5-alpha reductase converts testosterone to DHT at the follicle level, and Finasteride blocks this conversion by approximately 70%. Understanding this mechanism helps you interpret why your density data looks the way it does at month 3, month 6, and beyond, and why stabilization often matters more than regrowth in the early months.
The Enzyme: What 5-Alpha Reductase Actually Does
5-alpha reductase is an enzyme found in multiple tissues throughout the body, including the prostate, skin, and hair follicles. It exists in two primary forms:
| Isoenzyme | Location | Finasteride Inhibition | Dutasteride Inhibition |
|---|---|---|---|
| Type I | Skin, sebaceous glands, liver | Minimal | Strong |
| Type II | Hair follicles, prostate | Strong (70% reduction) | Strong (90%+ reduction) |
Finasteride (1mg, brand name Propecia) selectively inhibits the Type II isoenzyme. This is the form most active in hair follicles. By blocking Type II 5-alpha reductase, Finasteride reduces DHT concentration at the follicle level by approximately 70%, and serum DHT levels by about 65 to 70%.
Dutasteride (0.5mg, brand name Avodart) inhibits both Type I and Type II, reducing serum DHT by over 90%. This broader inhibition explains why Dutasteride is sometimes prescribed when Finasteride alone is insufficient, though it carries a higher side effect profile.
The Problem: How DHT Destroys Follicles
DHT is 5 times more potent than testosterone at binding to androgen receptors. When DHT binds to the androgen receptor in a genetically susceptible hair follicle, it triggers a cascade of molecular events:
- Receptor activation: DHT binds to the androgen receptor in the dermal papilla
- Gene expression changes: The receptor-DHT complex enters the cell nucleus and alters gene transcription
- Growth factor suppression: Key growth signals (including IGF-1) are downregulated
- TGF-beta increase: Transforming growth factor beta increases, promoting follicle regression
- Miniaturization: The follicle shrinks with each successive hair cycle
- Vellus conversion: Terminal hair is gradually replaced by fine, colorless vellus hair
- Follicle death: After enough cycles of miniaturization, the follicle ceases production entirely
This process takes years. A single follicle may go through 10 to 15 progressively shorter growth cycles before it stops producing visible hair. This slow timeline is why hair loss appears gradual and why early intervention with tracking data is so valuable.
The Geographic Pattern: Why Location Matters
Not all follicles are equally sensitive to DHT. The androgen receptor density varies dramatically across the scalp:
| Scalp Region | Androgen Receptor Density | DHT Sensitivity |
|---|---|---|
| Frontal hairline | High | Very sensitive |
| Crown (vertex) | High | Very sensitive |
| Mid-scalp | Moderate | Moderately sensitive |
| Temporal points | Variable | Variable |
| Occipital (donor area) | Low | Resistant |
This geographic variation explains the Norwood pattern. Hair loss follows a predictable map because DHT sensitivity follows a predictable map. The occipital region remains resistant because those follicles have inherently low androgen receptor expression, which is why transplanted grafts from the donor area survive permanently in the recipient zone.
When you track density with myhairline.ai, scanning multiple zones reveals which areas are actively losing density (high DHT sensitivity) and which are stable (lower sensitivity). This zone-by-zone data tells you more than a single overall density number.
How Finasteride Changes the Equation
Finasteride does not eliminate DHT. It reduces it by approximately 70%. For many follicles, this reduction is enough to drop DHT below the threshold that triggers miniaturization. The follicle stops shrinking and, in some cases, begins to recover.
Here is what happens at the follicle level after starting Finasteride:
Weeks 1 to 4: Biochemical Change, No Visible Effect
Serum DHT drops within 24 hours of the first dose. Scalp DHT follows within days. However, the follicle is already in its current growth cycle phase. The reduced DHT level does not instantly reverse miniaturization. Your density scans will show no change during this period.
Months 1 to 3: The Shedding Phase
Some users experience increased shedding during this period. This is not a sign of failure. Finasteride can cause miniaturized follicles to shed their thin, short hairs and re-enter a new anagen phase. The new growth cycle, now under reduced DHT conditions, will produce a thicker hair.
Your density readings may temporarily dip by 3 to 8% during this phase. This is normal and expected.
Months 3 to 6: Stabilization Begins
The most important signal in your tracking data appears here. If Finasteride is working, your density decline stops. The month-over-month trend line flattens. This stabilization means DHT suppression has dropped below the miniaturization threshold for your follicles.
