Wondering if anyone has this experience. I’m a NW3. I was previously on 1mg oral finasteride for 3 years and had good stabilization. But I was getting fed up with some of the side effects and switched to a 7%min/0.1% fin solution 1mL per day (so roughly 1mg of topical fin applied directly to hairline, front tuft, and crown). It’s been 6 months since switching to this new protocol.
Everything seemed fine the first three months. However I’ve seen a sharp density decline over the last 3 months. I was wondering if it could possibly be a combination of some synchronous shedding (since I had never applied min to the hairline/front tuft before) and TE (since I did a 15 week calorie deficit losing about a pound per week). I went to a dermatologist and she said it was definitely not TE since tufts of hair weren’t coming out, and she doesn’t believe topical fin works. She wanted to put me on oral min instead, as if that would help stop DHT related loss…
Idk I’m dubious of her opinion and inclined to believe chat GPT that stated stress+synchronous shed is more likely if my hairline shape has maintained and it’s mostly a density drop. I am seeing a lot of thin new growth throughout the front tuft and hairline that’s longer than vellus but still thin and lightly pigmented. I’ve heard those are supposed to shed and grow back thick. What do you guys think?
I just hope this wasn’t permanent loss ground on my baseline and even moreso I don’t want to keep blindly moving forward with topical if it is indeed not working
1)post pictures if possible. 2) if topical finasteride is not cutting it, you need under the guidance of a doctor oral dutasteride or oral finasteride. 3) it is well known that topical finasteride is inferior to oral finasteride despite blocking more DHT on the scalp to oral finasteride, topical finasteride is better in my opinion as an adjust treatment to oral finasteride at 1-1.25mg for that purpose. 4) This is the most important: you need to get a trichoscopy done to evaluate whether the shed/diffusing presents with miniaturization of hairs, keep in mind sometimes the miniaturization is observed in alopecia areata and telogen effluvium however in almost all of the cases it is due to AGA (androgenetic alopecia aka male pattern baldness). The 4) is the most important, that is the only way to be sure. Neither your doctor nor chatgpt can answer this, either get a trichoscopy done or pray that you are not balding, this is all I can say if I were to be rational. Also diffuse thinning or any type of thinning in the context of hair loss cannot be cured with any variant of minoxidil. Minoxidil exerts its effect on hair follicles through the SULT1A1 pathway and opens the potassium channels of the cell membranes which in turn hyperpolarizes the cell membranes and decrease the probability of (effectively closing) the voltage dependent calcium channels. With the closure of calcium channels there exists less intracellular calcium to activate calmoludin. With the failure of activation of calmoludin due to lack of intracellular calcium there exists less activation of myosin light chain kinase. With the decrease in myosin light chain phosphorylation due to lack of activation myosin light chain kinase, the vascular smooth muscles can no longer contract, effectively their relaxation thus occurs. This is how vasodilation occurs with the minoxidil. Now for unknown reasons, minoxidil does not have any effect on follicles themselves but only the minoxidil’s active form that had been converted to minoxidil sulfate on follicles or in liver via the SULT1A1 enzyme has. In fact, SULT1A1 enzyme amount is used as a predictor of treatment success. My hypothesis is that the precise mechanism through which minoxidil induces angiogenesis through the upregulation of VEGF it grows capillary networks around the hair follicle and thus signal to follicle to enter into anagen, while I believe increased blood flow is not its primary mechanism of action as most vasodilators don’t grow hair and that minoxidil does not exert any effect upon the capillaries however most KATP openers do indeed create some hair growth (hypertrichosis), minoxidil being the most famous of them. Thus the minoxidil is not a potent antiandrogen and cannot reliably stop hair loss. While there exists some research on its small antiandrogenic effects, it is nowhere near a competitor to finasteride/dutasteride.
Your dermatologist is inferior in knowledge to contemporary medical and pharmacological knowledge in the treatment of AGA, I am sorry to inform you. Minoxidil is NOT used for the prevention or progression of androgenetic alopecia. It is there to stimulate regrowth.
Precise pharmacology of minoxidil’s effect on blood pressure below to my knowledge to this date:
Minoxidil → SULT1A1 → Minoxidil Sulfate → Opening of potassium channels → Closure of Voltage Gated Calcium Channels → Hyperpolarization of cell membranes → Reduction of intracellular calcium (ca2+) → Decrease in formation of calcium calmoludin protein-ligand complex → Reduced activation of myosin light chain kinase → Reduced phosphorylation of the myosin light chains → (this is where minoxidil differentiates, blood pressure vs hair growth medicine)Failure to contract vascular smooth muscles → Relaxation of arterioles → Significant drop in blood pressure (typically at high dose only though, eg. above 5mg).
Myosins are protein structures in (sarcomere to be more precise) muscles that provide ability for muscle to contract.
It is not known how minoxidil works exactly for hair growth though unlike for blood pressure. Possibly may involve angiogenesis, but that is just my hypothesis.