To T or Not To T: Should We Treat Low Testosterone in Men with Obesity?

Whether to treat low testosterone in men with obesity will be the topic of “Low Testosterone in Obesity: Should We Treat or Not?” a debate session at ENDO 2026 that is sure to be somewhat vigorous as two experts in the field take sides in a session moderated by Endocrine Society Past-President Stephen Hammes, MD, PhD.

The question might seem simple enough: Should we treat low testosterone in men with obesity? Yet the questions only accrue from here. The field remains divided not only on whether to treat it but also on how — and even on what to call it. This standoff is why an upcoming ENDO session in Chicago promises to be one of the meeting’s most spirited exchanges. On Sunday, June 14, two leading experts in andrology will face off in a structured debate, moderated by a physician who says he is “fortunate to know them personally” and anticipates a lively morning.

“They are both extremely intelligent and know their field well,” says moderator and Endocrine Society Past-President Stephen Hammes, MD, PhD. “They also have larger-than-life personalities that I think will lead to a fun and spirited debate.” Hammes is the Louis S. Wolk Distinguished Professor of Medicine, chief of the Division of Endocrinology, Diabetes and Metabolism, and executive vice-chair of the Department of Medicine at the University of Rochester, in New York. He has been attending the Endocrine Society meeting for over 20 years and has moderated many debate sessions.

“How do you even define low testosterone in individuals with obesity, who have physiologic reasons to explain some of the lab results? If you think testosterone is indeed low, do you give testosterone to everybody or just those who are symptomatic? Or do you focus on lifestyle changes or prescribe weight loss drugs? Ask five endocrinologists and you will get 10 answers.” — Stephen Hammes, MD, PhD, Louis S. Wolk Distinguished Professor of Medicine; chief, Division of Endocrinology, Diabetes, and Metabolism; executive vice-chair, Department of Medicine at the University of Rochester, Rochester, N.Y.

Franck Mauvais-Jarvis, MD, PhD, professor of medicine, Price-Goldsmith Professor of Nutrition, Tulane University School of Medicine, in New Orleans, La., argues for the treat side. David Handelsman, MBBS, PhD, FRACP, of the ANZAC Research Institute at the University of Sydney, in Australia, argues the opposite: don’t treat. The two have already engaged directly in print on this topic with an Approach to the Patient paper, a Letter to the Editor on that paper, and an author’s response to the letter published in the Journal of Clinical Endocrinology & Metabolism in the fall of 2025, and the live debate promises to be every bit as pointed.

What is the Controversy?

The “whether to treat” question raises questions of its own that the two debaters answer very differently: What is happening hormonally in a man with obesity and low testosterone? And is the relationship bidirectional (and if so, which direction carries the greater clinical weight)? The answers determine everything else.

For Handelsman, the phenomenon has both a name and a clear physiologic explanation. “Pseudohypogonadism describes the hormonal state of simple obesity — low testosterone proportionate to low serum sex hormone–binding globulin (SHBG) with normal serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH), verifying the eugonadal state,” he says. In other words, the hypothalamic–pituitary–testis (HPT) axis is functioning normally; the low testosterone reading is a downstream consequence of obesity-related SHBG suppression, not a sign of gonadal failure. “That must be distinguished from genuine pathologic hypogonadism, which usually warrants testosterone treatment,” says Handelsman.

Mauvais-Jarvis takes issue with this framing as well as the terminology. “Pseudohypogonadism is a concept that has no scientific foundation,” he says, preferring the term “testosterone deficiency (TD).” “I don’t use the term ‘hypogonadism’ because gonadal function involves sperm and T production, but in most patients, we don’t measure spermatogenesis, we measure T.”

“Misguided testosterone treatment often arises from inadequate patient evaluation by measuring serum testosterone in isolation on the erroneous belief that this can diagnose androgen deficiency. Such overprescribing of testosterone for obesity has been a major driver of excessive testosterone prescribing, which rose 100-fold over recent decades, without a single new approved indication.”  — David Handelsman, MBBS, PhD, FRACP, emeritus director, ANZAC Research Institute at the University of Sydney, Australia

He uses the framework of “functional” TD, a concept that acknowledges that some forms of TD are reversible, as opposed to organic hypogonadism due to structural abnormalities. He also pushes back on the implication that reversibility makes a condition benign. “In reality, ‘functional forms’ of TD caused by obesity or chronic disease are rarely reversible and represent over 95% of patients today.”

Hammes, true to his moderating role, frames the definitional problem as the very reason this debate is worth having. “How do you even define low testosterone in individuals with obesity, who have physiologic reasons to explain some of the lab results?” he asks. “If you think testosterone is indeed low, do you give testosterone to everybody or just those who are symptomatic? Or do you focus on lifestyle changes or prescribe weight loss drugs? Ask five endocrinologists and you will get 10 answers.”

What Does the Literature Tell Us?

The definitional divide is not merely semantic; it reflects a genuine divergence in how each side reads the evidence (or lack thereof).

“Using testosterone to treat obesity is widely practiced but lacks objective evidence of efficacy or safety, as well as being fundamentally mistaken in treating a symptom (low testosterone) rather than the underlying disease, if any (often none),” explains Handelsman. He points to what he sees as a diagnostic problem upstream: “Misguided testosterone treatment often arises from inadequate patient evaluation by measuring serum testosterone in isolation on the erroneous belief that this can diagnose androgen deficiency.” He also situates the debate within a broader pattern he has tracked across his career. “Such overprescribing of testosterone for obesity has been a major driver of excessive testosterone prescribing, which rose 100-fold over recent decades, without a single new approved indication.”

