Understanding Obesity and Diabetes

March 11, 2023

What Is Obesity?

Obesity is a chronic disease that is currently defined as a body mass index (BMI) greater than 30.¹ BMI is a system used to estimate body fat and compare weights independent of stature across a population. It is calculated by dividing body weight (kg) by the square of height (m²).

Classification	BMI (kg/m²)
Underweight	<18.5
Normal	18.5-24.9
Overweight	25.0-29.9
Obesity	30.0-39.9
Extreme Obesity	>40

What Is the Prevalence of Obesity?

According to the 2021 National Health and Nutrition Examination Survey, the prevalence of obesity among adults (age >20 years) in the U.S. was 41.9% between 2017-2020, increasing from a prevalence of 30.5% between 1999-2000.² Prevalence in children and adolescents (age 2-19 years) was 19.7%.

What Causes Obesity?

1) Lifestyle Causes – Lifestyle, behavioral, and environmental factors are key causes of obesity.³ Excess dietary consumption relative to energy expenditure is most commonly the direct cause. The promotion of processed and high caloric foods and the decrease in physical activity in the recent decades contribute to the obesity epidemic. Decreased quality or quantity of sleep (sometime caused by medical conditions such as obstructive sleep apnea) can also contribute to weight gain by promoting hormonal, metabolic, and behavioral disturbances.⁴

2) Genetic & Medical Causes – Underlying genetic factors, neuroendocrine causes, and other medical conditions such as Hypothyroidism, Cushing syndrome, polycystic ovarian syndrome, and male hypogonadism can also lead to weight gain.⁴ A small percentage of obesity is attributed to monogenetic disorders such as Prader-Willi syndrome, Bardet-Biedl syndrome, and Leptin receptor deficiency. A relatively sudden weight gain may suggest an underlying neuroendocrine condition.

3) Psychosocial Causes – Studies have shown that mental health and social networks may be linked to obesity.^3,4 Mental health disorders such as depression, anxiety, and binge-eating disorders are known to be associated with obesity. Stress can also increase appetite and cause individuals to seek comfort food, and the stigma associated with weight can lead to further stress and overeating, exacerbating weight gain.⁴ Research has also shown that individuals are more likely to become obese if they have close relationships with other who are obese (eg, spouses, siblings, friends).³

What Are the Health Effects of Obesity?

Globally, obesity is one of the leading causes of morbidity and mortality. ⁵ In 2015, 4.0 million deaths (7.2% of all-cause deaths) globally were attributed to excess weight. Obesity is known to be associated with dyslipidemia, coronary artery disease, diabetes, sleep apnea, liver disease, and certain types of cancers.⁶ The leading causes of BMI-related deaths were cardiovascular disease (CVD) and diabetes.

What Is the Link Between Obesity and Diabetes?

There is strong evidence suggesting that obesity is the greatest risk factor for developing prediabetes and type 2 diabetes mellitus (T2DM), with estimates that nearly 90% of T2DM can be attributed to obesity.⁷ Excess visceral and abdominal adiposity are associated with metabolic abnormalities linked with the development of T2DM such as insulin resistance, pancreatic b-cell dysfunction, and dyslipidemia.^8,9 Studies have consistently demonstrated abdominal obesity as being a major risk factor for CVD as well.^10,11

Both obesity and T2DM are associated with insulin resistance.¹² Increases in intra-abdominal fat mass can disrupt the release of hormonal factors that regulate metabolism.^7,12–14 It is postulated that increases in plasma free fatty acid (FFA) levels (from increased adiposity and dietary intake) encourage cellular uptake and utilization of lipids instead of glucose, leading to a persistent hyperglycemic state and insulin resistance. Additionally, abdominal adiposity is associated with greater insulin resistance than peripheral adiposity, as abdominal fat is more metabolically active and lipolytic, actively releasing FFAs into the bloodstream.

In response to insulin resistance and persistent hyperglycemia, the body increases both the function and mass of pancreatic b-cells to produce more insulin to control blood glucose levels. However, as insulin resistance exacerbates and chronic hyperglycemia, hyperlipidemia, and hyperinsulinemia persist, pancreatic b-cells undergo damage through various pathological processes.¹⁵ The resulted insulin resistance and impaired insulin secretion are key characteristics of T2DM.^15,16

What Should Obese Individuals With Diabetes Do?

The current guidelines by the American Diabetes Association (ADA) recommend that adults with prediabetes or T2DM who are overweight (BMI >25 kg/m²) or obese (BMI >30 kg/m²) to achieve and maintain a >5% weight loss.^17,18

1) Lifestyle Changes – The ADA emphasizes the importance of making significant lifestyle changes to achieve appropriate weight loss and glycemic control.¹⁹ Making dietary changes and engaging in physical activity to create a 500-700 kcal/day energy deficit are recommended. Modest and sustained weight loss in overweight or obese individuals with T2DM has shown to improve glycemic control, blood pressure, and lipid profile.

