Male and female pattern hair loss

SUMMARY

Androgenetic alopecia, commonly referred to as male or female pattern hair loss, is a prevalent condition encountered in clinical practice. It is important to identify potential underlying causes and differentiate it from other forms of hair loss, which may require referral to a dermatologist for management.

Pharmacological treatments for female pattern hair loss include minoxidil (topical and oral) and antiandrogens such as spironolactone. For male pattern hair loss, minoxidil and 5-alpha-reductase inhibitors (e.g. finasteride, dutasteride) can be used. Combination therapy is commonly employed, with clinical improvement typically requiring a minimum of 6 months. 

Supplements and other treatments have varying levels of evidence, and counselling is important to help patients make informed decisions about their management.

 

Introduction

Hair is deeply intertwined with a person’s identity. Hair loss therefore can have a profound psychological impact and induce feelings of low self-worth, lack of physical attractiveness and fear of social rejection.^1,2 Androgenetic alopecia (AGA), otherwise known as pattern hair loss, is the most common form of hair loss in both men and women. It is characterised by progressive hair thinning in a defined pattern that is genetically regulated, driven by sensitivity to androgens.¹ The primary androgen involved in AGA is dihydrotestosterone.

In brief, the hair cycle consists of 3 main phases: anagen (growth), catagen (transitional) and telogen (resting), with hair follicles cycling between these stages to produce and shed hair over time. In AGA, alterations in the hair cycle include shortening of anagen and lengthening of telogen, resulting in reduced hair growth.³ Subsequent miniaturisation of hairs results in conversion of mature thick terminal hairs into fine vellus hairs on the scalp. Together with a truncated hair growth cycle, this results in reduced hair density.^4,5

There are 2 forms of alopecia: scarring (where the follicles are permanently lost) and non-scarring. AGA is a non-scarring alopecia. As the follicular unit is preserved, AGA is considered at least partially reversible.^3-5 A full discussion of other forms of alopecia will not be covered in this article.

 

Presentations and causes of male and female pattern hair loss

The prevalence of AGA increases with age. Male pattern hair loss is thought to affect 80% of males by the age of 80.² Female pattern hair loss affects approximately 12% of women aged between 20 and 29 years to 40% of women by age 50.⁶

Both males and females with AGA report hair thinning. Female patients may report progressive hair shedding and loss of ponytail volume, and male patients may report hairline recession. A positive family history or a history of thyroid dysfunction may be present. There may also be an association with polycystic ovary syndrome.

The causes of hair loss are diverse and varied, although the distribution of hair loss observed can provide clues about potential triggers. Severe psychological stress, systemic illness, endocrinological abnormalities, nutritional deficiencies, infections and malignancy can all contribute to hair loss, and a detailed history and thorough clinical examination can help differentiate potential causes.^4,7,8 For example, the development of female pattern hair loss in men may indicate an underlying testosterone deficiency.⁹

Physical examination findings

On examination, in female pattern hair loss, there is diffuse hair thinning with the temporal and occipital scalp usually preserved. Widening of the central part with frontal accentuation (i.e. Christmas tree pattern) may be noted. In male pattern hair loss, there is usually bitemporal hairline recession with or without scalp vertex hair loss. Commonly used classification scales include the Norwood–Hamilton scale for male pattern hair loss, and the Ludwig scale and Sinclair scale for female pattern hair loss.¹⁰

The hair pull test and dermoscopy of the scalp (also known as trichoscopy) can assist in the clinical diagnosis of AGA. The hair pull test involves holding approximately 60 hairs between the index finger and thumb and pulling these hairs away from the vertex, parietal and occipital areas of the scalp. A positive hair pull test is defined when more than 2 hairs are removed from the scalp.¹¹ In AGA, the hair pull test is negative, unless other conditions are also present.

Trichoscopy of AGA demonstrates miniaturised hairs, with a reduction of hairs per follicular unit; the follicular openings (ostia) are preserved.

Scalp biopsies are not routinely performed; however, they may be used if there is diagnostic uncertainty.¹²

Differential diagnoses

There are multiple differentials for AGA. For example, telogen effluvium presents as abrupt hair loss following pregnancy or a severe psychological or physical stressor. The hair pull test is positive and empty follicles may be seen on trichoscopy. Alopecia areata presents as well-circumscribed patches of hair loss in adults or children; trichoscopy may reveal black dots and exclamation mark hairs. AGA can present simultaneously with other forms of hair loss, such as telogen effluvium. Referral to resources such as DermNet for photographs can aid in the diagnosis.

Symptoms such as scalp pain, itch or burning, extensive hair loss, or rapid hair loss in the absence of a preceding trigger, warrant urgent escalation of care to a dermatologist.

It is important that the primary care physician is able to identify scarring alopecias to allow early referral to a dermatologist for treatment, as these can lead to permanent hair loss.¹³ The key finding in scarring alopecia is the loss of follicular ostia which is best determined on trichoscopy. Scaling or folliculitis may also be present.

If hormonal abnormalities are suspected that cannot be managed in the primary care setting, general practitioners (GPs) may consider the involvement of an endocrinologist to optimise patient management.

