Male Pattern Baldness: Genetics, DHT and the Norwood Scale

Male pattern hair loss, clinically androgenetic alopecia, is the most common cause of hair loss in men. Around half of men show some degree of it by their fifties, and a proportion see the first signs well before thirty.

It is not a disease and it is not a deficiency. It is an inherited sensitivity to a normal hormone, expressed in a predictable pattern over years. Understanding the mechanism makes the treatment options, and the limits of those options, much easier to make sense of.

What is actually happening

Every follicle on your scalp cycles independently: a growth phase lasting several years, a brief transition, then a resting phase before the hair is released and the cycle restarts.

In male pattern hair loss, the growth phase progressively shortens in susceptible follicles. Each cycle produces a hair that is slightly finer, slightly shorter and slightly less pigmented than the one before. Over many cycles the follicle continues to exist but produces hair too fine and short to contribute to visible coverage.

This process is called miniaturisation, and it is the actual mechanism of pattern hair loss. Hair is not falling out and failing to return. It is returning progressively smaller each time until it is effectively invisible.

Two implications follow. First, the loss is gradual rather than sudden, which is why it often goes unnoticed until a fair amount of ground has been given. Second, there is a window in which follicles are miniaturising but still alive, and a point past which there is nothing left to preserve.

See the hair growth cycle explained.

The role of DHT

The hormone driving miniaturisation is dihydrotestosterone, or DHT.

DHT is converted from testosterone by an enzyme called 5-alpha reductase. It has normal and necessary functions in male development. In susceptible scalp follicles, it binds to androgen receptors and progressively shortens the growth phase.

The critical word is susceptible. DHT does this only to follicles that are genetically sensitive to it, which is why the loss follows a pattern rather than affecting the whole scalp.

This explains the most important fact about hair transplant surgery. Follicles at the back and sides of the scalp are largely resistant to DHT, which is why most men who lose hair on top retain hair around the sides for life. When one of those follicles is moved to the front, it keeps its resistance. That property is called donor dominance, and it is the entire basis of the procedure.

Two misconceptions worth correcting:

High testosterone does not cause baldness. Men with pattern hair loss do not generally have elevated testosterone. What differs is follicular sensitivity to DHT. You cannot infer anything about your hormone levels from your hairline.

Blood flow is not the cause. Reduced scalp circulation has been proposed and is not supported as a primary mechanism. Products claiming to reverse hair loss by improving circulation are addressing something that is not the problem.

The genetics

Pattern hair loss is polygenic, meaning multiple genes contribute rather than a single one.

The androgen receptor gene sits on the X chromosome, which men inherit from their mother. This is the origin of the belief that baldness comes from your mother's side, and it is partly true.

It is not the whole picture. Genome-wide studies have identified a substantial number of loci associated with androgenetic alopecia, spread across many chromosomes, inherited from both parents.

The practical consequence: looking at male relatives on both sides of your family gives a better indication of your likely trajectory than looking at your mother's father alone. It is an indication, not a prediction. Siblings with the same parents frequently follow different courses.

What is largely inherited is the age of onset, the speed of progression, and the eventual pattern. Those three things are also exactly what a surgeon needs to estimate before operating, which is why family history comes up at consultation.

The Norwood Scale

The Norwood Scale, sometimes called the Hamilton-Norwood Scale, is the standard classification for the extent and pattern of male hair loss. It is used clinically to describe where someone currently sits and to discuss where they may be heading.

Stage I. An adolescent or juvenile hairline with no meaningful recession. Most men do not stay here into adulthood.

Stage II. Slight recession at the temples, creating a mild triangular retreat. This is usually a maturing hairline rather than the onset of baldness. The hairline typically settles around a finger's width above the highest forehead crease, and stopping there is normal.

Stage III. The earliest stage considered clinically significant. Recession at both temples is deeper and the hairline forms a distinct M, U or V shape. A variant, Stage III vertex, describes the same temporal recession accompanied by loss at the crown.