Mauvais-Jarvis takes a different view: “If you have to pick one marker that best summarizes the health status of a man, it’s T,” he says. “TD in men is not solely a problem of sexual dysfunction; it’s the best predictor of chronic disease, including metabolic syndrome, visceral obesity, type 2 diabetes, osteoporosis, anemia, depression, cognitive decline, cardiovascular disease, and overall mortality. In addition, it’s a cause of marital dysfunction and professional loss of productivity. It is a public health problem.”

His case for treatment draws on his clinical research into testosterone’s role in metabolic function as well as direct patient experience with treating hundreds of male veterans with TD.

Hammes, for his part, declines to adjudicate between the camps, at least in advance. “Overall, the level of evidence that treatment with testosterone helps patients with obesity-related low testosterone long-term is low but not zero,” he observes. “Then again, evidence that treatment with testosterone is harmful is also low. During this debate, we will hear about many of these studies.”

What’s a Clinician to Do?

The sharpest fault line between the two sides is whether low testosterone in men with obesity constitutes a condition that warrants treatment in its own right.

Handelsman’s position is categorical: “Valid testosterone treatment should be reserved for pathologic hypogonadism due to structural or genetic disorders of the HPT axis, not for reversible functional states (like obesity) accompanied by lowered serum testosterone.” For him, “the threshold for testosterone treatment is whether there is or is not pathologic hypogonadism, regardless of obesity status or testosterone level.”

He argues for treating what is actually wrong. “Serum testosterone is a dynamic hormone that is lowered by non-gonadal conditions like obesity and sleep apnea, for which there are better, effective treatments, rather than testosterone.”

Most patients with TD caused by obesity or chronic disease have a condition that is “rarely reversible,” counters Mauvais-Jarvis, and the treatment gap has real consequences for patients who are suffering now. His position is that testosterone therapy combined with a proper lifestyle program is the most effective approach, addressing both the hormonal deficiency and its metabolic context simultaneously.

Wondering what the harm would be in just going ahead and treating the low T? “‘Don’t treat’ obesity with testosterone because valid and established therapies can be used, whereas testosterone treatment of obesity is not effective and conveys undefined safety risks including accelerating cardiovascular and prostate disease as well as iatrogenic androgen dependence,” warns Handelsman.

“If you have to pick one marker that best summarizes the health status of a man, it’s T. TD in men is not solely a problem of sexual dysfunction; it’s the best predictor of chronic disease, including metabolic syndrome, visceral obesity, type 2 diabetes, osteoporosis, anemia, depression, cognitive decline, cardiovascular disease, and overall mortality. In addition, it’s a cause of marital dysfunction and professional loss of productivity. It is a public health problem.”   — Franck Mauvais-Jarvis, MD, PhD, Professor of Medicine, Price-Goldsmith Professor of Nutrition, Tulane University School of Medicine, New Orleans, La.

Hammes sees the treatment question as genuinely still open. “I think everybody focuses on weight loss as the best overall treatment,” he says, “but where people differ is in defining what it means to have a low testosterone in the setting of obesity, and then whether treatment with testosterone is appropriate or effective.” There are, he notes, few absolute contraindications — but also few absolute indications. “Our job as physicians is to mitigate these uncertainties as best we can for each individual patient and their unique situation.”

What Role Might GLP-1 RAs Play?

No discussion of obesity treatment in 2026 is complete without accounting for glucagon-like peptide 1 (GLP-1) receptor agonists, so what might these agents mean for the testosterone question?

On the “treat” side, Mauvais-Jarvis is skeptical: “GLP-1 RAs do not decrease body weight enough — approximately 10% — to improve TD in obese men with symptomatic TD.” He also raises a separate concern: “In addition, they cause a loss of lean mass that persists after discontinuation, although fat mass rebounds.” Thus, GLP-1 RA therapy may further complicate the metabolic picture.

Although Handelsman did not specifically address this issue, implicit in the “don’t treat” argument is that if effective weight loss is achieved, testosterone should organically normalize. However, the mechanism of weight loss (e.g., lifestyle changes, surgery, pharmacotherapy) might well have other known or as-yet unknown effects.

What Should Attendees Expect?

Handelsman is direct about his objectives: “My hope for this session is that it will reinforce the good practice that testosterone treatment should be used for pathologic disorders of the HPT axis and that testosterone treatment for obesity is futile and overlooks effective treatments with better defined efficacy and safety.”

Mauvais-Jarvis has a slightly different goal for attendees: “If they like boxing fights when one gets a knockout, they’ll enjoy,” he jokes. “Just kidding.”

For his part, Hammes is hoping for something the literature has not yet provided: A clear look at all the relevant evidence, argued by two people who know it better than almost anyone. “I would like to listen to these two very intelligent and experienced physicians discuss all points of view regarding low testosterone in obesity,” he says, “starting with the pathophysiology that leads to low testosterone, then discussing how we diagnose low testosterone in this population, and finally what options we have for treatment, along with the evidence to support these options.”

For any clinician who has ever faced a symptomatic, overweight patient with a low testosterone level and no clear roadmap for what to do next, which is to say, nearly all of them, the session should represent a long overdue conversation. “Right now, in my opinion, there is no specific standard of care for low testosterone in obesity,” Hammes says, “which is why this will be a wonderful debate as well as a great education session for the audience.”

As for his own position? Hammes, for now, is “doing a little sidestep,” in his words, but if the debate delivers what he’s hoping for, the audience will be able to draw their own conclusions about whether to T or not to T.

Horvath is a freelance writer based in Baltimore, Md., and a frequent contributor to Endocrine News. In the May issue, she wrote about two ENDO 2026 sessions: “Weight Loss: Friend or Foe for Bone & Muscle?” and “’Hot and Flashy’: Topics in Menopause.”