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Trying it for all of us, concluding my experiment


#1

So that everybody could find out about follica through me, I ran the experiment fairly close to the vest. Here are the details.

Last Monday night at about 9:00 PM, I abraded the frontal area UNDER my NW 3 hairline.

I had taken cyclosporin that morning (150 mgs). Cyclosporin’s presence in serum is markedly increased by drinking grapefruit juice (suprisingly tasty) by a factor of probably 2-to-3. I took divided doses of 50 mgs of cyclo (one in the morning, one at night), thereafter. This should equate to approximately 200-300 mgs per day, which is about the dosage given to psoriasis patients.

On Saturday night, 5 days post-wounding, I started taking about 2/3 a getfitinib tablet. Getfitinib is metabolized by the same enzyme that cyclosporin is (some CYA34-something-or-other), and its serum presence will be increased by drinking grapefruit juice (as many drugs serum percentage is increased by it also). I still was taking cyclosporin at this time.

I took both cyclo and getfitnib together for four days (Nine days of immuno-suppression). I was then out of cyclo, but took getfitinib one day beyond that, and will again (last time) tonight. That will be nearly 8 days of getfitnib). I have taken oral doses of lithium chloride on Monday, Wednsday, and Thursday (basically a pinch of the stuff).

I did not shampoo my hair from Monday before the wounding, until the NEXT Tuesday morning before work. This was approximately 8.5 days post wounding. I intended to only get the back of my head wet and not to let water hit the abraded area. To my dismay, some of my wet hair fell on what would have been the abraded area. I hope there was no intereference with the experiment here. It was an “oops” moment. Im going to wash my hair Saturday, because that will have been 12 full days since the wounding. Ive not allowed my abraded area to get wet since Tuesday morning. The only other time that excessive moisture might have impeded the goings-on in the abraded area is the steam from the shower touching it. This is a concern. Sunday morning, I actually thought about this and started wearing a baseball cap in the shower to lessen any moisture getting to touch my frontal scalp. I hope it helped.

So in conclusion I took cyclosporin internally, getfitinib internally, and pretty much didn't let any water touch the abraded area until at least 8 days past-the wound date. If I abraded deeply enough (I abraded in several quarter-sized wounds all over the frontal scalp), I SHOULD get something. If I don't, its my conclusion that we will simply have to wait on follica as I eliminated about every variable I could think of. It SUCKED going around with oily-hair for almost two weeks. I used a fine tooth comb (which I washed every night) to comb through my hair and physically remove as much oil as possible. I avoided any food with quercetin in it after three days in the experiment for fear of inhibiting wnt (no tea, apples, onions, etc.). I can't think of anything I left out. I used minoxidil ON THE TOP of my head, and below the abraded area (not touching it) on Sunday, Monday, and Tuesday, and Thursday nights).

So…I hope this gets it tried for all of us. If it doesn’t work on me, we will probably have to wait on Follica to be honest. I’d be willing to try it again if one of you guys has success growing something using various naturals and topicals, but for myself…I dont think Im willing to fool with it again. Ive had much LESS side effects this time, and only a couple of acne lesions (my nose is pretty inflammed right now though) from the getfitinib. The Cyclosporin will make you tired, which is why many people give up on cyclosporin. Ive had some diarreaha with the getfitinib, which I expected. I did use some TCA peels on the back of my neck and behind my ears on my wound date, but water had no doubt hit these areas in the shower. Any growth I got there would be considered a plus, but I wanted to see if TCA was a good wounding method. I left the 25% TCA on for exactly three minutes in these areas before washing it off.

I guess in about a month or so, I’ll know if I had any success. Other than the water mistake at 8.5 days, inusufficient amounts of cyclosporin, or if I screwed up the wounding (I doubt it, as I peeled which is good evidence of enough wounding), shower steam, perhaps sweating (I did pump iron during this time) interefering with the process are the only things I can think of that would have inhibited any hair formation.


#2

Well done. If it fails, I still wouldn’t lose hope for this protocol. As Follica has begun its human trials with a study on abrasion techniques, I think the depth of abrasion is important, and something that can’t really be done with any precision at home.


#3

» So that everybody could find out about follica through me, I ran the
» experiment fairly close to the vest. Here are the details.

