this is is for today people; every gene affected and a chemical to counteract each problem gene.
this is (again old info) taken from an old post; if anyone's interested in using any of the following chemicals and their uses in a kitchen sink approach please also read the two full regimen approaches which i posted before with pics....
here: - https://www.gourmetstylewellness.com/intera...alc-fibrosis-pdg-pge2-warning-complex.112286/
-------------------------------------------------------------------------------
and the following info below is taken taken from here:-
https://www.baldtruthtaIk.com/threa...reasons-why-we-balding-men-are-balding/page18
here is the info............................
updated list:
Experimental small molecule pharmalogical solutions for Androgenetic Alopecia by topical/oral route administration in order of descending preference(would be updated from time to time):
1): All affected genes indicated in the Scoliosis study:
TATA <= Topical Calcitirol/Calcipotriol
HNF4 <= Topical Carbamazepine(direct activator of SHBG for disactivating circulating sex hormones with highest affinity for DHT=>increased bone resorption in the balding skull. Has sides), Topical Valproic acid(Androgen Receptor Blocker, Wnt/B-catenin agonist, CD34 upregulator and several other pro-hair growth properties. Has sides if taken orally), Topical RU58841(Androgen Receptor Blocker- less systemic side effects), topical CB(Androgen Receptor Blocker), topical/oral Dutasteride(5A Redutase Inhibitor to decrease circulating DHT. Used carefully- will dramatically slow down, but not stop- Androgenetic Alopecia and increase 'free' Testosterone levels for the muscles), topical/oral Finasteride(5A Redutase Inhibitor to decrease circulating DHT- almost the same profile as Dutasteride but with less potency), oral Spironolactone(Androgen Receptor Blocker, Aldosterone Inhibitor=> Less sodium reabsorption in kidneys=>less vasoconstriction=>increased blood supply to hair follicles. Has feminizing sides.), topical Ethyl Estradiol (potently upregulates SHBG levels)
RAR <= Ultra low dose topical Tretinoin (0.01%-0.0005%. Ultra low doses of it induces hair shaft differentation at a stabilised rate with stem cells as the fuel while increasing dosages depletes stem cells rapidly and leads to apoptosis instead. Is also toxic when used in dosages above a certain threshold- and this 'threshold' is very low.), topical Valproic acid
RXRA <= Topical Calcitriol/Calcipotirol(Calcitriol-binded VDR is needed for full transcription of PPAR Alpha, Beta and Gamma. VDR-null cells on the scalp diverts pluripotent stem cells to the sebocyte(sebum) and sudoriferous(sweat) lineage).
STAT <= Topical Calcitriol/Calcipotriol(Calcitriol acts as a modulator of this central inflammation pathway- the JAK-STAT pathway.), topical/oral Sulfasalazine(via inhibiting TH1 cytokines), most anti-inflammatory drugs modulates this pathway to a certain degree.
BATF <= Topical Calcitirol/Calcipotriol(Calcitriol acts as a modulator of this TH17 cytokines regulatory gene), topical/oral Sulfasalazine(via inhibiting TH17 cytokines).
COMP <= Topical Calcitirol/Calcipotriol, topical Valproic acid(Both Calcitriol and Valproic acid increase expression of this gene- and it is upregulated only in haired-scalp.)
VDR <= Topical Calcitirol/Calcipotriol(Calcitriol's own receptor. It is a receptor that regulates, modulates and thus- controls hundreds of genes(900+ genes) involved with Immunity, Calcium homeostasis, Bone formation/resorption(in synergy with BMPs) and many, many more in the human body.)
HDAC2 <= Topical Valproic acid(inhibitor of HDAC2- which inhibits Androgenetic Alopecia-afflicted hair follicles stem cell renewal's function), topical Trichostatin A
CART1 <= Topical Calcitriol/Calcipotriol
FOXA <= FOXA2 inhibits pre-adipocyte differentiation. oral Sirt 1 activators like Resveratrol inhibits Foxa2 expression.
