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For Baccy


#1

In case u don’t see my other post.

mikey66walters@gmail.com — email me your address and I will send u a bottle this week. I’m 37, NW 2.5 I would say with a diffusing top. I am not the worse case here. I would say I’m somewhere in the middle. I’ve been battling this for years and it’s been an up and down battle. I’ve tried RU, Minox, fin, T4, TB4, PS1, curcumin, my own homebrew, dut, natural route and the list keeps going. I’ve had my ups and down I tell you and mixing these things up is nothing new to me. I wouldn’t worry too much about topical immunos as I don’t think it did anything beneficial.


#2

This is what I understand from this chart:

  1. Mice of all ages regenerated anywhere from 0 to 102 new follicles with wounding alone.

  2. Mice that had WNTs inhibited via Dkk1 during the 1st 17 days grew 0 follicles

  3. Mice that had WNTs inhibited between 11-14 days post wound grew 3 follicles

  4. Mice that had WNTs inhibited between 12-15 days post wound grew 2 follicles

  5. Mice that had WNTs inhibited between 0-10 days post wound had an average of 97 new follicles! Thats ~3X as many follicles. Now remember that lithium boosts WNT not inhibits them. We need something to inhibit wnt from days 0-10.

  6. Mice with no beta-catenin had 0 follicles

  7. Mice with extra wnt7a had an average of 100 new follicles.


So if ur trying to make sense of all this, well if u upregulate wnt7a I get 100 new follicles but if I inhibit wnt7a for the 1st 10 days I get 97 follicles. What do I do? Well in the case where they inhibited the wnt for the 1st 10 days the quality of hair was better(pigmentation) so if given the choice between 100 crap new hairs (like what I got) and 97 great hairs…which would you take? Additionally you have to ask yourself why a year later did they remove lithium from the 2nd patent and add all the EGFR stuff? Personally I think in that year they found the jackpot for human skin… wound+EGFR. The key is #5 above! I did not inhibit wnt the 1st 10 days post wounding and got crap growth as a result but growth none the less when you compare the topical route to the internal route.


#3

http://www.wipo.int/pctdb/en/wo.jsp?IA=US2007020842&wo=2008042216&DISPLAY=DESC

That is the follica patent. Here is the “human skin” experiment (Experiment number 7) in the patent that put HUMAN skin on the backs of immunocompromised SCID mice:

Example 7: EDIHN induces new hair follicles in human skin. Grafting. Discarded human adult scalp from the preauricular area obtained from plastic surgery was grafted onto immunodeficient (scid) mice. The graft was bandaged and allowed to heal, then was used in the wound healing study 3 months after grafting.

Results: To determine whether human skin responded to EDIHN as did mouse skin, human skin was grafted onto SCID (immuno-defϊcient) mice and subjected to depilation by plucking and wound induction three days later. Seven days following wound induction, formation of new HF was observed in the human skin (Figure 2 IA; arrows indicate new HF) by hematoxylin and eosin staining of paraffin embedded tissue sections.

In additional experiments, adult human skin was grafted onto mice, abraded, and examined at 7 days post-abrasion. New HF were generated in the human skin, which mimicked normal hair follicle formation during fetal development, as evidenced by staining for S100A6 or S100A4 (Figure 21B).

The results of this Example show that EDIHN can be used to generate hair growth in human skin as for mouse skin.

Human skin apparently re-epilithializes faster after dermabrasion than the skin of a mouse if its done “right”.

This verbiage is also “in the patent”:

The area of reepithelialization can be, for example, between 0-2 millimeteres (mm) in width (e.g., 1 mm, 2 mm, 3 mπij or greater), 0-2 centimeters (cm) in width (e.g., 1 cm, 1.5 cm, and 2.0 cm) or greater. Optionally, the area of reepithelialization can be interfollicular. In some aspects of the invention, it is desirable to administer the compounds of the invention at a particular phase of reepithelialization. Stages at which compounds of the invention may preferably be administered and/or activated include periods:

■ after completion of the reepithelialization process (e.g., 3-12 days, or 9- 11 days after having disrupted the skin),[/color]

That shows timelines for human skin re-epilithialization following laser and dermabraion. Its usually 60% complete at day 6 if its done “right”, but by going just a bit deeper, the skin might take much longer to re-epilithialize. It really is kind of a crap shoot depending on your skin’s individual characteristics. Ive finally “fully” peeled, but I wounded 13 friggin’ days ago. I wonder if I ran out of cyclo too soon, thus screwing up the whole thing (I also got my frontal scalp wet mistakenly at day 8.5). This is such a “delicate” process, and getting the “window” right is probably everything.


