In a spirited session at Obesity Week 2025 in Atlanta, two experts took different views on the term “metabolically healthy obesity” (MHO) and whether it describes a scientific paradigm shift or a medical myth. 

Samuel Klein, MD, of Washington University, St. Louis, supported the concept. He acknowledged that the literature on MHO is limited, however, with more than 30 different definitions leading to “confusion and misinterpretation,” which he aimed to help set straight.

Eric Ravussin, PhD, of Pennington Biomedical Research Center in Baton Rouge, Louisiana, challenged the concept of MHO, although he started by acknowledging that it exists by changing his title slide from “Obesity is Never Healthy” to “Obesity Is ‘Rarely’ Healthy.”

The two debaters pointed to similar issues standing in the way of confirming the validity of MHO, including the lack of a standard definition, a strong potential for people to “transition” from MHO to metabolically unhealthy obesity (MUO), and the presence of nonmetabolic health conditions such as cancer or heart disease, which still raise health risks for those with purported MHO. 

While there was more agreement than disagreement in their presentations, both experts made compelling points with clinical implications

Klein’s position was that MHO is “real and good” — though probably not very common. MHO prevalence is difficult to assess because of varied definitions, he said. In addition, “the population being studied is a major factor, because women tend to be more metabolically healthy than men, and young people are more metabolically healthy than older people, and there are racial/ethnic differences, as well.”

These variables likely underlie the large variability in reported MHO, ranging from 6% to 60% of adults with obesity, depending on the study.

In most studies, said Klein, MHO has been defined as having two or fewer of five metabolic syndrome components, including high systolic and diastolic blood pressures, high plasma triglyceride concentration, low HDL-C concentration, high fasting blood glucose, and a large waist circumference. Consequently, people said to have MHO often are not truly healthy but simply have fewer cardiometabolic abnormalities than those classified as having MUO.

For example, “people could have type 2 diabetes according to some definitions and still have MHO as long as they didn’t have hypertension or dyslipidemia,” Klein explained. “But these people are not really metabolically healthy.”

Also problematic is that many people convert from MHO to MUO. “The stability of MHO is questionable in people who are not that healthy to begin with, such as those with two metabolic conditions,” said Klein. And MHO stability is likely affected by the normal decline in metabolic health associated with increasing age, problems from prolonged excess adiposity, and the tendency to gain weight throughout middle age. 

Data from longitudinal studies suggest that approximately 30%-50% of people with MHO convert to MUO after a median of 14 years of follow-up, he continued. 

“Major factors associated with the conversion of MHO to MUO are a decline in insulin sensitivity and an increase in fasting blood glucose,” he said. 

Although other factors also contribute to the conversion (eg, high BMI, more severe metabolic dysfunction, a poor lifestyle index), Klein said, “what’s really important is to look at [Homeostasis Model Assessment of Insulin Resistance] HOMA-IR, a crude measure of insulin sensitivity, because insulin resistance is the underlying pathology that’s responsible for the metabolic complications of obesity.”

Notably, he said “about 50% of people with obesity are metabolically healthy when healthy is defined as the absence of the metabolic syndrome, whereas only approximately 5% are metabolically healthy when healthy is defined as the absence of any metabolic syndrome components and normal insulin sensitivity, as assessed by HOMA-IR.”

Therefore, “understanding people who are not insulin-resistant is an important part of determining who’s really metabolically healthy or not,” he continued. “If we can understand why some people who are obese with excess adiposity are resistant to the adverse effects of that excess adiposity, we will understand a lot more about the pathogenesis of the metabolic complications of obesity.” 

Klein described a patient with a BMI of 38 who gained 32 kg (70 pounds) — 32% of her body weight — over 5 years, raising her BMI to 50. “That’s a huge amount of weight gain and body fat, but there was no change in her fasting glucose, her 2-hour glucose, her triglycerides, or her insulin sensitivity measured with the clamp procedure,” he said. 

“We don’t know what happens to a person like this long term, because these people have never been studied. But this small number of people are the ones who really are MHO,” he said. “Although there’s no evidence of what happens to them long term, in our hands, people like this with remarkable weight gain are still okay 5 years later.” 

