Published
9 minute read
If your hairline is moving backwards or the crown is becoming easier to see, you probably want to know two things:
Why is this happening, and can I stop it?
For most men with gradual hairline recession or crown thinning, the answer is androgenetic alopecia, better known as male pattern hair loss.
It is driven primarily by genetics and the way susceptible hair follicles respond to dihydrotestosterone, or DHT. Those follicles gradually become smaller and produce progressively finer, shorter hairs. This process is called miniaturization. [1]
But not every man losing hair has male pattern baldness.
Stress, illness, rapid weight loss, medications, autoimmune disease, inflammation and other medical problems can cause very different types of hair loss.
That's why my first question isn't:
“What treatment do you want?”
It's:
“What kind of hair loss do you actually have?”
Male pattern hair loss is primarily the interaction between genetics and androgen signalling.
Testosterone is converted into DHT by an enzyme called 5-alpha-reductase. In genetically susceptible follicles, particularly around the hairline, mid-scalp and crown, DHT contributes to progressive miniaturization. [1,2]
The important word is susceptible.
You don't simply go bald because you have “too much testosterone.”
Two men can have similar circulating testosterone levels and completely different hair patterns because their follicles respond differently to androgen signalling.
Male pattern hair loss is also polygenic. There isn't one baldness gene, and you don't inherit it exclusively from your mother's father. Modern genetic research has identified hundreds of genetic regions associated with androgenetic alopecia. [1]
So blaming Grandpa on your mother's side is medically convenient, but not particularly accurate.
A surprising number of things get blamed for hair loss.
Wearing a hat does not cause androgenetic alopecia.
Normal shampooing does not cause androgenetic alopecia. Washing your hair may make shedding hairs more visible because hairs already at the end of their growth cycle come out in the shower.
Hair products do not usually cause male pattern baldness. Certain harsh practices can damage or break the hair shaft, but that is different from genetically driven follicular miniaturization.
Stress doesn't create male pattern baldness. Significant physical or emotional stress can cause a separate condition called telogen effluvium, where more hairs enter the shedding phase. That may temporarily make existing pattern loss look much worse.
And again:
Male pattern baldness does not simply mean your testosterone is unusually high.
The problem is the response of genetically susceptible follicles to androgen signalling.
Classic male pattern hair loss usually develops gradually.
You may notice:
If your hair is suddenly coming out everywhere, falling out in patches, or associated with redness, scaling, pain, itching or scarring, I want to think differently.
Rapid diffuse shedding can occur after illness, surgery, major stress, rapid weight loss or significant nutritional change.
Patchy hair loss may suggest an autoimmune condition such as alopecia areata.
Inflammation and scarring require particular attention because some scarring alopecias can permanently destroy follicles.
Not every man with a typical receding hairline needs extensive bloodwork. But when the history or pattern is unusual, targeted investigation can be appropriate.
Diagnosis comes first.
If DHT is helping drive the problem, reducing DHT is one of the most logical ways to slow it.
The two medications most commonly discussed are finasteride and dutasteride.
Both inhibit 5-alpha-reductase, the enzyme involved in converting testosterone into DHT.
Finasteride primarily blocks type II 5-alpha-reductase. Finasteride 1 mg is authorized in Canada for male androgenetic alopecia. [3]
Dutasteride inhibits both type I and type II forms of the enzyme and suppresses DHT more substantially. Studies generally find dutasteride more effective for hair growth than finasteride, although oral dutasteride is used off-label for hair loss in Canada. [4]
This doesn't mean every patient should automatically take dutasteride.
Medication is an individual discussion involving expected benefit, sexual side effects, fertility considerations, medical history and patient preference. [3]
But if I am trying to preserve a man's native hair over the long term, controlling DHT is often an important part of that conversation.
Minoxidil works differently.
It does not block DHT.
Instead, it acts on the hair-growth cycle and can help maintain hairs in their active growth phase longer.