Well done! Hopefully, you get something out of this, as you took a big enough risk.

Random thoughts:

Back when you were discussing trying this, I had wondered if the cyclosporine would help control the acne flare from gefitinib.

How did you wound the hairline?

You mentioned that you avoided foods containing quercetin. During my experiment I ate a lot of broccoli…in retrospect, I wish I hadn’t.


#4

» Well done. If it fails, I still wouldn’t lose hope for this protocol. As
» Follica has begun its human trials with a study on abrasion techniques, I
» think the depth of abrasion is important, and something that can’t really
» be done with any precision at home.

Thank you fckhrls for the kind words. You are quite correct about the precision of the dermabrasion. Ive seen a study, and posted a link on it, whereby re-epilithialization happened in 60% of dermabrasion patients by day 6 vs. hardly any at all who had CO2 laser resurfacing. Thats with professional instruments. I only had sandpaper.
I realize follica’s team (an impressive bunch of people) has a much greater chance to make this go than I ever would. Im afraid, but hope Im wrong, that they may find very intense immuno-suppression (as in 1000 mgs of cylco a day, like an organ recipient patient) per day might be necessary along with increased EDAR signalling, increased wnt, egf-antagonism, potassium channel openers, and all that jazz to really get good results in humans consistently.
My hope is that they will have success back in the donor area…where more “donor” hair can be made for FUE or FIT or whatever up to the front.

Ive been willing to “piddle” with this, because its the only thing anywhere close that we could try at home.


#5

»
» Well done! Hopefully, you get something out of this, as you took a big
» enough risk.
»
» Random thoughts:
»
» Back when you were discussing trying this, I had wondered if the
» cyclosporine would help control the acne flare from gefitinib. That very well might be it. I know the immune system gets involved in acne. I have a feeling that acne might be started via the hyperkeratinization of certain hair follicles, and the ensuing immuno-response to the dead keratiniocytes muddled in the excess sebum, that would begin to host some micro-organisms and all that is downstream of it. Cyclo does make one drowsy though. I was “bone” tired after my loading dose the first night. I dont see how some of these people who have to take 500 mgs or so for several months for various conditions can stand it. I honestly think my acne flare up the first time might have been caused by my washing my face and hair and back with nizoral. Ketoconazole and getfitinib aren’t supposed to be used together. My scalp had lesional acne on it the first time round. I thought the keto would have helped the acne, but I didn’t know then what I know now about how the two drugs interact. »
» How did you wound the hairline? sandpapering it. There was no blood, but it was very pink. It peeled. »

» You mentioned that you avoided foods containing quercetin. During my
» experiment I ate a lot of broccoli…in retrospect, I wish I hadn’t.
I remember that when mice were given wnt DURING re-epilithialization, they had pigmented hair as opposed to white hair. Mice dont have pigmented skin, but this shows me one other important thing: what happens during re-epilithialization (immunosuppression), might be important to the final result. Henceforth I only ate things that might inhibit wnt for the first three days post wounding since I didn’t want to inhibit wnt after re-epilithialization was done. I like tea and apples.


#6

Benji thanks a lot for trying this yourself. You followed what i believe is the best “home” approach of follica’s patent. I wish you have great results for you and for us :slight_smile:

By the way did you take (or already have) any before pictures?


#7

Good luck.

The most direct concern I have about your experiment this time would be insufficient immune suppression. Not that I think you pussied out or anything. But I also wonder if the necessary level of immune suppression might indeed be brutal enough for an organ donor.

It actually makes a lot of sense to me if that were indeed the case. We’re basically trying to form some new organs under our immune system’s nose and not get them rejected. This may not really be THAT different from an organ transplant situation, at least in the short term.

But even such a brutal round of cyclo, temporarily, doesn’t strike me as being any more objectionable than a 4000-graft strip-scarring hair transplant is already.

As for the topical issues you mentioned, it really doesn’t concern me. You’ve already kept the main idea of the issue by not shampooing or anything. I doubt the cancer patients were very careful about keeping their head/face clear of all foreign influences. And I can’t imagine they never hit their head/face with plain water during any of the vital timeframes. If your current experiment fails, topical interference is not gonna be what I first suspect.