FOXP1 <= Topical Valproic acid, Ultra low dose topical Tretinoin(0.01% - 0.0005%)(FOXP1 regulates stem cells levels in the hair)
GATA <= Topical Calcitriol/Calcipotriol, Oral Montelukast, Oral Zafirlukast(GATA3 is the master regulator TH2 cytokines profileration and differentiation.)
H6 family homeobox 2 <= ? (Has got more to do with inner ear functions than to hair on the balding scalp)
IRF <= Topical Calcitriol/Calcipotriol
PAX5 <= Topical Calcitriol/Calcipotriol(PAX5 is the master regulator of B cells profileration and differentiation.).
P300 <= Topical Calcitriol/Calcipotriol
2):
Top 5 upregulated genes in haired-scalp and Top 5 downregulated genes in haired-scalp as indicated by Dr Cotsarelis's patent in order of descending preference:
Upregulated in haired-scalp:
GPRC5D <= Ultra low dose topical Tretinoin(0.01% - 0.0005% )
CDT6<= Topical Calcitriol/Calcipotriol
LY6G6D<= Closest that could be found for small molecules addressing this extremely-rarely-described gene is Valproic acid(seeing how Valproic acid has an overwhelming pro-hair growth effect when used topically, this means it probably upregulates it to a certain degree.).
S100A3<= Topical Calcitriol/Calcipotriol
COMP<= Topical Calcitriol/Calcipotriol, topical Valproic acid
3):
Downregulated in haired-scalp:
CCL19<= Topical Calcitriol/Calcipotriol
FOSB<= Topical Valproic acid
c-FOS<= Topical Valproic acid(via inhibiting Protein Kinase C), Topical/oral Verapamil(Calicum channel blocker with lower half-life), topical Cilnidipine(Calcium cahnnel blocker with half-life of 24hrs), topical D609(research chemical).
PTGDS<= Topical/oral TM30089(Long half-life- allowing once/day applications High potency. Analog of Ramatroban.) topical/oral Setipiprant(Newest CRTH2 inhibitor in trials, topical/oral Ramatroban(Short half-life, Demanding twice/day applications to keep itch and pain away continuosly. 1% topical is sufficient.), topical/oral OC(Shortest half-life and lowest out of the four listed here potency. Twice/day applications.)
CORIN<= Topical Valproic acid(indirectly via antagonising Progesterone), Topical Carbamazepine, topical Phenytoin(the active ingredient of Proxiphen. Phenytoin is also associated with drug-induced hypertrichosis of the face. Has some deadly sides in those predisposed to), topical Curcumin(Upregulates Serpina1- another gene upregulated by 5.721 folds in haired-scalp which in turns inhibits the production of Corin that equautes to 1-32BNP(pro-hairgrowth) production instead of 4-32 BNP production- via trypsin inhibition. it is also a GSK3B inhibitor.), Oral Spironolactone(indirectly by antagonising Aldosterone=> CORIN downregulation=> FURIN-Cleaved proBNP=> 1-32 BNP(the pro-hair growth form of BNP) => hair pigmentation + keratinization)
4):
Three 'endpoint' genes indicated by Dr Cotsarelis's patent that are significantly-upregulated in haired-scalp:
CD200<== Topical Cacitirol/Calcipotriol(Calcitriol increases both CD200's expression in the balding scalp and balding skull. In the latter's case, without adequate CD200's expression- bone resorption is severely-impaired that leads to ever-increasing bone formation in the balding skull.)
CD34<== Topical Valproic acid(via existing cell self-renewal), Topical 16,16-Dimethly-PGE2(via homing from bone marrow), Topical PGE2(PGE2=>EP2 Receptor=>Survivin=>CD34. Also- PGE2=>EP4 Receptor=>BMP-2=>SMAD1/5/8=>SMAD4=>DLX3=>RUNX2=>Hair shaft differentiation), Topical Butaprost(This is a selective EP2 receptor and EP4 receptor agonist. An PGE2 analog), topical/oral Sulfasalazine(Upregulates PGE2 while inhibiting COX-2), Minoxidil sulfate(via mPGE2).
