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Why Is Obesity Considered a Disease?
Weight Loss

Why Is Obesity Considered a Disease?

In the United States, about 42% of all adults live with obesity, and two-thirds of U.S. adults meet the body mass index (BMI) criteria for overweight (>25 kg/m2) or obesity (>30 kg/m2).1,2 According to National Health and Nutrition Examination Survey (NHANES) data from 2017 to 2018, nearly 20% of U.S. children ages 2 to 19 have obesity.3

Until recently, clinicians were very limited in their options to treat this chronic disease. While surgical procedures to treat obesity have become safer, medical options were, until recently, scarce.

Obesity has many contributing causes, and it is a risk factor for over 200 other diseases, including cardiovascular disease, type 2 diabetes, fatty liver disease, sleep apnea, arthritis, depression, and certain types of cancer.4  

In 2013, the American Medical Association joined the World Health Organization, the American Association of Clinical Endocrinology,5 the U.S. Food and Drug Administration, and the U.S. National Institutes of Health and designated obesity as a disease after much discussion and debate, which opened the door for advancing evidence-based approaches to obesity treatment and prevention.6

What is obesity?

Obesity is a chronic disease that is diagnosed based on BMI. BMI measures your weight in relation to your height. It is a very imperfect measurement because it does not differentiate between lean body mass and body fat.

Many people fall into the range of overweight and obesity because they have increased muscle mass as a result of targeted exercises to increase muscle.

Obesity is a health risk because an excess accumulation of body fat increases your risk for other chronic diseases.

A doctor holding the word obesity

Why do people have obesity as a chronic disease?

Obesity is not just a result of overeating or a lack of willpower to control diet and exercise. Genetic predisposition, metabolic factors, living in an obesogenic environment, socioeconomic and sociocultural factors, individual behaviors, and lifestyle factors all affect whether a person is at an increased risk for obesity.

An excess of body fat can occur when calorie intake exceeds calorie expenditure. While, in simplest terms, obesity is described as an imbalance between calories in and calories out, it is not completely accurate to describe obesity in this way. This is referred to as the energy balance model.

Energy balance is controlled by a complex interaction between the brain, fat tissue, the gut, liver, pancreas, and other organs.7

If energy balance fully explains how calories are stored in your body, then you would lose one pound for every 3,500 kcal you burn over what you consume.8 Most people can attest that they have tried this and did not experience the steady weight loss they expected.

Adult body weight is remarkably stable, and there are complex physiologic mechanisms that conserve body fat and resist weight loss.8,9  However, it is important to note that body weight in the U.S. population has steadily increased since the 1960s. The average U.S. adult male has increased in weight from 165 pounds to 198 pounds.10

Genetic predisposition is also an important risk factor. A child with one parent who has obesity has a three-times higher risk of developing obesity as an adult. This increases to 10-fold when both parents have obesity.11

More research is needed to understand the pathophysiology of obesity. However, it is clear that once weight gain begins, your body works hard to resist attempts at weight loss.12

The words "obesity crisis"

What treatments are used to treat obesity?

Medications used to treat obesity are typically used in concert with lifestyle interventions, such as consuming a nutritious, reduced-calorie diet, managing stress, getting 7 to 9 hours of restful sleep each night, and incorporating movement throughout your day.


A meta-analysis of 14 popular dietary programs found that low-carbohydrate and low-fat diets had similar effects on weight loss (average 9 to 10 pounds over one year), with weight loss benefits diminishing after 12 months.13 Researchers found that with all specialized diets, including intermittent fasting options, there were initial weight loss benefits that diminished over time.14,15 The key to any diet is adherence, not the specific diet.16


Exercise reduces the risk of cardiovascular disease and improves overall health.17 Exercising regularly can help you lose body fat while retaining muscle mass, but exercise does not seem to prevent the slowly decreasing metabolic rate associated with weight loss.18

Weight loss is not typically commensurate with the number of calories burned with exercise. It is usually much less. Increased calorie consumption or decreased activity the rest of the day after exercising could both explain this. 19

It takes a lot of exercise to burn the calories consumed in a single meal. Most experts advise that diet has a much bigger impact on weight loss than exercise. You can’t exercise away the results of a poor diet.  


