Hormone Replacement Therapy (HRT), Testosterone Pellets, and Hair Loss in Women
The review explains how hormone-sensitive follicles may respond differently to testosterone exposure.
William Gaunitz, WTSClinical Trichologist · Expert Reviewer
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The review explains how hormonal signaling can influence follicular growth and stability.
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Hormone Replacement Therapy (HRT), Testosterone Pellets, and Hair Loss in Women
Introduction
Testosterone therapy is increasingly being incorporated into hormone replacement strategies for women, particularly during perimenopause and menopause. In addition to traditional estrogen and progesterone therapy, some clinicians now prescribe testosterone, often delivered through creams, injections, or long-acting pellets, to address symptoms such as fatigue, low libido, and loss of muscle mass.
At the same time, trichology clinics are seeing a growing number of women reporting increased hair shedding or thinning after starting testosterone therapy, particularly with pellet-based delivery. This raises an important clinical question: does testosterone therapy cause hair loss, or does it accelerate androgen-sensitive thinning in individuals who are already predisposed?
Understanding how hair follicles respond to hormonal shifts is essential for answering this question and helping patients balance both hormonal health and hair health.
Hair Follicles Are Highly Hormone Sensitive
Hair follicles are among the most hormonally responsive structures in the body. Unlike many tissues that respond primarily to circulating hormone levels, hair follicles respond to local hormone signaling, receptor sensitivity, and enzyme activity within the follicular environment.
This helps explain why the same hormone can produce very different effects depending on the individual and the location of the follicle.
Several major hormone groups influence follicular behavior, including1:
- Androgens
- Estrogens
- Thyroid hormones
- Cortisol
- Insulin
These signals help regulate the duration of the anagen (growth) phase, the transition into telogen (resting), and the size and productivity of the follicle itself.
When hormone levels shift, whether due to natural aging, endocrine conditions, or hormone therapy, hair follicles are often among the first tissues to respond.
In women, testosterone is not an abnormal hormone. It is naturally produced in small amounts by the ovaries, adrenal glands, and through peripheral conversion of other steroid hormones2.
Under normal physiological conditions, testosterone plays roles in bone density, muscle maintenance, mood regulation, and libido3. What matters for hair biology is not simply the presence of testosterone, but how it is regulated, transported, and metabolized.
Androgens do not affect all hair follicles the same way. In some areas of the body, androgens stimulate hair growth, such as in the eyebrows, underarms, and facial hair. On the scalp, however, follicles along the frontal hairline, part line, and crown may be genetically sensitive to androgen signaling and respond with progressive thinning4.
Testosterone Pellets vs Other HRT Delivery Methods
An overlooked factor in how testosterone therapy may influence hair is the method of hormone delivery. Different delivery systems can produce very different hormone exposure patterns, which may influence how hair follicles respond.
Testosterone pellets, which are inserted subcutaneously and release hormone continuously over several months, have become particularly popular in some hormone optimization practices. These pellets offer convenience and eliminate the need for daily dosing. However, one important limitation is that once a pellet is inserted, the dose cannot be easily adjusted if side effects occur. Blood levels may also peak early after insertion before gradually declining, which can result in periods of relatively high androgen exposure5,6.
This limitation is one reason pellets are viewed differently from topical testosterone in many clinical guidelines. The Global Consensus Position Statement notes that its recommendations do not apply to injectables, pellets, or formulations that produce supraphysiologic testosterone concentrations; ISSWSH guidance similarly centers transdermal therapy for women with HSDD and recommends against routes likely to produce sustained supraphysiologic exposure. The American College of Obstetricians & Gynecologists (ACOG) has also emphasized the practical problem that pellets cannot be easily removed once inserted and recommends preparations other than pellet therapy when testosterone delivery is being considered7–9.
By comparison, other delivery methods such as topical creams or gels allow for much more flexibility. Dosing can be adjusted gradually, paused if needed, or discontinued quickly if symptoms such as hair shedding or acne develop10.
Similarly, injectable testosterone may produce peaks and troughs depending on dosing intervals, but dosing adjustments can still be made more easily than with pellets.
