Testosterone does not directly “cause” migraines in the way a trigger like red wine or bright light might, but its levels appear to strongly influence how vulnerable your brain is to migraine attacks. Research consistently points in one direction: higher testosterone is associated with fewer and less severe migraines, while lower testosterone tracks with increased susceptibility. The relationship helps explain why migraines strike women two to three times more often than men, and why testosterone therapy has shown early promise as a treatment in several small clinical studies.
Why Women Get Far More Migraines Than Men
The most obvious clue that sex hormones are involved in migraine is the sheer size of the gap between men and women. After puberty, migraine becomes roughly three to four times more common in women, with a global prevalence of about 21% in women compared to 10% in men.1PubMed Central. Sex and gender differences in migraines: a narrative review Women also report longer attacks, greater disability, and a longer recovery time.2PubMed. Sex differences in the epidemiology, clinical features, and pathophysiology of migraine Before puberty, the rates are roughly equal between boys and girls. The gap opens when sex hormone levels diverge in adolescence, peaks during the reproductive years, and narrows again after menopause. That pattern alone strongly suggests that estrogen and testosterone are not bystanders. The question is how each one contributes.
Estrogen has received the most research attention, partly because the menstrual cycle provides a natural experiment: many women experience migraines in the days surrounding their period, when estrogen drops sharply. But testosterone’s role, though less studied, is increasingly recognized as equally important. The two hormones appear to push in opposite directions, with estrogen fluctuations promoting migraine and testosterone providing a buffer against it.
What Testosterone Does Inside Pain-Sensing Neurons
Your trigeminal nerve is the main highway for head and face pain signals, and it turns out that its neurons are studded with androgen receptors, the docking stations testosterone uses to exert its effects. In mouse studies, roughly half of the neurons in the sensory ganglia (the clusters of nerve cell bodies) expressed androgen receptors, spanning small, medium, and large nerve fiber types.3PubMed Central. Androgen receptors expressed in the primary sensory neurons regulate mechanical pain sensitivity When researchers knocked out those receptors in male mice, the animals became significantly more sensitive to mechanical pain, behaving more like female mice in their pain thresholds. The greatest effect was seen in neurons that produce CGRP, a molecule you may recognize from migraine drug commercials. CGRP is a key driver of migraine attacks: it dilates blood vessels in the brain’s covering and triggers the inflammatory cascade that produces throbbing head pain.
Testosterone appears to dampen CGRP activity. Animal studies show that androgens reduce CGRP release from sensory neurons and boost the expression of µ-opioid receptors, your body’s built-in pain-relief system, in the trigeminal ganglion.4Neurobiology of Pain. The role of androgens in migraine pathophysiology In one experiment, a particular inflammatory pain pathway driven by IL-17A caused mechanical sensitivity only in female mice. Treating those females with testosterone blocked the sensitization entirely, while giving males an androgen receptor blocker made them vulnerable to it. The implication is that testosterone is not just passively absent in migraine-prone individuals; it actively suppresses the signaling pathways that produce migraine pain.
Cortical Spreading Depression and the Androgen Shield
Migraine with aura involves a wave of abnormal electrical activity that spreads across the brain’s cortex, called cortical spreading depression. This wave is thought to be the trigger for the visual disturbances and sensory changes many people experience before the headache phase. In mice genetically engineered to carry a human familial hemiplegic migraine mutation, researchers found that removing the testes (and thus the primary testosterone source) made these waves easier to trigger. Restoring testosterone with chronic replacement reversed the effect in a way that depended on androgen receptors, meaning it was a direct hormonal action, not a side effect.5PubMed Central. Androgenic suppression of spreading depression in familial hemiplegic migraine type 1 mutant mice
Testosterone’s metabolites add another layer. When testosterone is broken down in the body, some of its byproducts act on GABA receptors, the brain’s main inhibitory system, while others interact with estrogen receptors. Both of these downstream effects could help quiet the overexcitable neural circuits that set off cortical spreading depression.6Frontiers in Pain Research. Molecular mechanisms of hormones implicated in migraine and the translational implication for transgender patients So testosterone’s protective effect on migraine is not a single action at a single site. It works through multiple routes: calming pain-sensing neurons, reducing CGRP, dampening cortical spreading depression, and modulating the brain’s excitatory-inhibitory balance.
