The Science of Stimulating Hair Growth: Evidence-Based Approaches for Treating Hair Loss

Hair loss, and specifically androgenetic alopecia, is among the most common dermatological complaints in both men and women. The psychological impact of hair loss can be significant and has led to a multi-billion dollar market of treatments, ranging from scientifically proven medicines to supplements without convincing evidence.

This article discusses the current state of interventions that stimulate hair growth. It covers both the biological basis of hair growth and the efficacy of various treatment approaches. For dermatologists, it remains important to explain to patients the distinction between medically substantiated therapies and products sold as hair growth remedies without adequate clinical substantiation.

Understanding the hair growth cycle

Hair growth is not a continuous process, but rather occurs in cyclical phases that repeat throughout life. The classic hair growth cycle consists of three primary phases: anagen, the active growth phase which can last several years for scalp hair; catagen, a short regression or involution phase lasting a few weeks; and telogen, a resting phase typically lasting a few months. Functionally, an exogen phase is often distinguished: the phase in which the telogen hair is shed and falls out. Hair follicles undergo these phases asynchronously, with the ratio of hairs in anagen, catagen, telogen, and exogen partly determining the clinically observable hair density.10

The regulation of this cycle relies on a complex network of signaling pathways and growth factors, including insulin-like growth factor 1 (IGF-1), fibroblast growth factors such as FGF-7/KGF, and Wnt/β-catenin signaling transduction.^{10, 12} The dermal papilla, a specialized mesenchymal structure at the base of the hair follicle, interacts closely with the follicular epithelium through epithelial-mesenchymal interactions and acts as an important regulatory signaling center within the hair cycle.^11,12 It is important to note that no single growth factor is solely responsible; hair growth is the result of a dynamic interplay of multiple activating and inhibitory signals.^10,12

In addition, oxidative stress has been increasingly investigated as a factor that can contribute to the disruption of hair follicle homeostasis. Reactive oxygen species can promote cellular damage, inflammatory signaling, and disruption of the hair cycle, and have been linked in the literature to androgenetic alopecia, alopecia areata, and telogen effluvium, among others.13 These insights have increased interest in antioxidative strategies as a potential supplementary approach, although their clinical substantiation varies by indication and intervention.13

EMA-approved treatments: the gold standard

Minoxidil

Topical minoxidil remains one of the most researched and widely used treatments for androgenetic alopecia. The drug was originally developed as an oral antihypertensive treatment, after which its hair growth-promoting effect was noted due to the occurrence of hypertrichosis. Multiple systematic reviews and meta-analyses have confirmed the efficacy of topical minoxidil, with both 2% and 5% formulations proving superior to placebo in clinical studies.^1,2,3

The exact mechanism of action of minoxidil has not yet been fully elucidated and appears to be multifactorial. Described mechanisms include the opening of ATP-sensitive potassium channels, effects on vascularization and VEGF expression, stimulation of dermal papilla cells, and activation of Wnt/β-catenin-related signaling pathways.^10,12 The primary clinical effect is generally attributed to the induction and/or prolongation of the anagen phase of the hair growth cycle, with an increase in the diameter and/or number of terminal hairs.

For men, topical 5% minoxidil is considered an established first-line treatment for androgenetic alopecia. For women, topical 2% minoxidil was traditionally the classic registered option, while in clinical practice—depending on country, registration, formulation, and tolerance—5% preparations are also used.^2,3,6 In practice, both minoxidil lotion and minoxidil foam are applied, depending on tolerance, ease of use, preference, and formulation composition. Lotion is often well-suited for patients who desire a liquid, precisely dosed application, while foam is better tolerated by some patients, especially when irritation from excipients such as propylene glycol plays a role.

