The same hormone that thickens hair on your jaw thins it on your scalp

Here's the part almost nobody explains. The same hormone, working through the same enzyme, pushes hair in opposite directions depending on where the follicle sits. On your jaw it makes hair coarser. On a genetically susceptible scalp it makes hair finer. Same molecule, same enzyme, opposite results.

That's not a curiosity. It's the thing that decides what any hair product can and can't do, and it's why "hair growth" isn't one process. Once you can see it, most of the marketing in this category stops being confusing and starts being obviously wrong.

This page explains the cycle underneath it. Every mechanism below carries a note saying what kind of study it came from — human, animal, or cells in a dish. That distinction does most of the work, and leaving it out is how honest sentences end up misleading people.

What are the phases of the hair growth cycle?

There are four, and each one is a distinct job rather than a stage of the same job. This is established human physiology — histology and decades of clinical observation, not an ingredient claim.

Anagen, catagen and telogen are the three classical phases. Exogen was described later as a separate, actively regulated shedding step rather than something that just happens at the end of rest. That's why some older sources list only three.

What decides how long a hair grows?

Time in anagen. That's very nearly the whole answer.

A follicle builds hair at a fairly steady rate — around a centimetre a month on the scalp, less at most other sites. So the length a hair reaches is basically growth rate multiplied by how long the follicle stays in growth before it shuts down.

Scalp follicles stay in anagen for years, so scalp hair can reach a metre or more. Eyelash follicles stay in anagen for a few weeks, so a lash reaches about a centimetre and stops. Neither follicle is working harder than the other. One just has a longer shift.

This is also why you can't make a hair grow past its own terminal length by leaving it alone for longer. Each follicle has a length it's programmed to reach. It reaches it and stops. Only something that lengthens the growth phase changes that ceiling. Nothing else does.

What decides how thick a hair is?

The diameter of the hair bulb, which is set by the size of the follicle and by how many cells are dividing in it.

Hairs come in two broad types. Vellus hairs are short, fine, pale and barely visible — the hair on most of a child's body, and on the parts of an adult's body that read as hairless. Terminal hairs are longer, thicker, pigmented and obvious — scalp, eyebrows, lashes, and in adults the beard, underarm and pubic hair.

A follicle isn't fixed as one or the other. The same follicle can convert from producing vellus hair to producing terminal hair, and back again. That conversion is behind almost every change in body hair people notice in adult life, and it's where hormones come in.

Why aren't all your hairs growing at the same time?

Because human follicles cycle independently of each other, in what's called a mosaic pattern. Right now some of your follicles are in anagen, some in catagen, some resting, some shedding.

Most animals shed in coordinated waves. People don't. If we did, we'd moult.

Two practical consequences follow, and they explain nearly every realistic timeline in hair care. First, only the follicles currently in anagen can be influenced by anything you apply — the resting ones aren't listening. Second, because they enter and leave anagen at different times, any effect builds gradually as each follicle comes into range, rather than appearing all at once.

So a fortnight isn't a test of anything. It's also why consistency beats intensity. The point is to be present when each follicle restarts, not to apply more of something on any given day.

Why does the same hormone make hair grow in one place and thin in another?

This is the genuinely counterintuitive part, and it's well established rather than controversial. What follows is human physiology and human clinical data, not ingredient research.

Testosterone is converted inside tissues, including skin, into a considerably more potent androgen called dihydrotestosterone, or DHT. The enzyme that does the converting is 5-alpha-reductase. The enzyme does one job everywhere it's found. What differs is how the follicle responds to the DHT that results.

On androgen-dependent follicles of the face, jaw, chest, abdomen and inner thighs, DHT drives the vellus-to-terminal conversion described above. More androgen signalling at those sites produces more hair, and coarser, darker hair.

On genetically susceptible follicles at the crown and temples, DHT does the reverse. Successive cycles produce progressively smaller follicles and finer, shorter hairs — a process called miniaturisation. More androgen signalling at those sites produces less hair.

The clearest demonstration is a drug rather than an argument. Finasteride inhibits 5-alpha-reductase. In the same person, at the same dose, it tends to thicken scalp hair and reduce body hair. One molecule, one enzyme, opposite directional effects, decided entirely by which follicle is receiving the signal.