Men With Chronic Migraine Have Lower Testosterone
If testosterone protects against migraines, you would expect men who get frequent migraines to have lower levels. A small clinical study measured total testosterone in 14 men with chronic migraine (15 or more headache days per month) and compared them to published age-matched norms. The men with chronic migraine had a mean testosterone level of 322 ng/dL, compared to 384 ng/dL in the reference population, a statistically significant difference. Nearly half of the migraine patients, 43%, fell below the normal range entirely.7PubMed Central. Testosterone levels in men with chronic migraine
This is a small study and cannot prove that low testosterone caused the migraines rather than the other way around. Chronic pain itself can suppress testosterone production through the stress hormone axis, so there may be a vicious cycle at work. Still, the finding fits the broader pattern from animal research and from the epidemiological sex gap. It also raises a practical question for men who suffer from severe, frequent migraines: is it worth getting your testosterone checked? The evidence is not yet strong enough for major headache societies to recommend routine testing, but individual clinicians have begun considering it, especially in men who also have other symptoms of low testosterone like fatigue, reduced muscle mass, or low libido.
Does Testosterone Therapy Help Migraines?
Several clinical observations suggest it can, though the evidence is still preliminary. In a pilot study of 27 women with documented migraines, both pre- and post-menopausal, treatment with subcutaneous testosterone pellet implants led to a striking improvement. Ninety-two percent of the women reported reduced headache severity over a three-month period, and 74% reported no migraines at all during that window. The improvement was equally strong in the pre- and post-menopausal groups.8PubMed. Testosterone pellet implants and migraine headaches: a pilot study Those numbers are remarkable, but the study had no placebo control, and migraine is notoriously susceptible to placebo effects. Larger, controlled trials have not yet followed up.
Data from transgender individuals receiving gender-affirming hormone therapy provides a different angle. A case report of two transmasculine patients found that testosterone therapy reduced migraine frequency or intensity in both.9PubMed Central. Effect of testosterone therapy on migraine frequency and disability in two transgender patients: a case report A larger cross-sectional study of people undergoing hormone therapy for gender transition found that about 26% of testosterone users reported improvement or resolution of their headaches, while only about 8% of estrogen users did. Conversely, new or worsening headaches were far more common in estrogen users (67%) than in testosterone users (27%).10PubMed Central. Headache in individuals undergoing hormone therapy for gender transition: A cross-sectional, observational study These observations are consistent with the idea that raising testosterone helps and raising estrogen can hurt, though gender-affirming hormone therapy changes many hormones simultaneously, making it hard to isolate testosterone’s specific contribution.
Nobody should start testosterone therapy purely for migraines based on current evidence. The side effects of testosterone supplementation are real and include cardiovascular risks, mood changes, and fertility suppression. But for people already considering or receiving testosterone for other reasons, the potential migraine benefit is worth discussing with a doctor.
How Testosterone Affects Blood Vessels in the Brain
Migraine has long been linked to changes in cerebral blood vessel behavior, even though the older “vascular theory” of migraine as purely a blood vessel problem has been largely replaced by a more nuanced neural-vascular model. Testosterone has measurable effects on these vessels. In rat studies, physiological levels of circulating testosterone increased vascular tone in the middle cerebral arteries, the vessels that supply much of the brain. This appeared to happen through suppression of an endothelium-derived relaxing factor, meaning testosterone made the arteries less likely to dilate.11PubMed. Testosterone suppresses endothelium-dependent dilation of rat middle cerebral arteries
How this fits into migraine is not entirely straightforward. During a migraine attack, blood vessels in the brain’s coverings dilate partly in response to CGRP and other inflammatory signals. If testosterone keeps baseline vascular tone higher, it could make it harder for those vessels to swing into the dilated state that accompanies a migraine. This is speculative, and rat cerebral arteries are not identical to human ones, but it adds another plausible mechanism to the testosterone-migraine story.
Genetics, Estrogen Receptors, and Migraine Risk
The hormonal picture is complicated by genetics. A meta-analysis of sex hormone receptor gene variants found that certain polymorphisms in the estrogen receptor gene ESR-1 are associated with increased migraine risk. Two specific variants raised migraine risk by roughly 16% to 37%, with an even larger effect (40–60% increased risk) when the analysis was limited to migraine with aura or migraine without aura subtypes.12PubMed Central. Sex Hormone Receptor Gene Polymorphisms and Migraine: A Systematic Review and Meta-Analysis Interestingly, polymorphisms in the progesterone receptor gene did not show an association.