2) Pharmacotherapy & Surgery – Although individuals and their health care team should carefully consider the pros and cons of weight loss medications, pharmacotherapy may be effective as adjuncts to lifestyle changes in individuals with T2DM and BMI >27 kg/m².¹⁹ Additionally, metabolic surgery (also known as bariatric surgery, a procedure that makes modifications to the stomach or intestines with the goal of facilitating weight loss) may be considered in conjunction with lifestyle changes for adults with T2DM and BMI >40 kg/m² (BMI >37.5 kg/m² in Asian Americans) and with BMI >35.0-39.9 kg/m² (BMI >32.5-37.4 kg/m² in Asian Americans) without improvements in weight or comorbidities. Individuals who undergo surgical procedure should receive long-term support and monitoring of metabolic and nutritional status.

References:
1. Purnell JQ. Definitions, Classification, and Epidemiology of Obesity. In: Feingold KR, Anawalt B, Blackman MR, et al., eds. Endotext. MDText.com, Inc.; 2000. Accessed February 16, 2023. http://www.ncbi.nlm.nih.gov/books/NBK279167/
2. Stierman B, Afful J, Carroll MD, et al. National Health and Nutrition Examination Survey 2017–March 2020 Prepandemic Data Files Development of Files and Prevalence Estimates for Selected Health Outcomes. National Center for Health Statistics (U.S.), ed. National Health Statistics Reports. 2021;(158). https://stacks.cdc.gov/view/cdc/106273
3. Wright SM, Aronne LJ. Causes of Obesity. Abdom Radiol. 2012;37(5):730-732. doi:10.1007/s00261-012-9862-x
4. van der Valk ES, van den Akker ELT, Savas M, et al. A Comprehensive Diagnostic Approach to Detect Underlying Causes of Obesity in Adults. Obs Rev. 2019;20(6):795-804. doi:10.1111/obr.12836
5. Health Effects of Overweight and Obesity in 195 Countries over 25 Years. N Engl J Med. 2017;377(1):13-27. doi:10.1056/NEJMoa1614362
6. Mitchell N, Catenacci V, Wyatt HR, Hill JO. OBESITY: OVERVIEW OF AN EPIDEMIC. Psychiatr Clin North Am. 2011;34(4):717-732. doi:10.1016/j.psc.2011.08.005
7. Verma S, Hussain ME. Obesity and Diabetes: An Update. Diabetes Metab Syndr. 2017;11(1):73-79. doi:10.1016/j.dsx.2016.06.017
8. Magkos F, Fraterrigo G, Yoshino J, et al. Effects of Moderate and Subsequent Progressive Weight Loss on Metabolic Function and Adipose Tissue Biology in Humans With Obesity. Cell Metab. 2016;23(4):591-601. doi:10.1016/j.cmet.2016.02.005
9. Zheng Y, Ley SH, Hu FB. Global Aetiology and Epidemiology of Type 2 Diabetes Mellitus and Its Complications. Nat Rev Endocrinol. 2018;14(2):88-99. doi:10.1038/nrendo.2017.151
10. Paley CA, Johnson MI. Abdominal Obesity and Metabolic Syndrome: Exercise as Medicine? BMC Sports Sci Med Rehabilitation. 2018;10(1):7. doi:10.1186/s13102-018-0097-1
11. Pedersen BK, Saltin B. Exercise as Medicine – Evidence for Prescribing Exercise as Therapy in 26 Different Chronic Diseases. Scand J Med Sci Sports. 2015;25(S3):1-72. doi:10.1111/sms.12581
12. Kahn SE, Hull RL, Utzschneider KM. Mechanisms Linking Obesity to Insulin Resistance and Type 2 Diabetes. Nature. 2006;444(7121):840-846. doi:10.1038/nature05482
13. Rochlani Y, Pothineni NV, Kovelamudi S, Mehta JL. Metabolic Syndrome: Pathophysiology, Management, and Modulation by Natural Compounds. Ther Adv Cardiovasc Dis. 2017;11(8):215-225. doi:10.1177/1753944717711379
14. Han TS, Lean ME. A Clinical Perspective of Obesity, Metabolic Syndrome and Cardiovascular Disease. JRSM Cardiovasc Dis. 2016;5:2048004016633371. doi:10.1177/2048004016633371
15. Galicia-Garcia U, Benito-Vicente A, Jebari S, et al. Pathophysiology of Type 2 Diabetes Mellitus. Int J Mol Sci. 2020;21(17):6275. doi:10.3390/ijms21176275
16. Ke C, Narayan KMV, Chan JCN, Jha P, Shah BR. Pathophysiology, Phenotypes and Management of Type 2 Diabetes Mellitus in Indian and Chinese Populations. Nat Rev Endocrinol. 2022;18(7):413-432. doi:10.1038/s41574-022-00669-4
17. Standards of Medical Care in Diabetes—2016 Abridged for Primary Care Providers. Clin Diabetes. 2016;34(1):3-21. doi:10.2337/diaclin.34.1.3
18. American Diabetes Association. 5. Lifestyle Management: Standards of Medical Care in Diabetes—2019. Diabetes Care. 2018;42(Supplement_1):S46-S60. doi:10.2337/dc19-S005
19. American Diabetes Association Professional Practice Committee. 8. Obesity and Weight Management for the Prevention and Treatment of Type 2 Diabetes: Standards of Medical Care in Diabetes—2022. Diabetes Care. 2021;45(Supplement_1):S113-S124. doi:10.2337/dc22-S008

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