You mention having nose acne. Man, I hope that doesn’t lead to “nose hair” like that cancer patient! (The idea that their new hair had formed because of sunburns serving as accidental “wounding” . . . it occurs to me that this idea was never really anything but unconfirmed guesswork on our part . . . )


#8

The reasons I think immunosuppression might be necessary are these:

1) The mice that had human skin transplanted on their backs, had no EGF-antagonism in experiment 7, yet they grew hair. The only difference between them and us is that we have an immune system

2) The two what getfitinib patients had been on chemotherapy, and had severely compromised immune-status. There are other EGF-antagonists like lefloumonide that have been in usage for other stuff for years. Surely somebody on lefloumonide has had a sunburn. Why no whack hairgrowth on shoulders, necks, arms, etc?

3) Many men take finasteride and use minoxidil. Many of these same men go to the beach every year and get that Florida sunburn. None of them have hairy shoulders in two months. They peel from the burns that should perfectly fit epidermal disruption and indeed sunburns are even mentioned in the patent. We know the mice with human skin on their backs did NOT have any egf-inhibition, yet grew hair. These men didn’t have EGF inhibition either, so where is their new hair.
NOTE: I once burned in Florida so bad my entire FACE peeled. My biceps and shoulders and back peeled. I used minoxidil still back then on my head (this is right before I got on finasteride). I didn’t get any whack hair anywhere.

4) Harold once posted at h…l…t… that neo-natal mice didn’t form hair when inflammation was present. He had he study. It should be there somewhere. The immune system is going to inflame any topical wound to kill any would-be invaders. It just stands to reason that if someone isn’t on a powerful immunosuppressant, or uses one topically, that the immune system is going to inflame a dermabraded area. Corscosteroids have effects on the immune system, and perhaps these were administered to the dermabrasion patients that Kligman noted de noveau hairgrowth on back in the seventies.

I’d like to be wrong about what I propose above, believe me…I’d love to be wrong about it. However TAGOHL (a very smart guy), Cal (another very smart guy), and myself (all thumbs but I can follow instructions) have tried egf-antagonism after wounding, and none of us got anything. So its either shampoo/water or the immune system in all likelihood. I doubt all three of us missed THE ENTIRE embryonic window which likely lasts for 2-3 days.

Like you Cal, if I failed this time…I believe its probably because I didnt suppress my immune system enough. Im pretty sure out of all the area I abraded, I’d have gotten it right in one of the temples in a large enough area somewhere. I do worry about that residue water from my hair that got on my temples at day 8.5. This water would have been soapy, and that is right in the middle of the time frame that things were going to go one way or another up there. Its a concern. Its funny that while I was on cyclo, I had no acne from the getfitinib at all, but now that Ive been off of cyclo for a few days…Ive got like five white heads. Two on the forehead, a big one on my nose, and two on my neck. My nose is inflammed. EGF antagonism causes hyperkeratinization through one pathway or another…and while my immune system was sort of suppressed, I had no inflammation from this, but now that its regained its strength, these sites are quite inflammed. I took my last getfitinib last night. I’d have taken cylco longer, but I only had 20 tablets. I used four the first day, and two every day thereafter, so I was on it for nine days. I probably got a tenth carry-over day of reasonable suppression. I healed more slowly this time though…probably because my last wound date was in late September. I did give it “the college try” though. I hope you Cal, can try it once more if I strike out with better immunosuppression. I had this “window” in my schedule where I could pull this post-Thanksgiving, but in this next year…yikes, I just don’t see much downtime at all. Even if I failed, it would be six months before I think I could wrangle the time again.


#9

Yeah, if your round here fails, then the logical thing for me to do next is hit the cyclo harder.

I’m willing & able to do it harder as long as it’s not too medically dangerous. As long as it doesn’t render me a total shut-in at my apartment for a week or more, frantically washing everything in sight. Just being in public for a week with unwashed hair and little red wounds doesn’t slow me down in any big way.

WNT and EGF details might affect characteristics and all that, but the basic growth has gotta be present with one good EGF + immune wallop during a wound re-epithialization. If growth isn’t coming from that, then we’re still doing something incorrect with the basics.

