When someone comes to see me about hair loss, the first question is often:
“What can I use to make my hair grow?”
That is understandable.
But before choosing a medication, supplement, injection or procedure, I think there is a more important question:
What is happening to the hair follicle?
Hair loss is not one disease.
Some forms are nonscarring, meaning the follicle remains present. Others are scarring, meaning inflammation or another destructive process can damage and eventually destroy the follicle itself.
And many patients have more than one hair-loss process occurring at the same time.
That is why I often think in terms of what is dominant.
A patient's hair loss may be nonscarring-dominant today but have an inflammatory or scarring component that requires attention. Another patient's scarring process may be the immediate threat even though androgenetic hair loss is also present.
“Dominant” is not another diagnosis.
It simply asks:
Which process is most important in determining what we should do right now?
And the dominant process can change over time.
Before we talk about regrowth, therefore, we need to ask:
Is the follicle still there—and what condition is it in?
The hair that you see above your scalp is the finished product.
The structure responsible for producing it—the hair follicle—extends beneath the skin.
A follicle may be:
Two people can therefore have areas that look similarly thin but possess very different possibilities for preservation or regrowth.
That is why every thinning scalp should not automatically receive the same “hair-growth treatment.”
With nonscarring alopecia, the follicle has not been destroyed by scar tissue.
Common examples include:
Pattern hair loss illustrates the concept particularly well.
A follicle may progressively produce hair that becomes:
Thick → thinner → shorter → finer → less visible
The follicle may still be present even when its hair has become so fine or short that it contributes very little to the visible appearance of the scalp.
This produces an important principle:
Nonscarring does not automatically mean fully regrowable.
A severely miniaturized or long-inactive follicle may have limited ability to produce cosmetically meaningful hair even though scar tissue has not destroyed it.
But the opposite is equally important:
Long-standing does not automatically mean hopeless.
The number of years that hair loss has been present does not, by itself, tell us what remains possible.
A better question is:
What is the condition of that follicle today?
Hair loss associated with GLP-1–based medications has become an increasingly common patient concern.
Patients now ask about semaglutide (Wegovy® / Ozempic®) and tirzepatide (Zepbound® / Mounjaro®) and whether these medications can cause hair loss.
Current evidence suggests that there is a real association, particularly with the more effective weight-loss medications, although the biology is still being clarified.
The leading explanation is often telogen effluvium—a nonscarring shedding process that may follow rapid or substantial weight loss, reduced caloric or protein intake, nutritional changes or other metabolic stress. Telogen effluvium can also make a previously subtle case of androgenetic alopecia suddenly become much more visible.
This distinction matters.
A patient who begins shedding after substantial weight loss should not automatically conclude:
“The medication destroyed my follicles.”
But we should not automatically dismiss the complaint either.
We should ask:
Is this temporary diffuse shedding?
Has underlying pattern hair loss become more visible?
Is nutrition adequate?
Is another medical problem contributing?
Or is there something occurring on the scalp that has nothing to do with the GLP-1 medication?
And if there is itching, burning, tenderness, focal loss or evidence of scarring, I would be especially reluctant to explain everything away as “GLP-1 hair loss.”
This rapidly evolving subject deserves a separate discussion:
GLP-1 Hair Loss: What We Know About Semaglutide, Tirzepatide and Telogen Effluvium
Scarring hair loss—also called cicatricial alopecia—is fundamentally different.
Here, inflammation or another destructive process damages the follicle itself.
If the process continues long enough, the progression may become:
Inflammation → follicular damage → scarring → permanent follicular loss
Examples include:
CCCA is particularly important in my practice and is an important cause of scarring hair loss among Black women.
With a scarring alopecia, the treatment conversation changes.
The first priority may not be:
“How do we make more hair grow?”
It may be:
“How do we prevent additional follicles from being permanently lost?”
That gives us one of the central principles of my approach:
Control what is active. Preserve what is threatened. Then pursue additional growth where possible.
Once a follicle has been completely destroyed and replaced by scar tissue, current medications cannot recreate that follicle.
That makes timing important.
Patients understandably judge treatment by regrowth.
But in a progressive hair disorder, preventing additional loss may itself represent successful treatment.
Imagine that you first sought treatment ten years ago and your hair today looks approximately the way it did then.
You might understandably conclude:
“Nothing happened.”
That may not be true.
If the untreated disease would otherwise have continued destroying or progressively miniaturizing follicles, something important may have happened:
Your hair may have been preserved.
That is why I ask two different questions:
How much hair did we grow?
and
How much hair did we save?
Both matter.
Hair-loss diagnoses are not mutually exclusive.
A patient may have:
CCCA + female pattern hair loss
or
traction alopecia + androgenetic alopecia
or
an inflammatory scarring process + telogen effluvium
or even several processes together.
This explains why treating one diagnosis may improve the hair without completely restoring it.
A growth-promoting medication may strengthen miniaturized living follicles while untreated inflammation continues threatening others.
Conversely, controlling inflammation may successfully preserve threatened follicles without fully reversing a separate pattern of androgenetic miniaturization.
This is precisely why the word dominant becomes useful.
The dominant process can change over time.
And treatment should change accordingly.
Traction alopecia beautifully demonstrates why the scarring-versus-nonscarring distinction matters.
Repeated pulling from braids, twists, extensions, weaves, wigs, locs, ponytails or other styling practices may initially injure follicles without permanently destroying them.
At that stage, removing or reducing the mechanical force may permit recovery.
But chronic traction can eventually result in follicular dropout and permanent scarring.
So a patient with thinning “edges” may have neighboring follicles that are:
healthy → stressed → injured but viable → severely damaged → permanently lost
That creates another principle:
Remove damaging traction before asking the follicle to grow.