That evidence is about as strong as evidence gets: large human clinical trials and decades of prescribing. It's worth being clear about what it is, though. Finasteride is a prescription medicine taken orally. It isn't a cosmetic, it isn't an ingredient in anything ungro makes, and no topical cosmetic does what it does. It's here as proof that site dependency is real, and for no other reason.

So the useful sentence is this: the follicle's response depends on where it is. "Hair growth" isn't one process happening at different intensities around the body. It's different local programmes running on the same hardware.

Are eyebrows and eyelashes affected the same way?

No, and this is worth stating clearly because it gets blurred constantly.

Brow and lash follicles aren't classic androgen-dependent follicles, and they aren't the site where DHT-driven miniaturisation happens. They're their own category: very short anagen, a short programmed terminal length, and a cycle that turns over in months rather than years.

What that means practically is that the scalp-versus-body contrast is an illustration of site dependency. It isn't a description of what happens on a lash line. Anyone who tells you a lash product works because of androgens is extending the story further than the evidence goes.

What does appear to matter at these sites is more general follicle biology: local blood supply, and the growth-factor signalling that keeps a follicle in anagen. Vascular endothelial growth factor and keratinocyte growth factor are both associated with sustaining the growth phase, and dermal papilla cells — the small cluster at the base of the follicle that acts as its control centre — are where much of that signalling is received.

Be careful with that last paragraph, including when ungro writes it. Most of the work mapping those signals was done in cell culture and in animals. It's good biology and it's the reason growth-factor ingredients get formulated at all. It is not a demonstration that applying something to a lash line changes a lash.

Why does the same enzyme turn up in products that reduce hair and products that support it?

Because 5-alpha-reductase is a step in a pathway, not an outcome. Change the pathway, and the result depends on the follicle you changed it in.

Several plant extracts interact with that enzyme. Saw palmetto is the best documented. Safflower floret extract has been reported to inhibit it too — in the same body of work that describes it doing several other things.

Here's that work, stated properly. Safflower floret extract (Carthamus tinctorius) makes dermal papilla cells and keratinocytes multiply faster, raises VEGF and keratinocyte growth factor, and suppresses TGF-beta, a signal associated with pushing follicles out of growth. It also inhibits 5-alpha-reductase. That's from Junlatat & Sripanidkulchai (2014), Phytotherapy Research 28:1030–1036.

What kind of study was that? Cells in a dish, plus cultured mouse follicles. Specifically: dermal papilla cells, HaCaT keratinocytes, and hair follicles taken from newborn mice and grown in culture. No people were involved at any point. Nothing in it concerns brows or lashes.

There's a second study, separate from that one: safflower floret extract loaded into nanostructured lipid carriers and applied to C57BL/6 mice, published as Hair growth promoting activity of Carthamus tinctorius florets extract-loaded nanostructured lipid carriers in the International Journal of Pharmacy and Pharmaceutical Sciences. It reports hair growth in the mice. That's an animal study, not a human one, and the delivery system tested was a nanostructured lipid carrier — a different vehicle from a conventional cosmetic emulsion. Two gaps there, not one.

So the honest summary of safflower is: interesting cell-culture mechanism, one supporting animal result, no human data, nothing lash-specific. That's a real reason to put an ingredient in a formula. It isn't a reason to promise anything.

Read the reduction and support findings side by side and it looks like a contradiction. It isn't. It's the site-dependency point again, plus a second point worth keeping hold of: most botanical extracts act on several pathways at once, and the enzyme is rarely the main event. A product's behaviour is the sum of what it does, not one line item from a mechanism paper.

The honest position, which isn't the position most of this category takes, is that enzyme mechanisms explain why an ingredient was chosen. They don't by themselves predict what a finished product will do to your face or your lashes. That requires testing the finished product.

What does this mean if you want less hair in one place and more in another?

It means the two goals aren't in conflict, and that no single product covers both.

Wanting a smoother jaw and fuller brows is an extremely common combination, and people are sometimes made to feel it's inconsistent. It isn't. Those are two different follicle populations, running two different programmes, responding differently to the same signals. Treating them differently is the biologically correct thing to do.