#4

Mike,

Ive went through the follica patent a good deal in the past few months.

Experiment 7, whereby hair follicle “placodes” were noticed in HUMAN skin grafted onto SCID mice has been the experiment (or example) that Ive focused on.

In humans, skin-re-epilithialization usually happens faster than it does in mice. For what reason I dont know, but I even found one study showing cold dressings following wounding got one subset of human skin to fully re-epilithialize by day 4.6 on average. Ive seen it be described as 7.9 days on average.

Then again Ive seen it average 10-12 days with other types of wounding using various laser and whatnot.

So I personally only used things that would have inhibited wnt for the first three days after wounding myself for fear of the risk of inhibiting it for too long. I have a bad feeling I screwed up my own experiment as I feel I re-epilithialized way too slowly this time, and frankly ran out of cyclosporin too soon. I also got my head wet on day 8.5, at a very crucial time.

To make this work for someone, I wanted to use the exact things follica used in the patent that are known to work in vivo in human beings running no risk of using any “anti-infective, ointment, or dressing normally administered to a wound” that is talked about in the patent. I figure soap is an anti-infective. This is the patent verbiage that left this impression upon me:

"Optionally, the skin, following the epidermal disruption, is not contacted for a period of time with any substance (e.g., ointment, a bandage, or a device) that is normally administered to an abrasion or wound to prevent infection.

Here the skin is not contacted with any substance until, for example, the ■ •■ - epidermal disruption -has healed (e.g., any time between 2 days and 3 weeks). Alternatively, the skin can be contacted with a cast or bandage (e.g., resulting in increased blood flow to the disrupted skin or decreased transdermal water loss or decreased mass transfer of gases into the skin and from the skin (e.g. oxygen, carbon dioxide, water vapor), decreased heat transfer from the skin (e.g. resulting in an increased temperature of the skin surface) or increased pressure on the skin.

Prior to disruption, the skin can depilated or epilated. The depilation or epilation can be accomplished through, for example, waxing, plucking, an abrasive material, a laser, electrolosis, a mechanical device, or thioglycolic acid.

The disruption of the epidermis can be induced between 3-12 days (e.g., 4-12, 5-12, 4-11, 6-11, 6-10, 6-9, 7-8, 5-11, 5-10, or 7-10 days) prior to the addition of the compositions of the invention."

TO make a long story short, every incidence of new growth associated with human skin was either on a SCID mouse (no immune system) or humans who had been in extensive chemotherapy (decimated immune status). The mice in experiment 7 didn’t even have egf-inhibitors used on them, injected in them, or placed in their chow. They simply were abraded and allowed to heal with human skin on their backs. EGF-antagonism merely made “more” hair with the little creatures. This is why I think (and wish I was wrong about it) that immunosuppression may be the key for the whole thing to work. I probably didn’t have enough cyclo myself anyway to be honest, as Im going to “guess” that one will need about 4-500 mgs of cyclo a day to get immunity compromised enough for t-cells not to use cytokines and all the other weapons at their disposal to inflame the wound sites. Harlodo once posted a study that showed in neo-natal mice, no new hair forms if inflammation is present. They get born hairless. The immune system inflames wounds, thats part of what it does, so that the inflammation and heat kill would-be invaders until the wound heals. I think we probably have to “scotch” it. As Ive said earlier, I’d like to be wrong about that, but five different immunosuppressants are mentioned as “adjuvants” in the patent. One is internal cyclosporin. They are discussed at some length. Why would follica even bother?

