Generally, much of the blame for obesity’s widespread existence in Western society is placed upon poor lifestyle. In the case of the former, the increasing pervasiveness of a sedentary lifestyle, characterized by long periods of inactivity (such as sitting in an office) with little to no exercise, in addition to a decreasing amount of leisure time being spent on physical activity, as opposed to video games and television viewing. (Bleich, et. al., 2007)
In the case of the latter, over-eating remains a problem, despite advances in nutritional awareness. Additionally, the increasing reliance on fast-food meals, with their energy dense composition, have quadrupled the calorie intake of the average American over the period between 1977 and 1995. (Lin, et. al., 1999)
Genetics also play a part in the development of obesity. Excess calorie intake and how it translates into body mass is affected by various factors such as the genes which regulate metabolism, appetite and adipokine. Additionally, there are various genetic conditions that have been identified as symptomatized by obesity (e.g. Bardet-Biedl syndrome, leptin receptor mutations and MOMO syndrome). Farooqi & O’Rahilly (2006) have also noted that obesity has a hereditary component.
Obesity may also be affected by medical illnesses such as Cushing’s syndrome, growth hormone deficiency and hypothyroidism. The treatment of some illnesses may also lead to fluctuations in weight, as a side effect of medication taken (e.g. antipsychotics, fertility meds). Quitting smoking has also been recognized as a cause of moderate weight gain, due to the resulting loss of appetite suppression. Also, some psychological disorders such as bulimia or binge disorders contribute direct risks of obesity.
The mechanisms of neurobiology also contribute to the development of obesity. In addition to leptin (which regulates the intake and expenditure of energy) substances such as ghrelin (which regulates short-term appetite) are linked with the maintenance of obesity. (Flier, 2004). Other such substances include adiponectin which regulates glucose, cholecystokinin which stimulates the digestion of fat and protein, and PYY 3-36 which responds to food intake by reducing appetite.
Finally, social determinants contribute to obesity by significantly affecting the habits formed that contribute to obesity. In a 2004 study, it was noted that there was an inverse correlation between wealth and obesity, suggesting that lower income individuals rely on cheaper fast food for nourishment. (Zagorsky, 2004). Also, a 2007 study followed more than 32,500 individuals over a span of 32 years and found that changes in body mass of friends, and siblings were reliable predictors of changes in subjects, regardless of geographical distance, suggesting that the acceptance of one’s body mass has an influence on changes in body size. (Christakis & Fowler, 2007)
Bleich, S., Cutler, D., Murray, C. & Adams, A. (2007) Why Is The Developed World Obese?. Annual Review of Public Health, Volume 29. Retrieved May 5, 2008 from: http://www.nber.org/papers/w12954.pdf
Lin, B.H., Guthrie, J. & Frazao E. (1999) “Nutrient contribution of food away from home”. In: Frazao, E. (Ed). America’s Eating Habits: Changes and Consequences. Agriculture Information Bulletin No. 750, US Department of Agriculture, Economic Research Service, Washington, DC, pp. 213–239.
Farooqi, S., O’Rahilly, S. (2006) Genetics of obesity in humans. Endocrine Review, Volume 27.
Chakravarthy, M.V., Booth, F.W. (2004). Eating, exercise, and “thrifty” genotypes: connecting the dots toward an evolutionary understanding of modern chronic diseases. Journal of Applied Physiology, Volume 96.
Flier, J.S. (2004). Obesity wars: molecular progress confronts an expanding epidemic. Cell, Volume 116, Issue 2, pp. 337-350.
Zagorsky, J.L. (2004) Is Obesity as Dangerous to Your Wealth as to Your Health? Res Aging Volume 26, pp. 130-152.
Christakis, N.A., Fowler, J.H. (2007) The Spread of Obesity in a Large Social Network over 32 Years.”