Maura Fox, DO 
2023 Namey/Burnett Preventive Medicine Writing Award Winner, First Place

Sponsored by the ACOFP Foundation, with winners selected by the ACOFP Health & Wellness Committee, the Namey/Burnett Preventive Medicine Writing Award honors the memory of Joseph J. Namey, DO, FACOFP, and John H. Burnett, DO, FACOFP—dedicated advocates for osteopathic medicine—and recognizes the best preventive medicine blog posts submitted by osteopathic family medicine students and residents.

Obesity is a worldwide problem that affects greater than 100 million Americans or 68.5% of the adult population. Obesity is defined as a BMI greater than or equal to 30 kg/m². Recent data from the US National Health and Nutrition Examination survey indicate that obesity affects around 35% of adult men and 40.4% of adult women in the US. Among the pediatric population aged 2-19 years old, the prevalence of obesity in 2011-2014 was 17%1. Obesity is linked to many chronic diseases, including but not limited to heart disease, cancer, and type 2 diabetes mellitus (T2DM). Obesity also increases vulnerability to mortality from other diseases, as we’ve seen in the COVID-19 pandemic.

Research has proven that there are genetic, environmental, and behavioral factors that influence the development of obesity – yet obesity is stigmatized in both the general public and among health professionals. Current evidence shows stigmatization of obese individuals poses risks to their psychological and physical health, generates health disparities, and interferes with implementation of effective obesity prevention efforts2. As family physicians, we have a unique opportunity to treat individuals with obesity as well as combat obesity’s associated stigma while working with both the pediatric and adult populations. It is time that we treat obesity as a chronic disease, and use the goal of weight loss as a prevention and treatment of complications to enhance health and mitigate morbidity and mortality3 .

Measuring Obesity

As obesity is classified through BMI, it is important to address limitations associated with this measurement. BMI is a measure of body weight adjusted for height and it is useful at a population-level. BMI is problematic as it is unable to distinguish weight associated with muscle versus fat. Measuring the fat distribution helps identify higher risk individuals as increased visceral fat predicts the development of metabolic syndrome, T2DM, etc., better than total body fat alone. Body fat scales can be expensive and have large interindividual variations, but measuring waist circumference is cost-effective and can be superior at detecting those with increased visceral fat. Utilizing waist circumference, in combination with BMI, can provide a way to incorporate weight distribution into measures of obesity, helping to better predict individuals with obesity who are most at risk for comorbid conditions4.

Increased Adiposity of Obesity

The excess of adipose tissue seen in obesity is problematic due to adipose tissue being a metabolically active organ. White adipose tissue releases inflammatory cytokines (termed adipokines) such as free fatty acids, TNF-alpha, and IL-6. These adipokines, as well as the macrophages that tend to infiltrate adipose cells, lead to inflammation, insulin resistance, hyperglycemia, and result in further endothelial dysfunction, atheroma formation, plaque, and thrombosis. Collectively these changes contribute to chronic low-grade systemic inflammation, metabolic syndrome, oxidative stress and endothelial function5. These processes ultimately culminate in insulin resistance, type 2 diabetes, hypertension, atherosclerosis which all constitutes metabolic syndrome6.Treating Obesity as a Complex Disease

Treating Obesity as a Complex Disease

There are a number of misconceptions regarding obesity among patients and providers alike: “obesity is not a disease”, “patients have the primary responsibility for the problem and for its treatment”, and “prevention is more important than treatment”4. Misconceptions are largely based on observational data, and trials that don’t isolate effects and therefore aren’t definitive. Media coverage about obesity is extensive, and promotes claims filled with circumstantial evidence7. Misconceptions fail to look at the complexity of obesity, and simplify it to an equation of energy in minus energy out. It’s a much more complicated equation than that. We must stop perceiving obesity as a side effect of our choices and discipline, and start classifying it as a disease, so we can successfully treat it and those who are affected by it.

Obesity is a disease of the energy balance, driven by dysregulated interactions involving satiety factors and the central nervous system resulting in increased caloric intake and an excess in adipose tissue. Simplified, energy balance consists of energy intake and energy expenditure. Energy intake is derived by eating, and energy expenditure consists not only of physical activity, but also of basal metabolism and adaptive thermogenesis8. Energy intake is impacted by hunger (orexigenic) and satiety (anorexigenic) hormones. Satiety hormones consist of GLP-1, leptin, CCK, PYY, 5-HT and the main hunger hormone is ghrelin (see Figure 1). These signaling hormones are part of the melanocortin pathway which play a key role in the development of obesity9. When an individual loses weight, by either decreasing calories or increasing activity, the body has a physiologic response that results in compensatory weight gain (see Figure 2). This response includes a decrease in metabolism, an increase in hunger hormones, and a decrease in satiety hormones. It is this physiologic response that can make weight loss, and maintenance of weight loss, extremely difficult.



