Curis, P&g, And The Lost Baldness Cure

[Dimitri001]

It's written in his regimen

Where is that? (maybe I'm being obtuse here)

 

[John Difool]

When I was doing around 8mg topical dutasteride, 80mg estriol, and 50mg spironolactone, along with all the other AAs it started affecting my libido. I since dropped it back down to 4mg topical dutasteride, 40mg estriol, and 25mg sprionolactone, while everything else is the same. That was the only side effect I've had. It didn't kill my libido, but it had an impact.

You therefore found out that even with its heavy molecules Duta topical worked and penetrated the skin deep enough to go systemic. I do make my own vials with Duta castor oil and Benzyl alcohol that I inject intradermal once a week. The slow release ID provides and the relatively long half life of Dutasteride should cover my AA needs.

 

[sonictemples]

Where is that? (maybe I'm being obtuse here)

where you wrote noting

 

[sonictemples]

Seriously Dimitri? Disliking someone who is trying to explain something that is so simple even kindergarten kids could easily understand? And you have been here for the past year too. Despite taking your time to spread hate towards someone who is trying to aid you, here is a more comprehensive explanation. Let me know if you got it this time.

 

[Dimitri001]

where you wrote noting

This is trying to help?

 

[sonictemples]

He didn't mention O MNX anywhere, or am I missing it?

Yes. Find more interesting things to do as an adult than disliking people lmao

 

[sktboiboi]

Well then why don't you try it yourself hoss? That guy on the other forum obviously had some thickening in the front.

cos they r lazy f**kers who jsut want somebody else to find the cure for them(and prove it's the cure)

 

[John Difool]

Now that I've tried high and low doses a few times, low doses work better. I will stick with that now. .1-.5%.

Which drug? Sorry with the detractors it's hard to follow the flow.

 

[sktboiboi]

@pegasus2 - If you haven't used tretinoin before, I would use a small amount on the other temple area (assuming you are only using SAG in one small area at the moment). Within 2-3 days of tretinoin gel (lowest concentration) first application, you will likely get red & irritated in that area. This will give you an idea of the effect you'll get. You can then decide if you really want to use it on the SAG temple. Once an area is irritated, you'll have to stop using anything in that area until it calms down. It will also likely peel. Might even have to use a bit of hydrocortisone to calm it down. And, the reservoir effect of tretinoin I believe is 3-4 days. Eventually, your skin will develop a resistance to the irritation, and, won't get as irritated. Even if you're only going to use it once a month, I would first test it on the non-SAG side. Also, if you do use tretinoin, don't go out in the sun without some kind of sun screen. Tretinoin makes your skin very vulnerable to uv radiation.

dont listen this

 

[pegasus2]

Which drug? Sorry with the detractors it's hard to follow the flow.

SAG.

 

[sktboiboi]

SAG.

hey c****, can u get b to the group pls, got some questions for u

 

[John Difool]

hey c****, can u get b to the group pls, got some questions for u

Wtf

 

[John Difool]

dont listen this

Why? This guy sounds like a subject matter expert with his Tretinoid advices. Lol

 

[sktboiboi]

Why? This guy sounds like a subject matter expert with his Tretinoid advices. Lol

that crap destroys cartilage, induces autoantigen-homing on the hair follicle outer rooth sheath(and cartilage in the joints)- and is upregulated in balding scalps. ALso, the balding scalp has been shown to be excessively thin when compared to normal hairy scalps in MRI scans.

https://www.researchgate.net/public...p_for_the_Evaluation_of_Androgenetic_Alopecia

my analysis of this- is that bony layer, the skull(the dark matter in the MRI scan)- replaces the connective tissue above it- n that is loose cartilage. SHH ups SOX(- master regulator chondrogenesis http://genesdev.cshlp.org/content/16/21/2813.full and all things cartilage amd is a direct target of SHH.

https://pubmed.ncbi.nlm.nih.gov/20034104/

Regulation of Sox9 by Sonic Hedgehog (Shh) is essential for patterning and formation of tracheal cartilage
Jinhyung Park 1, Jennifer J R Zhang, Anne Moro, Michelle Kushida, Michael Wegner, Peter C W Kim
Affiliations

• PMID: 20034104
  
• DOI: 10.1002/dvdy.22192

Free article
Abstract


We report that Sonic Hedgehog (Shh) regulates both formation and patterning of tracheal cartilage by controlling the expression pattern and level of the chondrogenic gene, Sox9. In Shh(-/-) tracheo-esophageal tubes, Sox9 expression is transient and not restricted ventrally to the site of chondrogenesis, and is absent at the time of chondrogenesis, resulting in the failure of tracheal cartilage formation. Inhibition of Hedgehog signalling with cyclopamine in tracheal cultures prevents tracheal cartilage formation, while treatment of Shh(-/-) tracheal explant with exogenous Shh peptide rescues cartilage formation. Both exogenous Bmp4 and Noggin rescue cartilage phenotype in Shh(-/-) tracheal culture, while promoting excessive cartilage development in wild-type trachea through induction of Sox9 expression. The ventral and segmented expression of Sox9 in tracheal primordia under Shh modulated by Bmp4 and Noggin thus determine where and when tracheal cartilage develops. These results indicate that Shh signalling is a critical determinant in tracheal cartilage development.