Adherence is essential for treatment success: the treatment must be continued long-term and continuously, as the achieved hair growth can usually be lost within a few months after discontinuation.^3,6 The most common side effects of topical minoxidil are local reactions such as pruritus, erythema, irritation, scaling, and contact dermatitis. Hypertrichosis, or unwanted hair growth outside the intended treatment area, is also a known side effect and can occur when the product unintentionally gets on surrounding skin or is absorbed systemically.^2,3,6

Adherence in topical treatment of AGA

In practice, adherence is an important consideration in topical treatments for androgenetic alopecia.17 Patients may prematurely discontinue treatment if they are not adequately prepared for the necessary treatment duration, the absence of immediate visible results, temporary shedding, local side effects, or practical objections to daily use.^3,6,17 With hair growth-stimulating interventions such as minoxidil, initial effects can appear within a few weeks, but a clinically significant assessment usually requires several months of consistent use; in practice, an evaluation point after approximately 3 to 6 months is often assumed.^2,3,6

Clear instructions on correct use, realistic expectation management, and accessible support for questions or side effects can contribute to better adherence.17 In this context, a structured guidance approach, such as that offered by DermaDomein, can practically support patients with evidence-based therapies through usage instructions, expectation management, and accessible support where needed.

Finasteride

Finasteride is approved for the treatment of male androgenetic alopecia. The drug primarily inhibits 5-α-reductase type II, the enzyme that converts testosterone to dihydrotestosterone (DHT). In genetically susceptible individuals, DHT plays a central role in the progressive miniaturization of hair follicles, thus contributing to the typical pattern of androgenetic alopecia.3 By lowering DHT levels, finasteride can inhibit further miniaturization and promote stabilization or regrowth in some patients.^2,3

The standard dosage for male androgenetic alopecia is 1 mg per day.^2,6,7 A 2022 network meta-analysis showed that oral finasteride was significantly more effective than placebo.7 Although finasteride is generally well-tolerated in clinical studies, in 2025 regulatory authorities drew additional attention to potential sexual and psychiatric side effects, including mood changes and suicidal thoughts. Therefore, it is important that patients are well-informed in advance about the potential risks and contact their doctor if new symptoms arise.^2,6,7 Finasteride is not indicated for use in women and is contraindicated during pregnancy, due to the risk of disrupting the development of a male fetus; therefore, appropriate precautions must be taken when used by women of childbearing age.¹⁸

Finasteride spray

In addition to oral administration, there is growing interest in topical finasteride, including finasteride cutaneous spray (Finjuve®). In several EU countries, finasteride has also been registered since 2020 for topical/cutaneous use as a spray solution at a strength of 2.275 mg/ml for the same indication: early-stage male androgenetic alopecia.¹⁸

The registration study with topical finasteride 0.2275% spray solution was a randomized, double-blind, double-dummy phase III study of 24 weeks in adult men with androgenetic alopecia. Topical finasteride resulted in a significantly greater increase in target area hair count than placebo, with an effect numerically comparable to oral finasteride 1 mg. At the same time, systemic exposure was clearly lower: the maximum plasma concentration of finasteride was more than 100 times lower than with oral finasteride, and the reduction in serum DHT was less pronounced than with oral treatment.19

For dermatologists, finasteride spray is therefore a relevant development within the broader category of hair growth products. The lower systemic exposure can theoretically reduce the risk of systemic side effects, but does not completely exclude them; a clinically relevant decrease in serum DHT was also observed with topical application. Therefore, its positioning in routine practice remains dependent on availability, formulation, patient preference, tolerance, correct application, and further long-term data.^18,19

Other emerging treatments

Dutasteride

Dutasteride is a related 5-α-reductase inhibitor that inhibits both type I and type II, while finasteride primarily inhibits type II. Due to this broader enzyme inhibition, dutasteride leads to stronger suppression of DHT. However, for androgenetic alopecia in Europe, dutasteride does not have a similarly established registration status as finasteride, meaning its use for this indication is generally considered off-label.^6,7

Studies and meta-analyses suggest that dutasteride may be more effective than finasteride. One network meta-analysis reported that dutasteride 0.5 mg per day was more effective than finasteride 1 mg per day, with an average difference of 7.1 hairs per cm².⁷ This potential added value must be weighed in clinical practice against the off-label nature of the treatment, the longer half-life of dutasteride, and the same category of concerns regarding sexual, psychiatric, and reproductive side effects.^6,7,18 Dutasteride, like finasteride, is contraindicated during pregnancy and should not be used by women who are pregnant or may become pregnant without adequate precautions.¹⁸

Oral minoxidil (Low Dose Oral Minoxidil or LDOM)