I have a relative with a heart transplant. He’s an energetic guy now, even dancing at parties and all that. If he can live on rejection-level doses of oral cyclo for the rest of his life then surely I can do it for a week. F*ck feeling lethargic, I want my hair back.


#10

a poster named “sothatslife” at h…l…t was kind enough to mail this to me:

"I read about your new experiment at hairsite.

The documentary I mentioned in my last PM to you, kinda pointed towards that it was the immune system that was keeping the body from regeneration it self. The healing process have cells that keep what they called supercells(the ones needed for regeneration) away from the wounded area. And that when removing/weakling the immune system, the supercells get access to the wounded area. Therefor control over the immune function was something the researchers looked in to, and probably is what follica is looking into right now.

It makes a lot of sense doesn’t it?

I mean lefloumonide has been on the market and used for YEARS now Cal. Surely one or two patients have gotten a sunburn and peeled on it by now. Why no whack hair growth?

I keep going back to those SCID mice. They were merely wounded, they had no EGF inhibition, yet the human skin on their backs made new human hair.


#11

This is exactly how I’ve been feeling for a long time too - It’s the immune system that’s really standing in the way.

In the big picture, we’re trying to regenerate (or at least repair) our hair follicles without our immune system stopping it. Once we get the follicles a few days/weeks of critical immune-shielded construction time, I’m reasonably confident that they’ll be safe from bodily rejection once the immune system is back online. All the research points to this fabled “critical window” that we’ve been chasing as the important factor that has kept mankind bald for thousands of years even when we get scalp injuries during life.

The EGF-R and WNT issues seem more like they’re just gears to play with once the main hair growth engine has been fired up. There will be a couple of real problems with WNT/EGF-R to avoid (like park and reverse gears). But the majority of ways the gears can be ordered & timed would still basically push hair growth forwards with varying degrees of success.

The question is - can Folica realistically do all this topically with a product? The immune suppression? The EGF-R and WNT issues?


#12

» So that everybody could find out about follica through me, I ran the
» experiment fairly close to the vest. Here are the details.
»

Thanks for the details! Successful or not, your experiments provide us with a lot of information.

However, I would not venture as far as to say that we have exhausted our options in regard to the internal follica route. There are so many variables to consider and tweak; timing, wound depth, dosages, substances, immunosuppression, etc. I realize that you’ve had enough for now, considering all the sides you put up with. You have done more than enough! Perhaps someone else can pick up where you left off.

But may I ask why you are not taking the topical route since it appears to be more successful and has less side effects? On this board alone, we have had several reports from people with some sort of result (Baccy, mikewalters, frankiebaby, coffee etc). Intuitively, one might think that the internal route ought to be more “powerful” but observations tell us otherwise. And after all, science is about observations, not opinions. :wink:


#13

» » So that everybody could find out about follica through me, I ran the
» » experiment fairly close to the vest. Here are the details.
» »
»
» Thanks for the details! Successful or not, your experiments provide us
» with a lot of information.
»
» However, I would not venture as far as to say that we have exhausted our
» options in regard to the internal follica route. There are so many
» variables to consider and tweak; timing, wound depth, dosages, substances,
» immunosuppression, etc. I realize that you’ve had enough for now,
» considering all the sides you put up with. You have done more than enough!
» Perhaps someone else can pick up where you left off.
»
» But may I ask why you are not taking the topical route since it appears to
» be more successful and has less side effects? On this board alone, we have
» had several reports from people with some sort of result (Baccy,
» mikewalters, frankiebaby, coffee etc). Intuitively, one might think that
» the internal route ought to be more “powerful” but observations tell us
» otherwise. And after all, science is about observations, not opinions. :wink:

Personally, I’m not convinced everthing needs to be systematic like egfr inhibitor (getfitnib), WNT booster (lithium), WNT inhibitor (can someone please tell what I can use topically for this?) and immunos. Things I took internally was only Dut/fin and anti-histimine. Just keep trying…Not to knock anybody doing the internal route, I personally would go with the direction that at least gave me something positive, however small it is.


#14

» WNT inhibitor (can someone please tell what I can use topically for this?)