So the fibrotic and hard, slicky look in severe Androgenetic Alopecia = the bony layer expanding at the expense of the loose, cartilagenous layer

anything that thins the skin and destroys cartilage- is bad for Androgenetic Alopecia and tretinoin does exactly that.



https://pubmed.ncbi.nlm.nih.gov/31217429/

"Interestingly, the transcript levels of PGC1a, PPARγand RAR-a were found to be concomitantly up-regulated with AR expression (Fig. 3A and Supp. Fig. 2A,B). "

https://en.wikipedia.org/wiki/Retinoic_acid_receptor_alpha

also, upregulating SHH in the scalp only in bare, minimum amounts wont likely cause https://en.wikipedia.org/wiki/Basal-cell_carcinoma , since:

https://www.hairlosstalk.com/intera...ive-study-gene-expression-differences.113659/

= SOnic hedgehog is indeed downregulated in balding scalps

 

[Photon]

I'm out of SAG - I didn't see any improvement

 

[sktboiboi]

that crap destroys cartilage, induces autoantigen-homing on the hair follicle outer rooth sheath(and cartilage in the joints)- and is upregulated in balding scalps. ALso, the balding scalp has been shown to be excessively thin when compared to normal hairy scalps in MRI scans.

https://www.researchgate.net/public...p_for_the_Evaluation_of_Androgenetic_Alopecia

View attachment 147038
View attachment 147036

my analysis of this- is that bony layer, the skull(the dark matter in the MRI scan)- replaces the connective tissue above it- n that is loose cartilage. SHH ups SOX(- master regulator chondrogenesis http://genesdev.cshlp.org/content/16/21/2813.full and all things cartilage amd is a direct target of SHH.

https://pubmed.ncbi.nlm.nih.gov/20034104/

Regulation of Sox9 by Sonic Hedgehog (Shh) is essential for patterning and formation of tracheal cartilage
Jinhyung Park 1, Jennifer J R Zhang, Anne Moro, Michelle Kushida, Michael Wegner, Peter C W Kim
Affiliations

• PMID: 20034104
  
• DOI: 10.1002/dvdy.22192

Free article
Abstract


We report that Sonic Hedgehog (Shh) regulates both formation and patterning of tracheal cartilage by controlling the expression pattern and level of the chondrogenic gene, Sox9. In Shh(-/-) tracheo-esophageal tubes, Sox9 expression is transient and not restricted ventrally to the site of chondrogenesis, and is absent at the time of chondrogenesis, resulting in the failure of tracheal cartilage formation. Inhibition of Hedgehog signalling with cyclopamine in tracheal cultures prevents tracheal cartilage formation, while treatment of Shh(-/-) tracheal explant with exogenous Shh peptide rescues cartilage formation. Both exogenous Bmp4 and Noggin rescue cartilage phenotype in Shh(-/-) tracheal culture, while promoting excessive cartilage development in wild-type trachea through induction of Sox9 expression. The ventral and segmented expression of Sox9 in tracheal primordia under Shh modulated by Bmp4 and Noggin thus determine where and when tracheal cartilage develops. These results indicate that Shh signalling is a critical determinant in tracheal cartilage development.




So the fibrotic and hard, slicky look in severe Androgenetic Alopecia = the bony layer expanding at the expense of the loose, cartilagenous layer

anything that thins the skin and destroys cartilage- is bad for Androgenetic Alopecia and tretinoin does exactly that.



https://pubmed.ncbi.nlm.nih.gov/31217429/

"Interestingly, the transcript levels of PGC1a, PPARγand RAR-a were found to be concomitantly up-regulated with AR expression (Fig. 3A and Supp. Fig. 2A,B). "

https://en.wikipedia.org/wiki/Retinoic_acid_receptor_alpha

also, upregulating SHH in the scalp only in bare, minimum amounts wont likely cause https://en.wikipedia.org/wiki/Basal-cell_carcinoma , since:

https://www.hairlosstalk.com/intera...ive-study-gene-expression-differences.113659/

