Research Blog

The reason people look for a topical DHT blocker is simple: oral finasteride works, but a minority tolerate it badly. The question worth asking is whether topical achieves the same thing at the follicle without the systemic footprint.

The published data is fairly consistent on this. A phase III randomised controlled trial of a topical finasteride spray found efficacy comparable to oral dosing while producing markedly lower systemic exposure and a much smaller effect on serum DHT. Earlier dose-ranging work on scalp versus serum DHT showed the same pattern — scalp DHT suppression with a fraction of the plasma concentration.

Mechanically this makes sense. Finasteride inhibits type II 5-alpha reductase. Applied to the scalp it acts where the enzyme is doing the damage, and only the fraction that crosses into circulation affects serum DHT. Oral dosing floods the whole system to reach the same follicle.

What that means in practice

• Lower plasma exposure is the entire point — it's why the sexual and mental side effect profile is generally milder
• Lower exposure is not zero exposure. Topical is not side-effect free, just further from the systemic end of the curve
• Consistency matters more than concentration. A missed week undoes more than a weak dose does
• Apply to a dry scalp, and leave it alone for about four hours so it actually absorbs rather than transferring to your pillow

Minoxidil is a vasodilator. It extends the growth phase of the follicle and increases blood flow to the dermal papilla, which is why it produces results and why those results fade when you stop.

5% versus 10%

5% twice daily is the most heavily studied protocol and remains the default. 10% once daily is a reasonable choice for people who won't reliably dose twice, or who want a shorter routine. Higher concentration is not automatically better — it also means more propylene glycol and alcohol on the scalp, which is the usual source of irritation and flaking.

Application that actually works

• 1 ml per application, on a dry scalp — water dilutes it and slows absorption
• Part the hair and get it on skin, not on the shaft
• Leave about four hours before washing
• Wash your hands afterwards, and be aware of transfer to partners and pets

The part people quit over

Expect a shedding phase somewhere around weeks two to six. It is a synchronisation effect, not a failure — follicles cycling into a new growth phase push out the old shaft. Early vellus growth appears around month two to three, visible improvement from month four, and maximum benefit around month twelve.

Androgenetic alopecia gets all the attention, but a meaningful share of shedding has an inflammatory component sitting on top of it. Seborrhoeic dermatitis — flaking, itch, redness at the hairline and brows — is driven by Malassezia overgrowth, and inflamed scalp tissue is a poor environment for a follicle.

Ketoconazole 2% shampoo addresses that directly. It's antifungal, and it also has a local anti-androgenic effect that has made it a long-standing adjunct in hair protocols.

How to use it without wrecking your scalp

• 2–3 times weekly, not daily
• Massage in, leave three to five minutes — contact time is what does the work
• Rinse thoroughly and follow with a normal conditioner; ketoconazole is drying
• Give it four to six weeks before judging whether it's helping the flaking

Most people abandon a protocol during the exact phase where it's working. Here's what to actually expect if you're consistent.

• Weeks 0–2: nothing visible. Possibly minor irritation while your scalp adjusts
• Weeks 2–6: shedding. This is the synchronisation effect and it is expected
• Months 2–3: fine vellus hairs at the hairline and temples, often only visible in photos
• Months 4–6: vellus converting to terminal, density becomes noticeable to other people
• Months 6–12: maximum benefit. Past twelve months you are maintaining, not improving

For a three-product routine that covers the three separate mechanisms — growth stimulation, DHT blockade and scalp inflammation — see the Beauty category.

Tretinoin, azelaic acid and estriol all do different things and they can be used together — but not all at once, and not from day one.

Order of application

Thinnest to thickest, always. Water-based serum first, then gel, then cream. Hyaluronic acid goes onto damp skin, not dry — it needs water to hold.

Timing

• Tretinoin: night only. It's photo-unstable and it thins the stratum corneum, so sunscreen becomes non-negotiable
• Azelaic acid: morning or night, and it layers fine with tretinoin
• Estriol: once daily, either time
• Hyaluronic acid: on damp skin, before anything occlusive

If you're new to tretinoin

Start twice weekly, buffered over moisturiser, and build to nightly over six to eight weeks. A pea-sized amount covers the whole face — more is not better, it's just more peeling. The purge around weeks two to four is real and it does end.

Lyophilised peptides are remarkably stable. Reconstituted peptides are not. Almost every "my peptide stopped working" story traces back to that difference.

Before reconstitution

• Store at −20°C, or −80°C for long-term. A domestic freezer is fine for months
• Keep away from light — the amber or opaque vial is not decoration
• Minimise freeze-thaw cycles; pull out what you need rather than warming the whole box repeatedly
• Lyophilised powder is stable for the shelf life on the label if kept cold and dry

After reconstitution

• Refrigerate at 2–8°C
• Use within about 30 days
• Do not freeze once mixed — ice crystal formation aggregates the peptide
• Swirl, never shake. Agitation denatures
• Inject the water down the vial wall, not onto the powder cake

Cloudiness, visible particles, or a gel-like texture after mixing all mean the same thing: start again.

BPC-157 is a 15-amino-acid fragment derived from a gastric protein, and it is one of the most studied peptides in the tissue-repair literature.

Mechanisms reported in models

• Upregulation of VEGFR2 signalling, driving new blood vessel formation into injured tissue
• Increased eNOS activity and improved local perfusion
• Enhanced fibroblast migration and collagen deposition
• Modulation of the local inflammatory response rather than blanket suppression of it

Where it's been studied

The bulk of the work is in tendon and ligament repair models, muscle crush injury, and gastrointestinal mucosal healing — unsurprising given its gastric origin. Rodent models dominate, which is worth keeping in mind when reading confident claims.

SARMs are selective androgen receptor modulators. The name describes the entire proposition: receptor activation with more tissue selectivity than a traditional anabolic steroid.

What's different in principle

• Tissue selectivity — the intent is anabolic effect on muscle and bone with less prostate and sebaceous gland activity
• Oral bioavailability for most compounds, so no injection
• Generally not substrates for aromatase, so no oestrogenic conversion
• No 5-alpha reduction to a more potent metabolite

What's different in practice

Selectivity is a spectrum, not a switch. Most SARMs still suppress the HPTA to some degree, which is why a post-cycle plan is still relevant. And the human evidence base is far thinner than for testosterone or nandrolone — much of what gets repeated is extrapolated from small trials and animal work.

The formula is one line, but people get it backwards constantly, so here it is with real numbers.

Volume of water = peptide mass ÷ desired concentration

A 10 mg vial at a target of 5 mg/ml takes 2 ml of water. A 5 mg vial at 2 mg/ml takes 2.5 ml. That's the whole calculation.

Drawing a dose

Concentration 5 mg/ml is 5000 mcg/ml. A 250 mcg dose is therefore 0.05 ml, which on a U-100 syringe is 5 units. On a U-40 syringe the same volume reads as 2 units — always check which syringe you have.

The calculator on the home page does both of these for you.