# The Impact of Commonly Used Medications on Erectile Dysfunction: Which Drugs Deserve Particular Attention?

## TL;DR

This paper reviews how common medications for chronic conditions can cause erectile dysfunction and highlights which drugs are most likely to contribute to this side effect.

## Contribution

The paper systematically evaluates drug classes and their mechanisms in causing erectile dysfunction, offering clinical guidance for minimizing sexual side effects.

## Key findings

- Antipsychotics and beta-blockers are strongly linked to erectile dysfunction through hormonal and vascular mechanisms.
- Opioids significantly impact sexual function by disrupting the hypothalamic-pituitary-gonadal axis.
- Renin-angiotensin system inhibitors and calcium channel blockers are associated with neutral or beneficial effects on erectile function.

## Abstract

Erectile dysfunction (ED) is a common but often underrecognized side effect of numerous medications prescribed for chronic conditions, particularly cardiovascular, psychiatric, and neurological disorders. This article reviews the impact of various drug classes on erectile function, focusing on mechanisms and clinical implications. Antipsychotics, widely used in schizophrenia, frequently cause ED through dopamine inhibition and increased prolactin levels, affecting libido and erectile capacity. Beta-blockers, especially older non-selective agents, contribute to ED by causing vascular constriction and hormonal alterations, while newer agents like nebivolol may improve erectile function via nitric oxide release. Diuretics, particularly thiazides, show mixed evidence regarding their effect on erectile function, though aldosterone receptor antagonists such as spironolactone are linked to antiandrogenic side effects. Centrally acting antihypertensives, antiepileptics, non-steroidal anti-inflammatory drugs (NSAIDs), lithium, and opioids also play significant roles in sexual dysfunction, primarily through hormonal disruption, vascular effects, and central nervous system pathways. Notably, opioids exert profound effects on the hypothalamic-pituitary-gonadal axis, leading to high rates of ED in younger men. In contrast, renin-angiotensin system inhibitors and calcium channel blockers generally exhibit neutral or beneficial effects on sexual function. Understanding these drug-related risks is crucial for clinicians to tailor therapies that minimize sexual side effects, thereby enhancing patient adherence and overall quality of life. Further research is warranted to clarify mechanisms and develop effective management strategies for medication-induced ED.