Does Radioactive Iodine Affect Fertility? Key Points to Consider

Radioactive iodine (RAI) is commonly used to treat hyperthyroidism and thyroid cancer, but its effects on fertility are a concern for many patients. Since the thyroid regulates metabolism and hormone balance, any disruption from RAI treatment could impact reproductive health.

Understanding how RAI interacts with the body helps clarify its potential effects on male and female fertility.

Mechanisms Of Radioactive Iodine In The Body

Radioactive iodine (RAI), primarily iodine-131 (I-131), is absorbed by thyroid tissue due to the gland’s natural affinity for iodine. Once administered, I-131 is taken up by thyroid follicular cells, where it emits beta and gamma radiation. The beta particles cause localized cellular damage, destroying thyroid tissue. This targeted effect makes RAI effective for treating hyperthyroidism and thyroid cancer by reducing hormone production or eliminating cancerous cells.

However, I-131 is also distributed systemically before being excreted, primarily through urine. Within 48 hours, approximately 80% of the administered dose is eliminated, but residual radiation exposure persists in various tissues, including the salivary glands, gastric mucosa, and reproductive organs. The extent of exposure depends on dosage, renal clearance, and individual iodine metabolism.

While gonads do not actively concentrate iodine, small amounts of circulating I-131 can reach the testes and ovaries. Research published in The Journal of Clinical Endocrinology & Metabolism has documented transient increases in gonadal radiation dose following high-dose RAI therapy, particularly in thyroid cancer patients. The biological effects vary, with some studies indicating temporary alterations in cellular function and others suggesting potential long-term effects depending on cumulative radiation exposure and individual susceptibility.

Thyroid Hormone Regulation And Fertility

Thyroid hormones, primarily thyroxine (T4) and triiodothyronine (T3), influence reproductive function by interacting with the hypothalamic-pituitary-gonadal (HPG) axis. Disruptions in thyroid function, whether from disease or RAI treatment, can alter the hormonal balance required for normal reproduction.

In women, thyroid hormones regulate gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus, influencing follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels. Disruptions in this signaling cascade can lead to menstrual irregularities, anovulation, or luteal phase defects. A study in The Journal of Clinical Endocrinology & Metabolism found that hypothyroid women experienced prolonged menstrual cycles and reduced luteal progesterone levels, impairing fertility. Hyperthyroidism, on the other hand, has been linked to shortened cycles and increased miscarriage risk due to altered endometrial receptivity.

In men, thyroid hormones influence spermatogenesis and testicular function by regulating testosterone synthesis and sperm maturation. Research from the American Society for Reproductive Medicine found that hyperthyroid men exhibited reduced sperm motility and increased oxidative stress in seminal plasma, while hypothyroid men had lower sperm concentration and abnormal morphology.

RAI therapy can induce transient or permanent hypothyroidism, depending on the dose and extent of thyroid tissue destruction. Patients often require thyroid hormone replacement therapy, but stabilizing hormone levels can take time. A longitudinal study in Thyroid found that women with poorly managed hypothyroidism post-RAI had lower conception rates than those maintaining stable thyroid hormone levels with levothyroxine.

Ovarian Function Changes

RAI therapy can affect ovarian function by exposing ovarian tissue to radiation, potentially influencing follicular dynamics and hormonal balance. While the ovaries do not concentrate iodine, circulating I-131 can reach ovarian tissue. The extent of exposure depends on dosage, iodine metabolism, and renal clearance. Higher cumulative doses, particularly for thyroid cancer treatment, may have a more pronounced effect.

One primary concern is the potential impact on ovarian reserve—the pool of viable oocytes available for future ovulation. Research indicates that high-dose RAI treatment may temporarily reduce anti-Müllerian hormone (AMH) levels, a biomarker of ovarian reserve. A study in Human Reproduction found that AMH levels declined in some patients post-RAI but often recovered within 12 months, suggesting short-term suppression rather than permanent damage, particularly in younger women.

Menstrual irregularities, including transient cycle disruptions or prolonged amenorrhea, have also been reported. These changes may result from direct radiation effects or secondary hormonal shifts due to thyroid dysfunction. Some patients experience delayed ovulation and luteal phase defects, affecting fertility in the months following treatment. While most menstrual cycles normalize within a year, women planning pregnancy soon after RAI therapy may need close monitoring.

Testicular Function Changes

RAI therapy raises concerns about testicular function due to potential radiation exposure to germ cells. While the testes do not accumulate iodine, small amounts of circulating I-131 can reach gonadal tissue. The degree of exposure depends on dosage, renal clearance, and individual metabolism. Spermatogenesis, a continuous and highly sensitive process, can be affected by radiation.

Some studies have documented temporary declines in sperm concentration, motility, and morphology following high-dose RAI therapy, particularly in thyroid cancer patients. These changes likely result from low-level radiation exposure affecting the seminiferous tubules. However, sperm parameters typically recover within 12 to 18 months post-treatment. For those planning conception, sperm banking before RAI therapy may be advisable, especially for higher cumulative doses.

Reproductive Hormone Dynamics

RAI therapy can influence reproductive hormone production and secretion, affecting fertility. While the thyroid does not directly regulate reproductive hormones, its disruption can create secondary hormonal imbalances.

In women, alterations in estrogen and progesterone levels often result from thyroid dysfunction. Hypothyroidism can disrupt GnRH pulsatility, leading to fluctuations in FSH and LH secretion. This may cause irregular ovulation, lower progesterone production, and potential delays in conception. Some patients report transient menstrual cycle changes, though these usually resolve with thyroid hormone replacement. Higher cumulative RAI doses may prolong hormonal imbalances, making close monitoring advisable for women planning pregnancy.

In men, temporary reductions in testosterone have been observed, likely due to mild testicular radiation exposure affecting Leydig cell function. This can lead to short-term declines in libido, energy levels, and spermatogenesis efficiency. However, testosterone levels generally return to baseline within months to a year. For men with prolonged hormonal disturbances, endocrinological evaluation may be necessary.

Given the potential for reproductive hormone fluctuations, both men and women undergoing RAI therapy should be aware of these effects when considering family planning.