 

Treatment of male and female pattern hair loss

As hair loss affects a person’s physical appearance, it is important that patients are counselled appropriately about treatment expectations, including the risks and benefits of treatments, so that they can make informed decisions about their management.

In most cases, treatments are not curative and are designed to slow progression of hair loss and stimulate hair growth. Concurrent conditions such as tinea capitis or seborrhoeic dermatitis must be addressed, and nutritional deficiencies such as iron deficiency, or metabolic disorders such as thyroid dysfunction, must be treated prior to starting treatment for hair loss.

Most pharmacological treatments take at least 6 months to show a response and may need to be continued long term. Referral to dermatologists may then be considered if there is no response to treatment after 6 months. Serial photography can assist with monitoring response to treatment. Nonpharmacological management should be encouraged, and this includes the use of healthy hair care practices, creative hair styling and the use of cosmetic camouflage (e.g. natural keratin fibres).^4,5,14-16 Because of increased scalp exposure, sun protection measures such as use of a broadbrim hat and sunscreen should be encouraged.⁵

Pharmacological treatments

Pharmacological treatments may stimulate hair growth and/or prevent further hair loss (Table 1). Treatment options for mild AGA can include initiation with monotherapy such as topical minoxidil, which can be obtained over the counter; however, pharmacists should encourage patients to see their medical practitioner to exclude scarring alopecias, correct any underlying nutritional and metabolic deficiencies, and access additional prescribed medications.

Table 1 Pharmacological treatments for male and female pattern hair loss

	Drug treatment	Dosage and administration	Mechanism of action	Adverse effects and precautions
Female pattern hair loss	Minoxidil	2% lotion: Apply approximately 1 mL to the scalp twice daily for 6 to 12 months and assess response. 5% foam/lotion: Apply approximately half a capful of foam (or 1 mL of lotion) to the scalp once daily for 6 to 12 months and assess response. Avoid application on forehead because of the risk of hypertrichosis. Sublingual or oral minoxidil 0.25 to 1 mg tablets (compounded): take orally once daily.	The mechanism of action of minoxidil is not fully understood. Minoxidil is a potent vasodilator thought to improve blood flow to the hair follicle, thereby promoting hair growth. Studies have shown variable hair density improvement with low-dose oral minoxidil, ranging from 12% at 24 weeks to much higher.17,18	Minoxidil is generally well tolerated and treatment is continued indefinitely. The main adverse effects reported are hypertrichosis, and allergic and irritant contact dermatitis.19 Many patients report reactive hair shedding for 2 to 3 months; however, this generally settles. The lotion contains propylene glycol, a preservative that can irritate the scalp, in which case the 5% foam may be better tolerated as it does not contain propylene glycol. If hypertrichosis is a concern, reducing to 2% may be considered.19 Sublingual or oral minoxidil may cause postural hypotension, fluid retention and hypertrichosis. Sublingual administration bypasses hepatic metabolism, increases bioavailability and may reduce the systemic effects of oral minoxidil. Avoid if there is a history of cardiac disease.
	Spironolactone	Generally started at 25 mg daily orally, and slowly up-titrated with renal function monitoring to a maximum dose of 100 mg daily.	Spironolactone is a mineralocorticoid receptor antagonist that has antiandrogenic properties. It prevents hair loss effectively in the majority of patients and results in hair growth that is generally noticeable after 6 months.20	As spironolactone is a potassium-sparing diuretic, hyperkalaemia is a serious adverse effect that has been noted, particularly in patients with renal insufficiency or congestive heart failure. Hypotension, increased urinary frequency, low energy and irregular menstruation are other potential adverse effects. It is contraindicated in pregnant women due to risk of feminisation of the male fetus. Contraception should be highly encouraged in women of childbearing potential and co-prescribed if possible.
Male pattern hair loss	Minoxidil	5% foam/lotion: Apply approximately half a capful of foam (or 1 mL of lotion) to the scalp twice daily for 6 to 12 months and assess response. Avoid application on forehead because of the risk of hypertrichosis. Sublingual or oral minoxidil 2.5 to 5 mg tablets (compounded): take orally once daily.	As above for female pattern hair loss	As above for female pattern hair loss
	5-alpha-reductase inhibitors (finasteride or dutasteride)	Finasteride: 1 mg orally once daily for at least 2 years Dutasteride: 0.5 mg orally once daily; used off label for hair loss [NB1]	5-alpha-reductase converts testosterone to dihydrotestosterone. Therefore, inhibition of 5-alpha-reductase prevents the formation of dihydrotestosterone, which improves hair growth and slows hair loss. Finasteride inhibits the type II isoform of 5-alpha-reductase while dutasteride inhibits type I and type II.	Adverse effects mainly relate to sexual dysfunction (e.g. erectile dysfunction, low libido, anorgasmia), gynaecomastia and lower blood pressure. These rarely persist and are generally reversible with discontinuation of the medication. 5-alpha-reductase inhibitors can reduce prostate serum antigen (PSA) concentrations by up to 50%;21 therefore, PSA concentrations require adjustment to obtain the ‘true’ PSA concentration.
NB1: Dutasteride is approved by the Therapeutic Goods Administration (Australia) for the treatment of benign prostatic hyperplasia.

