Cortisol is a hormone produce by the body in response to daily events and circumstances. It is produce when you get out of bed, go to work or when you exercise. Cortisol is also released in response to acute stress and in studies, it has been linked to one of the reasons behind stress eating [1-5].
One of cortisol’s important functions is to regulate your metabolism and energy reserves. It helps select the type and amount of nutrients required by our body to function correctly. In fact, this hormone selects which fat, protein or carbohydrates we should use as energy.
Chronic levels of this hormone can cause your body to resist insulin [6, 7]. This resistance can negatively impact your metabolism and appetite. In particular, it can have a disastrous effect on people trying to lose weight, often making weight loss impossible to achieve . In fact, scientists have found that a high level of cortisol present in the blood can produce high levels of glucose. This increase in glucose in turn raises the level of insulin in the blood, and subsequently cells build up a resistance to it over time [9, 10].
Insulin is required by the body to provide energy to its cells. If the cells resist insulin, the glucose produced for those cells continue to circulate in your body until the body realises there is too much and converts it to fat, which is then stored in your fat cells.
As this energy (glucose) is not being used by the cells your metabolism or the rate at which your body burns energy is reduced. Furthermore, each time your fat cells become full, they release a hormone known as leptin. Research has found this hormone to influence our feeling of hunger [11-13]. It basically, is used to signal the brain to stop eating, or in other words, I am full! This is the normal process of our body, however when chronic levels of leptin are received by the brain, due to this feedback loop (increase cortisol -> glucose -> insulin -> fat storage) the brain starts to resist this hormone, prolonging hunger and requiring more food to feel full [14, 15]. Leptin resistance not only makes us more hunger, but results in a domino effect where the body doesn’t think it getting enough nutrients. Subsequently reducing energy expenditure in our body, or in other words further reducing our metabolism [12, 13, 15].
1. Adams CE, et al. Lifestyle Factors and Ghrelin: Critical Review and Implications for Weight Loss Maintenance Obesity Review. (May 2011): Vol. 12, No. 5, electronic publication.
2. Manzoni GM, et al. Can Relaxation Training Reduce Emotional Eating in Women with Obesity? Journal of the American Dietetic Association (Aug. 2009): Vol. 109, No. 8, pp. 1427–32.
3. Mathes WF, et al. The Biology of Binge Eating Appetite. (June 2009): Vol. 52, No. 3, pp. 545–53.
4. Spencer SJ, et al. The Glucocorticoid Contribution to Obesity. Stress (Feb. 6, 2011): Vol. 14, No. 3, pp. 233–46.
5. Vicennati V, et al. Stress-Related Development of Obesity and Cortisol in Women. Obesity (Sept. 2009): Vol. 17, No. 9, pp. 1678–83.
6. Rizza RA, Mandarino LJ, Gerich JE 1982 Cortisol-induced insulin resistance in man: impaired suppression of glucose production and stimulation of glucose utilization due to a postreceptor detect of insulin action. J Clin Endocrinol Metab 54:131–138
7. Dinneen S, Alzaid A, Miles J, Rizza R 1993 Metabolic effects of the nocturnal rise in cortisol on carbohydrate metabolism in normal humans. J Clin Invest 92:2283–2290
8. The National Institute of Diabetes and Digestive and Kidney Diseases Health Information Center. Prediabetes and Insulin Resistance. https://www.niddk.nih.gov/health-information/diabetes/types/prediabetes-insulin-resistance
9. Sharon S Elliott, Nancy L Keim, Judith S Stern, Karen Teff, and Peter J Havel. Fructose, weight gain, and the insulin resistance syndrome. http://ajcn.nutrition.org/content/76/5/911.full
10. Gisela Wilcox, Monash University Department of Medicine & Clinical Nutrition & Metabolism Unit. Insulin and Insulin Resistance. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1204764/
11. Ahima RS. Revisiting leptin’s role in obesity and weight loss. The Journal of Clinical Investigation. 2008;118(7):2380-2383. doi:10.1172/JCI36284.
12. Allison MB, Myers MG Jr. 20 years of leptin: connecting leptin signaling to biological function. http://www.ncbi.nlm.nih.gov/pubmed/25232147
13. Hyeong-Kyu Park, Rexford S. Ahima. Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism. http://www.metabolismjournal.com/article/S0026-0495(14)00241-8/abstract?cc=y=
14. Schwartz MW, Woods SC, Porte D Jr, Seeley RJ, Baskin DG. Central nervous system control of food intake. http://www.ncbi.nlm.nih.gov/pubmed/10766253
15. Jean L. Chan, Kathleen Heist, Alex M. DePaoli, Johannes D. Veldhuis and Christos S. Mantzoros. The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men. http://www.jci.org/articles/view/17490