Male pattern baldness is a household phrase. The clinical name is androgenetic alopecia (AGA). They mean the same thing: a genetically inherited sensitivity of certain hair follicles to androgens, primarily dihydrotestosterone (DHT), that gradually shrinks those follicles until they stop producing visible hair.
It is by far the most common cause of hair loss in adult men. Roughly half of men show visible signs by age 50, and the underlying process can begin as early as the late teens or twenties. This page covers what's actually happening biologically, how the condition progresses, and what the staging system clinicians use looks like.
If you're looking for treatment-focused content, see our guides on how minoxidil works and the broader how to stop hair loss framework.
The hormonal driver: DHT
Testosterone, the primary male sex hormone, is converted into a more potent androgen called dihydrotestosterone (DHT) by an enzyme called 5-alpha reductase. DHT plays important roles during development and adulthood, but on the scalp of men with androgenetic alopecia, it's also the key driver of hair loss.
Genetically susceptible follicles, primarily on the top, front, and crown of the scalp, have receptors that bind DHT readily. When DHT binds, it triggers a cascade that progressively shrinks the follicle, a process called miniaturization. The follicles on the back and sides of the head, which is why hair transplants take grafts from there, are genetically resistant to DHT and don't undergo the same shrinkage.
This is why androgenetic alopecia produces a recognizable pattern: the genetically vulnerable follicles thin out, while the resistant ones at the sides and back are spared.
What miniaturization actually looks like
A healthy hair follicle cycles through three phases:
- Anagen: the active growth phase, lasting 2 to 6 years.
- Catagen: a brief transition phase, about 2 weeks.
- Telogen: a resting phase of 2 to 4 months, after which the hair sheds and a new one grows from the same follicle.
In a healthy scalp, around 85 to 90 percent of follicles are in anagen at any given time, producing the thick, pigmented hair you see.
In androgenetic alopecia, DHT progressively shortens the anagen phase. Each successive cycle, the new hair grows for less time, so it ends up shorter, thinner, and lighter in color. The follicle itself also shrinks. Eventually the cycles get so short that the hair is barely visible (sometimes called "vellus" or "peach fuzz" hair), and at end stage the follicle stops producing visible hair entirely.
This is critical to understand: the follicle doesn't disappear instantly. It dies a slow death over years. Treatment can intervene at any point along this curve, but the earlier you start, the more follicles are still producing visible hair worth saving.
The Norwood scale: how progression is staged
Clinicians and researchers use the Norwood-Hamilton scale to describe how far male pattern hair loss has progressed. It runs from Stage 1 (no visible loss) to Stage 7 (advanced, with only the horseshoe of hair around the sides and back remaining).
Roughly:
- Stage 1: full hair, no visible recession. This is the baseline.
- Stage 2: slight recession at the temples, often a normal "maturation" of the hairline rather than true pattern loss.
- Stage 3: clear "M-shaped" recession at the temples. This is generally considered the first stage of true pattern hair loss. Stage 3v adds early thinning at the crown.
- Stage 4: deeper temple recession plus an obvious thinning patch on the crown, with a band of hair still separating them.
- Stage 5: the temple and crown areas start to merge as the band between them thins.
- Stage 6: the band is essentially gone; significant baldness across the top of the scalp.
- Stage 7: only the horseshoe of hair around the sides and back remains.
Most men who develop androgenetic alopecia don't progress all the way to Stage 7, and the pace of progression varies a lot. Some men sit at Stage 3 for decades; others move from Stage 3 to Stage 5 in a handful of years.
The genetics of it
Androgenetic alopecia is highly heritable. Twin studies suggest the heritability is about 80%. The genes involved are spread across multiple chromosomes, but the most important known one is on the X chromosome (which men inherit from their mother). The popular advice to "look at your maternal grandfather" is based on this, but it's an oversimplification: paternal genes matter too, and so do many smaller-effect genes.
Practically, this means: family history is informative but not deterministic. Plenty of men with bald fathers and grandfathers keep most of their hair, and plenty of men from unbalding families lose theirs. If hair matters to you, the right move is to track your own scalp with photos and consult a physician at the first signs of recession or thinning.
Why "androgenetic alopecia" matters as a label
The clinical name distinguishes pattern hair loss from other types that look similar but require different treatment:
- Telogen effluvium (stress-triggered diffuse shedding) resolves on its own once the trigger is removed.
- Alopecia areata (autoimmune patchy loss) requires immunomodulatory treatment, often steroids.
- Scarring alopecias (where follicles are destroyed by inflammation) can progress to permanent loss and require dermatologist evaluation.
- Traction alopecia (from prolonged tension on hair, e.g. tight hairstyles) requires removing the tension, not medication.
Establishing that what you have is androgenetic alopecia is the first job of a physician reviewing your case. It's the type with the strongest, most predictable response to telehealth-friendly medications. Curekey's process explicitly screens for the other types and refers them to in-person care when needed.
Treatments that target the underlying process
Because androgenetic alopecia has a clear biological mechanism (DHT-driven follicle miniaturization), the most effective treatments target that mechanism directly:
5-alpha reductase inhibitors. These block the enzyme that converts testosterone to DHT, lowering scalp DHT levels significantly. Two are commonly used:
- Finasteride (1 mg/day): blocks Type II 5-alpha reductase. The most prescribed drug for AGA. Reduces scalp DHT by roughly 60-70%.
- Dutasteride: blocks both Type I and Type II 5-alpha reductase, lowering DHT more profoundly. Used off-label for hair loss when finasteride isn't enough or to maximize results.
Minoxidil. Doesn't address DHT directly, but extends the active growth phase of the hair cycle and improves follicle size and pigmentation. Used in topical or low-dose oral form. Most effective when combined with a 5-alpha reductase inhibitor. See our in-depth minoxidil guide for the science.
Microneedling. Adjunctive: enhances absorption of topical minoxidil and may stimulate follicle activity directly. Typically used 1 to 2 times per week with a 0.5mm to 1.5mm dermaroller.
The common combination ("finasteride plus topical minoxidil") has the strongest evidence base, and it's what most dermatologists recommend as a starting point for men with progressing AGA.
What treatment can and can't do
A realistic frame:
- What treatment does well: stops or slows progression in the large majority of patients who use it consistently. Often produces visible regrowth in areas where follicles are still active (Norwood 2-4, sometimes 5).
- What treatment does less well: reverses fully advanced loss (Norwood 6-7). At those stages, follicles in the bald regions have typically been miniaturized to the point of inactivity, and medication can't reliably bring them back. Hair transplants, which move DHT-resistant follicles from the back of the scalp to the front, are the option at that point.
- What treatment can't do: change the underlying genetics. As long as you have susceptible follicles and your body produces DHT, the process is ongoing. Stopping treatment means losing the hair that was preserved by it, usually within 3 to 6 months.
This is why androgenetic alopecia is a long-term management situation, not a one-time fix.
When to seek treatment
The honest answer: as soon as you notice recession at the temples, thinning at the crown, or a wider part. Earlier is better because more follicles are still producing visible hair, and those are the easiest to keep.
A consultation with a licensed physician through Curekey gives you a medical opinion on whether your hair loss is androgenetic alopecia, what stage you're at, and what combination of treatments fits your case. The assessment takes about 5 minutes online.
Related reading
- Hair loss overview: the broader context, other causes, and treatment options
- Hair loss in men: a men-specific guide
- Receding hairline: when temple recession is maturation versus when it's the start of AGA
- How to stop hair loss: a treatment decision framework
- How minoxidil works: the science of the most-studied treatment
- Topical vs. oral minoxidil: choosing between formulations