Recent research has increased interest in low-dose oral minoxidil as an alternative or supplementary option for androgenetic alopecia. LDOM is typically used in dosages of approximately 0.25 to 5 mg per day, with lower dosages usually applied in women and dosages in the order of 2.5 to 5 mg per day more often investigated in men.^5,20

For female pattern hair loss, studies have been published with oral dosages ranging from 0.25 to 1 mg per day. A randomized study showed that oral minoxidil 1 mg per day was more effective than 0.25 mg per day after 24 weeks of treatment.²¹ In men with androgenetic alopecia, a randomized study showed that oral minoxidil 5 mg once daily did not demonstrate superiority over topical minoxidil 5% twice daily after 24 weeks, although clinical improvement was seen in the oral group and the drug was generally well-tolerated.²² More recent dose-comparative data in men suggest that 2.5 mg and 5 mg oral minoxidil may have similar effects, but further confirmation and longer-term follow-up are still needed. ²³

LDOM currently has no EMA-approved indication for hair loss, and its use in androgenetic alopecia should therefore be considered off-label.⁵ The treatment requires careful patient selection and counseling, partly due to dose-dependent side effects such as hypertrichosis, headache, ankle edema, palpitations, and potential cardiovascular effects.^5,22

Other emerging treatments

Topical combination therapy of minoxidil with finasteride appears particularly interesting. Studies combining topical finasteride with topical minoxidil show that the combination can yield better results than minoxidil monotherapy.⁸ Clinical data with the combination of 5% minoxidil lotion and 0.2275% finasteride spray also indicate higher clinical and instrumental effectiveness than monotherapy, with a comparable safety and tolerability profile.^21,22

When considering combination therapy, a combination of a registered topical finasteride spray (Finjuve®) once daily with topical minoxidil once daily is pharmacologically and practically logical. This combines two agents with different mechanisms of action: minoxidil as a hair growth stimulating treatment and finasteride as a local 5-α-reductase inhibitor. Such an approach is, in principle, preferable to unregistered compounded combinations, because with compounded preparations, efficacy, stability, skin penetration, and follicular availability depend on the chosen base, concentration, excipients, and preparation quality. With untested or unstable bases, it is uncertain to what extent finasteride actually reaches the relevant follicular structures.

Additionally, clinical experience with both topical finasteride and low-dose oral minoxidil is increasing. This provides dermatologists with a broader treatment palette in which registered topical finasteride, topical minoxidil, and, where appropriate, off-label oral minoxidil can be rationally positioned, depending on the indication, patient preference, tolerability, risk assessment, and availability.^5,6,21

Low-level laser/light therapy (LLLT)

Low-level laser/light therapy (LLLT) devices, usually based on red light or near-infrared light, have also shown a statistically significant increase in hair density in pattern hair loss in sham-controlled clinical studies and meta-analyses. Several home-use LLLT devices, particularly in the United States, are FDA-cleared for pattern hair loss. However, the clinical evidence is device-dependent and less robust than that for established pharmacological treatments such as minoxidil and finasteride. Most studied devices use wavelengths in the red light spectrum, often around 630–660 nm, although other wavelengths and device types have also been investigated. The place of LLLT in clinical practice therefore remains dependent on the device, treatment protocol, patient selection, cost, adherence, and the limited availability of long-term data.²⁴

Platelet-rich plasma (PRP)

Platelet-rich plasma (PRP), in which concentrated platelets from autologous blood are injected into the scalp, has also received significant attention as a non-pharmacological intervention for androgenetic alopecia. Systematic reviews and meta-analyses predominantly report favorable effects on hair density, with a good safety profile and few serious side effects. However, the effects on hair diameter, hair thickness, and other follicle parameters are less consistent, and clinical relevance varies between studies.^25,26

The evidence for PRP is primarily limited by significant heterogeneity. PRP is not a standardized product: blood collection, centrifugation, platelet concentration, leukocyte content, activation, injection technique, treatment interval, and maintenance protocol vary widely between studies. This makes it difficult to compare results or identify an optimal protocol. PRP can therefore be considered a potentially useful adjunctive treatment for selected patients with androgenetic alopecia, but its place relative to established therapies such as minoxidil and 5-α-reductase inhibitors remains dependent on patient selection, availability, cost, treatment burden, and further standardization of clinical protocols.^{25, 26}

