Semaglutide: separating myths from evidence

Everyone from endocrinologists to fitness bloggers is talking about semaglutide, and the number of myths surrounding it is growing faster than the number of studies. The editors checked the most popular claims for compliance with scientific data.

Where do myths come from

Semaglutide became the first drug for the treatment of obesity, which is widely talked about outside the medical environment. His name is heard on talk shows, fitness blogs and forums where "experience" is exchanged. In this information noise, it is easy to confuse the results of clinical studies with personal impressions and marketing.

Myths about semaglutide have two opposite poles. Some portray it as a magic pill that solves the problem of weight effortlessly and forever. Others are a dangerous poison that inevitably causes cancer, destroys muscles and "eats" the face. The truth, as always, is more complicated.

The editors selected the most common claims and verified them against data from randomised trials, official guidelines and regulatory assessments. We do not give advice on application - we only analyze what science knows.

Below is a brief table, followed by a detailed breakdown of each myth.

Myth 1-2: "it's insulin" and "it burns fat"

Semaglutide is not insulin. It is a synthetic analog of the GLP-1 hormone, which is naturally released by intestinal cells after eating. Its molecule has been modified so that it binds to albumin and is resistant to the DPP-4 enzyme, resulting in a half-life of about a week (Drucker, 2018).

The drug does increase insulin secretion, but only when the glucose level is elevated. Therefore, semaglutide itself rarely causes hypoglycaemia. The risk increases when combined with insulin or sulfonylurea derivatives.

The second myth is that semaglutide "burns" fat like thermogenics. In fact, the main mechanism of weight loss is to reduce food consumption. The drug acts on the appetite centres in the hypothalamus and brain stem, increases the feeling of satiety and reduces cravings for high-calorie food.

No significant direct impact on energy consumption was found in the studies. That is, a person loses weight not because "metabolism accelerates", but because he eats less. This fact is important: without reducing the caloric content of the diet, the drug does not work as a "fat burner".

Myth 3: "the effect is forever"

One of the most common expectations is to pass a "course" and keep the result. Research data suggests otherwise. In the STEP 4 study, participants first received semaglutide for 20 weeks, after which some were switched to placebo. In the placebo group, body weight began to return, while in the continuation group, it continued to decrease (Rubino et al., 2021).

Follow-up after the completion of STEP 1 showed a similar picture: a year after withdrawal, the participants regained a significant part of the lost weight, and cardiometabolic indicators also returned towards baseline.

This does not mean that the drug "doesn't work". Obesity is a chronic disease with powerful biological mechanisms that strive to regain lost weight. Semaglutide inhibits these mechanisms only as long as it is active.

Therefore, modern guidelines consider medical treatment of obesity as a long-term therapy, not a short course. The question of duration of treatment is decided by the doctor together with the patient.

Myth 4: "only muscles lose weight"

With any significant weight loss, a person loses not only fat, but also a part of fat-free mass - muscles, water, glycogen. This applies to diets, bariatric surgery, and medications. In the densitometry (DXA) STEP 1 substudy, most of the mass lost was from fat, but the proportion of lean mass was appreciable.

So, the statement "only muscles lose weight" is not true, but the problem should not be ignored either. For the elderly and people with sarcopenia, the loss of muscle mass has real clinical significance.

Lean mass according to DXA is not only skeletal muscles, but also water, organs, and connective tissue. Therefore, the direct identification of "fat-free mass = muscles" is a simplification. There are still few studies that precisely measure skeletal muscles and their function.

What helps to preserve muscles against the background of weight loss:

• strength training 2-3 times a week;
• adequate protein intake agreed with a doctor or nutritionist;
• gradual, not sharp reduction in calories;
• control of body composition, not just weight on scales.

Myths 5-6: Cancer, Ozempic Face, and Other Fears

Caution for medullary thyroid cancer is based on data from rodent studies. In humans, the causal relationship has not been proven, but it has not been definitively disproved, so the drug is contraindicated for people with a relevant family history or MEN2 syndrome. Correct wording: "the risk has not been established, therefore the precautionary principle applies."

"The face of Ozempic" is a media term, not a medical diagnosis. It is about the loss of subcutaneous fat on the face during rapid weight loss, which can make the skin flabby. This is a consequence of weight loss as such, and not a specific toxic effect of the drug.

Regarding mental health: The EMA Pharmacovigilance Committee in 2024 reviewed reports of suicidal ideation and found no evidence of a causal relationship with GLP-1 agonists. At the same time, monitoring of the mental state during treatment remains recommended.

There are also rare risks that regulators have recognized. For example, the EMA in 2025 included non-arteritic anterior ischemic optic neuropathy (NAION) as a very rare side effect of semaglutide. Pancreatitis and gallbladder disease are also described.

And finally, the myth that semaglutide is only good for weight. The SELECT trial showed a reduced risk of major cardiovascular events in obese individuals with established cardiovascular disease without diabetes (Lincoff et al., 2023). This is one of the strongest arguments in favor of the drug in medical indications.

Editorial conclusions

Semaglutide is neither a magic pill nor a poison. It is an effective prescription drug with proven benefit for people with obesity and type 2 diabetes and with a known risk profile.

The main realistic expectations: weight loss occurs due to a decrease in appetite, the result is maintained only with long-term therapy and lifestyle changes, and part of the lean mass can be preserved with strength training and sufficient protein.

Be critical of loud headlines in both directions and check whether the claim is supported by research data.

We also recommend the materials "Contraindications to semaglutide", "Tirzepatide: mechanism of action and effects on the body" and "Status of semaglutide in WADA".

List of used literature

1. Drucker DJ. Mechanisms of action and therapeutic application of glucagon-like peptide-1. Cell Metab. 2018;27(4):740–756.
2. Wilding JPH, Batterham RL, Calanna S, et al. Once-weekly semaglutide in adults with overweight or obesity (STEP 1). N Engl J Med. 2021;384(11):989–1002.
3. Rubino D, Abrahamsson N, Davies M, et al. Effect of continued weekly subcutaneous semaglutide vs placebo on weight loss maintenance in adults with overweight or obesity: the STEP 4 randomized clinical trial. JAMA. 2021;325(14):1414–1425.
4. Wilding JPH, Batterham RL, Davies M, et al. Weight regain and cardiometabolic effects after withdrawal of semaglutide: the STEP 1 trial extension. Diabetes Obes Metab. 2022;24(8):1553–1564.
5. Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes (SELECT). N Engl J Med. 2023;389(24):2221–2232.
6. U.S. Food and Drug Administration. Wegovy (semaglutide) injection: prescribing information. Silver Spring (MD): FDA.
7. European Medicines Agency. Ozempic (semaglutide): summary of product characteristics. Amsterdam: EMA.