I think Baccy used Quercetin pills, crushed and dissolved in DMSO, and then mixed with a ALA cream topically. The Quercetin might inhibit WNT.


#15

»» Personally, I’m not convinced everthing needs to be systematic like egfr
» inhibitor (getfitnib), WNT booster (lithium), WNT inhibitor (can someone
» please tell what I can use topically for this?) and immunos.

Quercetin and curcumin. Problem with these are that they both inhibit EGF as well. My take on it is that you have to allow EGF to do it’s work for the first couple of days to epithelize the skin. EGF inhibition should only be applied after epithelization. I don’t know of anything we can take to inhibit wnt whilst not interfering with EGF. I would say that the way to go is to use quercetin and curcumin AFTER epithelization for a couple of days. This way you are theoretically inhibiting wnt and supplementing the action of the gefitinib on EGF. After a couple of days cease wnt inhibition and just go with the gefitinib. Also boost wnt if possible, maybe with lithium.

Thing I worry about with this wnt inhibition is overextending the wnt inhibition window and crossing into the phase where we should be BOOSTING wnt.


#16

» »» Personally, I’m not convinced everthing needs to be systematic like
» egfr
» » inhibitor (getfitnib), WNT booster (lithium), WNT inhibitor (can
» someone
» » please tell what I can use topically for this?) and immunos.
»
» Quercetin and curcumin. Problem with these are that they both inhibit EGF
» as well. My take on it is that you have to allow EGF to do it’s work for
» the first couple of days to epithelize the skin. EGF inhibition should only
» be applied after epithelization. I don’t know of anything we can take to
» inhibit wnt whilst not interfering with EGF. I would say that the way to go
» is to use quercetin and curcumin AFTER epithelization for a couple of days.
» This way you are theoretically inhibiting wnt and supplementing the action
» of the gefitinib on EGF. After a couple of days cease wnt inhibition and
» just go with the gefitinib. Also boost wnt if possible, maybe with
» lithium.
»
» Thing I worry about with this wnt inhibition is overextending the wnt
» inhibition window and crossing into the phase where we should be BOOSTING
» wnt.

What about Green tea powder mixed as a topical?

Same deal, green tea powder extract, everclear, ppg, distilled water and small amount of dmso. This shouldn’t stay in your body long.


#17

»
» What about Green tea powder mixed as a topical?
»
» Same deal, green tea powder extract, everclear, ppg, distilled water and
» small amount of dmso. This shouldn’t stay in your body long.

green tea inhibits epidermal growth factor and wnt:

1: Cancer Res. 2007 Jul 1;67(13):6493-501. Links
The inhibitory effect of (-)-epigallocatechin gallate on activation of the epidermal growth factor receptor is associated with altered lipid order in HT29 colon cancer cells.Adachi S, Nagao T, Ingolfsson HI, Maxfield FR, Andersen OS, Kopelovich L, Weinstein IB.
Herbert Irving Comprehensive Cancer Center and Department of Medicine, Columbia University Medical Center, New Yourk, NY 10032-2704, USA.

(-)-Epigallocatechin gallate (EGCG), a major biologically active constituent of green tea, inhibits activation of the epidermal growth factor (EGF) receptor (EGFR) and downstream signaling pathways in several types of human cancer cells, but the precise mechanism is not known. Because several plasma membrane-associated receptor tyrosine kinases (RTK) including EGFR are localized in detergent-insoluble ordered membrane domains, so-called “lipid rafts,” we examined whether the inhibitory effect of EGCG on activation of the EGFR is associated with changes in membrane lipid order in HT29 colon cancer cells. First, we did cold Triton X-100 solubility assays. Phosphorylated (activated) EGFR was found only in the Triton X-100-insoluble (lipid raft) fraction, whereas total cellular EGFR was present in the Triton X-100-soluble fraction. Pretreatment with EGCG inhibited the binding of Alexa Fluor 488-labeled EGF to the cells and also inhibited EGF-induced dimerization of the EGFR. To examine possible effects of EGCG on membrane lipid organization, we labeled the cells with the fluorescent lipid analogue 1, 1’-dihexadecyl-3,3,3’,3’-tetramethylindocarbocyanine perchlorate, which preferentially incorporates into ordered membrane domains in cells and found that subsequent treatment with EGCG caused a marked reduction in the Triton X-100-resistant membrane fraction. Polyphenon E, a mixture of green tea catechins, had a similar effect but (-)-epicatechin (EC), the biologically inactive compound, did not significantly alter the Triton X-100 solubility properties of the membrane. Furthermore, we found that EGCG but not EC caused dramatic changes in the function of bilayer-incorporated gramicidin channels. Taken together, these findings suggest that EGCG inhibits the binding of EGF to the EGFR and the subsequent dimerization and activation of the EGFR by altering membrane organization. These effects may also explain the ability of EGCG to inhibit activation of other membrane-associated RTKs, and they may play a critical role in the anticancer effects of this and related compounds.