No comparable meta-analysis exists yet for androgen receptor gene variants and migraine, which is a gap in the literature. What the estrogen receptor genetics tell us is that the hormonal contribution to migraine is partly hardwired. Your genes determine how sensitive your brain tissue is to estrogen fluctuations, and by extension, how much protection testosterone’s counterbalancing effects can provide. Two people with the same testosterone level might have very different migraine susceptibilities depending on their estrogen receptor genetics. This helps explain why testosterone is not a simple on-off switch for migraines. It is one variable in a system with many moving parts.
PCOS and the Paradox of High Androgens in Women
If testosterone protects against migraines, you might expect women with polycystic ovary syndrome, who typically have elevated androgen levels, to have fewer migraines. The reality is more complex. PCOS is associated with a higher incidence of migraine, not a lower one. Emerging research points to shared pathophysiology between the two conditions involving specific signaling molecules, particularly pituitary adenylate cyclase-activating polypeptide and the kynurenine pathway, which may promote migraine through mechanisms that overwhelm any protective effect of the elevated testosterone.13PubMed Central. Exploring the Role of Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) and Kynurenine Pathway Dysregulation in Migraine Pathophysiology Among Women With Polycystic Ovary Syndrome (PCOS)
PCOS also involves insulin resistance, chronic low-grade inflammation, and disordered estrogen metabolism, all of which can independently contribute to migraine. The lesson here is that you cannot treat hormone levels in isolation. A woman with PCOS may have higher testosterone than average and still get more migraines because the metabolic and inflammatory environment of her condition creates its own migraine risk. Testosterone’s protective effect, in other words, can be swamped by other factors. This is one reason researchers are cautious about framing testosterone as a simple migraine remedy.
Cluster Headaches and the Testosterone Connection
Cluster headaches are not migraines, but they are the other major headache disorder where testosterone keeps coming up. Cluster headache is sometimes called the most painful condition known, producing excruciating unilateral attacks that arrive in bouts (clusters) lasting weeks to months. Unlike migraine, cluster headache is much more common in men, with a ratio of roughly three to one. Despite this male predominance, research has found that men in active cluster periods tend to have lower-than-normal testosterone levels alongside elevated cortisol and suppressed melatonin.14PubMed. Steroid hormones in cluster headaches
The hypothalamus, which regulates circadian rhythms and also governs hormone release, is thought to be a central player in cluster headache. The low testosterone seen during active clusters may reflect hypothalamic dysfunction rather than a direct cause-and-effect relationship, but it underscores a broader theme: disrupted testosterone signaling is a recurring feature across the most severe headache disorders, not just migraine. For cluster headache patients, testosterone replacement has not been studied as rigorously as for migraine, but the shared hormonal terrain suggests that future treatment research in one condition may inform the other.
Why Testosterone Is Not Yet a Standard Migraine Treatment
Given everything above, you might wonder why neurologists are not already prescribing testosterone for migraines. Several practical and scientific barriers stand in the way. First, most of the mechanistic evidence comes from animal models, and mouse neurobiology does not always translate cleanly to humans. The clinical data in humans, while encouraging, consists of small uncontrolled studies and observational reports. The 27-woman pilot study and the transgender case reports are hypothesis-generating, not proof. The field needs randomized, placebo-controlled trials, and these are expensive and slow to organize for a hormone with complex systemic effects.
Second, testosterone supplementation carries its own health risks. In women, exogenous testosterone can cause acne, hair growth in unwanted places, voice deepening, and disruption of menstrual cycles. In men, it can suppress sperm production and may carry cardiovascular risk, though the latter is debated. For a condition that is usually managed with targeted medications like triptans, CGRP-blocking antibodies, or preventive drugs like topiramate, the risk-benefit calculus of adding testosterone is unclear. The newer anti-CGRP drugs are, in a sense, already targeting one of the downstream mechanisms that testosterone modulates, potentially making testosterone supplementation redundant for some patients.
Third, the PCOS paradox illustrates that testosterone’s effects depend heavily on context. A hormone that helps in one metabolic environment might not help in another. Personalized approaches that consider a patient’s full hormonal profile, genetic background, and metabolic health would be necessary, and headache medicine is not yet set up to deliver that level of individualization routinely. The research is promising enough that testosterone is on the radar of headache specialists, but it remains an area where the science is ahead of clinical practice by a considerable margin.