Does the Thyroid Affect Testosterone Levels?

Thyroid hormones have a direct and measurable effect on testosterone levels in both men and women. An underactive thyroid tends to lower free testosterone, while an overactive thyroid raises total testosterone but paradoxically reduces the amount your body can actually use. These effects operate through at least two distinct pathways: the thyroid acts on the cells that manufacture testosterone, and it also changes how much testosterone floats freely in the bloodstream versus how much gets locked up by a binding protein made in the liver. The relationship runs deep enough that some endocrinologists now argue thyroid function should be checked routinely when testosterone levels come back low.

What Happens to Testosterone When the Thyroid Is Underactive

In hypothyroidism, free testosterone drops. This has been documented across multiple studies, and the mechanism is fairly straightforward: the thyroid hormone triiodothyronine (T3) plays a hands-on role inside the testicular cells that produce testosterone, known as Leydig cells. When thyroid output falls, those cells get less of the molecular signal they need to maintain normal steroid production.¹ Reassuringly, treating the hypothyroidism with levothyroxine tends to bring free testosterone back to normal without the need for separate testosterone therapy.

The cellular story backs this up. T3 stimulates a protein called StAR inside Leydig cells, which is essentially the gatekeeper that moves cholesterol into the part of the cell where it gets converted into steroid hormones, including testosterone. When T3 levels are adequate, StAR protein and steroid output rise together. When T3 is deficient, the whole production chain slows.² Lab studies on isolated Leydig cells show that T3 boosts baseline testosterone output in a dose-dependent way, confirming that the thyroid isn’t just a passive bystander in reproductive hormone regulation.³

The Overactive Thyroid Paradox

Hyperthyroidism creates a confusing hormonal picture. Total testosterone goes up, which sounds like it would be beneficial, but the amount of testosterone available to tissues actually goes down. The reason involves a protein called sex hormone-binding globulin, or SHBG. Excess thyroid hormone tells the liver to ramp up SHBG production. SHBG grabs onto testosterone in the bloodstream and holds it in a form that tissues cannot use. So even though there is more total testosterone circulating, the biologically active fraction shrinks.⁴

The liver mechanism is well characterized. Thyroid hormones increase SHBG production indirectly by boosting levels of a liver transcription factor called HNF-4alpha and by reducing certain fatty acid levels in liver cells, both of which drive more SHBG to be made and released into the blood.⁵ This means that in hyperthyroidism, a standard blood test showing “normal” or even “high” total testosterone can be misleading. If you only check total testosterone without also measuring SHBG or free testosterone, you could miss the fact that the person’s usable testosterone is actually low.

Treatment reverses this. When hyperthyroid patients are given antithyroid medication to bring their thyroid levels back to normal, SHBG concentrations drop and settle at levels comparable to healthy individuals.⁶ The take-home point: both too little and too much thyroid hormone hurt your effective testosterone levels, just through different mechanisms.

Subclinical Thyroid Problems Still Matter

You don’t need a full-blown thyroid disorder for your testosterone to be affected. Subclinical hypothyroidism is a condition where thyroid-stimulating hormone (TSH) is mildly elevated but actual thyroid hormone levels still fall within the lab reference range. Many doctors regard this as a gray zone that doesn’t always need treatment, but its effects on testosterone appear to be real. One study found that even this mild degree of thyroid underactivity was associated with lower serum testosterone and lower levels of progesterone, which is a precursor the body needs to make testosterone. The researchers suggested that testosterone drops in part because the raw material for making it becomes scarce.⁷

This finding has practical implications for men who present with low testosterone symptoms like fatigue, reduced libido, and depressed mood but whose TSH is only marginally high. If the thyroid issue gets dismissed as subclinical and not worth treating, the testosterone angle could be missed entirely. It also complicates the question of whether to start testosterone replacement, because if thyroid correction alone restores testosterone, the extra prescription is unnecessary.

Why Symptoms Get Confused

One reason the thyroid-testosterone connection often gets overlooked is that hypothyroidism and low testosterone share a long list of symptoms. Fatigue, weight gain, brain fog, low mood, reduced sex drive, and even erectile difficulties show up in both conditions. A man walking into a clinic with those complaints could have either problem, or both at the same time.

Erectile dysfunction offers a useful case study. Research on men with erectile problems found that about three in ten had subclinical hypothyroidism. Interestingly, though, total testosterone levels in those men were not significantly different from those in men with normal thyroid function who also had erectile difficulties.⁸ This suggests that in some cases the thyroid itself may be driving sexual symptoms through pathways that don’t run primarily through testosterone, like changes in smooth muscle function, nerve signaling, or prolactin levels. It also means you can’t always assume that a normal testosterone result rules out a thyroid contribution to these symptoms.

The overlap is one reason some clinical reviews recommend checking thyroid function as part of the workup for men being evaluated for hypogonadism. A separate review on testosterone replacement therapy made the point that hypogonadism can be associated with both pituitary and thyroid dysfunction, and that checking thyroid status can uncover causes of low testosterone that would otherwise be treated with lifelong hormone replacement rather than a simpler thyroid correction.⁹

The Connection in Women

Testosterone matters for women too, playing roles in libido, bone density, energy, and mood. The thyroid-testosterone link is not limited to men. Women with hypothyroidism have been found to have significantly lower testosterone compared to women with normal thyroid function.¹⁰ A 2024 genetic analysis went further and found evidence for a causal relationship between hypothyroidism and decreased total testosterone in women, along with a reduction in SHBG levels.¹¹

That second finding is particularly interesting because of where the researchers found testosterone sitting in the causal chain. They concluded that the drop in testosterone mediates part of the link between hypothyroidism and depression in women. In other words, the thyroid problem leads to lower testosterone, and the lower testosterone contributes to depressive symptoms. This suggests that in some women being treated for hypothyroidism, persistent mood issues could be related to incomplete recovery of testosterone levels even after thyroid hormones normalize.