Intergrin A6<= Topical Valproic acid, Ultra low dose topical Tretinoin(0.01%-0.0005%. Tretinoin is the only small molecule that could be found to upregulate IntergrinA6(CD49F) with the other being the Parathyroid hormone-related protein(not a small molecule))
From Cotsarelis's patent:
Example 5 In Situ and Immuno-Histological Characterization of Novel HF Genes
In situ hybridization and immuno-histochemistry was next used to determine tissue patterns of expression of significantly enriched transcripts in the haired scalp, using human haired scalp samples from different patients than those used to generate the array and flow cytometry data.
Microarray showed that LRRC15 was upregulated 4.5 fold in the haired samples (FIG. 5B). LRRC15 is a transmembrane glycoprotein with leucine-rich repeats. To determine whether LRRC15 functions in cell migration, LRRC15 expression was measured in scalp samples by immuno-histochemistry. LRRC15 was present in Huxley's layer and the cuticle layer of the inner root sheath, especially at the lower follicle (FIG. 6A), which is an area of rapid cell movement during hair growth. Thus, LRRC15 functions in cell migration necessary for hair growth. <==topical Valproic acid
Serpin A was up-regulated 5.7 fold in the haired samples. Serpin A is, in another embodiment, a Glade A anti-protease in the same family as anti-trypsin and anti-chymotrypsin. Serpin A was expressed in the companion layer of the outer root sheath, as shown by immuno-histochemistry (FIG. 6B). <==oral Resveratol, topical Carbamazepine
GPR49 (LGF5, HG38), another leucine rich repeat-containing protein, was upregulated 6.8 fold in the haired samples, and was expressed in human outer root sheath cells, as shown by immuno-histochemistry. (FIG. 6C). GPR49 is known to be upregulated in the mouse bulge (outer root sheath), thus further confirming results of the present invention. Enrichment of this G-protein in anagen/terminal follicles show its utility as a drug target for stimulating hair growth. <==Topical Valproic acid, Topical Trichostatin A
The Angiopoietin-like gene CDT6 (upregulated 18 fold in the haired samples) is an anti-vascular factor that is also expressed in the cornea (Corneal Derived Transcript 6), and thought to maintain the avascularity of the cornea. CDT6 was expressed in the outer root sheath, as shown by immuno-histochemistry (FIG. 6D), which is also avascular. <== Topical Calcitirol/Calcipotriol 0.005%
GPRC5D (upregulated 19.5 fold in haired samples) is a homologue of RAIG-1 (retinoic acid inducible gene-1). GPRC5D was expressed in the inner root sheath and precortical cells of the hair, as shown by immuno-histochemistry (FIG. 6E). <== Topical Tretinoin(0.01%-0.0005%)
FGF18 (upregulated almost 6 fold in the haired samples; FIG. 5B) was found to be expressed in the inner root sheath, the companion layer, and to a lesser extent in the suprabasal outer root sheath of the bulge area (FIG. 6F-G). <== upregulated indirectly via FOXP1 by topical Valproic acid or topical Tretinoin(0.01%-0.0005%).
The genes identified in this Example are all enriched in haired scalp, and are thus therapeutic targets for stimulating hair growth.
*Dietary adjustments*
IMO adjusting your diet will never have much of an impact on Androgenetic Alopecia. The only thing to look out for would be anything that will cause vasocontriction. 1)Caffeine antagonises the Adenosine receptors and 2)Calcium will not only cause vasocontriction- it also is used as fuel to form our ever growing bones in the balding skull and also as mineral deposits on our fibrosising balding-scalp. Keep it at not more than 1 cup of coffee a day(I know it's hard to not drink coffee-including myself) and /or best of all- avoid milk/cheese consumption.