Prescription weight loss drugs are prescribed for weight management along with a reduced-calorie diet and increased physical activity for people with obesity (BMI ≥30 kg/m2) or overweight (BMI≥27 kg/m2) with at least one comorbid condition.

If you are not experiencing good weight loss results after using medication for three to four months, your doctor may consider an alternative medication or a dosage change.20


Orlistat is a selective pancreatic lipase inhibitor that decreases fat absorption by about 30%. Common side effects include decreased fat-soluble vitamin absorption, excessive gas, and a need to urgently have bowel movements. Mean weight loss when people take Orlistat is about 6.5 to 7.5 pounds per year, making it a less popular weight-loss treatment option.21,22


Combining an adrenergic agonist or stimulant (phentermine) and anti-seizure medication (topiramate) provides additional benefits for people with obesity and migraines. These medications combined have greater weight loss effects and fewer side effects than either one alone.7 

Phentermine/topiramate should not be used in people with uncontrolled high blood pressure, coronary artery (heart) disease, hyperthyroidism, glaucoma, or sensitivity to stimulants. Anyone who is pregnant or intends to become pregnant shouldn’t use the combination because it may cause congenital anomalies. An analysis of studies found an average weight loss of 14.5 to 19 pounds in one year.21,23


Bupropion/naltrexone (Contrave) combines a dopamine/norepinephrine reuptake inhibitor or antidepressant (bupropion) and an opioid receptor antagonist (naltrexone). It helps people resist cravings and food addictions. Do not use Bupropion/Naltrexone if you have uncontrolled high blood pressure, seizures, a history of eating disorders, or are withdrawing from drugs or alcohol. An analysis of studies found people taking bupropion/naltrexone experience an average weight loss of 10 pounds in a year.21


Liraglutide is a glucagon-like peptide 1 (GLP-1) receptor mimetic that is used to treat type 2 diabetes and obesity. By delaying stomach emptying, liraglutide helps you feel full longer. It may increase the risk of pancreatitis. An analysis of studies found that people taking liraglutide had an average weight loss of 12 pounds in one year.21


Like liraglutide, semaglutide is a glucagon-like peptide 1 (GLP-1) receptor mimetic that is used to treat type 2 diabetes and obesity. Semaglutide also delays stomach emptying and suppresses hunger. It may increase the risk of pancreatitis.

In three clinical trials, patients taking semaglutide attained a 15% to 18% weight loss over 68 weeks.24,25,26


Tirzepatide is used to treat type 2 diabetes and obesity. It is a glucagon-like peptide 1 (GLP-1) receptor agonist and a glucose-dependent insulinotropic polypeptide receptor agonist. In SURMOUNT 1, a 72-week phase 3 trial, people with obesity or overweight with a complication and without diabetes had a 15% to 21% weight loss over 72 weeks. The most common adverse events were gastrointestinal and occurred when the dose was increased.27 

Like other chronic diseases, such as high blood pressure, antiobesity medications should be continued as long as the benefits outweigh the risks.28 More clinical trials are needed to determine the ideal treatment length and dosage. Weight loss in the first three to four months of treatment is the best predictor of how well a weight-loss medication will work for you.29

A women with obesity talking with her doctor

Are most people receiving obesity treatment?

