I think I've hacked it

[NeedHairASAP]

Hi fred970

Well, instead of wasting your time reading my stuff here. I suggest you watch this movie, it's based on a true story

https://www.youtube.com/watch?v=tZV_bMgB-zA

never underestimate the power of a very motivated person

And always remember this:

"be the change you want to see in the world"

Hope you have a great day

What is so ironic is that Fred is accusing you of being a troll, whilst he himself is the biggest troll in this entire thread.

[FGF11]

I figured out a novel way to do my experiments in a much larger scale and for a longer amount of time, this is for me a very important time. So as of now I have decided to go ahead with this. (I may or may not however do this, also I may or may not post my results here), If I decide to go with it (after I totally get sure if it's safe), it probably will six or eight months, or even more till I get sure it works. Well, what I can say it's my hobby. Everyone has hobby, right? Anyways, here I wrote a last "scientific" reply further supporting it might be possible to reverse HF miniaturization. This time, I'm "REALLY" off this tread though. I appreciate those few critical responses I've got, from xyz123, chemical, swooping and everyone else for appreciating me writing my theory here. Good Luck.

Current drug treatments for MPP, Finasteride and Minoxidil, usually have only marginal effect on hair density. This is, despite the fact that, the bald region of scalp in MPB patients still retains the capacity for full regeneration of its hair follicles (1). In an experiment done by Krajcik et al, authors showed that not only hair follicles (HFs) from bald scalp can grow as fast as HFs from hairy scalp when transplanted onto the back skin of SCID mice, but also strikingly, they even produce a thicker shaft (2). Reversal of MPB has also been reported in patients on immune-related drugs (3). These data are promising as they provide the interested researcher with the much needed confidence that transformation of vellus hairs from bald region of scalp to terminal hairs, is indeed, possible. However, there are still contradictory data, around the possibility of restoring healthy cycle back to miniaturized HFs.


References

1. Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, et al. Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells. J Clin Invest. 2011 Feb;121(2):613-22.

2. Krajcik RA, Vogelman JH, Malloy VL, Orentreich N. Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice. J Am Acad Dermatol. 2003;48(5):752-9.

3. Fenton DA, English JS, Wilkinson JD. Reversal of male-pattern baldness, hypertrichosis, and accelerated hair and nail growth in patients receiving benoxaprofen. Br Med J (Clin Res Ed). 1982;284(6324):1228-9.

[NeedHairASAP]

may a proteasome inhibitor?

J Biol Chem. 2002 Sep 27;277(39):36570-6. Epub 2002 Jul 15.
Proteasome activity is required for androgen receptor transcriptional activity via regulation of androgen receptor nuclear translocation and interaction with coregulators in prostate cancer cells.

Lin HK1, Altuwaijri S, Lin WJ, Kan PY, Collins LL, Chang C.

Author information

Abstract
Upon binding to androgen, the androgen receptor (AR) can translocate into the nucleus and bind to androgen response element(s) to modulate its target genes. Here we have shown that MG132, a 26 S proteasome inhibitor, suppressed AR transactivation in an androgen-dependent manner in prostate cancer LNCaP and PC-3 cells. In contrast, MG132 showed no suppressive effect on glucocorticoid receptor transactivation. Additionally, transfection of PSMA7, a proteasome subunit, enhanced AR transactivation in a dose-dependent manner. The suppression of AR transactivation by MG132 may then result in the suppression of prostate-specific antigen, a well known marker used to monitor the progress of prostate cancer. Further mechanistic studies indicated that MG132 may suppress AR transactivation via inhibition of AR nuclear translocation and/or inhibition of interactions between AR and its coregulators, such as ARA70 or TIF2. Together, our data suggest that the proteasome system plays important roles in the regulation of AR activity in prostate cancer cells and may provide a unique target site for the development of therapeutic drugs to block androgen/AR-mediated prostate tumor growth.
PMID: 12119296 [PubMed - indexed for MEDLINE] Free full text
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[xyz123]

Good luck FGF11 - we will be awaiting your return in 6-8 months Your thread has gotten close to 10,000 views in less than 48 hours - which goes to show that you've gotten many people interested (not many journal articles can compete with those numbers ).

Pull this off and you'll grab the attention of the whole world - and become a billionaire in the process And if you don't - that's OK too - I think we've all learned from your posts.

Here's to hoping that you return with good news in mid-2016!

[youngin]

FGF11 - You have definitely done your research. I for one appreciate the self starting science you are doing. However, I do not think your path will be successful. As you know, when someone has started balding and is castrated they will not grow all of the miniaturized hair back. There is only a MINIMAL amount of active androgens without testicles. There is more going on here than just androgens. Something is causing a calcification/scarring type effect and also damaging the DNA of the cells. This has all been published. For many people minoxidil works much better than Finasteride for growth stimulation, which has nothing to do with androgens, but probably has more to do with removal of the scar like tissue by being a calcium channel blocker and also limiting collagen formation.

