We've covered how minoxidil works at a high level. This article goes deeper — into the follicle itself — to show exactly what's happening at each stage of the process. Think of it as zooming in from Google Maps street view to the cellular level.

The Players: Meet Your Hair Follicle

Before we add minoxidil to the picture, you need to know the key structures inside a hair follicle. Each one plays a specific role in what happens next.

Dermal Papilla (DP)

The command center of the follicle. A small cluster of specialized cells at the base of the follicle that receives blood supply and signals the surrounding cells to grow or rest. Think of it as the follicle's brain. Larger dermal papilla = thicker, more vigorous hair.

Outer Root Sheath (ORS)

The structural casing that surrounds the hair shaft as it grows. Contains the cells that form the hair itself. The outer root sheath also houses the enzymes that will become crucial in a moment — including sulfotransferase.

Hair Bulge Region

The stem cell reservoir of the follicle. Located in the upper portion of the follicle, the bulge contains multipotent stem cells that can regenerate the entire lower follicle during each growth cycle. These stem cells are why follicles can cycle through growth and rest phases repeatedly.

Perifollicular Capillaries

The network of tiny blood vessels surrounding the follicle. These deliver oxygen, nutrients, and hormones to the dermal papilla. The density and dilation of these capillaries directly affects how well-nourished the follicle is — and this is where minoxidil's primary action begins.

Arrector Pili Muscle

The tiny smooth muscle attached to the follicle that makes your hair "stand up" (goosebumps). Contains the smooth muscle cells whose potassium channels minoxidil will target. This muscle is a key access point for minoxidil's primary mechanism.

Before Minoxidil: The Dormant State

In a dormant beard follicle — the kind you're trying to activate — here's what you're starting with: a small dermal papilla that's receiving minimal blood supply, a follicle stuck in or cycling through short, ineffective anagen (growth) phases, and a hair shaft that's thin, short, and lightly pigmented — a vellus hair, if anything is growing at all.

The follicle exists. The stem cells in the bulge region are present. The machinery for growing a thick terminal hair is all there. It's just not being used. The dermal papilla is too small, the blood supply is insufficient, and the growth signal isn't strong enough to produce anything more than peach fuzz.

Now you apply minoxidil. Here's what happens, step by step.

Step 1: Sulfotransferase Converts Minoxidil to Its Active Form

Step 1

Enzymatic Activation

Minoxidil itself is actually a prodrug — it's not active in the form you apply it. It needs to be converted by the enzyme sulfotransferase into minoxidil sulfate, which is the biologically active compound. This conversion happens in the outer root sheath cells of the follicle and in surrounding skin tissue.

This step is critically important — and it's why approximately 30% of men don't respond to topical minoxidil. If your body doesn't produce sufficient sulfotransferase enzyme activity, the minoxidil you apply never gets converted to its active form. You're essentially applying an inert substance.

The non-responder problem: About 30% of men have insufficient sulfotransferase activity to adequately convert topical minoxidil into minoxidil sulfate. These men are often called "non-responders." Oral minoxidil bypasses this problem because the liver converts it systemically — but that requires a prescription and has different side effects. Read more about why minoxidil might not be working for you.

Step 2: KATP Channels Open

Step 2

Potassium Channel Activation

Minoxidil sulfate binds to ATP-sensitive potassium channels (KATP) in the smooth muscle cells of the arrector pili muscle and perifollicular blood vessels. Opening these channels causes hyperpolarization of the cell membrane — the cell becomes more negatively charged, which causes voltage-dependent calcium channels to close. With less calcium entering the cell, the smooth muscle relaxes.

This is the molecular event that starts the cascade. It's the same mechanism that makes oral minoxidil lower blood pressure — smooth muscle relaxation in blood vessel walls. But when it happens locally around a hair follicle, the effect is targeted vasodilation rather than systemic blood pressure reduction.

Step 3: Vasodilation and Blood Flow Increase

Step 3

Blood Vessels Dilate

The smooth muscle relaxation from Step 2 causes the perifollicular capillaries to widen. Wider capillaries = more blood flowing past the dermal papilla = more oxygen, glucose, amino acids, and growth factors being delivered to the follicle's command center. Simultaneously, minoxidil upregulates VEGF (vascular endothelial growth factor), which promotes the formation of entirely new capillaries around the follicle — not just widening existing ones but building new supply lines.