While obesity is a serious chronic disease, only a minority of people receive adequate treatment. In a study of nearly 15,000 people with obesity and nearly 2,800 healthcare providers, there was a lag of almost six years between when the patient met the criteria for having obesity and when their doctor first mentioned it.30

According to results from a large chart review, up to 90% of patients with obesity have not received a formal diagnosis, only half of patients who seek medical care for obesity receive a formal diagnosis,31 and only about one-fourth of patients will receive any follow-up care.32

Clinicians do not fully adopt weight-loss medication use. This is likely due to the significant side effects associated with previous generations of weight loss medications.33 Multiple studies have indicated that weight-loss medications are rarely prescribed to eligible patients.34,35

Invigor Medical offers a wide selection of prescription weight-loss medications. Talk to an Invigor Medical treatment specialist today to learn more about your options.

Get started today with a monthly subscription of Semaglutide.


While we strive to always provide accurate, current, and safe advice in all of our articles and guides, it’s important to stress that they are no substitute for medical advice from a doctor or healthcare provider. You should always consult a practicing professional who can diagnose your specific case. The content we’ve included in this guide is merely meant to be informational and does not constitute medical advice. 


1. The Organization for Economic Co-operation and Development. Obesity Update 2017.

2. Stierman B, Afful, J., Carroll, M. D., Chen, T.-C., Davy, O., Fink, S., Fryar, C. D. H., Gu, Q., Hales, C. M., Hughes, J. P., Ostchega, Y., Storandt, R. J., & Akinbami, L. J. National Health and Nutrition Examination Survey 2017–March 2020 Prepandemic Data  Files—Development of Files and Prevalence Estimates  for Selected Health Outcomes. Vol. 158. 2021.

3. Trust for America’s Health. The State of Obesity: Better Policies for a Healthier America. 2021:91.

4. Yuen M, Lui D, Kaplan L. A systematic review and evaluation of current evidence reveals 195 obesity-associated disorders (OBAD). Obesity Week. 2016

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11. Lin X, Li H. Obesity: Epidemiology, Pathophysiology, and Therapeutics. Review. Frontiers in Endocrinology. 2021 2021;12doi:10.3389/fendo.2021.706978

12. Albury C, Strain WD, Brocq SL, Logue J, Lloyd C, Tahrani A. The importance of language in engagement between healthcare professionals and people living with obesity: a joint consensus statement. Lancet Diabetes Endocrinol. May 2020;8(5):447-455. doi:10.1016/s2213-8587(20)30102-9

13. Ge L, Sadeghirad B, Ball GDC, et al. Comparison of dietary macronutrient patterns of 14 popular named dietary programmes for weight and cardiovascular risk factor reduction in adults: systematic review and network meta-analysis of randomised trials. Bmj. Apr 1 2020;369:m696. doi:10.1136/bmj.m696

14. Hajek P, Przulj D, Pesola F, et al. A randomised controlled trial of the 5:2 diet. PLOS ONE. 2021;16(11):e0258853. doi:10.1371/journal.pone.0258853

15. C, Roubal K, Veettil SK, et al. Intermittent Fasting and Obesity-Related Health Outcomes: An Umbrella Review of Meta-analyses of Randomized Clinical Trials. JAMA Netw Open. 2021;4(12):e2139558. doi:10.1001/jamanetworkopen.2021.39558

16. Bray GA, Heisel WE, Afshin A, et al. The Science of Obesity Management: An Endocrine Society Scientific Statement. Endocrine Reviews. 2018;39(2):79-132. doi:10.1210/er.2017-00253

17. Swift DL, McGee JE, Earnest CP, Carlisle E, Nygard M, Johannsen NM. The Effects of Exercise and Physical Activity on Weight Loss and Maintenance. Prog Cardiovasc Dis. 2018;61(2):206-213. doi:10.1016/j.pcad.2018.07.014

18. Johannsen DL, Knuth ND, Huizenga R, Rood JC, Ravussin E, Hall KD. Metabolic slowing with massive weight loss despite preservation of fat-free mass. J Clin Endocrinol Metab. 2012;97(7):2489-96. doi:10.1210/jc.2012-1444

19. Melanson EL, Keadle SK, Donnelly JE, Braun B, King NA. Resistance to exercise-induced weight loss: compensatory behavioral adaptations. Med Sci Sports Exerc. Aug 2013;45(8):1600-9. doi:10.1249/MSS.0b013e31828ba942

