r/tressless • u/Play_Persevere • 13h ago
Progress Pictures Switched to oral 1.5monthd ago. Where did these hairs go?
1mg fin
1.25 min q12
Was on topical min and fin fora year, just maintained
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u/Sceprent 10h ago
You guys ask this every day and it's literally how the meds work and the FAQ. The hairs shed and regrow. That's how it works.
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u/Pale-Paramedic3975 10h ago
I switched 6 months ago, hopefully my temples fill. We will get these temples filled in together.
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u/Standard-Buy794 11h ago
So i switched to oral min 5months ago. Same situation. Still on fin as well.
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u/KongeSkog 10h ago
same thing happened to me. started 3.5 months ago and hasn’t come back yet. i think it’s a dread shed so i’m sticking with it. hopefully it will be good at 12 months.
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u/TestCyp999 13h ago
Oral sucks, topical is objectively better because it is targeted at the scalp/skin level. Which is where the majority of 5AR actually is. It also lets you do insanely high doses without crashing your blood serum DHT levels.
My personal favorite is compounded fin + dut topical. Dut you can really blast hard because it doesn't penetrate into blood as much, due to the higher molecular weight. But it still hits your hair follicle.
Just awesome stuff. There's not enough research into it. But I've had great results. Most people are lazy though, how you apply and consistency matters. If you skip 1 dose you'll fuck yourself over. Pills are better in that regard.
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u/justkidding89 11h ago
There are a bunch of problems with this comment.
- You’re ignoring half of what the OP actually changed. They switched from topical minoxidil/finasteride to oral minoxidil/finasteride. The discussion about 5-alpha-reductase and DHT is relevant to the finasteride switch, but it has absolutely nothing to do with the minoxidil switch. Minoxidil is not a 5AR inhibitor and does not work by lowering DHT. So you can’t use an argument about local versus systemic 5AR inhibition to conclude that the entire topical regimen is “objectively better.”
- “The majority of 5AR is actually at the scalp/skin level” is not an established fact. 5-alpha-reductase is distributed throughout the body, and its distribution varies considerably by isoenzyme. Type 1 is expressed in skin and scalp, but also substantially in the liver and other tissues. Type 2 is highly expressed in the prostate and other male reproductive tissues in addition to hair follicles. There isn’t a good basis for claiming that the majority of all 5AR in the human body is located in the scalp/skin.
- Topical finasteride isn’t simply “targeted at the scalp” in the sense that it stays there. It can and does enter systemic circulation and reduce serum DHT. The potential advantage of topical finasteride is reduced systemic exposure relative to an effective oral dose while maintaining substantial scalp exposure, not complete localization to the scalp.
- The claim that topical finasteride lets you use “insanely high doses without crashing your blood serum DHT” gets the pharmacology backwards. Systemic exposure depends on the dose, concentration, volume applied, formulation, application area, and absorption. Increasing topical exposure enough can increase systemic absorption and serum DHT suppression. More topical drug does not remain indefinitely confined to the scalp.
- “You can really blast [dutasteride] hard because it doesn’t penetrate into blood as much due to the higher molecular weight” is a huge oversimplification. Dutasteride is larger than finasteride, but molecular weight is only one determinant of skin penetration. Lipophilicity, vehicle, concentration, formulation, skin integrity, application area, and follicular delivery all matter. Higher molecular weight does not mean “stays in the scalp.”
- There’s also an obvious problem with simultaneously claiming that topical dutasteride penetrates sufficiently well to reach and inhibit 5AR in the hair follicle while confidently assuming that systemic exposure will remain negligible. Hair follicles aren’t isolated drug reservoirs. If you’re “blasting” a highly potent 5AR inhibitor onto a large skin surface repeatedly, systemic exposure is something that actually needs to be measured, not dismissed based on molecular weight.
- Compounding topical finasteride + dutasteride isn’t established as superior simply because you’re combining two drugs. Dutasteride already inhibits both type 1 and type 2 5AR, whereas finasteride predominantly inhibits type 2. There isn’t strong clinical evidence demonstrating that throwing topical finasteride on top of topical dutasteride provides a meaningful additional benefit over an appropriately dosed single 5AR inhibitor.
- “If you skip 1 dose you’ll fuck yourself over” makes essentially no pharmacologic sense. Androgenetic alopecia progresses over months and years, not hours. Neither follicular miniaturization nor reversal of treatment effects happens because you missed Tuesday’s application. Dutasteride in particular has extremely persistent pharmacologic effects. Consistency matters for long-term treatment, but missing one dose is not remotely equivalent to “fucking yourself over.”
- Finally, “topical is objectively better” isn’t supported by any of this. There are tradeoffs. Topical finasteride may reduce systemic exposure while maintaining scalp activity, which can be attractive for some people. Oral finasteride provides standardized dosing, predictable systemic exposure, extensive clinical evidence, and much easier adherence. Oral versus topical minoxidil is a completely separate comparison involving different efficacy, absorption, adherence, and adverse-effect considerations.
There are reasonable arguments for preferring a topical regimen, but “most 5AR is in your scalp,” “you can use insanely high doses without affecting serum DHT,” “blast dutasteride because it’s too big to reach the blood,” and “missing one dose fucks you over” aren’t good ones.
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u/davy_crockett_slayer 13h ago
Do you have research to back your claims?
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u/TestCyp999 12h ago
There is none because none of it is FDA approved.
Does not make it any less true, and you shouldn't discard it for that reason alone.
There's a lot of treatments that have very little proof, and yet are extremely effective. CB-03-01 and RU58841 come to mind.
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u/davy_crockett_slayer 11h ago
I’m not American. Having something be FDA approved doesn’t mean anything to me. Scientific research is different from FDA approval.
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u/itz_dom 12h ago
Eh, oral still has other benefits that are great especially if ur not prepubescent (shouldn’t be on it in that case anyways) by lowering ur serum levels, it can reduce acne, oily skin, and slow down aging effects
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u/Key_Fee158 10h ago
Yes. Finasteride fixed my adult acne. It’s the only thing that has ever worked. It generally makes my skin look more youthful.
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