One difference worth noting is that in women, the direction of the SHBG change in hypothyroidism appears to be a decrease, at least based on genetic evidence, which contrasts with the SHBG spike seen in hyperthyroidism. The net result is still lower effective testosterone, but the mechanics shift depending on whether the thyroid is running too fast or too slow.

How Thyroid Levels During Development Shape Adult Testosterone Capacity

The thyroid’s influence on testosterone isn’t limited to adulthood. Animal research shows that thyroid hormone levels during early life affect how the adult population of Leydig cells develops in the testes, essentially setting the ceiling for how much testosterone the body can produce later on.

In rats, inducing hypothyroidism during the neonatal period reduced the proportion of Leydig cells in the testes dramatically at early ages. The percentage of Leydig cells was roughly 80% lower at 12 days of age and about two-thirds lower at 16 days compared to controls. Injection of T3 during that same period affected both Sertoli cell development and the formation of the adult Leydig cell population.¹² A related study confirmed that thyroid hormone is crucial for the onset of adult Leydig cell differentiation and found that transient neonatal hypothyroidism, where the thyroid was suppressed temporarily and then allowed to recover, led to roughly double the normal number of adult Leydig cells later in life.¹³

These are animal findings and cannot be directly extrapolated to humans, but they point to a window in early development when thyroid status shapes the reproductive system in lasting ways. Congenital hypothyroidism is screened for at birth in most developed countries precisely because untreated thyroid deficiency in newborns leads to severe developmental problems. The Leydig cell data add reproductive capacity to the list of things that can go wrong if that early thyroid deficiency is missed or corrected too late.

The Broader Hormonal Axis

Thyroid hormones don’t just act locally on the testes and liver. They also influence the brain’s hormonal control center. The hypothalamus and pituitary gland regulate both thyroid function and reproductive function, and disruptions in one axis can ripple into the other. Research in rats has shown that both hypothyroidism and hyperthyroidism alter the dynamics of the entire hypothalamic-pituitary-gonadal axis, changing how much luteinizing hormone (LH) and follicle-stimulating hormone (FSH) the pituitary releases, which in turn affects how strongly the testes are stimulated to produce testosterone.¹⁴

This matters because it means the thyroid affects testosterone at multiple levels simultaneously: at the level of the brain signaling the testes to produce, at the level of the testes responding to that signal, and at the level of the liver determining how much of the resulting testosterone remains biologically active. A problem at any one level can lower effective testosterone, and thyroid dysfunction has the unusual property of being able to disrupt all three at once.

Radioactive Iodine Treatment and Testosterone

Men who undergo radioactive iodine therapy for thyroid cancer often worry about effects on their reproductive hormones. The available evidence is reassuring on the testosterone front, though less so for other aspects of fertility. A meta-analysis of studies looking at gonadal function after radioactive iodine found that testosterone levels were slightly higher after treatment, but the difference was not statistically significant.¹⁵ An earlier study in thyroid cancer patients also found that all patients maintained normal testosterone levels after radioactive iodine treatment.¹⁶

Sperm counts and other measures of semen quality are more vulnerable to radioactive iodine, particularly in the months immediately following treatment. But for men specifically concerned about testosterone, the evidence suggests that radioactive iodine at standard therapeutic doses does not meaningfully impair the Leydig cells’ ability to produce it.

When Testosterone Feeds Back on the Thyroid

The relationship between these two systems is not a one-way street. There is emerging evidence that testosterone itself can influence thyroid autoimmunity. A study of men with Hashimoto’s thyroiditis, the most common autoimmune thyroid condition, who also had low testosterone, found that testosterone replacement reduced the levels of thyroid antibodies, the markers of the immune system’s attack on the thyroid gland. Treatment also appeared to improve one measure of the thyroid’s ability to produce hormones.¹⁷

This finding is preliminary and comes from a single study, so it would be premature to frame testosterone as a treatment for thyroid autoimmunity. But it does suggest a bidirectional relationship where low testosterone could, in some men, worsen the autoimmune process that damages the thyroid, which in turn further depresses testosterone levels. Breaking that cycle at either point, whether by treating the thyroid or supplementing testosterone, might benefit the other. Autoimmune thyroid disease is far more common in women than men, but when it does occur in men with concurrent low testosterone, this interplay may be clinically relevant.

What to Do With This Information

If you are experiencing symptoms consistent with low testosterone, asking your doctor to check thyroid function along with your hormone levels is reasonable. A basic thyroid panel (TSH and free T4) is inexpensive and widely available, and it can reveal a treatable cause of hormone disruption that might otherwise lead to a premature prescription for testosterone replacement. For men already on testosterone therapy who are not responding as expected, undiagnosed thyroid dysfunction is worth investigating as a contributing factor.

If you have a known thyroid condition and are being treated for it, keep in mind that full normalization of testosterone may lag behind normalization of thyroid hormones. SHBG levels, in particular, can take weeks to adjust after thyroid treatment begins. Checking testosterone and SHBG after thyroid levels have been stable for a few months gives a more accurate picture than testing during the early adjustment phase.

For women with hypothyroidism who experience persistent fatigue, low mood, or reduced libido even after their TSH normalizes, the possibility that testosterone has not fully recovered is worth discussing with a clinician, especially given the emerging evidence linking thyroid-mediated testosterone drops to depressive symptoms. Testosterone testing in women remains underused and sometimes controversial, but the science increasingly supports its relevance in this context.