Combination therapy (e.g. with antiandrogens) is more effective than monotherapy at minimising hair loss and may be considered for those with moderate to severe AGA. In female pattern hair loss, antiandrogen therapy may be considered particularly in those with signs of hyperandrogenism (e.g. hirsutism, acne).

For female pattern hair loss, introductory treatment regimens can include:

• topical minoxidil (2 to 5%) with oral spironolactone 25 to 50 mg
• oral minoxidil (compounded into 0.25 mg tablets) with oral spironolactone 25 to 50 mg²⁰
• sublingual or oral minoxidil 0.25 to 1 mg with oral spironolactone 25 to 50 mg and oral finasteride 1 mg in postmenopausal women.²²

Co-prescription of contraception with spironolactone is strongly encouraged (see Table 1).

5-alpha-reductase inhibitors can be used off label in postmenopausal women; however, evidence for its use is limited. This treatment is generally not recommended in premenopausal women due to the risk of feminisation of the male fetus.

For male pattern hair loss, introductory treatment regimens can include:

• topical minoxidil 5% with oral finasteride 0.5 to 1 mg
• sublingual or oral minoxidil (compounded into 2.5 to 5 mg tablets) with oral finasteride 1 mg.

Topical finasteride (0.1 to 0.25% solution or lotion, used once or twice daily) is being investigated as a treatment for AGA. In a phase 3 randomised controlled trial, the efficacy of topical finasteride 0.25% spray was compared with oral finasteride 1 mg as well as placebo. Although there was a significant improvement in target area hair count with topical finasteride compared with placebo, no difference in hair diameter was noted.²³ The safety profile of topicalfinasteride has been generally reassuring;²³ however, a recent alert from the US Food and Drug Administration highlighted rare adverse effects similar to those reported with oral finasteride including erectile dysfunction, anxiety and depression, which persisted after discontinuation of the topical medication.²⁴

Generally, treatment is continued according to patient preference and tolerance of medications. Stopping treatment leads to progression of AGA.

Supplements

Nutritional supplements such as zinc, vitamins B and D, and antioxidants have been used extensively for hair loss; however, evidence for their efficacy is highly variable.²⁵ Pumpkin seed oil and saw palmetto are used by patients to treat hair loss and are reported to exhibit antiandrogenic properties.²⁶ In a head-to-head open-label study comparing oral finasteride with saw palmetto, finasteride was shown to be superior, with 68% of patients treated with finasteride showing increased hair growth compared with 38% treated with saw palmetto.²⁷

It is essential that clinicians appropriately counsel patients as the benefits of nutritional interventions are unknown, their use may be expensive and lead to toxic effects at high doses, and they can interact with medications and test results, particularly biotin.^25,26

Other treatment options

There are several other treatment options that all have limited evidence.

Mesotherapy involves the intradermal injection of therapeutic agents and bioactive substances.²⁸ Various therapeutic agents, including dutasteride, botulinum toxin A, minoxidil and stem cells, have been administered via intradermal injections to the scalp and synergistic responses have been reported;²⁸ however, further research is required to determine the efficacy and safety of this treatment.

The use of platelet-rich plasma has been proposed for many dermatological disorders given its anti-inflammatory and regenerative properties through angiogenesis, cell differentiation and proliferation.²⁹ Although not completely understood, platelet-rich plasma is believed to have a therapeutic effect on hair loss through alpha granule activation and release of growth factors that bind to receptors on stem cells in the bulge area of the hair follicle. This results in follicular proliferation, differentiation, and a prolonged anagen phase of the hair cycle.^29,30

Low-level laser therapy devices emit low-power coherent monochromatic red light that has been shown to promote hair growth as a result of increased blood flow to the hair follicle.^31-33 Low-level laser therapy is typically administered through home‐use devices that are available in the forms of combs, helmets and caps,¹⁴ and can be used with other treatments such as minoxidil and finasteride. Results to date have shown a variable response and further research is needed to ascertain the efficacy of this treatment.

Patients in whom medical therapy has failed may consider surgical management, which involves hair transplantation and results in permanent hair restoration.¹⁴ Patients may choose to combine transplantation with medical therapy for improved cosmesis; however, cost and access can be major barriers.

 

Conclusion

Treatment of AGA involves a multipronged approach, where medical treatments are personalised to the patient, considering goals, cost and comorbidities. Referral to a dermatologist should be considered if the diagnosis is unclear, scarring alopecia is suspected, patients do not respond after 6 months of active pharmacological treatment, there is psychological distress due to hair loss, or if there are concomitant symptoms such as pain or discomfort. Patients should be counselled from the outset about the array of treatment options for AGA, and patient expectations should be guided with regard to response to treatments.

This article was finalised on 5 May 2025.

Conflicts of interest: Jane Li received an advisory payment from Bristol Myers Squibb in relation to deucravacitinib (for psoriasis), and received an honorarium from Cerave for delivering an educational presentation on eczema and seborrhoeic dermatitis.

Laxmi Iyengar has no conflicts of interest to declare.

This article is peer reviewed.

 

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