There is heterogeneity not only in the relationship between adiposity and metabolic dysfunction but also in the response to weight loss, Klein added. “The same weight loss in one person might cause a very different response in terms of metabolic function than in another person,” he said.

To underscore this point, he noted that “after people lose 18% of their body weight through either diet or bariatric surgery, they improve their insulin sensitivity by about 75% on average in our hands. But there’s incredible heterogeneity, where some people don’t improve their insulin sensitivity at all and some have a dramatic improvement. And this is related to whether you have MHO to begin with or not.”

Insulin sensitivity improves very little with weight loss in people with a high baseline insulin-stimulated glucose rate of disposal. “If your insulin sensitivity is not broken, you don’t get a beneficial effect from losing weight,” he explained. “And this again supports the concept that some small subset of people are MHO.”

All that said, Klein reminded the audience that MHO looks only at obesity related to cardiometabolic disease, not conditions such as cancer, arthritis, or sleep apnea. “There are many other reasons to treat obesity, not just for metabolic complications.”

Ravussin acknowledged that he and Klein share many of the same concerns about MHO, the definition of which Ravussin said is “a mess.” He agreed that lack of a standard definition makes studies on epidemiology problematic, and that demographic modulators such as age, sex, and ethnicity need to be taken into consideration when assessing MHO. 

He also concurred that the woman Klein described, who gained a large amount of weight but remained metabolically healthy, truly had MHO, and that the probability of transitioning from MHO to MUO is strong.

That said, MHO remains rare. Ravussin pointed to a study from Israel and published in Biology with more than 15,000 participants entitled, “Metabolically healthy obesity is a misnomer: components of the metabolic syndrome linearly increase with BMI as a function of age and gender.” For that study, being classified with MHO required zero metabolic syndrome components, resulting in only a 7.5% prevalence of complete metabolic health among those with a BMI above 30 overall, declining to less than 1% when considering those with a BMI of 36.”

Similarly, he said, studies have confirmed that MHO declines steeply with age. “The clinical implication is that we should pay attention to and take care of people with MHO to help them avoid the progression and transition to MUO.”

Arguments against using MHO as a classification include lack of a clinical feasible definition and diagnostic; danger of false reassurance, since the person is still at risk; instability and poor prognostic value of MHO; and the masking of inherent adiposity-driven risks beyond hypertension and cardiovascular disease, Ravussin said.

Arguments in favor of an MHO classification include its potential utility in risk stratification to prioritize resources and interventions and the potential for insights into the biology that protects against adverse metabolic consequences — eg, genetic variants in which adiposity-increasing alleles were simultaneously associated with lower cardiometabolic risks.

All that said, Ravussin proposed that instead of using MHO, the field should “start from a solid foundation, such as ‘preclinical obesity,’ as defined by the Lancet Commission on Clinical Obesity.” Preclinical obesity is confirmed by excess body fat using two different methods, with no evidence of reduced organ or tissue function due to obesity; it is associated with a variable level of health risks, but no ongoing illness. 

In response to a question, Ravussin reiterated that being MHO, even with the strictest criteria, does not mean an individual is healthy obese. 

“MHO is purely related to cardiometabolic factors,” he said. “It doesn’t mean you shouldn’t treat the obesity itself. You won’t improve the metabolic outcomes, potentially, if an individual is considered MHO. But you can improve the other obesity-related conditions, as well as quality of life.”

Klein disclosed an advisor relationship with Altimmune, Boehringer Ingelheim, and Merck, and a consultant relationship with Alnylam. 

Ravussin disclosed and advisor relationship with Amgen; consultant relationships with AbbVie, Amway, CinFina Pharma, Biophytis, Boehringer Ingelheim, Lilly, Energesis, Generian, Kintai Therapeutics, Merck, Orbimed, PakHealth, Structure Therapeutics USA, Summit Clinical Research, and YSOPIA; and researcher relationships with Boehringer Ingelheim, Eli Lilly, Novo Nordisk, Novartis, and Sanofi-Avantis. 

Marilynn Larkin, MA, is an award-winning medical writer and editor whose work has appeared in numerous publications, including Medscape Medical News and its sister publication MDedge, The Lancet (where she was a contributing editor), and Reuters Health.