Here is the patent verbaige on immunosuppressants (note how much longer this entry is than the entry for potassium channel openers, retinoids, anti-histamines, anti-androgens, etc.:

Imm unosuppressants

In certain embodiments, a nonsteroidal immunosuppressant can be used in the compositions, methods, and kits of the invention. Suitable immunosuppressants include cyclosporine, tacrolimus, rapamycin, everolimus, and pimecrolimus.

Cyclosporines

The cyclosporines are fungal metabolites that comprise a class of cyclic oligopeptides that act as immunosuppressants. Cyclosporine A is a hydrophobic cyclic polypeptide consisting of eleven amino acids. It binds and forms a complex with the intracellular receptor cyclophilin. The cyclosporine/cyclophilin complex binds to and inhibits calcineurin, a Ca2± calmodulin-dependent serine-threonine-specifϊc protein phosphatase. Calcineurin mediates signal transduction events required for T-cell activation (reviewed in Schreiber et al., Cell 70:365-368, 1991). Cyclosporines and their functional and structural analogs suppress the T cell-dependent immune response by inhibiting antigen-triggered signal transduction. This inhibition decreases the expression of proinflammatory cytokines, such as IL-2. Many different cyclosporines (e.g., cyclosporine A, B, C, D, E, F, G, H, and I) are produced by fungi. Cyclosporine A is a commercially available under the trade name NEORAL from Novartis. Cyclosporine A structural and functional analogs include cyclosporines having one or more fluorinated amino acids (described, e.g., in U.S. Patent No. 5,227,467); cyclosporines having

modified amino acids (described, e.g., in U.S. Patent Nos. 5,122,511 and 4,798,823); and deuterated cyclosporines, such as ISAtx247 (described in U.S. Patent Application Publication No. 2002/0132763 Al). Additional cyclosporine analogs are described in U.S. Patent Nos. 6,136,357, 4,384,996, 5,284,826, and 5,709,797. Cyclosporine analogs include, but are not limited to, D-Sar (α-SMe)3 Val2-DH-Cs (209-825), Allo-Thr-2-Cs, Norvaline-2-Cs, D- Ala(3-acetylamino)-8-Cs, Thr-2-Cs, and D-MeSer-3-Cs, D-SeI-(O-CH2CH2- OH)-8-Cs, and D-Ser-8-Cs, which are described in Cruz et al., Antimicrob. Agents Chemother. 44: 143 (2000).

Tacrolimus

Tacrolimus and tacrolimus analogs are described by Tanaka et al. (J. Am. Chem. Soc, 109:5031 (1987)) and in U.S. Patent Nos. 4,894,366, 4,929,611, and 4,956,352. FK506-related compounds, including FR-900520, FR-900523, and FR-900525, are described in U.S. Patent No. 5,254,562; O- aryl, O-alkyl, O-alkenyl, and O-alkynylmacrolides are described in U.S. Patent Nos. 5,250,678, 532,248, 5,693,648; amino O-aryl macrolides are described in U.S. Patent No. 5,262,533; alkylidene macrolides are described in U.S. Patent No. 5,284,840; N-heteroaryl, N-alkylheteroaryl, N-alkenylheteroaryl, and N- alkynylheteroaryl macrolides are described in U.S. Patent No. 5,208,241 ; aminomacrolides and derivatives thereof are described in U.S. Patent No. 5,208,228; fluoromacrolides are described in U.S. Patent No. 5,189,042; amino O-alkyl, O-alkenyl, and O-alkynylmacrolides are described in U.S. Patent No. 5,162,334; and halomacrolides are described in U.S. Patent No. 5,143,918. Tacrolimus is extensively metabolized by the mixed-function oxidase system, in particular, by the cytochrome P-450 system. The primary mechanism of metabolism is demethylation and hydroxylation. While various tacrolimus metabolites are likely to exhibit immunosuppressive biological

activity, the 13-demethyl metabolite is reported to have the same activity as tacrolimus.

Pimecrolimns Pimecrolimus is the 33-epi-chloro derivative of the macrolactam ascomyin. Pimecrolimus structural and functional analogs are described in U.S. Patent No. 6,384,073.