END
this is (again old info) taken from an old post; if anyone's interested in using any of the following chemicals and their uses in a kitchen sink approach please also read the two full regimen approaches which i posted before with pics....
here: - https://www.gourmetstylewellness.com/intera...alc-fibrosis-pdg-pge2-warning-complex.112286/
-------------------------------------------------------------------------------
and the following info below is taken taken from here:-
https://www.baldtruthtaIk.com/threa...reasons-why-we-balding-men-are-balding/page18
here is the info............................
updated list:
Experimental small molecule pharmalogical solutions for Androgenetic Alopecia by topical/oral route administration in order of descending preference(would be updated from time to time):
1): All affected genes indicated in the Scoliosis study:
TATA <= Topical Calcitirol/Calcipotriol
HNF4 <= Topical Carbamazepine(direct activator of SHBG for disactivating circulating sex hormones with highest affinity for DHT=>increased bone resorption in the balding skull. Has sides), Topical Valproic acid(Androgen Receptor Blocker, Wnt/B-catenin agonist, CD34 upregulator and several other pro-hair growth properties. Has sides if taken orally), Topical RU58841(Androgen Receptor Blocker- less systemic side effects), topical CB(Androgen Receptor Blocker), topical/oral Dutasteride(5A Redutase Inhibitor to decrease circulating DHT. Used carefully- will dramatically slow down, but not stop- Androgenetic Alopecia and increase 'free' Testosterone levels for the muscles), topical/oral Finasteride(5A Redutase Inhibitor to decrease circulating DHT- almost the same profile as Dutasteride but with less potency), oral Spironolactone(Androgen Receptor Blocker, Aldosterone Inhibitor=> Less sodium reabsorption in kidneys=>less vasoconstriction=>increased blood supply to hair follicles. Has feminizing sides.), topical Ethyl Estradiol (potently upregulates SHBG levels)
RAR <= Ultra low dose topical Tretinoin (0.01%-0.0005%. Ultra low doses of it induces hair shaft differentation at a stabilised rate with stem cells as the fuel while increasing dosages depletes stem cells rapidly and leads to apoptosis instead. Is also toxic when used in dosages above a certain threshold- and this 'threshold' is very low.), topical Valproic acid
RXRA <= Topical Calcitriol/Calcipotirol(Calcitriol-binded VDR is needed for full transcription of PPAR Alpha, Beta and Gamma. VDR-null cells on the scalp diverts pluripotent stem cells to the sebocyte(sebum) and sudoriferous(sweat) lineage).
STAT <= Topical Calcitriol/Calcipotriol(Calcitriol acts as a modulator of this central inflammation pathway- the JAK-STAT pathway.), topical/oral Sulfasalazine(via inhibiting TH1 cytokines), most anti-inflammatory drugs modulates this pathway to a certain degree.
BATF <= Topical Calcitirol/Calcipotriol(Calcitriol acts as a modulator of this TH17 cytokines regulatory gene), topical/oral Sulfasalazine(via inhibiting TH17 cytokines).
COMP <= Topical Calcitirol/Calcipotriol, topical Valproic acid(Both Calcitriol and Valproic acid increase expression of this gene- and it is upregulated only in haired-scalp.)
VDR <= Topical Calcitirol/Calcipotriol(Calcitriol's own receptor. It is a receptor that regulates, modulates and thus- controls hundreds of genes(900+ genes) involved with Immunity, Calcium homeostasis, Bone formation/resorption(in synergy with BMPs) and many, many more in the human body.)
HDAC2 <= Topical Valproic acid(inhibitor of HDAC2- which inhibits Androgenetic Alopecia-afflicted hair follicles stem cell renewal's function), topical Trichostatin A
CART1 <= Topical Calcitriol/Calcipotriol
FOXA <= FOXA2 inhibits pre-adipocyte differentiation. oral Sirt 1 activators like Resveratrol inhibits Foxa2 expression.