[pixels]

I'm with Fred.

How many pages was that for pretty much no information.

You can't bring pics to the table for some kind of ethical condumdrum?

Oh please. You can waste our time with pages of mumbo jumbo but when somebody asks for evidence you get all holy.

No thanks. Please just go away.

[Swooping]

@Chemical

Thank you. See where I'm heading at though? Let's hypothetically assume that these factors are indeed deeply implicated in AGA. How does one work around that? Direct modulation of these factors for instance is something you can't really do I guess due to very serious safety concerns. I find it also interesting that 17b-estradiol can regrow hair to great extent sometimes but not always. I have seen pictures of people that have regrown a very big amount of hair due to being on anti-androgen therapy + estrogen. I think Cotsarelis puts this nicely again;

Studies and case reports of transgender operations where men become women and receive high doses of estrogen show that a scalp that was almost completely bald can have, after castration and high estrogen supplementation, a tremendous amount of hair growth. The overall feeling is that the follicles can be thought of as being in three states. Either they’re terminal, and they’re large, or they’re miniaturized, and they’re small, and the hair they’re creating is microscopic, or they’re in between, called indeterminate. It’s thought that follicles reach a point where they’re producing a hair so small that at that point the chance of reversing that follicle is small. There seems to be a point of no return with respect to androgen removal; even if you castrate someone who’s bald he won’t regrow all his hair. If you give him estrogen, too, he might.

When you look at what estrogen actions are on the hair follicle it's quite broad; http://press.endocrine.org/doi/full/...0/er.2006-0020. Awesome study in relation to estrogen and the hair follicle. Some targets seem to be the likes of Cyclin D1, AP-1 (c-fos , c-jun proto-oncogenes), SHH, WNT's etc.

Does something stand out for you there? It does for me. All these targets of estrogen seem to be factors that control cell proliferation positively. And to no surprise estrogen is classified as a carcinogen and formulations of estrogen have a black box warning; http://www.cancer.org/cancer/cancerc...an-carcinogens.

Most of the actions of estrogens on the normal and abnormal mammary cells are mediated via estrogen receptors (ERs), including control of cell proliferation; however, there are also alternative pathways of estrogen action not involving ERs. Estrogens control several genes and proteins that induce the cells to enter the cell cycle (protooncogenes, growth factors); estrogens also act on proteins directly involved in the control of the cell cycle (cyclins)

When we look at AP1 for example induction of it can repress (antagonize) other factors like P53, P16 , P21 etc;

There is evidence that AP-1 proteins, mostly those that belong to the Jun group, control cell life and death through their ability to regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21cip1/waf1, p19ARF and p16. Amongst the Jun proteins, c-Jun is unique in its ability to positively regulate cell proliferation through the repression of tumor suppressor gene expression and function, and induction of cyclin D1 transcription. These actions are antagonized by JunB, which upregulates tumor suppressor genes and represses cyclin D1. An especially important target for AP-1 effects on cell life and death is the tumor suppressor p53, whose expression as well as transcriptional activity, are modulated by AP-1 proteins.

And all these factors P53, pRB, P21 etc. seem to act negatively on cell proliferation generally. Studies that I have shown that show these factors to be implicated in AGA.

Now there is way more to read upon these pathways how they interact with each other obviously. So this begs the question how do we fix this problem? Well I can only think that you can guinea pig yourself and start modulating these factors directly. But as one can imagine that would be incredibly dangerous due to obvious reasons.

To finish it off here are some examples where estrogen has regrown hair;









And there are more cases. On another forum a transgender also is regrowing hair from NW5 to NW2. Doesn't happen always but it can happen. Estrogen is obviously no option though for any men . It's interesting nonetheless I guess. Perhaps you might find something.

Swooping,

1) Yes, they don't go bald (Castrated Males) Why?

Since androgen as an initial signal is needed to get cells activated to produce cytokines in the first place.

When androgen is totally absent cytokines, are not made in the HFs, and the eventual add up of cytokines therefore never happen.

Now, imagine, when cytokines (or some other factors) levels are low, the activation of AR is majorly androgen dependent, while they start to add up, it become androgen independent, lessening and lessening the need for androgen-dependent signalling.

2) It's not only about cytokines, I'm talking the big picture here. AR, will lock other transcription factors such as FOXa2 and Beta-catenin, to have their normal function in the nucleus. So, It's knockdown will cause secretion a set of growth factors, such as WNTs, and activating epithelial stem cells in a co-ordinate manner to divide.

