mariniguy
Marini
- Joined
- Apr 6, 2026
- Posts
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Allot of people in this forum recommend minoxidil and finasteride. Both are cope. Here is exactly why and what you should actually be doing.
First. Know your mechanism.
There are two completely different reasons steroids cause hair loss depending on what you're running. Getting this wrong means your entire hair protocol does nothing.
If you are running testosterone your problem is DHT conversion via 5-alpha reductase.
If you are running SARMs or androgenic compounds your problem is direct androgen receptor activation.
These require completely different solutions.
Solution for Testosterone users-
Dutasteride 0.5mg daily, That is it!
Dutasteride is a dual 5 alpha reductase inhibitor. It inhibits both type I and type II isoforms simultaneously achieving over 90% suppression of DHT conversion across both pathways. On a test cycle where both isoforms are being driven hard by high testosterone load this dual blockade is the only approach that actually covers the full conversion pathway.
Olsen et al JAAD 2006 - 416 men randomised to dutasteride vs finasteride vs placebo for 24 weeks. After 24 weeks 56% of the dutasteride group had over 10% increased hair count versus 41% for finasteride versus 0% for placebo. Dutasteride won at normal testosterone levels. On cycle where type I activity is elevated by high testosterone volume the advantage over finasteride widens further.
PUBMED
The mistake behind taking finasteride-
Finasteride is a type II 5 alpha reductase inhibitor. What that means is it blocks the enzyme responsible for converting testosterone into DHT specifically in the hair follicle and prostate tissue. At natural testosterone levels this achieves around 60 to 70% scalp DHT suppression which is functional to a normie.
The problem on cycle is very simple. 5 alpha reductase has two isoforms, Type I and type II. Finasteride only inhibits type II where as Type I is the dominant isoform expressed in sebaceous glands in the scalp. When your circulating testosterone is above physiological levels the type I pathway alone produces enough DHT to continue miniaturising your follicles regardless of type II being fully blocked. The testosterone volume on cycle is so high that the open pathway compensates entirely. Finasteride was studied and dosed exclusively for men at physiological testosterone levels. It was never calibrated for exogenous androgen loads.
PUBMED
Solution for SARMs / Androgenic compound users-
Dutasteride and finasteride do nothing here because testosterone gets converted into DHT via 5 alpha reductase and DHT then binds to androgen receptors in dermal papilla cells triggering follicle miniaturisation where as SARMs/Androgenic compounds skip that conversion step entirely. They bind directly to the androgen receptor in dermal papilla cells without needing to convert to DHT first. 5 alpha reductase is not involved in the mechanism at all.
The solution for this is Clascoterone (CB-03-01) topical daily.
Clascoterone is a topical androgen receptor antagonist. Rather than blocking an upstream enzyme it competes directly with androgens at the androgen receptor itself inside the dermal papilla cell. Clascoterone occupies the receptor so the compound cannot bind and trigger miniaturisation. The data confirms that at therapeutic concentrations applied to the scalp systemic absorption remains negligible. The androgen receptor blockade stays localised to the follicle. Systemically your androgen receptors remain fully active meaning the anabolic signal from your compound is completely preserved.
Rosette et al JAAD 2021 - Phase III RCT. Statistically significant reduction in hair loss versus placebo confirmed.
PUBMED
used ai for spelling correction lolz & feel free to correct me
First. Know your mechanism.
There are two completely different reasons steroids cause hair loss depending on what you're running. Getting this wrong means your entire hair protocol does nothing.
If you are running testosterone your problem is DHT conversion via 5-alpha reductase.
If you are running SARMs or androgenic compounds your problem is direct androgen receptor activation.
These require completely different solutions.
Solution for Testosterone users-
Dutasteride 0.5mg daily, That is it!
Dutasteride is a dual 5 alpha reductase inhibitor. It inhibits both type I and type II isoforms simultaneously achieving over 90% suppression of DHT conversion across both pathways. On a test cycle where both isoforms are being driven hard by high testosterone load this dual blockade is the only approach that actually covers the full conversion pathway.
Olsen et al JAAD 2006 - 416 men randomised to dutasteride vs finasteride vs placebo for 24 weeks. After 24 weeks 56% of the dutasteride group had over 10% increased hair count versus 41% for finasteride versus 0% for placebo. Dutasteride won at normal testosterone levels. On cycle where type I activity is elevated by high testosterone volume the advantage over finasteride widens further.
PUBMED
The mistake behind taking finasteride-
Finasteride is a type II 5 alpha reductase inhibitor. What that means is it blocks the enzyme responsible for converting testosterone into DHT specifically in the hair follicle and prostate tissue. At natural testosterone levels this achieves around 60 to 70% scalp DHT suppression which is functional to a normie.
The problem on cycle is very simple. 5 alpha reductase has two isoforms, Type I and type II. Finasteride only inhibits type II where as Type I is the dominant isoform expressed in sebaceous glands in the scalp. When your circulating testosterone is above physiological levels the type I pathway alone produces enough DHT to continue miniaturising your follicles regardless of type II being fully blocked. The testosterone volume on cycle is so high that the open pathway compensates entirely. Finasteride was studied and dosed exclusively for men at physiological testosterone levels. It was never calibrated for exogenous androgen loads.
PUBMED
Solution for SARMs / Androgenic compound users-
Dutasteride and finasteride do nothing here because testosterone gets converted into DHT via 5 alpha reductase and DHT then binds to androgen receptors in dermal papilla cells triggering follicle miniaturisation where as SARMs/Androgenic compounds skip that conversion step entirely. They bind directly to the androgen receptor in dermal papilla cells without needing to convert to DHT first. 5 alpha reductase is not involved in the mechanism at all.
The solution for this is Clascoterone (CB-03-01) topical daily.
Clascoterone is a topical androgen receptor antagonist. Rather than blocking an upstream enzyme it competes directly with androgens at the androgen receptor itself inside the dermal papilla cell. Clascoterone occupies the receptor so the compound cannot bind and trigger miniaturisation. The data confirms that at therapeutic concentrations applied to the scalp systemic absorption remains negligible. The androgen receptor blockade stays localised to the follicle. Systemically your androgen receptors remain fully active meaning the anabolic signal from your compound is completely preserved.
Rosette et al JAAD 2021 - Phase III RCT. Statistically significant reduction in hair loss versus placebo confirmed.
PUBMED
used ai for spelling correction lolz & feel free to correct me
