Why "Start Early" Isn't a Marketing gimmick - The Science of Hair Follicle Miniaturization

I was 23 years old when I first started noticing my hair fall off. You can read about that story in my previous article. However, it took me over one and a half years before I actually started using minoxidil and finasteride. But at this point I had a very prominent bald spot with very tiny baby hairs on my crown. And it was easily visible.

Throughout the next year of using the medication, I was able to grow back a considerable amount of hair and get back density. But even after almost 12 months of use, I still haven't been able to get to that very dense locks of hair that I used to have. There was a considerable improvement, however, not to how my hair originally was.

And this is why the old adage goes as such: you want to start treatment as early as possible. Because it is easier to stop the progress of hair loss than to actually regrow it. And next I'll run you through the science of why that is.

1. What Miniaturization Actually Is

Every hair on your scalp sits in a follicle that cycles through phases — a long growth phase (anagen), a short transition phase, and a resting phase (telogen) before the hair sheds and the cycle starts again. In a healthy follicle, anagen lasts years, which is why scalp hair can grow long. In a follicle exposed to DHT — the more potent form of testosterone that your enzyme 5-alpha reductase converts it into — something changes cycle over cycle. DHT binds to androgen receptors sitting in the dermal papilla, the tiny cluster of cells at the base of the follicle that essentially acts as the hair's engine room. That binding shortens the anagen phase a little each cycle, and the follicle itself gets a little smaller each time it restarts. Do this over enough cycles, and a follicle that used to produce a thick, pigmented terminal hair starts producing a short, fine, colourless vellus hair instead — the "baby hairs" I had on my crown before starting treatment. That's miniaturization: not the follicle dying in one dramatic event, but the follicle downgrading itself, cycle after cycle, until what it produces is barely worth calling hair.

Here's the dumbed-down version, because that paragraph reads like a textbook and none of us actually think in dermal papillae. Imagine your hair follicle is a phone battery. Every charge cycle it holds a little less than the one before — not because anything catastrophic happened, just wear, cycle after cycle. Early on, you don't notice: 98% capacity feels identical to 100%. By the time you're down to 40%, you're annoyed but the phone still basically works. DHT does the same thing to a follicle, except instead of "battery health," the number that's quietly dropping every cycle is hair thickness and growth duration — and unlike your phone, there's no settings menu warning you it's happening. You just wake up one day, someone tells you "adoh are you losing your hair," and you go check the drawer for the charger you thought you still had two years of life left on.

2. Follicular Atrophy — The Point of No Return

Here's the part that matters more than the metaphor: miniaturization doesn't happen smoothly. It's been described in the dermatology literature as a series of comparatively large step-changes rather than a gradual slide — each step driven by a further drop in the number of cells in the dermal papilla. And that number matters enormously, because every new hair cycle needs papillary cells to be recruited to kick it off. Fewer cells, weaker recruitment, smaller follicle, thinner hair — and the cycle repeats with less to work with each time.

Push this far enough, and you cross into what's called follicular atrophy: the follicle's dermal papilla has shrunk below the threshold needed to produce a visible hair shaft at all. At that point the follicle is still technically there, but functionally it's gone quiet — it isn't dying dramatically, it's just no longer got enough working parts to build anything. This is the "point of no return" people mean when they talk about hair loss becoming permanent. It's not a switch that flips on a certain birthday. It's a threshold that gets crossed quietly, follicle by follicle, usually years before it's visible in the mirror.

3. Why Medical Therapy Stops Progression Better Than It Reverses It

This is exactly why my own year on minoxidil and finasteride gave me real, meaningful improvement — but not a full return to my original density.

Finasteride works "upstream": it blocks the 5-alpha reductase enzyme, which means less testosterone gets converted to DHT in the first place, which means less DHT is available to keep shortening each cycle. That's excellent at halting further miniaturization. What it doesn't do is walk into an already-atrophied follicle and rebuild the dermal papilla cell count that's been lost. You can't un-shrink an engine room that's already been stripped for parts by switching off the thing that stripped it.

Minoxidil works differently and slightly more usefully for existing damage — it's thought to extend the anagen phase and improve blood flow to the follicle, which can genuinely thicken and re-lengthen follicles that are miniaturized but not yet atrophied. That's the regrowth people do see. But a follicle that's already crossed into atrophy has nothing left for minoxidil to stimulate — there's no papilla left to extend a cycle for.

Put the two together, which is what I was doing, and you get the actual real-world outcome I described above: meaningful regrowth in the follicles that were miniaturized-but-salvageable, and no regrowth at all in the follicles that had already crossed the line before I started. Not a treatment failure. A timing outcome.

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One of my buddies from uni — he's balding as well, and he happens to be a doctor too — when I told him to just get on minoxidil and fin, he simply retorted with "no bro, I'll just get a transplant later." This is a terribly misinformed and uninformed way of thinking, and coming out of a doctor's mouth, it shows how uninformed we are in general when it comes to hair regrowth. To know exactly why this is the wrong way to think about it, read my next article on hair transplants.

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Scientific Citations

1. Pathogenesis of Androgenetic Alopecia. Clinical Dermatology Review (2022). Describes the dermal papilla/dermal sheath cell disruption underlying follicular miniaturization, androgen receptor and 5-alpha reductase activity differences between balding and non-balding follicles, and the progressive shortening of anagen with constant/prolonged telogen. https://journals.lww.com/cddr/fulltext/2022/06020/pathogenesis_of_androgenetic_alopecia.3.aspx
2. Using the Mechanisms of Action Involved in the Pathogenesis of Androgenetic Alopecia to Treat Hair Loss. (2025). Details the DHT–androgen receptor binding process specifically within dermal papilla cells and how this transactivation process drives follicle miniaturization. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12608207/
3. Possible mechanisms of miniaturization during androgenetic alopecia or pattern hair loss. Journal of the American Academy of Dermatology (2001). Source for the "step-change rather than gradual" model of miniaturization, tied directly to reductions in dermal papilla cell number — the basis for the follicular atrophy / point-of-no-return framing above. https://www.sciencedirect.com/science/article/abs/pii/S0190962201432804
4. Effectiveness of Combined Oral Minoxidil and Finasteride in Male Androgenetic Alopecia: A Retrospective Service Evaluation. (2024). Confirms finasteride's mechanism of halting follicular miniaturization via 5-alpha reductase inhibition, and minoxidil's separate mechanism of enhancing follicular blood flow, extending anagen, and promoting thicker hair shafts — the basis for why the two drugs address different parts of the same problem. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829753/