signal is then sent to the hypothalamus, also in the brain. This region of the brain acts like a control centre, communicating with the rest of the body through the autonomic nervous system (ANS). Initially sending signals via the sympathetic nervous system (SNS) to the adrenal glands for the release of adrenaline in to the bloodstream. Adrenaline brings on a number of physiological changes including: increased heart rate, increased blood pressure, the opening up of smaller airways in the lungs and an increased breathing rate. This encourages the push of oxygenated blood to the muscles, heart, and other vital organs. As the extra oxygen is sent to the brain, alertness, sight, hearing, and other senses become sharper. This process is known as acute stress or the sympathetic-adrenal-medullary (SAM) axis.
This reaction occurs rapidly so is hardly noticed, but should the stressor continue to cause the stress response, the reaction goes from acute stress to chronic. This begins once the initial release of adrenaline subsides.
The chronic stress reaction also originates from the hypothalamus but the signals, previously sent to the adrenals, are now sent to the pituitary gland by a neurotransmitter called corticotropin-releasing hormone (CRH). The pituitary gland then reacts by releasing adrenocorticotropic hormone (ACTH). This travels to the adrenals and on this occasion causes the release of the stress glucocorticoid hormone known as cortisol (Harvard Health Publications, 2011). This process is known as chronic stress or the hypothalamic–pituitary–adrenal (HPA) axis.
Chronic stress and cortisol.
In modern day living we are constantly surrounded by pressures. Problems with finances, work, family, relationships and of course health are all ongoing stressors which a large number of people are exposed to on a daily basis, sometimes for years on end. This means the body is exposed to the stress hormone cortisol during this time. The primary effects of cortisol are:
- Providing the body with glucose by tapping into protein stores via gluconeogenesis in the liver.
- Reducing insulin effects.
- Reducing inflammation in the body.
- Suppression of the parasympathetic nervous system (PNS) and digestive functions.
- Blood vessel constriction and increasing blood pressure.
After a prolonged period each of these effects has a detrimental effect on the body’s functions, leading to physiological imbalance and associated systemic conditions.
I will be studying each of the following stress related systemic dysfunctions in more detail in the future, but here is a brief overview of the potential effects on each:
Blood glucose imbalance and insulin resistance.
Consistently high blood glucose levels from stress along with insulin resistance leads to cells that are starved of glucose, resulting in hunger signals being sent to the brain. This can lead to overeating. The unused glucose is stored as fat in the body’s adipose tissue (Aronson, 2009). This causes weight gain and can lead to obesity.
Further to this chronic stress also leads to the suppression of the hormone, insulin-like growth factor (lGF-1). The reduced IGF-1 levels contribute to impaired glucose metabolism and insulin resistance, with studies associating it to the development of diabetes type 2 (Innes et al, 2007).
Over time, the effects of cortisol to reduce inflammation also suppresses the immune system (Aronson, 2009). Stress and other lifestyle factors such as a poor diet cause inflammation in the body. This, as an internal stressor, maintains high cortisol levels, wreaking havoc on the immune system with the contradictory processes (Aronson, 2009).
This can lead to a multitude of physiological problems including increased susceptibility to bacterial or viral infections (such and cold or flu), increased risk of allergies (due to raised levels of histamines produced to reduce the inflammation), increased risk of gastrointestinal conditions (paired with the sympathetic nervous system reduction in digestive function), an increased risk of autoimmune diseases and cancer (Aronson, 2009).
Stress causes the activation of sympathetic nervous system (SNS) functions, this means that the parasympathetic nervous system (PNS) functions are stopped in order to do so. Digestion is one of the functions the PNS controls so is supressed in order to allow the SNS to respond to the stressor(s).
Stress has been shown to result in a an induced slowing of gastric emptying, increase in distal colonic motility, and acceleration of intestinal transit. Persistent alterations of the autonomic nervous system (both SNS and PNS) is likely to play a role in altered bowel habits and the most common gastrointestinal disorders; irritable bowel syndrome (IBS and functional dyspepsia (FD) (Mayer, 2000).
Short term moderate stress can enhance the risk of colonic inflammation. Studies have shown results which are consistent with a model in which the effect of the stressor is primarily mediated by autonomic responses (Whitworth et al, 2000).
Cortisol constricts the blood vessels and increases the blood pressure in order to improve the flow of oxygenated blood (Aronson, 2009). Further to this the changes in digestive functions and glucose levels contribute to the increased risk of cardiovascular diease. Whitworth et al (2005) states:
There is increasing evidence that cortisol contributes to cardiovascular risk, not only in Cushing’s syndrome (hypercortisolism), but more generally. Hypertension, truncal obesity, hyperglycemia, insulin resistance, and dyslipidemia are all important in this regard.
Persistently elevated cortisol levels from chronic stress can lead to erectile dysfunction or the disruption of normal menstrual cycles (Aronson, 2009).
Cortisol disturbs the activating effect of gonadotrophins in synthesizing sex steroids (oestrogens, progesterones, testosterone and other androgens) resulting in reduction of their synthesis. This appears to take place more so during chronic stress (Cwikel et al, 2004).
This sex hormone decrease disruption leads to the reduced function of reproductive organs in both men and women.
Although this is a mere snapshot of the effects of chronic stress the information detailed should give a good insight in to the overall detrimental effects of long term stress on the body. Both patients and practitioners should consider this while reviewing health concerns. By acknowledging relevant affecting factors, we should be able to find methods to manage and possibly counteract the effects from chronic stress.
Further research will be posted on each of the systems to highlight the prevalence of both chronic stress and post-traumatic stress disorder as an affecting factor in chronic diseases.
- Aronson, Dina. “Cortisol — Its Role In Stress, Inflammation, And Indications For Diet Therapy”. Todaysdietitian.com. N.p., 2009. Web. 9 Apr. 2017.
- Cwikel, J., Y. Gidron, and E. Sheiner. “Psychological Interactions With Infertility Among Women”. European Journal of Obstetrics & Gynecology and Reproductive Biology 117.2 (2004): 126-131. Web.
- Innes, Kim E., Heather K. Vincent, and Ann Gill Taylor. CHRONIC STRESS AND INSULIN RESISTANCE– RELATED INDICES OF CARDIOVASCULAR DISEASE RISK, PART I: NEUROPHYSIOLOGICAL RESPONSES AND PATHOLOGICAL SEQUELAE. 2007. Article. July/August 2007. Volume 13. Virginia.
- MAYER, E A. “The Neurobiology Of Stress And Gastrointestinal Disease”. Gut 47.6 (2000): 861-869. Web.
- Publications, Harvard. “Understanding The Stress Response – Harvard Health”. Harvard Health. N.p., 2011. Web. 9 Apr. 2017.
- Whitworth, Judith A et al. “Cardiovascular Consequences Of Cortisol Excess”. Vascular Health and Risk Management 1.4 (2005): 291-299. Web.