Rapamycin Rapamycin structural and functional analogs include mono- and diacylated rapamycin derivatives (U.S. Patent No. 4,316,885); rapamycin water-soluble prodrugs (U.S. Patent No. 4,650,803); carboxylic acid esters (PCT Publication No. WO 92/05179); carbamates (U.S. Patent No. 5,118,678); amide esters (U.S. Patent No. 5,118,678); biotin esters (U.S. Patent No. 5,504,091); fluorinated esters (U.S. Patent No. 5,100,883); acetals (U.S. Patent No. 5,151,413); silyl ethers (U.S. Patent No. 5,120,842); bicyclic derivatives (U.S. Patent No. 5,120,725); rapamycin dimers (U.S. Patent No. 5,120,727); O- aryl, O-alkyl, O-alkyenyl and O-alkynyl derivatives (U.S. Patent No. 5,258,389); and deuterated rapamycin (U.S. Patent No. 6,503,921). Additional rapamycin analogs are described in U.S. Patent Nos. 5,202,332 and 5,169,851.


#5

»»
»
» mikey66walters@gmail.com — email me your address and I will send u a
» bottle this week. I’m 37, NW 2.5 I would say with a diffusing top. I am
» not the worse case here. I would say I’m somewhere in the middle. I’ve
» been battling this for years and it’s been an up and down battle. I’ve
» tried RU, Minox, fin, T4, TB4, PS1, curcumin, my own homebrew, dut, natural
» route and the list keeps going. I’ve had my ups and down I tell you and
» mixing these things up is nothing new to me. I wouldn’t worry too much
» about topical immunos as I don’t think it did anything beneficial.

You get my mail Mike?


#6

» »»
» »
» » mikey66walters@gmail.com — email me your address and I will send u
» a
» » bottle this week. I’m 37, NW 2.5 I would say with a diffusing top. I
» am
» » not the worse case here. I would say I’m somewhere in the middle.
» I’ve
» » been battling this for years and it’s been an up and down battle. I’ve
» » tried RU, Minox, fin, T4, TB4, PS1, curcumin, my own homebrew, dut,
» natural
» » route and the list keeps going. I’ve had my ups and down I tell you
» and
» » mixing these things up is nothing new to me. I wouldn’t worry too much
» » about topical immunos as I don’t think it did anything beneficial.
»
» You get my mail Mike?

Got it! U r in the UK? I hope customs don’t… u know. I will mix up this week and send. My return address will be a dummy one.


