The Non-Surgical Stepladder for Hair Growth

Healthy hair isn’t an accident.  Small, interventions layered together over time (much like a good skincare routine or a well-tailored wardrobe) can help to maximise hair growth and condition.  While genetics, hormones and ageing play a large part, the tools available to support, maintain and in some cases restore hair density without surgery are both broader and more effective than ever. 

In this article I wanted outline my ‘stepladder’ approach to hair health, starting with the fundamentals and moving upwards to more intensive clinic-based options.  Think of it as a progression, with each step supporting the one above, with the strongest results when they’re combined.

Understanding Hair Follicle Health and Growth

The hair follicle is not simply a static anchor for a strand of hair.  You can think of it as a remarkably active mini-organ, complete with its own stem cell niche, blood supply, sebaceous gland and sensory nerve network (in histology it’s referred to as the ‘pilosebaceous unit’).  At its base, the dermal papilla directs the entire growth process, communicating constantly with the surrounding follicular cells.  For hair to grow well, the follicle needs not just energy and amino acids, but also hormonal balance, adequate microcirculation and a healthy extracellular matrix to anchor and nourish the bulb.  Even subtle disruptions in these systems, from inflammation in the scalp to changes in local hormone signalling, can push follicles out of growth mode. 

Hair growth occurs in a repeating cycle with three main phases: anagen (the active growth phase), catagen (a short transitional period where growth stops) and telogen (the resting phase before the hair is shed).  On a healthy scalp, the vast majority of follicles are in anagen at any given time, producing strong, pigmented hairs.  

Problems arise when the anagen phase shortens or when a disproportionate number of follicles enter telogen prematurely, leading to thinning or shedding.  This shift can be triggered by a range of factors, from nutritional deficiencies, hormonal changes, systemic illness or significant stress, which often explains why shedding appears a few months after the underlying trigger.

A key hormonal player in many patterns of hair loss is dihydrotestosterone (DHT), a metabolite of the androgen hormone testosterone (the key male sex hormone) produced by the action of the 5-alpha-reductase enzyme within the skin and hair follicles.  In genetically susceptible individuals, DHT binds to androgen receptors in the dermal papilla and alters the follicle’s normal growth cycle, gradually shortening the anagen phase and miniaturising the hair shaft over successive hair cycles.  The process doesn’t destroy the follicle outright, which is why medical intervention can sometimes reverse it, but it progressively produces finer, less pigmented hairs until they become barely visible.  Not all follicles are equally sensitive to DHT: those on the scalp’s frontal and crown regions are far more vulnerable than those on the occipital scalp (back of the head), which is why androgenetic alopecia follows such a recognisable pattern.

In women, particularly during and after menopause, hormonal changes shift the playing field.  Falling oestrogen and progesterone levels remove their natural protective influence on the hair cycle.  Oestrogen helps to prolong anagen, supports scalp blood flow, and moderates androgen activity; progesterone also has an anti-androgenic effect at the follicle.  When both decline, androgens like DHT have a relatively greater impact, leading to diffuse thinning over the crown with preservation of the frontal hairline in many women.  Menopause can also change the scalp’s microenvironment: reduced sebum output can make the scalp drier and more sensitive, while changes in pH and barrier function can increase susceptibility to inflammation, all of which can subtly influence follicular performance.

Thyroid hormones, in particularl thyroxine (T4) and triiodothyronine (T3) are another crucial, if often overlooked, factor. They regulate the metabolic rate of virtually every cell, including those within the follicle. Both hypo- and hyperthyroidism can disrupt the normal hair cycle, often pushing a higher proportion of follicles into telogen and producing diffuse shedding.  Hypothyroidism tends to cause coarse, brittle hair and thinning of the outer third of the eyebrows, whereas hyperthyroidism can result in finer more fragile strands. Subclinical thyroid dysfunction that is not severe enough to trigger obvious systemic symptoms can still have a measurable effect on hair density and quality.

From a more holistic perspective, supporting hair therefore means thinking beyond the strand of hair itself.  We must consider scalp environment (inflammation, barrier function, sebum production), systemic health (thyroid status, ferritin, vitamin D, sex hormones) and lifestyle influences (dietary quality, stress, sleep, medications, smoking, alcohol).  A treatment plan that overlooks these elements risks treating only the symptom.

When we address follicle biology, local scalp health, and whole-body wellness in tandem, we create the best possible conditions for both regrowth and long-term maintenance.