It also means you should be sceptical of any product marketed as acting on "hair growth" without saying where. The site isn't a detail. The site is the mechanism.

How long before anything changes?

Longer than most people expect, and the cycle tells you roughly how much longer.

Because only follicles in anagen are available to be influenced, the sensible unit of patience is one cycle at the site in question. Not one week, and not one bottle.

None of this is maintenance-free. Follicles keep cycling regardless of what you put on them, so any cosmetic effect on the cycle holds only while you're still applying the product. Stop, and over the following cycles things return to whatever is normal for you.

Where ungro's products sit in this

ungro makes three things, and they act on three different states of the same structure.

The Ingrown Hair Oil is for a hair that's growing normally but can't get out — an occluded follicle, or a hair that has curled back into the skin. Nothing about the cycle is wrong. The exit is blocked. The actives are a lipid complex selected on supplier data ungro hasn't independently reviewed, plus mandelic acid at 0.3% for an antibacterial contribution. That's a low dose, well below an exfoliating one, and the antibacterial evidence behind it is laboratory work rather than a human trial.

The Smooth Gel is for hair that's growing normally and isn't wanted, on the body and face. Its actives are described by their suppliers as acting on the timing of the cycle and on the local androgen pathway, so that regrowth returns finer. Those mechanisms are cellular and enzymatic — measured in assays and cell systems. ungro is standing on supplier dossiers for the outcome, and has asked for the study designs behind them.

The brow & lash serum is for hair that's wanted, at a site with a naturally short growth phase. It's built around a botanical oil-phase active from roselle flower and safflower floret. It isn't on sale yet, and the next section is about it.

Three products, three states, one structure. That's the whole range, and there's no fourth step.

What ungro's brow & lash serum has not been shown to do

This is the section most brands don't write. Read it as the standard you should hold every brand in this category to, including this one.

There is no human study on the finished formula. None. ungro has not tested this product on people for efficacy and has no consumer assessment, no instrumental measurement and no photographic study on file.

There is no lash-specific trial of anything in it. Not of the finished serum, not of the supplier's active, not of the botanicals. Every study described above was done on scalp-type follicles or on cells, in dishes and in mice. Brow and lash follicles are a different population with a different cycle, and adjacency isn't evidence.

There is no published human data on the roselle half of the active. Roselle has long traditional use in hair preparations. Traditional use is a reason to look at something. It isn't a mechanism and it isn't a result.

The ingredient was selected on mechanism and supplier data. That's the honest description of how this formula came to exist: a documented cell-culture mechanism, one animal study, and a supplier's efficacy dossier at a stated use level. It's a legitimate basis for choosing an ingredient. It's not a basis for telling you what will happen to your lashes.

So ungro isn't going to tell you. No length claim, no density claim, no count, no "clinically proven" anything. When there's human data on the finished product, this page will say so, will say how many people and over how long, and will say who paid for it. Until then this paragraph stands.

Two things follow that are worth taking with you. Ask any lash brand what was tested — the finished product, the ingredient, or neither — and how many people were in it. Most can't answer. And note that ungro's serum contains no prostaglandin analogue, which is the ingredient class behind the darkening, irritation and iris-colour concerns this category is known for. That one is simply a fact about the ingredient list, and you can check it yourself.

What this page is not

This is an explanation of normal follicle biology. It is not a diagnosis and it is not advice about your own hair.

ungro's products are cosmetics. They are not a treatment for hirsutism, polycystic ovary syndrome, alopecia or any hormonal or medical condition, and they are not a substitute for medical care. If your hair has changed noticeably or quickly, in either direction, or if the change came with other changes, that is a conversation for a doctor rather than a cosmetic purchase. Sparse lashes or brows that have thinned suddenly are also worth having looked at, because there are medical causes.

Nothing on this page describes a way to remove hair permanently, and nothing on it describes a way to make a follicle grow a hair it is not programmed to grow. Anyone claiming either from a topical product is overselling, and that alone tells you what the rest of their claims are worth.

Published by the ungro lab. ungro formulates and makes its products in small batches in New Zealand. Every mechanism on this page states what kind of study it came from. This article is general information, not medical advice.