Nutritional approaches: potential and limitations

The role of nutrition and micronutrients in hair health has garnered significant interest, and a large number of supplements are marketed with claims to reduce hair loss or stimulate hair growth. However, the clinical evidence for nutritional interventions remains mixed. Systematic reviews suggest that certain supplements or correction of deficiencies may be beneficial in selected patients, but interpretation is limited by small study populations, heterogeneous interventions, the absence of active comparators, potential commercial bias, and methodological shortcomings.^9,14

It is particularly important that supplementation is rational when there is a documented or clinically plausible deficiency, for example of iron/ferritin, vitamin D, or zinc, or when diet, comorbidity, malabsorption, medication use, or increased physiological need warrants it. In patients without deficiency, the added value of routine supplementation is less well-supported and must be weighed against costs, expectations, safety, possible overdose or interactions, and the risk that proven treatments may be delayed.^9,14

Vitamins and minerals for hair loss

The question of which vitamins and minerals play a role in hair loss frequently arises in clinical practice. Observational studies and systematic reviews have linked deficiencies or imbalances of, among others, vitamin D, iron/ferritin, zinc, and certain B vitamins to various forms of hair loss, including androgenetic alopecia and telogen effluvium. However, interpretation remains cautious, as association does not automatically imply causality and supplementation is primarily rational when there is a documented or clinically plausible deficiency.^9,14

Vitamin D3

Vitamin D deficiency has been linked to various forms of hair loss in observational studies. A study on oral vitamin D3 supplementation in women with telogen effluvium reported improvement in 82.5% of participants after treatment with vitamin D³, but this finding must be interpreted cautiously due to the nature of telogen effluvium, which often resolves spontaneously, and due to limitations in study design and generalizability.²⁷

Iron and zinc tablets

Iron is relevant for rapidly dividing cells, including cells in the hair follicle matrix. Low ferritin levels or iron deficiency can therefore be clinically relevant in diffuse hair loss, especially when anamnesis, menstrual pattern, diet, comorbidity, or medication use provides a reason for it.^9,14 Supplements combining iron with other nutrients have shown benefits in some studies as an addition to standard treatment. For example, a study with a supplement based on amino acids, iron, selenium, and marine hydrolyzed collagen reported improvement in patients with androgenetic alopecia, female androgenetic alopecia, or telogen effluvium, but such results must be considered in light of product-specific composition, study design, and potential commercial bias.¹⁵

Zinc deficiency can be associated with hair loss, fragility, and thinning hair. However, the results of zinc supplementation are inconsistent: supplementation may be rational in cases of deficiency or low baseline values, but in cases of normal zinc status, the added value is less well-supported.^9,14

Biotin and hair loss

Biotin is one of the most commercialized supplements for hair loss, but convincing controlled studies on biotin as monotherapy are lacking, except in situations of actual biotin deficiency or rare metabolic disorders.^9,28 It is also important to note that biotin supplementation can interfere with laboratory tests, including troponin measurements and hormonal immunoassays, which can lead to diagnostic errors.²⁹

Antioxidants and botanicals

Vitamin A, C and E

Given the possible role of oxidative stress in disrupting hair follicle homeostasis, antioxidants such as selenium and vitamins A, C, and E are regularly included in supplements claiming to support hair growth. However, the clinical evidence for such combinations remains limited and product-specific. A study on a combination of fish oil, blackcurrant seed oil, vitamin E, vitamin C, and lycopene in women with hair loss reported improvement in hair density and telogen percentage, among other things, after 6 months, but these findings must be interpreted cautiously due to methodological limitations and risk of bias.^9,30

Furthermore, excessive supplementation is not without risk. In particular, an excess of vitamin A has been linked to hair loss, while high doses of fat-soluble antioxidants and minerals, including vitamin E and selenium, can cause unwanted effects or interactions. Supplementation should therefore primarily be considered in cases of documented or clinically plausible deficiency, and not as a generic replacement for evidence-based treatment.^9,13

Pumpkin seed oil and saw palmetto extract

Botanical interventions with proposed anti-androgenic or 5-α-reductase inhibiting properties include pumpkin seed oil and saw palmetto extract. A randomized placebo-controlled study with pumpkin seed oil in men with androgenetic alopecia reported a greater increase in hair count than placebo after 24 weeks.³¹ The study is interesting, but the evidence remains limited by its relatively small size, short duration, and the fact that the studied supplement is not directly equivalent to all commercial pumpkin seed oil products.31

For saw palmetto, positive signals also exist from small clinical studies and reviews, but the literature is characterized by heterogeneous preparations, different dosages, combination products, and limited long-term data.^9,32 Botanicals can therefore be considered clinically interesting, but for now supportive interventions in selected patients. They do not currently have the same evidence position or predictability as established treatments such as minoxidil and 5-α-reductase inhibitors.