Think of this like upgrading a follicle's supply chain from a single dirt road to a four-lane highway. The follicle's dermal papilla has been surviving on minimal nutrition. Now it's flooded with resources it hasn't seen before.

Step 4: Dermal Papilla Enlargement

Step 4

The Command Center Grows

With increased blood supply and nutrient delivery, the dermal papilla cells begin proliferating. The papilla physically enlarges — more cells, larger structure, stronger signaling capacity. A larger dermal papilla is directly correlated with a thicker hair shaft. This is the structural change that eventually produces a visible difference: the follicle's output changes because its core has grown.

This doesn't happen overnight. Dermal papilla enlargement is a gradual process that begins in the first few weeks but takes months to translate into visibly different hair output. This is why the first few months of minoxidil use often show no visible change — the changes are happening below the surface, at the cellular level, before you can see them in the mirror.

Step 5: Anagen Phase Prolongation

Step 5

The Growth Phase Extends

Hair follicles cycle through three phases: anagen (growth), catagen (transition), and telogen (rest). In dormant beard follicles, the anagen phase is short — the follicle grows a small vellus hair for a brief period and then goes back to rest. Minoxidil, through increased VEGF expression and prostaglandin E2 (PGE2) upregulation, extends the anagen phase. The follicle grows for longer. A longer growth period = a longer, thicker hair.

PGE2 is particularly noteworthy. Prostaglandin E2 is a known hair growth stimulant, while prostaglandin D2 (PGD2) is a known suppressor. Minoxidil tips this balance toward growth by upregulating PGE2. This is a secondary mechanism — separate from the vasodilation effect — that contributes to the overall growth stimulus.

This is also the mechanism behind the shedding phase at months 2–4. Minoxidil pushes follicles in telogen (resting) phase prematurely into a new anagen (growth) phase. The old resting hair sheds to make room for the new, better-nourished growth cycle. Shedding is the transition — not a failure.

Step 6: Vellus to Terminal Conversion

Step 6

The Hair Transforms

With a larger dermal papilla, extended anagen phase, better blood supply, and increased growth factor signaling, the follicle begins producing a progressively thicker, longer, and more heavily pigmented hair shaft. What started as a thin, light vellus hair darkens, thickens, and elongates over successive growth cycles. This is the vellus-to-terminal conversion — the visible payoff of everything that's been happening below the surface.

This conversion is partially androgen-dependent. Once minoxidil enlarges the dermal papilla and extends the growth cycle, DHT in the beard area helps sustain the terminal state. This is why the permanence theory centers on the androgen paradox — beard follicles are DHT-dependent, so once they reach terminal state with androgen support, they may no longer need minoxidil to stay that way.

The full conversion takes months — typically 6 to 12 months from first visible vellus growth to fully terminal hairs. Each successive growth cycle produces a slightly thicker, darker hair until the follicle reaches its maximum output.

Why Some Men Don't Respond: The Full Picture

Now that you understand the complete cascade, you can see exactly where it can break down:

Failure at Step 1: No sulfotransferase

Minoxidil never gets converted to its active form. Everything downstream never starts. This is the most common reason for non-response (~30% of men). Solution: oral minoxidil bypasses this step entirely.

Failure at Step 6: Low androgen sensitivity

Minoxidil does everything it's supposed to — enlarges papilla, extends anagen, increases blood flow — but low androgen receptor sensitivity limits the terminal conversion. Hairs may improve but never reach full terminal status. Solution: may require TRT evaluation if testosterone is clinically low.

Failure at the follicle: No follicles present

Minoxidil cannot create new follicles. If an area of your face has zero follicles (rare, but possible), no amount of minoxidil will produce hair there. Most "bare" areas actually have dormant follicles — but truly follicle-free zones exist.

Start the Cascade

Every terminal beard hair starts with Step 1: getting minoxidil to your follicles. Happy Head makes it easy with prescription-backed formulations.

Get Started with Happy Head → Browse Minoxidil Foam →

Enhance the Process

Dermarolling activates the Wnt/β-catenin pathway and creates microchannels that support Step 3's blood flow effects. Combined with minoxidil, it produced 4x more growth in the Dhurat 2013 study.

Browse Derma Rollers →