These differences matter because hair follicles often respond more strongly to peak androgen exposure and free hormone availability than to average hormone levels alone11. Rapid increases in circulating testosterone past physiologic female ranges can increase conversion to DHT in susceptible individuals.
Pharmacokinetic data helps explain why pellet-associated cases can look more dramatic in practice. In one study of subcutaneous testosterone implants in women, serum testosterone averaged 299.36 +/- 107.34 ng/dL four weeks after insertion and 171.43 +/- 73.01 ng/dL when symptoms returned, with substantial inter-individual variability. This means two patients can receive similar pellet dosing but experience very different androgen exposure. In a woman with low SHBG, insulin resistance, PCOS history, or strong follicular androgen sensitivity, that early high-exposure window may be enough to trigger both a diffuse telogen shed and acceleration of patterned miniaturization12.
None of these suggests that one delivery method is universally inappropriate. Rather, it highlights that delivery method, dosing strategy, and individual susceptibility all influence how hair follicles may respond to hormone therapy.
Importantly, testosterone therapy does not typically create androgenetic alopecia where it did not exist genetically. Instead, it accelerates the expression of underlying androgen sensitivity in individuals who are already predisposed. This distinction is critical because it reframes testosterone not as a direct cause of hair loss, but as a potential modifier of follicular signaling in susceptible patients8.
Why Some Women Lose Hair and Others Do Not
One of the most important clinical realities of testosterone therapy is that not all women experience hair changes, even at similar hormone levels. Some patients maintain stable hair density despite treatment, while others notice increased shedding or thinning within months.
One of the most important variables is genetic androgen sensitivity. Hair follicles differ in how strongly their androgen receptors respond to hormones like testosterone and DHT. Some women may have relatively resistant follicles, while others may have hypersensitive ones.
Another important factor is the activity of the enzyme 5-alpha reductase, which converts testosterone into DHT. Individuals with higher activity of this enzyme produce greater amounts of DHT locally, even when circulating testosterone levels are similar to those of other patients. Because DHT is the primary androgen involved in follicular miniaturization, local enzyme activity can significantly influence outcomes.
The balance of another enzyme, aromatase, may also play a role. Aromatase converts testosterone into estradiol, which can have protective effects on hair follicles13. Individuals with higher aromatase activity may partially buffer increases in testosterone by converting more of it into estrogen.
The balance between testosterone and estrogen is also important. Estrogen is generally considered supportive of hair growth because it helps prolong the anagen phase and supports follicular density. When testosterone levels increase without adequate estrogen balance, the relative reduction in estrogen signaling may remove some of this protective influence on the follicle14.
Levels of sex hormone–binding globulin (SHBG) also contribute to individual variability. SHBG binds circulating testosterone and limits the amount of free hormone available to tissues. Lower SHBG levels can result in higher levels of free testosterone reaching hair follicles, increasing the likelihood of androgen-related hair changes15.
Metabolic health is another often overlooked contributor. Insulin resistance can lower SHBG levels and increase androgen availability, while also promoting inflammatory signaling16.
Women with metabolic conditions such as polycystic ovary syndrome (PCOS) may already have underlying androgen sensitivity and may therefore be more vulnerable to changes in androgen exposure during testosterone therapy17.
Finally, systemic inflammation may influence how follicles respond to hormonal changes. Chronic low-grade inflammation can alter follicular signaling and may amplify the effects of androgen exposure in susceptible individuals.
Understanding this variability allows practitioners to move away from oversimplified conclusions and instead focus on individualized assessment when hair changes occur during hormone therapy.
Telogen Effluvium vs Androgenic Thinning
When hair changes occur after starting testosterone therapy, it is important to distinguish between telogen effluvium (TE) and androgenetic thinning, as these processes have different mechanisms and clinical implications.
Telogen effluvium may occur following hormonal shifts, dose adjustments, or metabolic adaptation to therapy. This typically presents as diffuse shedding across the scalp, often beginning 2–4 months after a hormonal change. TE is usually temporary and may stabilize once the body adjusts to the new hormonal environment18.
In contrast, androgen-related thinning tends to present more gradually and follows recognizable patterns, such as:
- Widening of the part line
- Reduced density at the crown
- Progressive miniaturization of hair
This reflects follicular sensitivity to androgen signaling rather than a temporary shift in the hair cycle19.