Critical evaluation of the evidence

When evaluating nutritional interventions for hair loss, several limitations must be considered. Many studies lack an active comparator, comparing only with placebo or baseline rather than with proven treatments. In addition, patient numbers are often small, heterogeneous interventions and subjective outcome measures are used, and a systematic assessment of the baseline nutritional status is often missing.^9,14 In conditions such as telogen effluvium, which can resolve spontaneously, it is also difficult to attribute improvement to supplementation rather than natural recovery.²⁷

Supplementation seems most rational when a documented or clinically plausible deficiency is corrected. However, routine screening for micronutrient deficiencies in all patients with hair loss remains a subject of discussion; a targeted history, dietary history, and clinical risk assessment are important here.^9,14 Furthermore, the quality of supplements varies, and due to less stringent regulatory control, it is not always certain that products actually contain the ingredients, dosages, or purity stated on the label.^9,29

In contrast, the evidence for minoxidil and 5-α-reductase inhibitors like finasteride is considerably more robust, with multiple randomized studies, systematic reviews, and meta-analyses demonstrating efficacy in androgenetic alopecia.^1,2,4,7 For topical finasteride spray, a randomized phase III study is also available, showing significant efficacy compared to placebo and clearly lower systemic exposure than oral finasteride.^18,19 These agents have been much more stringently researched for effectiveness, safety, dosage, and pharmacological basis than most nutritional or botanical supplements.

In clinical practice, there is therefore a sharp distinction between medically supported treatments and products with a predominantly cosmetic or nutritional positioning. Many hair growth products are presented as if they have a comparable basis of evidence, while the clinical basis is limited, product-specific, or absent. For many dermatologists, it is essential to inform patients well about the difference between agents with convincing evidence, such as topical minoxidil, oral finasteride, and products that primarily rely on plausible mechanisms, limited studies, or marketing claims.^{1,2,4,7,9,14,19}

Conclusion

The landscape of hair growth stimulating treatments ranges from rigorously researched, registered medicines to supplements with widely varying levels of evidence. Topical minoxidil, oral finasteride, and finasteride spray are among the best-substantiated treatments for androgenetic alopecia, supported by decades of clinical experience and multiple systematic reviews and meta-analyses showing a clear effect.^1,2,4,7 Emerging approaches such as low-dose oral minoxidil and combination therapy are promising and can offer benefits in specific situations, but require careful positioning based on indication, availability, safety, tolerability, and long-term data.^5,6,8,19,23

Nutritional interventions hold a less certain position. While certain micronutrients are relevant for hair health and deficiencies can contribute to hair loss, the evidence for supplementation in individuals without a demonstrable or clinically plausible deficiency remains limited.^9,14 Supplements can at best play a complementary role, particularly when used alongside proven therapies or to correct deficiencies, but should not be considered a substitute for evidence-based treatment.^9,14,15

For patients experiencing hair loss, the most sensible approach remains consultation with a doctor or dermatologist to determine the underlying cause, assess deficiencies as needed, and establish a treatment plan based on the strength of the evidence. Understanding the biological mechanisms of hair growth and the quality of the underlying research enables more rational decision-making for this common complaint.

The field continues to evolve, with ongoing research into new mechanisms and treatment strategies. As knowledge of hair follicle biology increases, new therapeutic targets are likely to emerge. However, the fundamental principle remains unchanged: treatment choices should be guided by the quality and strength of scientific evidence, with realistic expectations about efficacy and the understanding that long-term therapy is usually necessary to maintain results.

Frequently asked questions

What are the best-supported treatments to stimulate hair growth in androgenetic alopecia?