FOXP1 <= Topical Valproic acid, Ultra low dose topical Tretinoin(0.01% - 0.0005%)(FOXP1 regulates stem cells levels in the hair)
GATA <= Topical Calcitriol/Calcipotriol, Oral Montelukast, Oral Zafirlukast(GATA3 is the master regulator TH2 cytokines profileration and differentiation.)
H6 family homeobox 2 <= ? (Has got more to do with inner ear functions than to hair on the balding scalp)
IRF <= Topical Calcitriol/Calcipotriol
PAX5 <= Topical Calcitriol/Calcipotriol(PAX5 is the master regulator of B cells profileration and differentiation.).
P300 <= Topical Calcitriol/Calcipotriol
2):
Top 5 upregulated genes in haired-scalp and Top 5 downregulated genes in haired-scalp as indicated by Dr Cotsarelis's patent in order of descending preference:
Upregulated in haired-scalp:
GPRC5D <= Ultra low dose topical Tretinoin(0.01% - 0.0005% )
CDT6<= Topical Calcitriol/Calcipotriol
LY6G6D<= Closest that could be found for small molecules addressing this extremely-rarely-described gene is Valproic acid(seeing how Valproic acid has an overwhelming pro-hair growth effect when used topically, this means it probably upregulates it to a certain degree.).
S100A3<= Topical Calcitriol/Calcipotriol
COMP<= Topical Calcitriol/Calcipotriol, topical Valproic acid
3):
Downregulated in haired-scalp:
CCL19<= Topical Calcitriol/Calcipotriol
FOSB<= Topical Valproic acid
c-FOS<= Topical Valproic acid(via inhibiting Protein Kinase C), Topical/oral Verapamil(Calicum channel blocker with lower half-life), topical Cilnidipine(Calcium cahnnel blocker with half-life of 24hrs), topical D609(research chemical).
PTGDS<= Topical/oral TM30089(Long half-life- allowing once/day applications High potency. Analog of Ramatroban.) topical/oral Setipiprant(Newest CRTH2 inhibitor in trials, topical/oral Ramatroban(Short half-life, Demanding twice/day applications to keep itch and pain away continuosly. 1% topical is sufficient.), topical/oral OC(Shortest half-life and lowest out of the four listed here potency. Twice/day applications.)
CORIN<= Topical Valproic acid(indirectly via antagonising Progesterone), Topical Carbamazepine, topical Phenytoin(the active ingredient of Proxiphen. Phenytoin is also associated with drug-induced hypertrichosis of the face. Has some deadly sides in those predisposed to), topical Curcumin(Upregulates Serpina1- another gene upregulated by 5.721 folds in haired-scalp which in turns inhibits the production of Corin that equautes to 1-32BNP(pro-hairgrowth) production instead of 4-32 BNP production- via trypsin inhibition. it is also a GSK3B inhibitor.), Oral Spironolactone(indirectly by antagonising Aldosterone=> CORIN downregulation=> FURIN-Cleaved proBNP=> 1-32 BNP(the pro-hair growth form of BNP) => hair pigmentation + keratinization)
4):
Three 'endpoint' genes indicated by Dr Cotsarelis's patent that are significantly-upregulated in haired-scalp:
CD200<== Topical Cacitirol/Calcipotriol(Calcitriol increases both CD200's expression in the balding scalp and balding skull. In the latter's case, without adequate CD200's expression- bone resorption is severely-impaired that leads to ever-increasing bone formation in the balding skull.)
CD34<== Topical Valproic acid(via existing cell self-renewal), Topical 16,16-Dimethly-PGE2(via homing from bone marrow), Topical PGE2(PGE2=>EP2 Receptor=>Survivin=>CD34. Also- PGE2=>EP4 Receptor=>BMP-2=>SMAD1/5/8=>SMAD4=>DLX3=>RUNX2=>Hair shaft differentiation), Topical Butaprost(This is a selective EP2 receptor and EP4 receptor agonist. An PGE2 analog), topical/oral Sulfasalazine(Upregulates PGE2 while inhibiting COX-2), Minoxidil sulfate(via mPGE2).