Step 1

Lifestyle considerations for hair growth: Setting the Stage

Before we even think about supplements, serums or sophisticated in-clinic treatments, it’s worth acknowledging that hair follicles are exquisitely sensitive to the rhythms and stresses of daily life.  In the same way that a chronically sleep-deprived, over-stressed body struggles to heal a wound, it also struggles to maintain the demanding cellular activity of hair growth.

Sleep is the quiet architect of hair repair and its influence on hair is twofold.  Firstly, adequate restorative sleep (ideally 7–9 hours per night) supports the circadian regulation of hormones including cortisol, melatonin, growth hormone and thyroid hormones, all of which have downstream effects on the hair cycle.  Secondly, it helps to keep inflammation in check; poor sleep is associated with higher systemic inflammatory markers, which can compromise the scalp’s microenvironment.

Stress management is equally critical. Chronic psychological stress raises cortisol and can dysregulate the hypothalamic–pituitary–adrenal (HPA) axis, which in turn impacts the hair follicle’s stem cell niche.  High levels of the stress hormone cortisol is known to prematurely shift follicles from anagen into catagen, the first step towards shedding.  Aside from chronic stress, acute stress can trigger telogen effluvium, a sudden, diffuse loss that becomes apparent two to three months after the stressful event, while persistent low-grade stress can subtly thin the hair over years.

Other lifestyle choices matter too.  Regular exercise improves scalp blood flow and insulin sensitivity, both of which help nourish follicles.  Excessive heat styling or tight hairstyles can cause mechanical damage or traction alopecia, while over-washing with harsh products can strip the scalp’s protective lipid barrier.  Even hydration plays a modest role; while it won’t make hair grow faster, it supports overall cellular function and helps maintain the scalp’s barrier integrity. 

Step 2

Nutrition: Feeding the Follicle

Hair is built in the follicle.  Hair follicles are metabolically active and require a constant supply of nutrients to function optimally.  Protein is non-negotiable: keratin production relies heavily on sulphur-containing amino acids like cysteine and methionine, along with lysine for both shaft structure and iron absorption.  Animal proteins including eggs, poultry, lean meat and fish tend to be the most efficient source, as they contain all essential amino acids in generous amounts.

Well-constructed plant-based diets can still meet needs, but they require complementary protein pairing with, for example, lentils with rice, or soy with whole grains to achieve the same amino acid completeness.  Other dietary pillars include omega-3 fatty acids (from oily fish, flax, chia), iron, zinc, vitamin D and vitamin C to aid collagen production.

Crash dieting, severe caloric restriction or rapid weight loss (including that sometimes seen with GLP-1 inhibitors such as semaglutide) can tip follicles into telogen (the shedding phase) within weeks due to reduced protein and calorie availability.  In short: before investing in expensive treatments, ensure your diet supports your biology.

Step 3

At-Home Topicals: Minoxidil and Beyond

Once you’ve ensured the follicle is adequately nourished from within, the next rung is supporting it externally with evidence-based topicals.  The gold standard here remains minoxidil, originally developed as a blood pressure medication and later observed to stimulate hair regrowth as an unexpected side effect.  Its precise mechanism is still being unraveled, but we know it acts as a potassium channel opener, causing vasodilation and improving microcirculation around the follicle.  More intriguingly, it appears to directly stimulate dermal papilla cells, prolonging the anagen (growth) phase and increasing follicular size, leading to thicker, more pigmented hair shafts.  It’s available as a foam or solution, in strengths from 2% to 5% (and sometimes higher under prescription) and results generally begin to show at around the three-month mark, with optimal outcomes at 6–12 months.  Consistency is key: stopping minoxidil usually means losing the gains within months.

Beyond minoxidil, a new wave of topical serums is showing promise.  Peptide-based formulations, for example those containing copper tripeptide-1 aim to signal the follicle’s stem cell niche to initiate growth and improve extracellular matrix quality.  Caffeine-based serums may work by inhibiting an enzyme called phosphodiesterase, which can counteract some of the effects of DHT (dihydrotestosterone) at the follicular level, with small in vitro studies showing stimulation of hair shaft elongation.  Botanicals like saw palmetto extract (rich in fatty acids and phytosterols) are proposed to reduce local DHT activity, although the clinical evidence is more modest than for pharmaceuticals.

