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Reproductive Biomedicine
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Volume 24, Issue 9 (September 2026)
Int J Reprod BioMed. 2026, 24(9): 859-860 |
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Nasirian M. Can injectable glucose-lowering agents affect erectile function in men? A letter to the editor. , Int J Reprod BioMed.. 2026; 24 (9) :859-860
URL: http://ijrm.ir/article-1-3956-en.html
URL: http://ijrm.ir/article-1-3956-en.html
Department of Psychiatry, Research Center of Addiction and Behavioral Sciences, Non-Communicable Diseases Research Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. , nasirian90@gmail.com; m.nasirian@ssu.ac.ir
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Dear Editor
Erectile dysfunction (ED), one of the most common male sexual dysfunctions, is defined as the persistent inability to attain or maintain an erection sufficient for satisfactory sexual performance. Although it has historically been referred to as “impotence”, this term is now used less frequently because of its imprecision and negative connotations. ED may arise from psychogenic, organic, or mixed mechanisms (1-3).
ED has a substantial negative impact on men’s quality of life. It may reduce self-esteem and sexual confidence, contribute to avoidance of intimacy, and increase anxiety and depressive symptoms, all of which may further worsen sexual dysfunction. In addition, ED can adversely affect partner relationships, leading to sexual dissatisfaction and impaired psychological well-being within couples (1, 3).
The pathophysiology of ED is multifactorial and involves vascular insufficiency, impaired penile blood flow, endothelial dysfunction, oxidative stress, neurogenic disturbances, hormonal alterations, metabolic abnormalities, and psychogenic contributors. Lifestyle and behavioral factors such as smoking, alcohol use, sedentary habits, obesity, and chronic psychological stress may further increase vulnerability to ED and contribute to its persistence over time (2, 3).
ED frequently coexists with obesity, insulin resistance, hypertension, dyslipidemia, and other cardiovascular disorders, supporting the concept that erectile function is closely linked to systemic vascular and metabolic health. In this context, ED has also been recognized as a potential clinical marker of underlying vascular disease and future cardiovascular events (2).
In recent years, newer injectable glucose-lowering agents have gained increasing attention in the treatment of type 2 diabetes, obesity, and metabolic disorders. These therapies include glucagon-like peptide-1 (GLP-1) receptor agonists and dual incretin-based agents such as tirzepatide. Given their beneficial effects on body weight, glycemic control, insulin sensitivity, and several cardiometabolic parameters, an important question arises as to whether these medications may also influence male sexual function, particularly erectile function (4, 5).
This possibility is biologically plausible. Erectile function depends heavily on vascular integrity, endothelial health, metabolic balance, and hormonal regulation, all of which may be favorably influenced by GLP-1-based therapies. Improvements in obesity, insulin resistance, chronic inflammation, and endothelial dysfunction may theoretically translate into better erectile outcomes in some men (4, 5).
At present, however, the available evidence does not support a definitive conclusion. Some emerging data suggest that GLP-1-based therapies may improve erectile function through weight reduction, improved endothelial function, and broader cardiometabolic benefits (4, 5). Conversely, recent observational and pharmacovigilance findings have raised the possibility of an association between some of these agents and male sexual dysfunction, including ED. However, such findings do not establish causality and may be influenced by residual confounding, baseline disease burden, or concurrent comorbidities (6, 7). Therefore, the relationship between injectable glucose-lowering agents and erectile function may be heterogeneous and context-dependent rather than uniformly beneficial or harmful.
Given the expanding use of these medications among men of reproductive and sexually active age, their potential effects on sexual function deserve more focused investigation. Future studies should move beyond general metabolic outcomes and directly evaluate erectile function as a clinically meaningful endpoint. A clearer understanding of this issue would be valuable not only for sexual medicine but also for the broader delivery of comprehensive cardiometabolic care in men.
Acknowledgments
The author declares no financial, professional, or personal interests in any product, service, or company. I am solely responsible for the content and writing of the paper. I also acknowledge the assistance of AI (ChatGPT) utilized in this article for enhancing grammar and readability.
Conflict of Interest
The author declares that there is no conflict of interest.
Erectile dysfunction (ED), one of the most common male sexual dysfunctions, is defined as the persistent inability to attain or maintain an erection sufficient for satisfactory sexual performance. Although it has historically been referred to as “impotence”, this term is now used less frequently because of its imprecision and negative connotations. ED may arise from psychogenic, organic, or mixed mechanisms (1-3).
ED has a substantial negative impact on men’s quality of life. It may reduce self-esteem and sexual confidence, contribute to avoidance of intimacy, and increase anxiety and depressive symptoms, all of which may further worsen sexual dysfunction. In addition, ED can adversely affect partner relationships, leading to sexual dissatisfaction and impaired psychological well-being within couples (1, 3).
The pathophysiology of ED is multifactorial and involves vascular insufficiency, impaired penile blood flow, endothelial dysfunction, oxidative stress, neurogenic disturbances, hormonal alterations, metabolic abnormalities, and psychogenic contributors. Lifestyle and behavioral factors such as smoking, alcohol use, sedentary habits, obesity, and chronic psychological stress may further increase vulnerability to ED and contribute to its persistence over time (2, 3).
ED frequently coexists with obesity, insulin resistance, hypertension, dyslipidemia, and other cardiovascular disorders, supporting the concept that erectile function is closely linked to systemic vascular and metabolic health. In this context, ED has also been recognized as a potential clinical marker of underlying vascular disease and future cardiovascular events (2).
In recent years, newer injectable glucose-lowering agents have gained increasing attention in the treatment of type 2 diabetes, obesity, and metabolic disorders. These therapies include glucagon-like peptide-1 (GLP-1) receptor agonists and dual incretin-based agents such as tirzepatide. Given their beneficial effects on body weight, glycemic control, insulin sensitivity, and several cardiometabolic parameters, an important question arises as to whether these medications may also influence male sexual function, particularly erectile function (4, 5).
This possibility is biologically plausible. Erectile function depends heavily on vascular integrity, endothelial health, metabolic balance, and hormonal regulation, all of which may be favorably influenced by GLP-1-based therapies. Improvements in obesity, insulin resistance, chronic inflammation, and endothelial dysfunction may theoretically translate into better erectile outcomes in some men (4, 5).
At present, however, the available evidence does not support a definitive conclusion. Some emerging data suggest that GLP-1-based therapies may improve erectile function through weight reduction, improved endothelial function, and broader cardiometabolic benefits (4, 5). Conversely, recent observational and pharmacovigilance findings have raised the possibility of an association between some of these agents and male sexual dysfunction, including ED. However, such findings do not establish causality and may be influenced by residual confounding, baseline disease burden, or concurrent comorbidities (6, 7). Therefore, the relationship between injectable glucose-lowering agents and erectile function may be heterogeneous and context-dependent rather than uniformly beneficial or harmful.
Given the expanding use of these medications among men of reproductive and sexually active age, their potential effects on sexual function deserve more focused investigation. Future studies should move beyond general metabolic outcomes and directly evaluate erectile function as a clinically meaningful endpoint. A clearer understanding of this issue would be valuable not only for sexual medicine but also for the broader delivery of comprehensive cardiometabolic care in men.
Acknowledgments
The author declares no financial, professional, or personal interests in any product, service, or company. I am solely responsible for the content and writing of the paper. I also acknowledge the assistance of AI (ChatGPT) utilized in this article for enhancing grammar and readability.
Conflict of Interest
The author declares that there is no conflict of interest.
Type of Study: Letter to Editor |
Subject:
Reproductive Urology
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