Stage IV. Temporal recession is more pronounced and there is definite loss at the crown. A band of hair still separates the two areas.

Stage V. The band between the front and crown narrows and thins. Both areas of loss are larger and the separation is becoming indistinct.

Stage VI. The bridge between front and crown has largely gone, leaving the two areas joined. Hair remains at the sides and back.

Stage VII. The most advanced stage. Only a band of hair remains around the sides and back of the scalp.

Why the stage matters for surgery

The Norwood stage is not just descriptive. It has direct consequences for what surgery can achieve.

Donor supply is finite and the demand grows with stage. Restoring a hairline at Stage III requires far fewer grafts than achieving meaningful coverage at Stage VI. At the more advanced stages, the area needing coverage may simply exceed what the donor region can supply, and the honest conversation becomes about partial coverage in the areas that matter most rather than full restoration.

Progression must be anticipated. A surgeon planning a hairline for a man at Stage III needs to consider where he will be at Stage V. Placing a low, dense hairline that looks appropriate now can look increasingly odd as the area behind it continues to thin.

Stability matters more than stage. A Stage III whose loss is progressing rapidly is a more difficult surgical case than a Stage V that has been stable for a decade, because the second is predictable and the first is not.

This is why surgeons ask about family history, rate of change, and whether you have photographs from a few years ago. The current stage is only half the information.

See are you a suitable candidate and how many grafts will I need.

What else contributes

Genetics sets the trajectory. Some other factors can influence how quickly it plays out, though none causes pattern hair loss in someone not predisposed.

Age. Progression continues over decades. The pattern at 30 is rarely the final pattern.

Anabolic steroids. Substantially raise androgen levels and can accelerate loss markedly in a susceptible man. Loss occurring during use does not simply reverse afterwards.

Smoking. Associated with earlier and more severe pattern loss in several studies.

Traction from tight hairstyles. Causes a separate condition, traction alopecia, which can compound pattern loss. See traction alopecia.

Nutritional deficiency. Iron deficiency in particular can contribute to shedding, though correcting it does not reverse pattern loss. See diet and hair health.

More detail on the accelerants in do protein powders, creatine and steroids cause hair loss and why so many men are losing hair in their twenties.

What it is not

Pattern hair loss is diagnosed partly by excluding other causes, and it is worth knowing what does not fit the picture.

Loss that is diffuse rather than patterned, patchy and circular, accompanied by scalp inflammation or scaling, sudden in onset, or occurring alongside other symptoms such as fatigue or weight change points elsewhere. Thyroid dysfunction, iron deficiency, telogen effluvium following illness or stress, alopecia areata and medication effects all present differently and several are reversible.

Getting the diagnosis right matters because the responses are not interchangeable.

See when hair loss isn't genetic.

What can be done

Realistically, three categories, and it is worth being clear about what each does.

Medical treatment can slow progression and in some cases produce partial regrowth in follicles that have miniaturised but not been lost. It requires ongoing use, since stopping generally results in resumed loss. Options have side effect profiles worth understanding and are a conversation for a doctor.

Surgery redistributes DHT-resistant follicles from the donor area to areas of loss. It does not stop ongoing loss elsewhere, which is why medical treatment and surgery are often used together.

Doing nothing is a legitimate choice. Pattern hair loss is a common, natural process and not everyone wants to intervene.

For an honest comparison, see hair loss treatments compared.

Getting assessed

If you want to know where you sit, what is driving it, and what your realistic options are, an examination is the way to find out. Assessment includes the pattern and extent of loss, density and calibre in both the recipient and donor areas, and the degree of miniaturisation present.

Dr Jassim Daood has practised for over 30 years and performs both FUE and FUT hair transplant surgery at our Bankstown clinic.

A GP referral is required before a cosmetic surgery consultation. Every surgical procedure carries risk, set out on our risks and complications page.

Book a consultation.

Related reading: how much hair loss is normal, age and hair transplants, hair transplant surgery in Sydney: the complete guide.