Green tea and wnt:

http://www.jbc.org/cgi/content/abstract/281/16/10865

Green tea wouldn’t be a good idea after re-epilithialization, which occurs earlier in humans than in mice.


#18

» »» Personally, I’m not convinced everthing needs to be systematic like
» egfr
» » inhibitor (getfitnib), WNT booster (lithium), WNT inhibitor (can
» someone
» » please tell what I can use topically for this?) and immunos.
»
» Quercetin and curcumin. Problem with these are that they both inhibit EGF
» as well. My take on it is that you have to allow EGF to do it’s work for
» the first couple of days to epithelize the skin. EGF inhibition should only
» be applied after epithelization. I don’t know of anything we can take to
» inhibit wnt whilst not interfering with EGF. I would say that the way to go
» is to use quercetin and curcumin AFTER epithelization for a couple of days.
» This way you are theoretically inhibiting wnt and supplementing the action
» of the gefitinib on EGF. After a couple of days cease wnt inhibition and
» just go with the gefitinib. Also boost wnt if possible, maybe with
» lithium.
»
» Thing I worry about with this wnt inhibition is overextending the wnt
» inhibition window and crossing into the phase where we should be BOOSTING
» wnt.

the only “natural” Ive seen in any literature that might inbhibit EGF without suppressing wnt also was silymarin isolated from milk thistle.

Copyright © 1998 Academic Press. All rights reserved.
Regular Article
Skin Cancer Chemopreventive Effects of a Flavonoid Antioxidant Silymarin Are Mediated via Impairment of Receptor Tyrosine Kinase Signaling and Perturbation in Cell Cycle Progression

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Nihal Ahmada, Hala Galia, Seema Javeda and Rajesh Agarwalb, c, a, 1

a Department of Dermatology, Skin Diseases Research Center, Case Western Reserve University, Cleveland, Ohio, 44106

b Skin Diseases Research Center, CWRU Ireland Cancer Center University Hospitals of Cleveland, Case Western Reserve University, Cleveland, Ohio, 44106

c Center for Cancer Causation and Prevention, AMC Cancer Research Center, Denver, Colorado, 80214

Received 23 April 1998. Available online 15 April 2002.

Abstract
Enhanced tyrosine kinase activity due to aberrant or overexpression of receptor and/or non-receptor tyrosine kinases has been implicated in a variety of human malignancies including cutaneous neoplasms. Epidermal growth factor receptor (EGFR)-mediated tyrosine phosphorylation may be a primary indicator of signal transduction regulating cell growth and proliferation. Recent studies have shown that skin tumor promoters such as phorbol ester and ultraviolet B radiation activate EGFR in mouse skin as well as in cell culture. Similarly, oxidative stress, which is implicated in skin tumor promotion, also activates EGFR-mediated cell signaling. Since this signaling pathway has been suggested to be involved in skin tumor promotion, its impairment by antioxidants may lead to an efficient way for skin cancer prevention and therapy. Recently, we showed that silymarin, a flavonoid antioxidant, affords exceptionally high to complete protection against several skin tumor promoters caused tumor promotion in mouse skin. Employing human epidermoid carcinoma cells A431 that contain overexpressed EGFR, in this study, we assessed whether the anti-skin tumor promoting effects of silymarin are due to its inhibitory effect on EGFR activation and down stream signaling pathway leading to perturbations in cell cycle progression. Treatment of cells with silymarin resulted in a significant inhibition of ligand-induced activation of EGFR with no change in its protein levels. Silymarin treatment also resulted in a significant decrease in tyrosine phosphorylation of Shc, an immediate downstream target of EGFR, but no change in the protein levels of Shc. The inhibition of EGFR activation by silymarin was associated with a highly significant to complete inhibition of EGFR intrinsic kinase activity. Cells treated with silymarin also showed a significant G2-M arrest in cell cycle progression, and a highly significant inhibition of DNA synthesis and cell growth in a dose-dependent manner. Taken together, these results suggest that skin cancer chemopreventive effects of silymarin are mediated via impairment of EGFR signaling which ultimately leads to perturbation in cell cycle progression resulting in the inhibition of proliferation and induction of growth arrest.