#7

» Mike,
»
»
» Ive went through the follica patent a good deal in the past few months.
»
»
» Experiment 7, whereby hair follicle “placodes” were noticed in HUMAN skin
» grafted onto SCID mice has been the experiment (or example) that Ive
» focused on.
»
»
» In humans, skin-re-epilithialization usually happens faster than it does
» in mice. For what reason I dont know, but I even found one study showing
» cold dressings following wounding got one subset of human skin to fully
» re-epilithialize by day 4.6 on average. Ive seen it be described as 7.9
» days on average.
»
» Then again Ive seen it average 10-12 days with other types of wounding
» using various laser and whatnot.
»
»
» So I personally only used things that would have inhibited wnt for the
» first three days after wounding myself for fear of the risk of inhibiting
» it for too long. I have a bad feeling I screwed up my own experiment as I
» feel I re-epilithialized way too slowly this time, and frankly ran out of
» cyclosporin too soon. I also got my head wet on day 8.5, at a very crucial
» time.
»
»
»
»
»
» To make this work for someone, I wanted to use the exact things follica
» used in the patent that are known to work in vivo in human beings running
» no risk of using any “anti-infective, ointment, or dressing normally
» administered to a wound” that is talked about in the patent. I figure soap
» is an anti-infective. This is the patent verbiage that left this impression
» upon me:
»
»
» “Optionally, the skin, following the epidermal disruption, is
» not contacted for a period of time with any substance (e.g., ointment, a
» bandage, or a device) that is normally administered to an abrasion or wound
» to prevent infection.
»
» Here the skin is not contacted with any substance until, for example,
» the ■ •■ - epidermal disruption -has healed (e.g., any time
» between 2 days and 3 weeks).
Alternatively, the skin can be contacted
» with a cast or bandage (e.g., resulting in increased blood flow to the
» disrupted skin or decreased transdermal water loss or decreased mass
» transfer of gases into the skin
and from the skin (e.g. oxygen, carbon
» dioxide, water vapor), decreased heat transfer from the skin (e.g.
» resulting in an increased temperature of the skin surface) or increased
» pressure on the skin.
»
» Prior to disruption, the skin can depilated or epilated. The depilation or
» epilation can be accomplished through, for example, waxing, plucking, an
» abrasive material, a laser, electrolosis, a mechanical device, or
» thioglycolic acid.
»
» The disruption of the epidermis can be induced between 3-12 days (e.g.,
» 4-12, 5-12, 4-11, 6-11, 6-10, 6-9, 7-8, 5-11, 5-10, or 7-10 days) prior to
» the addition of the compositions of the invention.”
»
»
»
»
»
» TO make a long story short, every incidence of new growth associated with
» human skin was either on a SCID mouse (no immune system) or humans who had
» been in extensive chemotherapy (decimated immune status). The mice in
» experiment 7 didn’t even have egf-inhibitors used on them, injected in
» them, or placed in their chow. They simply were abraded and allowed to heal
» with human skin on their backs. EGF-antagonism merely made “more” hair with
» the little creatures. This is why I think (and wish I was wrong about it)
» that immunosuppression may be the key for the whole thing to work. I
» probably didn’t have enough cyclo myself anyway to be honest, as Im going
» to “guess” that one will need about 4-500 mgs of cyclo a day to get
» immunity compromised enough for t-cells not to use cytokines and all the
» other weapons at their disposal to inflame the wound sites. Harlodo once
» posted a study that showed in neo-natal mice, no new hair forms if
» inflammation is present. They get born hairless. The immune system inflames
» wounds, thats part of what it does, so that the inflammation and heat kill
» would-be invaders until the wound heals. I think we probably have to
» “scotch” it. As Ive said earlier, I’d like to be wrong about that, but five
» different immunosuppressants are mentioned as “adjuvants” in the patent.
» One is internal cyclosporin. They are discussed at some length. Why would
» follica even bother?
»
»
»
»
»
»
» Here is the patent verbaige on immunosuppressants (note how much longer
» this entry is than the entry for potassium channel openers, retinoids,
» anti-histamines, anti-androgens, etc.:
»
» Imm unosuppressants
»
» In certain embodiments, a nonsteroidal immunosuppressant can be used in
» the compositions, methods, and kits of the invention. Suitable
» immunosuppressants include cyclosporine, tacrolimus, rapamycin, everolimus,
» and pimecrolimus.
»
» Cyclosporines
»
» The cyclosporines are fungal metabolites that comprise a class of cyclic
» oligopeptides that act as immunosuppressants. Cyclosporine A is a
» hydrophobic cyclic polypeptide consisting of eleven amino acids. It binds
» and forms a complex with the intracellular receptor cyclophilin. The
» cyclosporine/cyclophilin complex binds to and inhibits calcineurin, a Ca2±
» calmodulin-dependent serine-threonine-specifϊc protein phosphatase.
» Calcineurin mediates signal transduction events required for T-cell
» activation (reviewed in Schreiber et al., Cell 70:365-368, 1991).
» Cyclosporines and their functional and structural analogs suppress the T
» cell-dependent immune response by inhibiting antigen-triggered signal
» transduction. This inhibition decreases the expression of proinflammatory
» cytokines, such as IL-2. Many different cyclosporines (e.g., cyclosporine
» A, B, C, D, E, F, G, H, and I) are produced by fungi. Cyclosporine A is a
» commercially available under the trade name NEORAL from Novartis.
» Cyclosporine A structural and functional analogs include cyclosporines
» having one or more fluorinated amino acids (described, e.g., in U.S. Patent
» No. 5,227,467); cyclosporines having
»
» modified amino acids (described, e.g., in U.S. Patent Nos. 5,122,511 and
» 4,798,823); and deuterated cyclosporines, such as ISAtx247 (described in
» U.S. Patent Application Publication No. 2002/0132763 Al). Additional
» cyclosporine analogs are described in U.S. Patent Nos. 6,136,357,
» 4,384,996, 5,284,826, and 5,709,797. Cyclosporine analogs include, but are
» not limited to, D-Sar (α-SMe)3 Val2-DH-Cs (209-825), Allo-Thr-2-Cs,
» Norvaline-2-Cs, D- Ala(3-acetylamino)-8-Cs, Thr-2-Cs, and D-MeSer-3-Cs,
» D-SeI-(O-CH2CH2- OH)-8-Cs, and D-Ser-8-Cs, which are described in Cruz et
» al., Antimicrob. Agents Chemother. 44: 143 (2000).
»
» Tacrolimus
»
» Tacrolimus and tacrolimus analogs are described by Tanaka et al. (J. Am.
» Chem. Soc, 109:5031 (1987)) and in U.S. Patent Nos. 4,894,366, 4,929,611,
» and 4,956,352. FK506-related compounds, including FR-900520, FR-900523, and
» FR-900525, are described in U.S. Patent No. 5,254,562; O- aryl, O-alkyl,
» O-alkenyl, and O-alkynylmacrolides are described in U.S. Patent Nos.
» 5,250,678, 532,248, 5,693,648; amino O-aryl macrolides are described in
» U.S. Patent No. 5,262,533; alkylidene macrolides are described in U.S.
» Patent No. 5,284,840; N-heteroaryl, N-alkylheteroaryl, N-alkenylheteroaryl,
» and N- alkynylheteroaryl macrolides are described in U.S. Patent No.
» 5,208,241 ; aminomacrolides and derivatives thereof are described in U.S.
» Patent No. 5,208,228; fluoromacrolides are described in U.S. Patent No.
» 5,189,042; amino O-alkyl, O-alkenyl, and O-alkynylmacrolides are described
» in U.S. Patent No. 5,162,334; and halomacrolides are described in U.S.
» Patent No. 5,143,918. Tacrolimus is extensively metabolized by the
» mixed-function oxidase system, in particular, by the cytochrome P-450
» system. The primary mechanism of metabolism is demethylation and
» hydroxylation. While various tacrolimus metabolites are likely to exhibit
» immunosuppressive biological
»
» activity, the 13-demethyl metabolite is reported to have the same activity
» as tacrolimus.
»
» Pimecrolimns Pimecrolimus is the 33-epi-chloro derivative of the
» macrolactam ascomyin. Pimecrolimus structural and functional analogs are
» described in U.S. Patent No. 6,384,073.
»
» Rapamycin Rapamycin structural and functional analogs include mono- and
» diacylated rapamycin derivatives (U.S. Patent No. 4,316,885); rapamycin
» water-soluble prodrugs (U.S. Patent No. 4,650,803); carboxylic acid esters
» (PCT Publication No. WO 92/05179); carbamates (U.S. Patent No. 5,118,678);
» amide esters (U.S. Patent No. 5,118,678); biotin esters (U.S. Patent No.
» 5,504,091); fluorinated esters (U.S. Patent No. 5,100,883); acetals (U.S.
» Patent No. 5,151,413); silyl ethers (U.S. Patent No. 5,120,842); bicyclic
» derivatives (U.S. Patent No. 5,120,725); rapamycin dimers (U.S. Patent No.
» 5,120,727); O- aryl, O-alkyl, O-alkyenyl and O-alkynyl derivatives (U.S.
» Patent No. 5,258,389); and deuterated rapamycin (U.S. Patent No.
» 6,503,921). Additional rapamycin analogs are described in U.S. Patent Nos.
» 5,202,332 and 5,169,851.

