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Semaglutide increases the risk of erectile dysfunction in obese patients without diabetes
Last reviewed: 02.07.2025
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In a newly published study in IJIR: Your Sexual Medicine Journal, researchers assessed the risk of erectile dysfunction (ED) in obese, non-diabetic men following treatment with semaglutide.
Semaglutide use for weight loss in obese non-diabetic patients is associated with an increased risk of erectile dysfunction: the TriNetX database study.
What is Semaglutide? Semaglutide is an incretin mimicking drug that increases the release of insulin from the pancreas and is therefore used to treat type 2 diabetes (T2D) and obesity.
Semaglutide is currently considered one of the most effective treatments for obesity, with some scientists describing its approval by the U.S. Food and Drug Administration (FDA) as a "paradigm shift" in obesity treatment. In addition to its benefits for type 2 diabetes and obesity, semaglutide has been clinically shown to reduce the risk of cardiovascular disease, heart attack, and stroke in obese men and women.
Despite these benefits, semaglutide use has been associated with sexual dysfunction, particularly in non-diabetic men. However, more research is needed to determine the risk of this side effect in patients prescribed semaglutide.
With semaglutide becoming a popular weight loss drug, it is important to take a closer look at its known side effects.
In the current study, researchers assessed the risks of sexual dysfunction associated with semaglutide use in obese men without diabetes. Study participants were recruited from the TriNetX, LLC Research Network, which includes electronic health records, demographic data, and insurance claims for 118 million people from 81 healthcare organizations.
Inclusion criteria for the study were adult men aged 18 to 50 years with medically confirmed obesity, defined as a body mass index (BMI) greater than 30, and without a diagnosis of diabetes. Individuals with a clinical history of ED, penile surgery, or testosterone deficiency were excluded.
Data were collected between June 2021 and December 2023 and included participants' medical and demographic records. Participants were divided into semaglutide users and controls, with outcomes measured including a diagnosis of ED one month or more after semaglutide use or a new diagnosis of testosterone deficiency after taking the drug.
The present study was almost entirely statistical and all statistical analyses were performed using the TriNetX platform. Univariate analyses included chi-square and t-tests with differences between groups tested using proficiency scoring.
Adjustments were made for known risk factors for ED and testosterone deficiency, such as tobacco use, alcohol use, sleep apnea, hyperlipidemia, or hypertension. A smaller group of participants were matched to their closest demographic counterparts before analysis to improve comparisons between groups.
Participant screening yielded 3,094 individuals who met inclusion criteria, who were then matched with an equal number of controls. Participant demographics showed a mean age of 37.8 years in both groups, with 74% being white. The main medical difference between the groups was BMI: the mean BMI in the case group was 38.7 kg/m2, while in the control group it was 37.2 kg/m2.
Among participants prescribed semaglutide, 1.47% were diagnosed with ED or prescribed a phosphodiesterase 5 inhibitor (PDE5I), a class of drugs commonly used to treat ED. In comparison, 0.32% of patients in the control group were diagnosed with ED or prescribed a PDE5I. Additionally, 1.53% of cases were diagnosed with testosterone deficiency after semaglutide prescription, compared to 0.80% of men in the control group.
The present study highlights a significant increase in the risks of both ED and testosterone deficiency in men prescribed semaglutide. However, this increase was only 1.47%, which may be acceptable to most patients given the weight loss and cardiovascular health benefits associated with semaglutide treatment.
Semaglutide may interact with Leydig cells, which express the glucagon-like peptide-1 (GLP-1) receptor and regulate GLP-1 secretion. By stimulating GLP-1 receptors present in cavernous tissue, semaglutide treatment may reduce pulsatile testosterone secretion and increase smooth muscle relaxation.
Because there is little research on the sexual side effects of semaglutide, all current explanations are speculative and require further investigation in basic science research and clinical trials.