1 Author for correspondence

this doesn’t mean it will not be overcome by natural processes in the body in respone to a wound, but it would be great if it didn’t. I’d much rather take milk thistle extract from the Grocery store than buy any more getfitinib.

BTW-----if you take getfitinib for x-amount of days, its actually WISE to take some cyclo. It will help you not have the mother of all acne breakouts. Interestingly, Silymarin inhibits Interleukin 1-alpha, which seems to help with the hyperkeratinization problem that egf-inhibitors cause, and hence the really bad acne associated with their usage. The dead kt cells dont “slough off” like they are supposed to in the hair follicle and cling to the infidulum walls, inviting a big inflammatory immune response–hence the acne inflammation and pus, etc.

Baccy If I were going the entire natural route…this is what I’d do. Id wound, not wash the hair for at least two full weeks (even water), take things that would inhibit wnt for 3 full days at least (quercetin), then I’d up wnt at day 6 or so with lithium chloride (just a pinch of it daily like salt) and start using silymarin (milk thistle) extract 2-3 times a day from day 5 onwards until day 14. I’d put minoxidil on the BACK OF MY HEAD at day 9 thru 11 like the patent hints at. I might take some anti-inflammatories during this time.

However, I really think follica is going to find that humans will have to have immunosuppression INTERNALLY (the immune systems cells travel the whole body, so I’ll be suprised if just inhibiting them at the point of wounding will be “enough”). We have had hair growth on human skin twice, both with chemo patients, and several times on human skin on immuno compromised mice.

SEVEREAL LEFLOUMONIDE PATIENTS HAVE NO DOUBT HAD SUNBURNS, but no strange hairgrowth…why? Immunosuppression is the only answer in my opinion.


#19

»
» Baccy If I were going the entire natural route…this is what
» I’d do. Id wound, not wash the hair for at least two full weeks (even
» water), take things that would inhibit wnt for 3 full days at least
» (quercetin), then I’d up wnt at day 6 or so with lithium chloride (just a
» pinch of it daily like salt) and start using silymarin (milk thistle)
» extract 2-3 times a day from day 5 onwards until day 14. I’d put minoxidil
» on the BACK OF MY HEAD at day 9 thru 11 like the patent hints at. I might
» take some anti-inflammatories during this time.
»
»
I’m actually trying topical gefitinib this time, very kindly mixed up by Mike.
On my successful attempt, I actually used milk thistle as an EGF inhibitor and Quercetin to inhibit wnt for the first couple of days after wounding.


#20

SEVEREAL LEFLOUMONIDE PATIENTS HAVE NO DOUBT HAD SUNBURNS, but no strange hairgrowth…why? Immunosuppression is the only answer in my opinion.

Bingo. My thoughts exactly.

Baccy, best of luck to you. It would be really beneficial if we could find topicals for as much of this stuff as possible. Oral cyclo is probably unavoidable (at least with the current anti-immune topicals), and I think that’s enough powerful oral drugs for one sitting if we can possibly help it IMHO.

I think your basic thrust here makes a lot of sense. The EGF-R and WNT effects in general sound like they could be topically do-able, if we could just make sure that we’re not cancelling out the effects we DO want with all the multiple effects of these things.

The Folica patents all say “non-natural EGF-R inihibitor.” But I really have never come up with any significant difference from the effects of naturals other than the single/multiple effects. Well, that and maybe the strength of the efficiacy in general. (Big deal. So maybe we’ll have to learn to crawl with the naturals before we learn to walk with something custom-brewed by Folica.)