= SOnic hedgehog is indeed downregulated in balding scalps


View attachment 147035

retinoic acid promotes bone profileration at the expense of cartilage(and fats).

also, it simply,, causes hair loss:

Cutaneous Retinoic Acid Levels Determine Hair Follicle Development and Downgrowth*

Junko Okano, Clara Levy, [...], and Maria I. Morasso

Additional article information

Abstract
Retinoic acid (RA) is essential during embryogenesis and for tissue homeostasis, whereas excess RA is well known as a teratogen. In humans, excess RA is associated with hair loss. In the present study, we demonstrate that specific levels of RA, regulated by Cyp26b1, one of the RA-degrading enzymes, are required for hair follicle (hf) morphogenesis. Mice with embryonic ablation of Cyp26b1 (Cyp26b1−/−) have excessive endogenous RA, resulting in arrest of hf growth at the hair germ stage. The altered hf development is rescued by grafting the mutant skin on immunodeficient mice.(cos RA triggers autoantigens on the hair follciles, resulting in the immune system attacking them- as mentioned above) Our results show that normalization of RA levels is associated with reinitiation of hf development. Conditional deficiency of Cyp26b1 in the dermis (En1Cre;Cyp26b1f/−) results in decreased hair follicle density and specific effect on hair type, indicating that RA levels also influence regulators of hair bending. Our results support the model of RA-dependent dermal signals regulating hf downgrowth and bending. To elucidate target gene pathways of RA, we performed microarray and RNA-Seq profiling of genes differentially expressed in Cyp26b1−/− skin and En1Cre;Cyp26b1f/− tissues. We show specific effects on the Wnt-catenin pathway and on members of the Runx, Fox, and Sox transcription factor families, indicating that RA modulates pathways and factors implicated in hf downgrowth and bending. Our results establish that proper RA distribution is essential for morphogenesis, development, and differentiation of hfs.



= too much RA prevents hair follcile downgrowth into the dermal layer of cartilage and fatty cushion to n anchor themselves firmly in .

 

[sktboiboi]

retinoic acid promotes bone profileration at the expense of cartilage(and fats).

also, it simply,, causes hair loss:

Cutaneous Retinoic Acid Levels Determine Hair Follicle Development and Downgrowth*

Junko Okano, Clara Levy, [...], and Maria I. Morasso

Additional article information

Abstract
Retinoic acid (RA) is essential during embryogenesis and for tissue homeostasis, whereas excess RA is well known as a teratogen. In humans, excess RA is associated with hair loss. In the present study, we demonstrate that specific levels of RA, regulated by Cyp26b1, one of the RA-degrading enzymes, are required for hair follicle (hf) morphogenesis. Mice with embryonic ablation of Cyp26b1 (Cyp26b1−/−) have excessive endogenous RA, resulting in arrest of hf growth at the hair germ stage. The altered hf development is rescued by grafting the mutant skin on immunodeficient mice.(cos RA triggers autoantigens on the hair follciles, resulting in the immune system attacking them- as mentioned above) Our results show that normalization of RA levels is associated with reinitiation of hf development. Conditional deficiency of Cyp26b1 in the dermis (En1Cre;Cyp26b1f/−) results in decreased hair follicle density and specific effect on hair type, indicating that RA levels also influence regulators of hair bending. Our results support the model of RA-dependent dermal signals regulating hf downgrowth and bending. To elucidate target gene pathways of RA, we performed microarray and RNA-Seq profiling of genes differentially expressed in Cyp26b1−/− skin and En1Cre;Cyp26b1f/− tissues. We show specific effects on the Wnt-catenin pathway and on members of the Runx, Fox, and Sox transcription factor families, indicating that RA modulates pathways and factors implicated in hf downgrowth and bending. Our results establish that proper RA distribution is essential for morphogenesis, development, and differentiation of hfs.



= too much RA prevents hair follcile downgrowth into the dermal layer of cartilage and fatty cushion to n anchor themselves firmly in .

atually, this has been mentioned ad naseum over the YEARS.

why does ppl keep bringing up Tretinoin as a remedy for Androgenetic Alopecia???? just becos some individual doctors formulated 0.025% tretinoin in minoxidil solutions, claiming it helps penetration?

 

[pegasus2]

I'm out of SAG - I didn't see any improvement

What dose?

 

[Photon]

What dose?

20mg every 3 weeks or so, right after wounding.

 

[pegasus2]

20mg every 3 weeks or so, right after wounding.

I think that dose is too high. My results slowed down on higher doses too. I'm sticking with 0.15% now. That dose seems to work best for me, and better the more often I use it.