Obesity

Obesity is defined as abnormal or excessive fat accumulation that may impair health measured by body mass index (BMI).1 Currently, one-third (37.7%) of US adults are considered to have obesity and are at an increased risk of obesity-related comorbidities, including cardiovascular disease, hypertension, and type 2 diabetes.2,3 

Given the significantly increased morbidity and mortality associated with obesity, the American Medical Association, the American Association of Clinical Endocrinologists, the FDA, and the World Health Organization have recognized obesity as a disease. This recognition is based on the criteria that it impairs the normal functioning of some aspects of the body, has characteristic signs or symptoms, and results in harm or morbidity.4-7 

Maintaining weight loss has been demonstrated to improve obesity-related comorbidities. The benefits of a 5% to 10% weight loss include reduction in risk of type 2 diabetes, reduction in cardiovascular risk factors, improvements in the blood lipid profile, and improvements in blood pressure.4

However, scientific evidence has shown that that physiological responses to intentional weight loss trigger weight regain. Weight loss in people with obesity causes changes in appetite hormones that actually increase hunger and the desire to eat for at least a one-year period following a reduction in weight. Hormones such as ghrelin, GLP-1, PYY, CCK, insulin, and leptin among others play an important role in appetite regulation. Long-term intervention is often required, and physician-initiated discussions can motivate patients to achieve significant and maintained weight loss.8-13  

Obesity

Obesity is defined as abnormal or excessive fat accumulation that may impair health measured by body mass index (BMI).1 Currently, one-third (37.7%) of US adults are considered to have obesity and are at an increased risk of obesity-related comorbidities, including cardiovascular disease, hypertension, and type 2 diabetes.2,3 

Given the significantly increased morbidity and mortality associated with obesity, the American Medical Association, the American Association of Clinical Endocrinologists, the FDA, and the World Health Organization have recognized obesity as a disease. This recognition is based on the criteria that it impairs the normal functioning of some aspects of the body, has characteristic signs or symptoms, and results in harm or morbidity.4-7 

Maintaining weight loss has been demonstrated to improve obesity-related comorbidities. The benefits of a 5% to 10% weight loss include reduction in risk of type 2 diabetes, reduction in cardiovascular risk factors, improvements in the blood lipid profile, and improvements in blood pressure.4

However, scientific evidence has shown that that physiological responses to intentional weight loss trigger weight regain. Weight loss in people with obesity causes changes in appetite hormones that actually increase hunger and the desire to eat for at least a one-year period following a reduction in weight. Hormones such as ghrelin, GLP-1, PYY, CCK, insulin, and leptin among others play an important role in appetite regulation. Long-term intervention is often required, and physician-initiated discussions can motivate patients to achieve significant and maintained weight loss.8-13  

Abbreviations: GLP-1: glucagon-like peptide-1; PYY: peptide tyrosine tyrosine; CCK: cholecystokinin

 

References

  1. National Heart, Lung, and Blood Institute. Assessing your weight and health risks. Available at: https://www.nhlbi.nih.gov/health/educational/lose_wt/risk.htm. Accessed May 2017.
  2. Prevalence of Obesity Among Adults and Youth: United States, 2011–2014. NCHS Data Brief, No. 219, November 2015.
  3. Managing Overweight and Obesity in Adults. Systematic Review From the Obesity Expert Panel, 2013. U.S. Department of Health and Human Services, National Institutes of Health, National Heart Lung and Blood Institutes.
  4. AMA. Is Obesity a Disease. 2013. https://www.ama-assn.org/sites/default/files/media-browser/public/about-ama/councils/Council%20Reports/council-on-science-public-health/a13csaph3.pdf. Accessed March 23, 2018.
  5. Mechanick et al. Endocr Pract. 2012;18:642–648.
  6. TOS Obesity as a Disease Writing Group. Obesity 2008;16:1161–77; 4. Available at: http://www.fda.gov/ohrms/dockets/98fr/010600a.txt.
  7. World Health Organization (WHO). Waist circumference and waist-hip ratio. 2008. Available at:
    http://apps.who.int/iris/bitstream/10665/44583/1/9789241501491_eng.pdf?ua=1.
  8. Sumithran P, Prendergast LA, Delbridge E, et al. Long-term persistence of hormonal adaptations to weight loss. N Engl J Med. 2011;365(17):1597-1604.
  9. Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes (Lond). 2010;34(suppl 1):S47-S55.
  10. Rosenbaum M, Kissileff HR, Mayer LE, Hirsch J, Leibel RL. Energy intake in weight-reduced humans. Brain Res. 2010;1350:95-102.
  11. Schwartz A, Doucet É. Relative changes in resting energy expenditure during weight loss: a systematic review. Obes Rev. 2010;11(7):531-547.
  12. Badman MK, Flier JS. The gut and energy balance: visceral allies in the obesity wars. Science. 2005;307(5717):1909-1914.
  13. Sumithran P, Proietto J. The defence of body weight: a physiological basis for weight regain after weight loss. Clin Sci (Lond). 2013;124(4):231-241.