Thanks for your response. I get what you mean though. I don't agree with this entirely though. Again, even if you castrate someone who is aggressively balding his hair loss stops as I have said. So even when the process has been ongoing and these things add-up like you put it it doesn't matter. Cause when you remove androgens or AR balding will stop. Now finasteride might not always cut it, but after all finasteride doesn't remove all androgens as you very well know. RU-58841 doesn't sufficiently antagonize the androgen receptor either. Castration is better but not a really viable option I guess . After all that is why I don't think what you say will work. Sure full AR silencing will work excellent in preventing AGA, but will not do much more than castration. At least that is what I think. The thing is when you act to late these factors have already done their job like I mentioned. So removing AR out of the question doesn't matter anymore at this point. You used cancer cells as an example to point out the fact that these cells can find ways around to get stimulated. That's true but remember one hallmark of cancer cells is adaptation. They like to survive.

Although targeting the androgen axis has clear therapeutic benefit, its effectiveness is temporary, as prostate tumor cells adapt to survive and grow.

[youngin]

I agree with Swoop that silencing AR is not going to do much more than stop the hair loss. The reason estrogen works may be because how it effects bone structures. It complete effect bone resorption as well as some forms of BMP. I bet the the transgender individuals ended up with skin changes as well, like being softer. Look at the bone structure difference in men and women, androgens have a huge affect on it. Even as an adult increasing androgens will increase bone density.

[youngin]

There are causes not being taken into consideration here. No one in this thread is addressing:
#1: Why does minoxidil work so well, and why does derma rolling increase its effectiveness. Look at PrettyFly83's results. This has nothing to do with androgens.
#2: Why does it present itself in a pattern. This has never been explained in a study.

[NeedHairASAP]

@Chemical

So removing AR out of the question doesn't matter anymore at this point. You used cancer cells as an example to point out the fact that these cells can find ways around to get stimulated. That's true but remember one hallmark of cancer cells is adaptation. They like to survive.

Swoop, what if estrogen down-regulates ARs? Then estrogen regrowing hair doesn't actually refute fg11's hypothesis.

http://www.ncbi.nlm.nih.gov/pubmed/3569146

[gainspotter]

Cute

[joachim]

yeah, fred doesn't know what he is talking about at all. of course, there are those side effects with minox. i've seen it in 4 of my friends who took it for months and then quit because of the sides in their face. swollen eyes and swollen face sometimes too, wrinkles and also headache from time to time.
it's all placebo effect would fred say. he's just a typical mr. know-it-all and if he doesn't have side effects then nobody will.
fred is probably also one of those guys who says that Fin is absolutely side-effect free and that the sexual/hormonal side effects are not real.

all bullshit. fred it's not the right and place here for you. you're just spreading bullshit around, and also drove the FGF11 guy away. he was obviously one very intelligent bioscience guy who brought some good ideas in. it's not comparable with the typical con artists like habemus/futurocabeludo or the chlorine dioxine guy.

[fred970]

i've seen it in 4 of my friends who took it for months and then quit because of the sides in their face. swollen eyes and swollen face sometimes too, wrinkles and also headache from time to time.

That's just a harsh allergic reaction, of course it can happen.

But wrinkles? Show me one scientific study that proves minoxidil gives wrinkles or even dark circles?

Don't bother, you won't find any.

[joachim]

That's just a harsh allergic reaction, of course it can happen.

But wrinkles? Show me one scientific study that proves minoxidil gives wrinkles or even dark circles?

Don't bother, you won't find any.

lol. why on earth should there be studies out there which show the negative side effects of minox, and especially wrinkles and dark circles? of course we won't find them. but there are hundrets of reports/opinions/posts and pics on the internet, and if you just don't want to believe they exist, then be it so. everyone has the right to be ignorant and just believe what they want.

[Chemical]

@Chemical
Does something stand out for you there? It does for me. All these targets of estrogen seem to be factors that control cell proliferation positively. And to no surprise estrogen is classified as a carcinogen and formulations of estrogen have a black box warning; http://www.cancer.org/cancer/cancerc...an-carcinogens.

When we look at AP1 for example induction of it can repress (antagonize) other factors like P53, P16 , P21 etc;

And all these factors P53, pRB, P21 etc. seem to act negatively on cell proliferation generally. Studies that I have shown that show these factors to be implicated in AGA.

Now there is way more to read upon these pathways how they interact with each other obviously. So this begs the question how do we fix this problem? Well I can only think that you can guinea pig yourself and start modulating these factors directly. But as one can imagine that would be incredibly dangerous due to obvious reasons.

I think we shouldnt mess around with p53 too much because it actually repairs DNA damage and we should be focusing on the detrimental byproducts of p53 which are ironically easier to tackle, like DKK1 with oleuropein.

I've decided to post a an analysis on Estrogens actions on hair in my thread seeing as this thread is becoming a flame war and we're deviating from the main topic. I think youre on to something and we could potentially exploit the estrogen pathway with readily available/easily acquired drugs to achieve the same regrowth as those transgender cases.

https://www.baldtruthtalk.com/threads/22104-Updated-Research-and-Knowledge-Cutting-Edge?p=224562&viewfull=1#post224562