Obesity: New definitions and practical implications to know

Recently, The Lancet Diabetes & Endocrinology’s expert panel on obesity bifurcated obesity diagnoses into either clinical obesity or preclinical obesity.¹ The panel defined clinical obesity as a chronic disease with active organ or tissue dysfunction or as a functional limitation (inability to perform activities of daily living) caused by excess adiposity, whereas preclinical obesity is defined as having excess fat without current dysfunction but with high future risk. This framework shifts focus from simple body mass index (BMI) measurements to identifying when fat creates functional harm. Additionally, the framework is largely an effort to address the limitations of using BMI as the sole anthropometric measure for diagnosis, to distinguish between those with excess adiposity having either normal or demonstrably abnormal organ function, and to more explicitly target interventions for those at highest risk.

Unless BMI is equal to or greater than 40, the panel recommends a second anthropometric measure to first establish excess adiposity (obesity), such as waist to height ratio of more than 0.5, waist to hip ratio of more than 0.90 in men and 0.85 in women, waist circumference of more than 40 inches in men and more than 35 inches in women, or direct measurement (where available) of subcutaneous and abdominal/intrahepatic fat mass by CT, MRI, dual-energy x-ray absorptiometry, or hydrostatic weighing. Thus, for patients with BMI of less than 40, establishing obesity writ large requires a BMI of 30 or more plus at least 1 additional abnormal measure.

As for demonstrating organ/tissue dysfunction to establish clinical obesity, the panel includes 18 diagnoses for adults and 13 for children. These include hypertension, heart failure with preserved ejection fraction, atrial fibrillation, nonalcoholic fatty liver disease with fibrosis, obstructive apnea/hypopnea, microalbuminuria with reduced glomerular filtration rate (kidney disease), urinary incontinence, polycystic ovary syndrome, chronic/severe knee and hip pain, and the combination of hyperglycemia, elevated triglyceride level, and low level of high-density lipoprotein cholesterol (3 of the 5 criteria for metabolic syndrome [MS], the others being hypertension and abdominal obesity). Of note—and controversially—type 2 diabetes (T2D) is not recognized as a functional consequence of clinical obesity.

The Endocrine Society has criticized the Lancet commission’s framework for multiple reasons, including practical difficulty of proving that organ dysfunction is directly caused by excess fat, which could stall timely weight-management interventions; the exclusion of T2D from the list of obesity-induced organ dysfunctions; and the lack of standardization and accuracy among anthropometric measures of adiposity in most primary care settings.² Pointedly, they argue that routine assessment of organ dysfunction or functional limitations exceeds the capacity of most primary care settings and that because detailed diagnostic assessments are often unavailable in settings that serve low-income, rural, and racial and ethnic minority groups, these stringent criteria risk worsening existing health care disparities.

The lead author of the Lancet position statement responded to the Endocrine Society’s criticism about the exclusion of T2D with the following retort: “The suggestion that diabetes should be a criterion for diagnosing clinical obesity may be the paper’s (Muniyappa et al) most telling mistake. Diseases are defined to identify discrete entities. They do not incorporate other independent diseases as their own diagnostic criteria.”³

My personal view is that this is a distinction without a difference. Overweight and obesity are the single most important risk factors for T2D, despite myriad other genetic and environmental influences implicated in the pathogenesis of T2D. The components of MS are given a pass by the Lancet commission, though patients diagnosed with MS and obesity by 1 or more metrics will invariably be categorized as having clinical obesity.

Interestingly, vision loss at least partly attributable to excess body weight (the commission specifically cites increased intracranial pressure with vision loss) is another independent criterion cited by the Lancet commission as organ/tissue dysfunction constituting clinical obesity. It is certainly the case that many patients with excess body weight are diagnosed with weight-associated ocular diseases, but we cannot be certain that for any particular patient with any ocular diagnosis (including pseudotumor cerebri), obesity is the cause. This strikes me as a glaring logical inconsistency vis-à-vis the exclusion of T2D.

What strikes me as a positive development from this report is renewed discussion about the inadequacy of BMI in isolation as well as increased focus on helping those with existing organ dysfunction strongly associated with obesity (diabetes and prevention of obesity-associated complications notwithstanding). On a practical level, better assessment of excess adiposity and its complications allows clinicians to tailor individual therapies for specific patients, such as those proposed by the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease.⁴

These include individual comparison of patient metrics with geography/region-specific norms for both BMI and waist circumference (easy to measure and standardize in virtually every setting); a caloric deficit of 500 to 700 kcal per day utilizing plant-based, sustainable diets; 150 minutes/75 minutes weekly of moderate/vigorous physical activity; lipid/glycemia assays with consideration of echocardiogram; and use of incretin (glucagon-like peptide-1/glucose insulinotropuc peptide receptor agonists) for those at highest risk (heart failure or atherosclerotic cardiovascular disease). Of course, these recommendations do not expressly reduce health care disparities engendered by an economic system that prioritizes infinite accumulation of wealth and assets and corporate personhood over the needs of the population at large, but I will leave this for another column.

References

1. Rubino F, Cummings DE, Eckel RH, et al. Definition and diagnostic criteria of clinical obesity. Lancet Diabetes Endocrinol. 2025;13(3):221-262. doi:10.1016/S2213-8587(24)00316-4

2. Muniyappa R, Chukir T, Desai D, et al. Defining disease or delaying care? a conceptual and clinical appraisal of the Lancet obesity framework. J Clin Endocrinol Metab. 2026;111(6):1503-1512. doi:10.1210/clinem/dgag097

3. Mohta A. A proposed shift in how obesity is defined is creating tension in the medical community. MDLinx. May 4, 2026. Accessed May 7, 2026. https://www.mdlinx.com/article/a-proposed-shift-in-how-obesity-is-defined-is-creating-tension-in-the-medical-community/1hl84VnNUdOOCfEMIRzJQs

4. Zahid S, Peng AW, Razavi AC, Yao Z, Blumenthal RS, Blaha MJ. B is for body fat: a practical implementation of the new clinical obesity definition into preventive cardiology clinic. Am J Prev Cardiol. 2025;23:101281. doi:10.1016/j.ajpc.2025.101281