Anti-obesity medications help offset the physiologic adaptations that resist weight loss and promote weight gain. Therapeutic agents target various components of the obesity signaling pathways. The first generation of anti-obesity medications that were FDA approved include orlistat, phentermine/topiramate ER, naltrexone ER/bupropion ER, and liraglutide 3 mg/day3 . Orlistat inhibits pancreatic lipase that reduces intestinal digestion of fat, but it has known and severe GI side effects including steatorrhea. Liraglutide is a GLP-1 agonist that extends the half-life of this hormone, from 1 to 2 minutes to 13 hours. It is contraindicated for those who have had pancreatitis or who have a family history of medullary thyroid carcinoma or MEN2. Phentermine/topiramate produces decreased appetite through phentermine’s action of increasing norepinephrine in the hypothalamus, and topiramate’s effect on GABA receptors. Phentermine is a sympathomimetic and long-term use in this class of drugs has unclear side effects, but generally recommended not to be given to individuals with a history of cardiovascular disease. Naltrexone/bupropion has satiety effects through bupropion action on adrenergic and dopaminergic receptors in the hypothalamus, and naltrexone’s action on the melanocortin receptor system. This combination medication can increase blood pressure, and further study is needed for examination of cardiovascular outcomes4. Surgical strategies for weight loss have evolved during the last 50 years. These procedures include sleeve gastrectomy, Roux-en-Y gastric bypass, laparoscopic adjustable gastric banding and others. Surgery has been shown to yield improvements in metabolic comorbidities like diabetes, hypertension, dyslipidemia, insulin resistance and inflammation – an effect not largely seen in the approved first generation medications. Surgery can also help slow the atherosclerotic process and reduce cardiovascular and all cause mortality10. Due to these benefits, some refer to weight loss surgery as “metabolic surgery.”

The first generation obesity medications fail to produce greater or equal to 10% of weight loss in the majority of patients. The American Association of Clinical Endocrinology obesity guidelines note that many complications of obesity require 10 to 20% weight loss to achieve therapeutic goals. The advent of second-generation obesity medications have proven to reach this goal percentage target and thus provide sufficient weight loss to ameliorate a broad range of complications4. Semaglutide 2.4 is a second generation medication with an average of 12.3% of weight loss. Semaglutide is a GLP-1 agonist in the same family as liraglutide. Terzepitide is a second generation medication that acts as a dual gastric inhibitory polypeptide (GIP) and GLP-1 receptor agonists that produce at least 10% of weight loss. Another class of medications, SGLT-2 inhibitors, were developed first for the management of blood sugar and diabetes. These medications act by inhibiting glucose intake in the kidney causing increased glucose excretion through the urine. These medications have proven to have weight loss benefits and be cardioprotective. The cardioprotective benefit is significant enough now that SGLT-2 inhibitors are part of goal-directed medical therapy in those with heart failure or at risk for heart failure. The second generation medications are exciting developments as the weight loss achieved is enough to treat or prevent sleep apnea, nonalcoholic fatty liver disease, type 2 diabetes mellitus, hypertension, cardiovascular disease risk, etc3 .


People-First and Obesity: A Disease

The future of obesity management is bright with these surgical and medical therapies on the horizon. In order to use them to their full potential, we must acknowledge that obesity is a complex disease, and stop the rhetoric of obesity simply being a side effect to our lack of discipline. Bias and obesity creates obstacles to quality patient care. Depending on the language practitioners use, this may influence how the patient feels about their condition and how likely they are to continue to seek medical care11. Using people-first language, addressing the person with a disease, rather than labeling them as their disease, is critical in order to combat weight stigma. If we continue to use stigmatizing language to describe people with obesity or refer to them as “the obese” we will only contribute to already pervasive weight bias in healthcare settings.

Disease stigma occurs when groups are blamed for their illnesses. If obesity was truly a matter of personal responsibility, as is the prevailing message in the media, there would not be the high rates of weight regain following weight loss despite maintenance of lifestyle changes. The blame on patients with obesity need to be replaced with messages that obesity is a chronic, complex disease and will likely be a lifelong condition–preventing weight regain is extremely challenging. Puhl and Heuer, completed a review of current evidence surrounding obesity stigma2. The paper states that obesity stigma is a social justice issue and priority for public health as stigmatization of obese individuals threatens health, generates health disparities, and interferes with effective obesity intervention efforts. At an individual level, the study shows patients experiencing stigma are more likely to engage in unhealthy eating behaviors and have lower levels of physical activity. It seems that supporting individuals with adaptive ways to cope with weight stigma, rather than using stigma as a perceived incentive to lose weight, can facilitate weight loss outcomes.

Weight Stigma

Unfortunately healthcare systems are a large source of weight stigma. Patients with obesity have reported feeling disrespected by providers, feel like they are not being taken seriously enough due to their weight, report that their weight is to blame for all other medical problems, and are reluctant to even address their weight concerns with their provider. A number of studies found that that obese persons are less likely to undergo age-appropriate preventative cancer screenings, an unfortunate side effect of stigma. There is substantial evidence that weight bias creates adverse outcomes for emotional functioning, personal relationships, educational attainment, employment and health care. cancer screenings. Puhl surmised that addressing the detrimental effects of weight stigma is essential to understand the cumulative impact of weight stigma on public health2. As obese individuals are at high risk for weight-related comorbidities, quality health care is essential. As physicians, we must do better.