You might be right as I tried topical tacro and it didn’t seem to aid the cause any. The results I got so far with the exception of temple that I had to further wound (not enough wounding the first time) was from my first try. I would still try topical immunos b4 I give up and go internal. When the skin start to heal is still up in the air for me. Like I said b4, I applied egfr 24 hours post wounding because I didn’t want to miss the window. if you have all the ingredients and you you don’t wound enough and if your timing is off then you might as well forget it. I don’t think follica is 100% sure on how human skin heals on a human body (not mice), hence the study at Harvard. There is no mention of applying egfr too early will be detrimental to the experiment so I took the “better be safe than sorry” route. You had no ill effects with internal cyclo? If I were to do this, I would cut that pill in halves or quarters. We are trying to introduce new organs (hair) to our bodies but it is our own organ not somebody elses. I guess it would be logical to say that the human body might treat the new hair cells like it would try to treat new cancer cell (for example) and try to fight it off. I kind of look at it like a transplanting hairs from one part of your own body to another, why would your body try to reject it from forming if its our own? If immunos are used I don’t think it would be in high doses. This is all speculation on my part. BTW, you know what I can inhibit WNT with? I’m thinking to inhibit wnt from days 0-10 and apply egfr on maybe day 3-4 this time around. But it wouldn’t be for several months as the skin on my temples are still a little red.