Then there’s the scalp environment itself, where shampoos and leave-on treatments can play a supportive if not directly transformative role.  Ingredients like ketoconazole (an antifungal agent) have been shown to reduce micro-inflammation in the scalp and may have mild anti-androgenic effects, making them useful adjuncts in androgenetic alopecia.   Piroctone olamine, another antifungal, is thought to reduce oxidative stress around the follicle, while salicylic acid shampoos help by clearing excess sebum and keratin debris from the follicular opening, theoretically improving penetration of active serums.

Barrier function in the scalp is important to consider, as much as it is with the skin elsewhere.  Indeed, humectants like glycerin or hyaluronic acid in scalp tonics can help maintain an optimal moisture balance, which supports a healthy barrier and reduces low-grade irritation, an often-overlooked contributor to chronic shedding.

While none of these topicals (with the exception of minoxidil) should be considered standalone ‘miracle’ cures, they form an important rung in the hair growth stepladder.  Used consistently and in combination with systemic support and in-clinic stimulation they can improve follicular conditions, reduce inflammation and prolong the life of each strand you have.

Step 4

Oral Supplements for hair growth: Closing Nutritional Gaps

If Step 2 ensures that the diet delivers a strong baseline of hair-friendly nutrients, Step 4 is about filling in the cracks deliberately, with evidence and using testing rather than guesswork.  The temptation to ‘cover all bases’ with an arsenal of hair supplements is understandable, but indiscriminate dosing can be counterproductive, wasteful and in some cases harmful.

The most common deficiencies I see in patients with hair concerns are low ferritin (the storage form of iron), vitamin D insufficiency, and zinc deficiency.

• Ferritin is particularly important because iron is integral to the enzymes involved in DNA synthesis, a process that is constant and rapid in the hair matrix.  Low ferritin can shorten the anagen phase and increase shedding, even if haemoglobin levels are normal.
• Vitamin D influences the hair cycle via its role in keratinocyte proliferation and immune modulation and low levels have been linked to several types of non-scarring alopecia. 
• Zinc is involved in protein synthesis and cell division, both critical for producing new hair shafts; a deficiency can lead to brittle, easily broken hair and a dry, flaky scalp.

Certain amino acids also deserve targeted mention.  L-lysine aids in iron absorption and contributes structurally to the hair shaft.  Methionine and cysteine, both sulphur-containing amino acids, are essential for keratin formation.  Cysteine, in particular, forms the disulphide bonds that give hair its tensile strength.  While these are abundant in animal proteins, a vegan or restrictive diet may benefit from supplementation if intake is insufficient and shedding is a concern.

Specialty hair supplements often combine these nutrients with additional B-vitamins, selenium, and sometimes marine collagen peptides.  While these can be useful in certain cases, they should be selected to address a known need, not as a blanket insurance policy.  Biotin, for example, is the poster child of the hair supplement industry yet true deficiency is vanishingly rare outside of specific medical conditions; high-dose supplementation is unlikely to improve hair in otherwise healthy individuals and can interfere with laboratory tests (particularly cardiac biomarkers) if not discontinued in advance.

The most effective approach is test, don’t guess.  A blood panel assessing ferritin, vitamin D, zinc, thyroid function and sometimes sex hormones will identify any true deficiencies or imbalances.  Supplementation can then be tailored in both dose and duration, often with a follow-up test after 3–6 months to confirm correction.  In this way, Step 3 acts as a targeted bridge between the foundational diet of Step 1 and the more intervention-heavy strategies that follow, ensuring the follicle has everything it needs internally to respond to topical and procedural treatments externally.

Step 5

Prescription Medicines for Hair growth: Targeting Hormonal effects on Hair Growth

For many patients, particularly those with androgenetic alopecia or hormonally driven shedding, the step from nutritional and topical support to prescription medicines is where the most substantial gains can be made.  These treatments work by directly addressing the hormonal signals that shorten the growth phase and miniaturise hair over time.