According to clinical data, 80 to 90% of men on Finasteride experience halted further loss within this timeframe.
Months 6 to 12: Early Regrowth in Responders
In approximately 65% of users, density begins to increase during this window. The increase is typically modest, in the range of 5 to 15% above the baseline. This regrowth represents follicles that were miniaturized but not yet dead, recovering to produce thicker terminal hairs under reduced DHT conditions.
Months 12 to 24: Peak Response
Maximum density improvement is usually reached between month 12 and month 24. After this point, density typically plateaus at a new, higher level that is maintained as long as Finasteride use continues.
Interpreting Your Tracking Data Through the DHT Lens
Your myhairline.ai data becomes much more meaningful when you understand the mechanism behind it. Here is how to read common patterns:
Pattern 1: Steady Decline Despite Finasteride
If density continues to decline after 12 months on Finasteride, the 70% DHT reduction may not be sufficient for your follicles. Your follicles may have:
- Exceptionally high androgen receptor density requiring more than 70% DHT reduction
- Significant Type I 5-alpha reductase activity that Finasteride does not block
- Non-androgenetic factors contributing to the loss
This pattern affects approximately 17% of Finasteride users and is the definition of a non-responder. Your tracking data identifies this early, at 6 to 9 months, rather than waiting the traditional 12 months.
Pattern 2: Stabilization Without Regrowth
Your density stops declining but does not increase. This is actually a successful outcome. It means DHT suppression is sufficient to prevent further miniaturization, but the existing miniaturized follicles have progressed too far to recover. You are in the 80 to 90% of responders, just in the stabilization subset rather than the regrowth subset.
Pattern 3: Initial Regrowth Then Plateau
Density increases for 12 to 18 months and then levels off. This is the ideal and most common responder pattern. The follicles that could be rescued have recovered, and the new density level will be maintained.
Pattern 4: Zone-Specific Response
Your frontal hairline stabilizes but your crown continues to thin, or vice versa. This reflects the variable androgen receptor density across zones. Some areas respond to 70% DHT reduction while others need more. Tracking by zone reveals this pattern that a single overall scan would miss.
The Role of Androgen Receptor Sensitivity
The CAG repeat length in the androgen receptor gene influences how sensitive each person's follicles are to DHT. Shorter CAG repeat sequences produce androgen receptors that bind DHT more effectively, making those individuals more susceptible to hair loss and potentially less responsive to partial DHT reduction.
This genetic variation explains why two men with identical DHT levels can have completely different hair loss patterns. It also explains why Finasteride works well for some men and inadequately for others. Your tracking data reflects your individual androgen receptor sensitivity without requiring genetic testing.
Combining Mechanism Knowledge With Tracking Strategy
Understanding the 5-alpha reductase mechanism informs a smarter tracking approach:
Scan multiple zones: Because androgen sensitivity varies by location, scanning only one area gives incomplete data. Track at least three zones (hairline, mid-scalp, crown) to identify zone-specific responses.
Give it time: The mechanism operates on hair cycle timescales (months, not weeks). Do not draw conclusions from less than 6 months of data.
Track thickness, not just count: DHT-driven miniaturization reduces hair diameter before reducing hair count. A shift from thin to thicker hairs in your scan is an early positive signal, even if the total count has not changed.
Log your dose and compliance: The 70% DHT reduction requires consistent daily dosing. Missed doses allow DHT to spike, and your tracking data will reflect inconsistent use as erratic density readings.
What the Science Means for Your Decision
If your tracking data shows stabilization or regrowth on Finasteride, the mechanism is working. Your 5-alpha reductase inhibition is reducing DHT below the miniaturization threshold for your follicles. Continue the medication and continue tracking.
If your data shows continued decline, the mechanism is working (DHT is reduced) but the reduction is insufficient for your follicle sensitivity. This is when to discuss Dutasteride (which blocks both Type I and Type II, achieving 90%+ DHT reduction) with your prescriber, supported by your tracking data as evidence.
Either way, the data guides the decision. Visit myhairline.ai/analyze to start tracking your response to DHT suppression with objective density measurements.
Medical disclaimer: This article is for informational purposes only and does not constitute medical advice. Finasteride and Dutasteride are prescription medications with potential side effects including sexual dysfunction in 2 to 4% of users. Consult your dermatologist or prescribing physician for personalized treatment recommendations. myhairline.ai is a tracking tool, not a diagnostic or treatment platform.