20. Gadde KM, Martin CK, Berthoud HR, Heymsfield SB. Obesity: Pathophysiology and Management. J Am Coll Cardiol. 2018;71(1):69-84. doi:10.1016/j.jacc.2017.11.011

21. Singh AK, Singh R. Pharmacotherapy in obesity: a systematic review and meta-analysis of randomized controlled trials of antiobesity drugs. Expert Review of Clinical Pharmacology. 2020 2020;13(1):53-64. doi:10.1080/17512433.2020.1698291

22. Srivastava G, Apovian CM. Current pharmacotherapy for obesity. Nature Reviews Endocrinology. 2018 2018;14(1):12-24. doi:10.1038/nrendo.2017.122

23. Apovian CM, Aronne LJ, Bessesen DH, et al. Pharmacological management of obesity: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. Feb 2015;100(2):342-62. doi:10.1210/jc.2014-3415

24. Rubino D, Abrahamsson N, Davies M, et al. Effect of Continued Weekly Subcutaneous Semaglutide vs Placebo on Weight Loss Maintenance in Adults With Overweight or Obesity: The STEP 4 Randomized Clinical Trial. JAMA. 2021;325(14):1414-1425. doi:10.1001/jama.2021.3224

25. Wadden TA, Bailey TS, Billings LK, et al. Effect of Subcutaneous Semaglutide vs Placebo as an Adjunct to Intensive Behavioral Therapy on Body Weight in Adults With Overweight or Obesity: The STEP 3 Randomized Clinical Trial. JAMA. 2021;325(14):1403-1413. doi:10.1001/jama.2021.1831

26. Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine. 2021 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183

27. Jastreboff AM, Aronne LJ, Ahmad NN, et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022 2022;387(3):205-216. doi:10.1056/NEJMoa2206038

28. Breton ER, Fuemmeler BF, Abroms LC. Weight loss—there is an app for that! But does it adhere to evidence-informed practices? Translational Behavioral Medicine. 2011;1(4):523-529. doi:10.1007/s13142-011-0076-5

29. Gadde KM, Pritham Raj Y. Pharmacotherapy of Obesity: Clinical Trials to Clinical Practice. Current Diabetes Reports. 2017 2017;17(5):34. doi:10.1007/s11892-017-0859-2

30. Caterson ID, Alfadda AA, Auerbach P, et al. Gaps to bridge: Misalignment between perception, reality and actions in obesity. Diabetes Obes Metab. Aug 2019;21(8):1914-1924. doi:10.1111/dom.13752

31. Crawford AG, Cote C, Couto J, et al. Prevalence of Obesity, Type II Diabetes Mellitus, Hyperlipidemia, and Hypertension in the United States: Findings from the GE Centricity Electronic Medical Record Database. Population Health Management. 2010 2010;13(3):151-161. doi:10.1089/pop.2009.0039

32. Kaplan LM, Golden A, Jinnett K, et al. Perceptions of Barriers to Effective Obesity Care: Results from the National ACTION Study. Obesity. 2018;26(1):61-69. doi:

33. Gribble FM, O’Rahilly S. Obesity therapeutics: The end of the beginning. Cell Metab. 2021;33(4):705-706. doi:10.1016/j.cmet.2021.03.012

34. Petrin C, Kahan S, Turner M, Gallagher C, Dietz WH. Current attitudes and practices of obesity counselling by health care providers. Obes Res Clin Pract. 2017;11(3):352-359. doi:10.1016/j.orcp.2016.08.005

35. Saxon DR, Iwamoto SJ, Mettenbrink CJ, et al. Antiobesity Medication Use in 2.2 Million Adults Across Eight Large Health Care Organizations: 2009-2015. Obesity (Silver Spring). Dec 2019;27(12):1975-1981. doi:10.1002/oby.22581

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Published: Aug 26, 2023


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