This will be explored further in:
Hairline & Edges: When Traction Becomes Hair Loss
Hair loss is not only something we see.
Sometimes the scalp tells us that something is happening.
Patients may say:
“My scalp itches.”
“My edges hurt.”
“It burns sometimes.”
“My scalp feels sore.”
“It is tender when I move my hair.”
Those statements matter.
Inflammation does not always announce itself with dramatic redness or dandruff.
And itching or soreness does not automatically mean that an inflammatory hair-loss disease is present.
Symptoms may also result from:
Therefore:
Itch or tenderness does not give us the diagnosis. It tells us to look for the diagnosis.
But there is an equally important opposite principle:
No itch does not prove that there is no inflammation.
Some inflammatory scarring alopecias can progress quietly.
This deserves its own discussion:
Itch, Tenderness or Soreness Changes the Plan
For now, remember:
A quiet scalp provides the best foundation for hair growth.
Sometimes the distinction is obvious.
Sometimes it is not.
One important clue is whether the normal openings from which hairs emerge—the follicular openings or ostia—remain visible.
Dermatologists may use trichoscopy, magnified examination of the scalp, to evaluate features such as:
But I think of the scalp as a map.
One area may contain relatively healthy follicles.
Another may contain severely miniaturized follicles.
Another may show active inflammation.
Another may already contain established scarring.
A single diagnostic label may not describe every area of the scalp equally well.
Sometimes history, examination and trichoscopy provide enough information.
Sometimes they do not.
A carefully selected scalp biopsy can help determine whether follicles demonstrate:
The purpose of biopsy is not merely to prove that hair loss exists.
A biopsy should answer a clinical question that may change treatment.
That leads to another principle:
Sometimes the most important next treatment is a better diagnosis.
A future article will explore this in:
Why Your Dermatologist May Recommend a Scalp Biopsy
Minoxidil (Rogaine® / minoxidil) can be extremely useful for appropriately selected patients.
But it is important to understand what minoxidil can—and cannot—do.
Minoxidil may stimulate living follicles.
It cannot recreate a follicle that has already been completely replaced by scar tissue.
It does not eliminate traction.
And it does not substitute for treatment of active inflammatory scarring alopecia.
Therefore, I prefer this sequence:
Diagnose → Preserve → Control disease → Stimulate → Measure
rather than:
“Hair is thinning. Add another growth product.”
Future discussions will address topical minoxidil, low-dose oral minoxidil (Loniten® / minoxidil), finasteride (Propecia® / Proscar® / finasteride), corticosteroids and other anti-inflammatory treatments, metformin (Glucophage® / metformin), tretinoin (Retin-A® / tretinoin), platelet-rich plasma (PRP), laser treatment, transplantation and other approaches.
Every treatment makes more sense once we first understand:
Which follicular problem are we trying to solve?
I ask patients coming for hair-loss evaluation to try to locate two older photographs before the visit.
The first should be an adult photograph from a time when you were reasonably happy with the appearance of your hair.
Not necessarily your childhood hair.
Not how your hair looked at age 12.
I want an adult appearance that represents a reasonable personal restoration target.
This photograph tells us:
Where would you like to be?
The second photograph should be from around the time your hair first concerned you enough to seek treatment.
That photograph gives us:
Where did this clinical journey begin?
Your current examination then gives us:
What may still be biologically possible today?
Together:
Past baseline → patient-perceived target → present follicular potential
Those old photographs can also answer another important question:
Has the hair loss progressed, stabilized or improved?
Once again:
How much hair did we grow?
And:
How much hair did we save?
When I evaluate hair loss, I ultimately want to answer five questions:
1. What hair-loss processes are present?
2. Which process is dominant now?
3. Which follicles remain healthy, threatened, miniaturized but viable, or permanently lost?
4. Where does enough potential for preservation or regrowth remain to make treatment worthwhile?
5. What has actually happened over time—progression, stabilization or improvement?
The diagnosis gives us the name of the disease.
These questions help determine:
What should we do about it?
The most important distinction in hair restoration is not simply:
“Do you have hair loss?”
It is:
Is the follicle still there?
With nonscarring-dominant hair loss, follicles remain present, although they may be miniaturized, temporarily inactive or functioning poorly.
With scarring-dominant hair loss, follicles may be threatened by an inflammatory or destructive process and can eventually be permanently lost.
Many patients have both.
And the dominant process may change.
That is why my approach to hair restoration begins with understanding the follicle rather than immediately choosing a product.
Preserve what is threatened.
Control what is active.
Strengthen what is viable.
Restore what remains possible.
The ultimate question is not merely:
“What is the name of my hair loss?”
It is:
This article is the starting point.
Future discussions in the Hair Preservation & Restoration series will explore:
Hairline & Edges: When Traction Becomes Hair Loss
Itch, Tenderness or Soreness Changes the Plan
Why Your Dermatologist May Recommend a Scalp Biopsy
CCCA: Control the Inflammation Before the Follicle Is Lost
Female Pattern Hair Loss: Miniaturized Does Not Necessarily Mean Dead
GLP-1 Hair Loss: What We Know About Semaglutide, Tirzepatide and Telogen Effluvium
Why Minoxidil Works Better for Some People Than Others
Low-Dose Oral Minoxidil: Benefits, Risks and Monitoring
Because the science changes.
And your treatment should be allowed to change with it.
Leon E. Brown, MD
Board-Certified Dermatologist
Practicing Dermatology Since 1982
This article is provided for general educational purposes and does not replace an individualized medical evaluation, diagnosis or treatment plan.