In men, the best-established intervention is finasteride, a prescription medication which selectively inhibits a en enzyme called 5-alpha-reductase.  This enzyme converts testosterone to dihydrotestosterone (DHT).  By reducing scalp DHT levels, finasteride protects susceptible follicles from the miniaturisation process described earlier.  Finasteride is taken orally at 1 mg daily, with data showing stabilisation of hair loss in over 80% of men and visible regrowth in many.  Dutasteride, another medication in the same ‘class’ inhibits both type I and type II 5-alpha-reductase (finasteride only inhibits type II) and is sometimes useful in more resistant cases.  Both finasteride and dutasteride are generally well-tolerated, but they are not without potential side effects.  In men, reported issues include reduced libido, erectile dysfunction and, more rarely, mood changes or depression.  These effects are reversible in most cases after discontinuation, though a small proportion of patients describe longer-lasting symptoms.  In women of childbearing potential, both drugs are contraindicated due to the risk of causing genital abnormalities in a male fetus so strict contraception is essential if prescribed off-label.  Dutasteride’s longer half-life means it lingers in the system for months after stopping, which is also worth considering when weighing its use.

Both drugs require ongoing use: if stopped, any hair preserved through treatment is typically lost over several months.  For those concerned about systemic exposure, topical finasteride and dutasteride has emerged as a promising option, delivering local scalp effects with lower circulating drug levels.

In women, especially those post-menopause, the hormonal picture is somewhat more complex.  Declining oestrogen and progesterone remove their protective effects on the follicle, allowing even normal DHT levels to exert a stronger influence.  Here, systemic anti-androgens such as spironolactone can be effective.  This works by blocking androgen receptors in the follicle and reducing androgen production in the adrenal glands.  

For women with confirmed androgen excess (for example, in polycystic ovary syndrome), oral contraceptives containing oestrogen and an anti-androgenic progestin can help stabilise shedding and improve density.  In select post-menopausal patients, hormone replacement therapy (HRT), tailored and monitored carefully, may provide indirect hair benefits by restoring some oestrogen and progesterone activity in the scalp, although its use is dictated more by systemic health considerations than hair alone.

Thyroid-related hair loss requires a different approach: no topical or anti-androgen will help if the underlying thyroid dysfunction remains untreated.  Both hypo- and hyperthyroidism can trigger diffuse hair shedding, and in these cases, restoring euthyroid status with the appropriate dose of levothyroxine (for hypothyroidism) or anti-thyroid medication (for hyperthyroidism) is key.  Even subtle imbalances can impact hair quality, so patients with persistent shedding despite good nutritional and topical support should have their thyroid function checked as part of a comprehensive work-up.

While prescription medicines can be highly effective, they are rarely the whole answer. For the best results, they should be layered with the nutritional, topical, and procedural strategies from earlier steps in the stepladder.

Step 5

In-Clinic Procedures for Hair Growth: Stimulating the Scalp

When the physiological groundwork is in place (Steps 1–5), clinic treatments become the accelerators: they recruit growth pathways, calm scalp inflammation and improve the follicle’s microenvironment so each growth cycle is longer and more productive.  None of these is a magic wand - they all work best as part of a layered plan.  What follows is how I frame the options, what to expect, and how I combine them.

Platelet‑Rich Plasma (PRP)

PRP takes a small sample of your blood, concentrates the platelets and re‑injects their growth‑factor payload into thinning scalp.  Platelet‑derived factors (PDGF, VEGF, TGF‑β) promote blood vessel growth and signal dermal papillary cells.  Clinical data showing meaningful gains in hair counts, especially when PRP is layered over minoxidil.  A 2024 meta‑analysis reported that PRP combined with minoxidil improved growth and patient satisfaction versus either alone, while another 2024 review found increased density (more follicles per cm²) even when shaft calibre didn’t change dramatically.  This is useful for patients who want better coverage as a first win.  My protocol in clinic is generally three to four monthly sessions, then maintenance every 4–6 months; the first visible change typically appears at 8–12 weeks, with consolidation by 6–9 months. Side‑effects are minimal and usually limited to transient tenderness and redness, although this is rare.

Microneedling of the scalp: controlled injury, constructive healing.

By creating precise micro‑channels in the scalp, microneedling is a simple tool that is known to activate wound‑healing cascades (Wnt/β‑catenin signalling, growth‑factor release) and improve penetration of proven topicals such as minoxidil and even PRP when performed in the same session.  Randomised trials show microneedling can increase terminal hair counts and rescue cases ‘refractory”’ to minoxidil, particularly when delivered in a structured course.  I favour medical‑grade devices at conservative depths (typically 0.8–1.5 mm depending on area) every 2–4 weeks for 3–6 sessions, then maintenance every 6 months or so.  Expect a pink scalp for 12–24 hours; it should not be done over actively inflamed conditions until these are controlled.