With immunos used, you have a very valid point. But, I’ll say this again, I got tons a baby hairs on my once bald temples. I’ve never had hair there b4 as I was going for a pretty boy or girls hairline however you want to call it. I honestly think I got new hair cells to form. My issue is why is growing like it doesn’t want to grow. It kind looks like I generated tons of vellous hairs that might remain that way and I don’t think immunos had anything to do with it in my case otherwise nothing would’ve been formed. Where I stand for myself right now is either a timing issue or a wnt inhibition issue in the 1st 10 days or a combination of both. Benji, I’m well aware of ur stance on immunos in follicas method and I tried it (tacrolimus), but not internally and they might very well play a part of the whole scheme of things. It just didn’t work for me any better than without it imho. If you did exactly what I did then you don’t need it to work any better. Now, if you tried a variation of what I did topically maybe you will see a more positive outcome. I don’t know, all we can do is keep trying and I don’t really think this is that hard to figure out. We just have a handful of guys here doing it and maybe a 100 “good” combinations to try. But I tell u that as sure as you are that internal cyclo is to be used, I am sure topical egfr is used, not internal. Why don’t you just wound/wait and take cyclo and see how much hair u get, no antaganist.


#8

Baccy, I’m concerned about the customs issue. Do have ppg and dmso on hand? The other ingredients are easily obtainable at the supermarkets and they are cheap as well. If not, I will go forward and mix/send this week.


#9

» Baccy, I’m concerned about the customs issue. Do have ppg and dmso on
» hand? The other ingredients are easily obtainable at the supermarkets and
» they are cheap as well. If not, I will go forward and mix/send this week.

I’ve got dmso but that is all. I’ve been sent a bottle of mix before by a guy on another forum who I think is based in the USA. There were no customs issues. It could be just a Christmas gift from a relative overseas.
When it comes to mixing up things myself, the only experience I’ve had is with my tin-pot experiments on here. Crushing tablets on a teaspoon and dissolving in dmso then mixing into emu oil.


#10

Mike, regarding your concerns about the effect of an ointment base on the wound, doesn’t ppg have an effect on wounds?


#11

Guys,

Wouldn’t it be easier just to find some herb that grows in the Brazilian rainforest that, when rubbed on the scalp, grows new follicles? :smiley:


#12

Baccy, I will try to mix up a batch and send to you on Wednesday.

MW


#13

» Baccy, I will try to mix up a batch and send to you on Wednesday.
»
» MW

Cheers for that m8.


#14

» » Baccy, I will try to mix up a batch and send to you on Wednesday.
» »
» » MW
»
» Cheers for that m8.

Baccy, your package is shipped via regular USPS mail. Let me know when you recieve it, I will email you when you do.

MW


#15

» » » Baccy, I will try to mix up a batch and send to you on Wednesday.
» » »
» » » MW
» »
» » Cheers for that m8.
»
» Baccy, your package is shipped via regular USPS mail. Let me know when
» you recieve it, I will email you when you do.
»
» MW

Roger that. And many thanks.