Testosterone does not directly cause hair loss. The actual culprit is DHT (dihydrotestosterone), a hormone derived from testosterone through an enzyme called 5-alpha reductase. Whether DHT causes your hair to thin depends on your genetic follicle sensitivity, not your testosterone levels.
This distinction matters because many men avoid treatments that affect testosterone when the real target is DHT conversion. Understanding the mechanism helps you make better treatment decisions.
Step 1: Understand the DHT Pathway
Testosterone circulates in the bloodstream and reaches hair follicles on the scalp. At the follicle, the enzyme 5-alpha reductase converts a portion of testosterone into DHT.
DHT binds to androgen receptors on genetically susceptible hair follicles. This binding triggers a process called follicle miniaturization: the follicle gradually shrinks, produces thinner and shorter hairs, and eventually stops producing visible hair entirely.
Key facts:
- DHT is 2 to 3 times more potent than testosterone at binding androgen receptors
- Only scalp follicles in the frontal and vertex regions are typically susceptible
- Follicles on the back and sides of the head (donor area) are genetically resistant to DHT
- This DHT resistance is why transplanted hair from the donor area is permanent
Step 2: Recognize That Testosterone Levels Are Not the Problem
A common misconception is that high testosterone equals more hair loss. Research does not support this.
Men with androgenetic alopecia often have normal testosterone levels. The determining factor is the density of 5-alpha reductase and androgen receptors in scalp follicles, both of which are inherited.
Two men with identical testosterone levels can have completely different hair loss outcomes. One may reach Norwood 7 (5,500 to 7,500 grafts needed for restoration) by age 40, while the other keeps a full head of hair for life. The difference is genetic follicle sensitivity, not hormonal levels.
This also means that testosterone replacement therapy (TRT) does not automatically cause hair loss. It may accelerate loss in men who are already genetically predisposed, but it does not create susceptibility where none exists.
Step 3: Learn How DHT Blockers Work
The primary pharmaceutical approach to androgenetic alopecia targets the DHT pathway directly.
Finasteride (1 mg daily):
- Blocks Type II 5-alpha reductase
- Reduces scalp DHT by approximately 60 to 70%
- Halts further hair loss in 80 to 90% of men
- Produces visible regrowth in approximately 65% of men
- Sexual side effects reported in 2 to 4% of users, typically reversible
- Onset of results: 3 to 6 months
Dutasteride (0.5 mg daily):
- Blocks both Type I and Type II 5-alpha reductase
- Reduces DHT by approximately 90%
- More effective than finasteride but with higher side effect incidence
- FDA approved for BPH, used off-label for hair loss
Neither medication lowers testosterone levels significantly. They specifically target the conversion of testosterone to DHT. This is why libido and muscle mass are generally unaffected in 96 to 98% of users.
Step 4: Map Your Genetic Risk
Androgenetic alopecia is polygenic, meaning multiple genes contribute. The androgen receptor (AR) gene on the X chromosome plays a significant role, which is why maternal family history is often predictive, though paternal genes also contribute.
Risk indicators:
- Father, maternal grandfather, or uncles with significant hair loss
- Early onset of temple recession (before age 25)
- Visible miniaturized hairs at the temples or crown
- Progressive thinning that follows the Norwood pattern
If you have strong genetic risk factors and are at Norwood 2 (800 to 1,500 grafts) or early Norwood 3 (1,500 to 2,200 grafts), starting finasteride early provides the greatest long-term benefit. Men who begin DHT-blocking treatment at earlier stages preserve more native hair and have better outcomes over 5 to 10 years.
Step 5: Combine Treatments for Maximum Effect
Blocking DHT addresses the root cause, but combining it with treatments that stimulate growth produces better results.
Optimal combination protocol:
- Finasteride 1 mg daily (blocks DHT production)
- Minoxidil 5% topical or low-dose oral (stimulates growth, 40 to 60% regrowth rate)
- Ketoconazole shampoo 2 to 3 times per week (reduces scalp DHT and inflammation)
This triple therapy is the strongest non-surgical protocol available. At Norwood 2 to 3, it can halt progression and produce meaningful regrowth in the majority of users.
For Norwood 4 and above (2,500 to 3,500+ grafts), medication maintains existing hair but surgical restoration (FUE, 90 to 95% graft survival, 7 to 10 day recovery) is typically needed for visible improvement.
PRP therapy ($500 to $2,000 per session, 30 to 40% density increase) can supplement either a medical or surgical plan.
The DHT Paradox: Body Hair vs. Scalp Hair
One of the more confusing aspects of DHT is that it stimulates hair growth on the body and face while causing hair loss on the scalp. This is because body hair follicles and scalp follicles respond differently to the same hormone.
Body hair follicles are androgen-dependent: they need DHT to enter and sustain the growth phase. Scalp follicles in genetically susceptible areas are androgen-sensitive in the opposite direction: DHT causes them to miniaturize.
This paradox explains why men with significant body hair can simultaneously experience significant scalp hair loss. The two processes are driven by the same hormone acting on different receptor configurations.
Know Your Current Stage
Understanding the DHT pathway is the foundation of treating androgenetic alopecia, but every treatment decision starts with knowing where you currently stand on the Norwood scale. Over 60% of men misidentify their own stage, leading to mismatched treatments.
Get a free, AI-powered assessment at myhairline.ai/analyze. Upload your photos and receive an objective Norwood classification in under 60 seconds.
Medical disclaimer: This article is for informational purposes only and does not constitute medical advice. Hormonal treatments for hair loss should be prescribed and monitored by a qualified medical professional. Do not adjust testosterone or DHT-related medications without consulting your doctor.