For androgenetic alopecia, topical minoxidil and 5-α-reductase inhibitors, particularly oral finasteride in men, remain the most well-supported treatments. For both, there are multiple randomized studies, systematic reviews, and meta-analyses demonstrating efficacy. The choice of treatment depends on gender, age, diagnosis, contraindications, patient preference, risk profile, and willingness for long-term therapy.

How does finasteride work for androgenetic alopecia?

Finasteride primarily inhibits 5-α-reductase type II, thereby reducing the conversion of testosterone to dihydrotestosterone (DHT). In genetically susceptible hair follicles, DHT plays a central role in progressive follicular miniaturization. By lowering DHT, finasteride can slow down further miniaturization and, in some patients, promote stabilization or regrowth.

What is the role of finasteride spray compared to oral finasteride?

Topical finasteride spray is not yet registered in the Netherlands but is in neighboring countries. It has been developed to locally inhibit 5-α-reductase with lower systemic exposure than oral finasteride. In the phase III registration study, topical finasteride spray showed a significant effect compared to placebo, similar to oral finasteride 1 mg, with systemic exposure significantly lower than with oral finasteride. This can be relevant in practice for patients for whom systemic exposure is a major concern. However, systemic effects are not entirely ruled out, as topical application can also lead to a decrease in serum DHT.

Which is better: minoxidil lotion or minoxidil foam?

There is no universally "better" option; the choice between minoxidil lotion and minoxidil foam mainly depends on tolerance, ease of use, patient preference, and the formulation's composition. Lotion can be practical for patients who prefer a liquid, precisely dosed application. Foam is better tolerated by some patients, especially when irritation from excipients such as propylene glycol is an issue. Both formulations can be effective if used correctly and consistently.

How long should minoxidil be used before assessing its effect?

A clinically meaningful assessment typically requires several months of consistent use. In practice, an evaluation point after approximately 3 to 6 months is often used, with further gains possible with longer use. Early discontinuation is common when patients are insufficiently prepared for the required duration of treatment, temporary shedding, or the absence of immediate visible results.

Does low-dose oral minoxidil have a place in androgenetic alopecia?

Oral minoxidil is increasingly used off-label for various forms of hair loss, including androgenetic alopecia. Available studies and consensus publications suggest potential benefits in carefully selected patients, but the drug does not have EMA-approved indication for hair loss. Therefore, this treatment requires careful patient selection, counseling, and attention to side effects such as hypertrichosis, edema, headache, palpitations, and cardiovascular risks.

Is combination therapy with minoxidil and finasteride useful?

Combination therapy is pharmacologically plausible because minoxidil and finasteride have different mechanisms of action. Minoxidil stimulates hair growth, among other things, through its effects on the anagen phase, while finasteride inhibits DHT-mediated miniaturization. Studies on combinations of topical minoxidil and topical finasteride show favorable results compared to minoxidil monotherapy. In practice, a combination with a registered topical finasteride spray is preferred over untested compounded combinations, because stability, skin penetration, and follicular availability of compounded preparations depend on the base, excipients, and quality of preparation.

What role do PRP and LLLT play in androgenetic alopecia?

PRP and low-level laser/light therapy can be considered as complementary interventions. For both, clinical studies and meta-analyses show positive signals, especially for hair density. However, the evidence is less robust than for minoxidil and finasteride. With PRP, comparison between studies is complicated by heterogeneous protocols, while for LLLT, effectiveness is device-dependent and long-term data are limited.

When are supplements useful for hair loss?

Supplements are primarily rational when there is a demonstrated or clinically plausible deficiency, for example of iron/ferritin, vitamin D, or zinc, or when diet, comorbidity, malabsorption, medication use, or increased physiological demand warrants it. In patients without deficiency, the added value of routine supplementation is less well-supported. Therefore, supplements should not be positioned as a substitute for evidence-based treatments such as minoxidil or finasteride.

Is biotin useful for hair loss?

Biotin is strongly positioned commercially, but convincing evidence for biotin as monotherapy for hair loss is lacking, except in cases of actual biotin deficiency or rare metabolic disorders. Additionally, biotin supplementation can interfere with laboratory tests, including troponin assays and hormonal immunoassays. This makes it important to actively inquire about biotin use in patients taking supplements.

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