Low‑level laser/light therapy (LLLT) photobiomodulation for hair growth 

LLLT devices (clinic or medical‑grade home caps) deliver red/near‑infrared light that raises ATP production in follicular mitochondria and modulates inflammatory mediators, nudging follicles into the anagen phase of hair growth and lengthening it.  Evidence has matured: systematic reviews and trials show statistically significant improvements in terminal hair density versus sham with regular use (commonly 3 times weekly for ~24–26 weeks).  I use LLLT as a low‑burden adjunct for patients who will actually use it; it is safe, synergistic with minoxidil/PRP and particularly helpful for maintenance between in‑clinic blocks.  I generally recommend the dermalux Flex MD for patients looking for an at home device.

Polynucleotides for hair growth

Well known in skin, polynucleotide injections are moving into hair because their biology is ideally suited for this purpose.  This includes fibroblast activation, angiogenesis and anti‑inflammatory signalling.  This matters to the scalp’s extracellular matrix and microvasculature when it comes to promoting growth and the anagen phase.  Early clinical work from Korea suggests polynucleotides can improve density in androgenetic cases, plausibly via improved dermal environment and anti‑apoptotic effects on follicular cells.  I position polynucleotides as an adjunct in patients who also care about scalp quality (itch, tightness, post‑inflammatory fragility) or who haven’t tolerated other actives.  Protocols typically mirror those for the skin skin: 3 sessions about 3–4 weeks apart, then space.  The treatments are quick but slightly uncomfortable as polynucleotides sting when they are injected.  As ever, expectations must be measured until larger trials are available.

Exosomes for hair growth

Exosomes, which are cellular nanovesicles carrying proteins and micro‑RNAs are compelling in preclinical hair models and early reports, with proposed effects on follicle stem cells and inflammation.  However, sourcing, standardisation and regulatory status are active issues; recent UK reporting has highlighted concerns around human‑origin exosomes in cosmetics and longer‑term safety/quality controls are still being defined.  In my clinic we use damascene rose derived exosomes and exosome‑like growth‑factor topicals as an adjunct, not a substitute, for evidence‑led care.

What we offer and where this sits in my clinics.

At my clinics we provide PRP programmes for male and female pattern hair loss, often in combination with medical therapy and at‑home regimens; we also offer polynucleotide programmes and medical microneedling where indicated, mapped to scalp health as much as strand count. Consultations are used to stage the alopecia correctly, exclude reversible triggers and decide which ‘stack”’ gives the highest yield for the least burden.

Step 7

Combination Protocols — The Modern Standard

By the time we reach this stage of the stepladder, the groundwork has been laid: nutrition is optimised, deficiencies corrected, topicals are in place, hormonal drivers addressed and in-clinic stimulation started.  Step 7 is about weaving those strands into a coherent, sustained programme.  As mentioned above, hair growth is an ongoing conversation between follicle biology, systemic health and the microenvironment of the scalp.  The more touchpoints we influence, the better the results.

The scientific rationale for combination therapy is compelling.  Follicles respond to multiple simultaneous cues: mechanical stimulation (microneedling), biochemical triggers (PRP, polynucleotides, peptides), improved microcirculation (minoxidil, LLLT) and hormonal modulation (finasteride, spironolactone, HRT where appropriate).  Each of these acts at a different point in the hair cycle or follicular signalling cascade.  Used together, they can stabilise shedding, increase the proportion of follicles in anagen, improve shaft calibre and optimise scalp health.  These are outcomes that are far harder to achieve with a single modality.

A typical combination plan might look like this: 

• Daily minoxidil (or compounded minoxidil/finasteride for men, minoxidil ± topical anti-androgens for women)
• Oral therapy to address DHT or thyroid imbalance where indicated
• Targeted supplementation for any proven nutrient gaps
• Three monthly PRP sessions with microneedling
• Polynucleotide injections for scalp regeneration
• Home use of an LLLT device three times weekly

Lifestyle anchors including adequate protein intake, stress regulation and restorative sleep remain in place throughout, because without them the gains are harder to maintain.  Maintenance then becomes the rhythm: in-clinic sessions every 4–6 months, continued home actives and periodic reassessment to adapt the plan as the hair and the patient’s life evolve.

The point of Step 7 is not to overwhelm the patient with an encyclopaedia of interventions but to identify the right combination for their stage, type and cause of hair loss.  For some, that will be a leaner regimen; for others, especially where the window to preserve follicles is narrowing, it will mean a more intensive stack.  Either way, the aim is the same: to shift the biology in favour of growth and keep it there for as long as possible.

