Immunotherapy, a revolutionary cancer treatment that harnesses the body’s immune system to fight tumors, raises important questions about its effects on fertility. Understanding whether immunotherapy affects fertility involves looking at how these treatments interact with reproductive organs and functions in both men and women.
For men, current evidence suggests that immunotherapy, particularly immune checkpoint inhibitors (ICIs), tends to have a **modest impact on sperm production**. Studies involving men treated with ICIs for cancers like melanoma have shown a decrease in sperm output by about one-third, with sperm concentration also declining by roughly 30%. However, sperm motility and morphology—the shape and movement of sperm—generally remain unchanged. Hormonal levels related to testicular function, such as testosterone and luteinizing hormone, tend to stay stable, although there may be slight increases in follicle-stimulating hormone (FSH), which can indicate some testicular stress. Rarely, autoimmune orchitis, an inflammation of the testes caused by immune system activity, has been reported but is not common. Overall, these findings indicate that while immunotherapy can reduce sperm quantity somewhat, it does not typically cause severe or permanent damage to male fertility or hormonal balance.
In women, the picture is somewhat different and more complex. Unlike chemotherapy, which is well-known to reduce ovarian reserve and potentially cause premature menopause, immunotherapy’s direct effects on ovarian function appear to be minimal based on recent research. Experimental studies combining genetic data analysis and laboratory tests on ovarian follicles have found that PD-1 inhibitors, a common class of ICIs, do not harm follicle viability or disrupt hormone production such as estradiol. This suggests that immunotherapy does not directly damage the ovaries or their ability to produce eggs and hormones. However, because immunotherapy can trigger immune responses, there is a theoretical risk of autoimmune effects on ovarian tissue, but this has not been widely observed or confirmed in clinical settings.
Despite these reassuring findings, fertility preservation remains an important consideration for cancer patients of reproductive age who are about to start immunotherapy. For women, standard fertility preservation methods like egg or embryo freezing are recommended before treatment begins, especially since other cancer therapies often accompany immunotherapy and may impact fertility more severely. Additionally, medications such as GnRH agonists can be used to protect ovarian function during chemotherapy, though their role alongside immunotherapy is less clear. For men, sperm banking before treatment is a straightforward and effective option to safeguard future fertility.
Another important factor is the timing and prognosis of the patient. Many younger patients treated with immunotherapy have good long-term survival prospects, making fertility and family planning relevant concerns. Some surveys and clinical practices are beginning to address fertility counseling and preservation proactively in patients receiving ICIs, but standardized guidelines are still evolving.
In summary, immunotherapy, especially immune checkpoint inhibitors, generally has **minimal to modest effects on fertility**. In men, sperm production may decline somewhat but without major hormonal disruption. In women, ovarian function appears largely preserved, with no clear evidence of direct ovarian toxicity from immunotherapy alone. Nonetheless, because cancer treatment often involves multiple modalities and because individual responses vary, fertility preservation strategies remain a prudent part of care for patients planning future pregnancies. Ongoing research continues to clarify the long-term reproductive effects of immunotherapy and to optimize fertility management in cancer survivors.