Topical minoxidil has longstanding evidence for male pattern hair loss and remains an established treatment. [2,5]
Low-dose oral minoxidil is increasingly used off-label in selected patients. It can be useful when topical treatment is inconvenient or poorly tolerated, but because minoxidil was originally developed as a blood-pressure medication, oral treatment requires appropriate medical assessment.
DHT blockers and minoxidil therefore solve different parts of the problem.
One primarily addresses the hormonal driver of miniaturization.
The other supports hair growth.
For some patients, combination treatment makes sense.
Platelet-rich plasma, or PRP, involves drawing the patient's blood, concentrating the platelet-containing plasma and injecting it throughout the scalp.
Meta-analyses suggest that PRP can improve hair density in androgenetic alopecia, but the literature is highly variable. Different studies use different preparation systems, platelet concentrations, activation protocols, injection depths and treatment schedules. The patient's own plasma also varies biologically. [6]
At FORM, when I want to add a procedure-based treatment to a medical hair-restoration program, I generally use Alma TED in lieu of PRP.
TED stands for trans-epidermal delivery. It uses low-frequency ultrasound and acoustic pressure to improve penetration of a defined topical formulation through the scalp without repeated needle injections.
For me, its appeal is partly reproducibility.
We remove several variables inherent to PRP: how the patient's plasma is constituted, how it is prepared and how consistently hundreds of injections are placed.
The important thing to note is that TED and PRP are used as adjuncts, not as a substitute for treating the underlying androgenetic alopecia.
There is legitimate evidence behind low-level light therapy, also called LLLT, red-light therapy or photobiomodulation.
A 2025 systematic review and meta-analysis involving more than 3,000 patients found that low-level laser and LED treatment significantly improved hair density in androgenetic alopecia compared with placebo. [7]
That doesn't mean any red light pointed at your head will regrow hair.
Devices differ considerably in wavelength, power, scalp coverage and treatment schedule.
And the evidence regarding whether LLLT meaningfully improves results on top of good medical therapy is mixed. Some analyses suggest an additional benefit with minoxidil, while others have not found a significant difference. [7]
I therefore view red light as another supportive tool, particularly for someone looking for a non-invasive adjunct.
I don't view it as a replacement for controlling progressive DHT-mediated hair loss.
A hair transplant does something none of these treatments can do:
It moves permanent donor hair into an area where hair has already been lost.
But a hair transplant does not stop future hair loss.
That distinction is critical.
If I transplant a beautiful frontal hairline while the native hair immediately behind it continues rapidly miniaturizing, we haven't solved the long-term problem.
This is why I generally want to understand and, where possible, stabilize the hair loss before transplantation. Current reviews of hair-transplant candidacy similarly emphasize medical optimization and long-term donor planning. [8]
Your donor hair is finite.
Whether we use manual FUE, device-assisted FUE or ARTAS robotic FUE, the fundamental questions are the same:
The extraction technology is a tool.
The strategy matters more.
Usually, it isn't one treatment.
My approach at FORM Face + Body in Toronto is to think about male hair restoration in stages.
First, diagnose the hair loss.
Is this androgenetic alopecia, temporary shedding, inflammation, a medical problem or something else?
Second, preserve what you have.
For androgenetic alopecia, that may involve a DHT blocker, minoxidil or both.
Third, add supportive treatments when they make sense.
That may include Alma TED or low-level red-light therapy.
Fourth, restore what medication cannot restore.
Once an area is substantially bald, medication cannot reliably recreate the density that used to be there. That's where hair transplantation may have a role.
The biggest mistake is waiting until you've lost most of your hair before thinking about preservation.
Hair restoration isn't only about putting hair back. It's about protecting the hair you still have and planning intelligently for the hair you may lose in the future.
A medical assessment is required to determine the cause of hair loss and which treatments are appropriate. Prescription medications have potential risks and contraindications and must be considered individually. This article is educational and is not a substitute for individual medical advice.
References