Hair Transplant

For some patients, even the most comprehensive programme of nutrition, supplementation, topical stimulation, hormonal optimisation and in-clinic treatments will eventually meet its biological limits.  Once follicles have miniaturised beyond recovery, there is no medical intervention that can coax them back into meaningful growth.  At that point, hair transplantation becomes the final, definitive option - not as a failure of the earlier steps, but as their logical conclusion.

I have been through this process myself.  My own transplant was carried out by Mr Christopher D’Souza at The D’Souza Clinic in London and I wrote about the experience for The Tweakments Guide.  Approaching surgery as both a doctor and a patient gave me a unique perspective on how meticulous planning, artistry and surgical precision come together in this field.  Dr D’Souza’s approach is based on an intrinsic understanding of hairline design as much as graft survival, the goal being a result that grows in harmony with the patient’s natural pattern, age and facial structure.  The surgery itself was uneventful and surprisingly comfortable, with the real transformation occurring gradually over the following year to eighteen months as transplanted hairs emerged, matured, and blended seamlessly with my existing hair.

This being said, a successful transplant is never a standalone solution.  It works best when the groundwork has been laid with lifestyle and other interventions.  This ensures that the native hairs surrounding the transplant are preserved, and that the new grafts grow in the healthiest possible conditions.  The process is not instant.  In the first few weeks there is often a temporary shedding of both transplanted and nearby native hairs, followed by a quiet phase where nothing seems to be happening.  Regrowth typically begins at around three to four months, with density and refinement building steadily over the next year to eighteen months.  The choice of surgical technique, whether follicular unit excision (FUE) or follicular unit transplantation (FUT), depends on the donor area, desired density, lifestyle considerations and the long-term preservation of the donor supply.

CONCLUSION

Hair restoration is about creating the right conditions, deploying the right interventions at the right time and sustaining them so the gains are both visible and lasting.  Whether you are taking your first step towards improving scalp health or are considering the final, surgical stage, the process begins in the same place: a thorough understanding of your hair’s biology, its challenges and the options available.  The best results come from a plan built specifically for you, grounded in evidence and executed with precision.  If you are ready to explore what that plan could look like, I would encourage you to book a consultation at one of my clinics, where we can assess your hair health in detail and chart the most effective, personalised course forward.

References

Waniczek, D., Ostrowska, K., Olszewska, A., Snela, S., Kaminska, M. and Lasek, W. (2024) ‘Efficacy of Platelet-Rich Plasma in Androgenetic Alopecia Combined with Minoxidil: A Meta-Analysis’, Journal of Cosmetic Dermatology, 23(1), pp. 15–28. Available at: https://pubmed.ncbi.nlm.nih.gov/38789807/ (Accessed: 15 August 2025).

Fabbrocini, G., De Vita, V., De Padova, M.P., Cacciapuoti, S., Sirico, A. and Lembo, S. (2014) ‘Androgenetic Alopecia Treatment Using PRP’, Dermatologic Therapy, 27(3), pp. 276–277. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC3746236/  (Accessed: 15 August 2025).

Avci, P., Gupta, A., Clark, J., Wikonkal, N. and Hamblin, M.R. (2014) ‘Low-Level Laser (Light) Therapy (LLLT) for Treatment of Hair Loss’, Lasers in Surgery and Medicine, 46(2), pp. 144–151. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC11023987/ (Accessed: 15 August 2025).

Kim, J.H., Seo, Y., Choi, M.R., Kang, B. and Lee, S. (2025) ‘Effectiveness of Polynucleotide Injections for Androgenetic Alopecia’, Journal of Dermatological Treatment, [Epub ahead of print]. Available at: https://pubmed.ncbi.nlm.nih.gov/39951159/ (Accessed: 15 August 2025).

Liu, Y., Jiang, X., Wang, M., and Yu, W. (2023) ‘Exosome Therapy for Hair Loss: Potential and Challenges’, Journal of Cosmetic Dermatology, 22(4), pp. 1234–1242. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC12305264/ (Accessed: 15 August 2025).

Smith, A. (2025) ‘Exosome Therapy for Hair Loss’, ResearchGate. Available at: https://www.researchgate.net/publication/391807226_Exosome_Therapy_for_Hair_Loss (Accessed: 15 August 2025).