The prevailing view that obesity is a choice that can be entirely reversed by voluntary decisions can exert negative influences on public health policy use, access to treatment, and research. A joint international consensus statement for ending the stigma of obesity was published in Nature Medicine in 2020. The goal was to review current literature and address the gap between stigmatizing narratives around obesity and current scientific knowledge regarding mechanisms of body weight regulation. This consensus statement is an attempt to best inform healthcare providers, policy makers, and the public about the stigma associated with obesity and came up with recommendations to eliminate weight bias12. This statement recognized the pervasive form of weight stigma in society, and commented that the idea that body weight is volitional is an unproven assumption that is inconsistent with current scientific evidence. Current evidence indeed demonstrates that body weight regulation is contributed by biological, genetic, and environmental factors. The bias and stigma associated with weight can result in discrimination, undermine human rights, social rights, and the health of affected individuals.

As family medicine physicians, we have an important role in treating those with obesity as well as combating the stigma against obesity. First, we must treat obesity as a disease, and recognize the complex interactions at play. This realization will help us better treat and manage this chronic disease. Second, we must treat obesity as we treat other chronic diseases if we hope to combat the comorbid conditions associated mortality with obesity. There are great therapies already FDA approved, and the research is growing. Understanding the complexity of obesity will help provide our patients with tools to achieve and/or maintain the weight loss needed to protect against comorbid conditions. Therapeutic agents are key to overcoming the physiologic adaptions that occur in weight loss. Last, we must use patient-first language and stop defining patients with obesity by their disease. We must make our healthcare settings a place where all patients feel safe, not where they feel stigmatized. We must provide the same healthcare to each individual, regardless of their BMI.


  1. National Center for Health Statistics (U.S.). (n.d.). National Health and Nutrition Examination Survey: analytic guidelines, 1999-2010.
  2. Puhl, R. M., & Heuer, C. A. (2010). Obesity Stigma: Important Considerations for Public Health. In Public Health (Vol. 100).
  3. Timothy Garvey, W. (2022). New Horizons. A New Paradigm for Treating to Target with Second-Generation Obesity Medications. In Journal of Clinical Endocrinology and Metabolism (Vol. 107, Issue 4, pp. E1339–E1347). Endocrine Society.
  4. Bray, G. A., Heisel, W. E., Afshin, A., Jensen, M. D., Dietz, W. H., Long, M., Kushner, R. F., Daniels, S. R., Wadden, T. A., Tsai, A. G., Hu, F. B., Jakicic, J. M., Ryan, D. H., Wolfe, B. M., & Inge, T. H. (2018). The science of obesity management: An endocrine society scientific statement. Endocrine Reviews, 39(2), 79–132.
  5. Andrade, F. B., Gualberto, A., Rezende, C., Percegoni, N., Gameiro, J., & Hottz, E. D. (2021). The Weight of Obesity in Immunity from Influenza to COVID-19. In Frontiers in Cellular and Infection Microbiology (Vol. 11). Frontiers Media S.A.
  6. Redinger Professor, R. (2007). The Pathophysiology of Obesity and Its Clinical Manifestations. In Gastroenterology & Hepatology (Vol. 3, Issue 11).
  7. Casazza, K., Fontaine, K. R., Astrup, A., Birch, L. L., Brown, A. W., Bohan Brown, M. M., Durant, N., Dutton, G., Foster, E. M., Heymsfield, S. B., McIver, K., Mehta, T., Menachemi, N., Newby, P. K., Pate, R., Rolls, B. J., Sen, B., Smith, D. L., Thomas, D. M., & Allison, D. B. (2013). Myths, Presumptions, and Facts about Obesity. New England Journal of Medicine, 368(5), 446–454.
  8. Spiegelman, B. M., & Flier, J. S. (2001). Obesity and the Regulation Review of Energy Balance. In Cell (Vol. 104).
  9. Wen, X., Zhang, B., Wu, B., Xiao, H., Li, Z., Li, R., Xu, X., & Li, T. (2022). Signaling pathways in obesity: mechanisms and therapeutic interventions. In Signal Transduction and Targeted Therapy (Vol. 7, Issue 1). Springer Nature.
  10. Iqbal Z, Adam S, Ho JH, et al. Metabolic and cardiovascular outcomes of bariatric surgery. Curr Opin Lipidol. 2020;31(4):246-256.
  11. Kyle, T. K., & Puhl, R. M. (2014). Putting people first in obesity. In Obesity (Vol. 22, Issue 5, p. 1211). Nature Publishing Group.
  12. Rubino, F., Puhl, R. M., Cummings, D. E., Eckel, R. H., Ryan, D. H., Mechanick, J. I., Nadglowski, J., Ramos Salas, X., Schauer, P. R., Twenefour, D., Apovian, C. M., Aronne, L. J., Batterham, R. L., Berthoud, H. R., Boza, C., Busetto, L., Dicker, D., de Groot, M., Eisenberg, D., … Dixon, J. B. (2020). Joint international consensus statement for ending stigma of obesity. Nature Medicine, 26(4), 485–497.

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