By: Dr. Chantell Groenewald (M.TechHom UJ)
Cortisol, the stress hormone that promotes the accumulation of abdominal fat. Overgaard et al.(2004) conducted a study amongst a group of 6 704 nurses to test the theory that an increased workload, and by association higher levels of stress, contributed to an increased level of weight gain. Overgaard then went further by publishing a novel where he illustrated, by means of reference to the decreased level of cerebrospinal corticotrophin-releasing factor, his theory with regards to over eating due to chronic stress and consequent weight gain. He proposed that individuals who suffer from chronic stress may over eat to reduce the level of activity in the chronic stress response network. Cortisol is a major glucocorticoid hormone in humans. It is secreted from the adrenal glands, situated on top of the kidneys, and is regulated by the Hypothalamic-pituitary-adrenal (HPA) axis in response to stress. It affects several systems in the body, including metabolic, central nervous system (CNS), immune system and iron transport. Alterations in the ability to respond to stressful situations, i.e. excessive and or prolonged exposure to stressors, lead to the development of stress syndrome. Stress syndrome refers to the collection of events and subsequent symptoms that occur following prolonged periods of stress. The key components of the stress syndrome are the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). The HPA axis comprises of chemical reactions that occur during a stressful situation. The series of events are explained thus. The hypothalamus (situated in the region of the brain involved in coordination of neural and endocrine functions) is triggered by stressors and subsequently releases corticotrophin-releasing hormone (CRH), as well as arginine vasopressin (AVP). These two hormones in turn stimulate the secretion of ACTH from the posterior pituitary gland. ACTH activates the noradrenic neurons of the locus caeruleas/norepinephrine (LC/NE) system of the brain. The LC/NE system is directly responsible for the ‘flight and fight’ response (release of adrenalin as well as nor-adrenalin), while the ACTH is responsible for releasing cortisol from the adrenal cortex (centre of the adrenal gland situated on top of the kidneys). The function of this HPS axis is primarily catabolic, i.e. to release all possible energy sources for the fight and flight response. Cortisol stimulates fat and carbohydrate metabolism i.e gluconeogenesis (process by which the level of glucose in the blood stream is increased), to supply the body with ‘fast’ energy during periods of stress. This leads to an increase in hepatic (liver)gluconeogenisis and plasma glucose concentration. Furthermore, lipolysis and protein degeneration offers even more potential energy. This response is necessary in an acute fight or flight reaction, however, when stressors become chronic, it may have adverse effects on these physiological functions. Responses that are not essential to the fight and flight response are curbed by elevated levels of cortisol, altering the immune system response and supressing the metabolism and the reproductive system. Long term exposure to elevated levels of cortisol translates into: · Weight gain (specifically abdominal fat) · Hormone imbalances · Insulin resistance · Increased appetite · Supressed immune system and repetitive colds and flu · Anxiety and depression · Difficulty sleeping · Problems with memory and concentration. Elevated levels of cortisol promotes the accumulation of abdominal fat, that is, fat deposition around the waist, termed visceral adipose tissue. This type of fat (adipose) cell is distinctly different form the fat cells in the rest of our bodies (subcutaneous fat). Visceral adipose tissue functions as an endocrine gland, secreting hormones that have an effect on our insulin metabolism as well as good cholesterol (HDL) vs. bad cholesterol (LDL) levels.Also secreted by visceral adipose tissue, are a number of inflammatory markers (including IL-6), that further contributes to the development of cardiovascular disease. A combination of insulin resistance, high LDL and low HDL, together with increased abdominal width, is termed metabolic syndrome. Metabolic syndrome is directly related to cardiovascular health, and a predictor for cardiovascular accidents as well as stroke. Metabolic syndrome, or syndrome X, encompasses the following features:
A diagnosis of the metabolic syndrome is made in the presence of three or more of the following features: · a waist circumference larger than 102 cm in males and 88 cm in females; · Triglyceride level greater than 150mg/dL; · HDL less than 40mg/dL in men and less than 50mg/DL in females; · blood pressure higher than 135/85 mmHg; and · a fasting glucose higher than 110mg/dL. All of the above factors are associated with chronic low-grade inflammation. As mentioned earlier, elevated levels of IL-6 inflammatory markers are illustrated in patients with increased abdominal width (<88cm in females), and this inflammation plays a crucial role in propagating diseases associated with being overweight, and is associated with hindering weight loss. A diet rich in anti-inflammatory foods have been shown to assist in reducing levels of IL-6, and associated markers of metabolic syndrome, thereby assisting weight loss. Lifestyle changes that may assist in reducing stress: · Relaxation breathing exercises · Drinking herbal teas that assist in bringing about calm (egchamomile tea) · Reducing caffeinated drinks · Taking 20min ‘me time’ per day · Take up a hobby so promote stress free activities · Getting 7-8 hours’ sleep per night · 20 minutes physical activity per day (keeping heart rate below 140 bpm) · Diet alterations that assist in reducingdiet related inflammation is an important factor in maintaining a healthy weight. Visit your health care practitioner annually for a thorough medical examination, to assess your general well-being.Prevention is better than cure. References: Goedecke, J., Jenning, C., Lambert, E. (2005). Obesity in South Africa. Chronic disease of lifestyle in South Africa since 1995-2005, 5: 65-79. Guilliams, T., Edwards, L. (2010). Chronic Stress and the HPA Axis: Clinical Assessment and Therapeutic Considerations. The Standard, 9(2): 1-12. Esposito, K., Giugliano, D. (2004). The metabolic syndrome and inflammation: association or causation. Nutrition. Metabolism and Cardiovascular disease, 14:228-232. Kyrou, I., Tsigos, C. (2009). Stress Hormones: Physiological Stress and Regulation of Metabolism. Current Opinion in Pharmacology, 9(6): 787-793. National Heart Lung and Blood Institute (2010). Overweight and Obesity-Risks. Available: http://www.nhlbi.nih.gov/health/health-topics/topics/obe/risks.html (Accessed 15 March 2012). Overgaard, D., Gamborg, M., Gyntelberg, F., Heitman, B. (2004). Psychological workload associated with weight gain between 1993 and 1999: analysis based on the Danish Cohort study. International Journal of Obesity, 28:1072-1081. http://www.health.harvard.edu/newsweek/Abdominal-fat-and-what-to-do-about-it.htm http://www.medicinenet.com/script/main/art.asp?articlekey=53304 http://www.mayoclinic.org/healthy-living/stress-management/in-depth/stress/art-20046037?footprints=mine http://dujs.dartmouth.edu/fall-2010/the-physiology-of-stress-cortisol-and-the-hypothalamic-pituitary-adrenal-axis#.UyBS__mSxAA
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AuthorsDr. Marike de Klerk Categories
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