Differentiation is important, as TE often self-stabilizes, while androgen-sensitive thinning may require longer-term management strategies.
Clinical Patterns
In clinical practice, several patterns are commonly reported among women who begin testosterone therapy, particularly those using pellet-based delivery. Some patients report increased shedding within 3–6 months of starting therapy, consistent with hormonal adjustment–related telogen effluvium.
Others describe more gradual changes such as widening of the part, decreased density at the crown, or increased scalp oil production.
Clinically, pellet-associated hair loss can look more abrupt and emotionally distressing than the slower thinning seen with physiologic topical dosing. Patients may report handfuls of hair in the shower, rapid visible widening of the part, new thinning at the temples or crown, and a sudden loss of ponytail volume.
The same visit may reveal other androgen clues such as dermatitis rash, acne, increased oil production, unwanted facial hair, or new body hair20.
Patients may also notice increased facial or body hair alongside scalp thinning, reflecting the location-specific effects of androgen signaling.
Supporting Hair While on Testosterone Therapy
When hair changes occur during testosterone therapy, the goal is not necessarily to discontinue treatment, but to evaluate how hormonal balance and follicular health can be supported simultaneously.
When the patient is using pellets, documentation becomes especially important. Practitioners should record:
- Insertion date
- Dose if known
- Symptom timeline
- Onset of shedding
- Scalp pattern
- Acne/oil/facial hair changes
- Available labs for: total testosterone, free testosterone, DHT, estradiol, and SHBG.
This timeline helps the prescribing clinician understand why the reaction may be continuing even after the patient recognizes the problem, and it helps distinguish a temporary telogen effluvium event from androgen-driven miniaturization.
Dose Optimization
Hair follicles are particularly sensitive to androgen exposure, so ensuring that testosterone levels remain within appropriate physiologic ranges for women may help reduce the likelihood of androgen-driven follicular changes. This is particularly relevant with delivery systems that may produce higher or less adjustable hormone levels.
Estrogen Balance
Estrogen supports the duration of the hair growth phase and contributes to follicular stability. When testosterone is introduced without balancing the ratios, relative shifts in hormone balance may influence how follicles respond.
Nutritional Status
Hair follicles require adequate protein, iron, micronutrients, and essential fatty acids to maintain growth, particularly during periods of hormonal transition. Ensuring nutritional sufficiency may help improve follicular resilience and reduce the likelihood of excessive shedding.
Scalp Care
Maintaining scalp barrier health, addressing irritation, and reducing inflammatory triggers may help protect follicles that are already adapting to hormonal changes. Stabilizing the scalp environment before introducing additional interventions is often a prudent strategy.
Periodic Monitoring
Evaluating total and free testosterone, SHBG, and related hormone parameters may provide useful context when hair changes occur. Collaboration between trichologists and prescribing clinicians can help ensure that both systemic health goals and hair-related concerns are appropriately considered.
Taken together, these approaches reflect an important Advanced Trichology principle: when hair changes occur in the context of hormone therapy, the focus should be on optimizing the internal environment rather than assuming that therapy must be abandoned.
Conclusion
Testosterone therapy is becoming an increasingly common component of hormone replacement strategies for women, offering meaningful benefits for energy, metabolic health, and quality of life in appropriately selected patients. At the same time, androgen exposure has significant effects on hair follicles.
Current evidence and clinical observation suggest that testosterone therapy does not universally cause hair loss. However, it accelerates androgen-sensitive thinning in women who are already biologically predisposed, while others may experience no hair changes at all. This variability reflects the complex interplay between genetics, hormone metabolism, metabolic health, and inflammatory signaling.
For trichologists, this reinforces the importance of approaching hair loss during hormone therapy with nuance rather than oversimplification. Careful history taking, recognition of shedding patterns, and collaboration with prescribing clinicians can help ensure that both hormonal health and hair health are addressed together. In many cases, adjustments to dosing, monitoring, and supportive care may help stabilize the follicular environment without requiring discontinuation of therapy.
With a systems-based approach, it is often possible to support both endocrine health and long-term follicular stability.
References
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