Intergrin A6<= Topical Valproic acid, Ultra low dose topical Tretinoin(0.01%-0.0005%. Tretinoin is the only small molecule that could be found to upregulate IntergrinA6(CD49F) with the other being the Parathyroid hormone-related protein(not a small molecule))
From Cotsarelis's patent:
Example 5 In Situ and Immuno-Histological Characterization of Novel HF Genes
In situ hybridization and immuno-histochemistry was next used to determine tissue patterns of expression of significantly enriched transcripts in the haired scalp, using human haired scalp samples from different patients than those used to generate the array and flow cytometry data.
Microarray showed that LRRC15 was upregulated 4.5 fold in the haired samples (FIG. 5B). LRRC15 is a transmembrane glycoprotein with leucine-rich repeats. To determine whether LRRC15 functions in cell migration, LRRC15 expression was measured in scalp samples by immuno-histochemistry. LRRC15 was present in Huxley's layer and the cuticle layer of the inner root sheath, especially at the lower follicle (FIG. 6A), which is an area of rapid cell movement during hair growth. Thus, LRRC15 functions in cell migration necessary for hair growth. <==topical Valproic acid
Serpin A was up-regulated 5.7 fold in the haired samples. Serpin A is, in another embodiment, a Glade A anti-protease in the same family as anti-trypsin and anti-chymotrypsin. Serpin A was expressed in the companion layer of the outer root sheath, as shown by immuno-histochemistry (FIG. 6B). <==oral Resveratol, topical Carbamazepine
GPR49 (LGF5, HG38), another leucine rich repeat-containing protein, was upregulated 6.8 fold in the haired samples, and was expressed in human outer root sheath cells, as shown by immuno-histochemistry. (FIG. 6C). GPR49 is known to be upregulated in the mouse bulge (outer root sheath), thus further confirming results of the present invention. Enrichment of this G-protein in anagen/terminal follicles show its utility as a drug target for stimulating hair growth. <==Topical Valproic acid, Topical Trichostatin A
The Angiopoietin-like gene CDT6 (upregulated 18 fold in the haired samples) is an anti-vascular factor that is also expressed in the cornea (Corneal Derived Transcript 6), and thought to maintain the avascularity of the cornea. CDT6 was expressed in the outer root sheath, as shown by immuno-histochemistry (FIG. 6D), which is also avascular. <== Topical Calcitirol/Calcipotriol 0.005%
GPRC5D (upregulated 19.5 fold in haired samples) is a homologue of RAIG-1 (retinoic acid inducible gene-1). GPRC5D was expressed in the inner root sheath and precortical cells of the hair, as shown by immuno-histochemistry (FIG. 6E). <== Topical Tretinoin(0.01%-0.0005%)
FGF18 (upregulated almost 6 fold in the haired samples; FIG. 5B) was found to be expressed in the inner root sheath, the companion layer, and to a lesser extent in the suprabasal outer root sheath of the bulge area (FIG. 6F-G). <== upregulated indirectly via FOXP1 by topical Valproic acid or topical Tretinoin(0.01%-0.0005%).
The genes identified in this Example are all enriched in haired scalp, and are thus therapeutic targets for stimulating hair growth.
*Dietary adjustments*
IMO adjusting your diet will never have much of an impact on Androgenetic Alopecia. The only thing to look out for would be anything that will cause vasocontriction. 1)Caffeine antagonises the Adenosine receptors and 2)Calcium will not only cause vasocontriction- it also is used as fuel to form our ever growing bones in the balding skull and also as mineral deposits on our fibrosising balding-scalp. Keep it at not more than 1 cup of coffee a day(I know it's hard to not drink coffee-including myself) and /or best of all- avoid milk/cheese consumption.
END
