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Yes, I did get a buzzcut before trying Minoxidil, so I would. Both to photograph and look for results, and to ensure product wasn't wasted on the hair instead of scalp. Heck, even the provokative columnist Katie Hopkins put vanity aside and put on 45 lbs of weight so she could lose it again to prove her point which is that fat people are just lazy. In case you do not get a buzzcut, please post weekly updates of also somebody with short hair and more severe balding. While you're saying "if it works well, it'll be visible on my longer hair", there might be indicators much more visible on those with less hair that says maybe it's working but needs some adjustments.
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What will be the exact dosage of IGF-1 in the Follicept treatment ? The IGF signaling pathway is implicated in some cancers so we should be careful about it. Also the sometomedin is basically known to promote cell and hormons growth, like isn't there any risk to see some irregular development of the bones or some other parts of the body?Comment
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StayHopeful, sorry man but this is a bit far stretched. Devon and Hsu are great people, but I don't think their solution will present a complete cure to androgenic alopecia. It's 50/50 chance that it will work or not. Odds are split.
Please don't "hype" the conversation. Please stay neutral and objective.
Let's hope it works but for now, let's not "hype" it .
Also, Hsu and Devon might be great people, but I won't make statues of them.
Baldness is a affliction that psychologically and physically impacts us all, but it's not as bad as cancer , multiple sclerosis or autism which completely debilitates you and your human dignity.
Please hold your horses and kindly please post to the thread when you have something "meaningful" or have scientific questions .
You are "equally" at fault as Swooping or Arashi for polluting this thread with your meaningless mumbo jumbo.
You pointed fingers at Arashi and others, look at yourself in the mirror man. I'm sure you'll find the reality hit hard.
Good luck, but please don't given others false hope or act like you know something about follicept others don't thus they should be excited or hyper like you .
I'm a skeptically/cautiously optimistic. I'm reserving my statements for after the trials and then I will led the firehoose loose of praises or proper critique .
Please keep our egos and emotions in control.
Thanks!Comment
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bro, loook carefully at how i qualified my statements. I stand by them. They are perfectly legitimate. I understand balding isn't cancer. But it is a SEVERE psychological issue in the type of society we live in today. you can't understate that. And what I said is IFFF it works like it says on their website... perfectly legit statement, but i understand what you're saying the general theme of it may be a little too strong given the trials haven't started, my badComment
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@devon,
what happened to mice 3 months post treatment? You didnt show that data in the presentation.
Just curious.
tnx and good luck!Comment
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Great, relevant question. This is why we are here. From Dr. Hsu:
This is an astute question! Maimonides is credited with the following teaching that I use to help my students not be afraid of not knowing the answer: "Teach thy tongue to say I do not know, and thou shalt progress." All scientific investigation begins with "Why..." or "How...," which implies "I do not know." It is also the inspiration to answer those questions.
I don't know if it is an accurate statement that there is a "universal type of initial shedding common to all good therapies." What current therapies are considered to be "good?"
We won't know with certainty how pulse stimulation will affect "semi-terminal follicles" that will eventually lose the ability to grow a hair shaft as they transition to telogen. Perhaps with enough longitudinal follow-up data on those on Follicept, the answer will reveal itself.
In the mouse study by Li et al 2014, a synchronized telogen was induced by application of a depilatory (well known property) in an 18-day study. "Semi-terminal follicles" in those with AGA in the thinning stage represent a population that are undergoing progressively shortened anagen that will eventually regress to telogen. However, they are not synchronized. Follicept may induce a new cycle of prolonged anagen in the population of "semi-terminal" follicles that are soonest to reach telogen marked by imminent hair loss.
I cannot offer as satisfying a conjecture regarding the effect of Follicept on other asynchronous follicle populations representing the continuum of increasingly shorter anagen cycles in the natural history of AGA. However, it makes sense that intermittent "pulse stimulation" cycles with intervening periods without Follicept application may be the most beneficial regimen for those with earlier stage AGA and thinning hair. The Follicept-free interval may be different for different men, but a regimen employing alternating cycles of on/off use would be a reasonable starting point. In this sense, each user will be an investigator studying his/her own pattern of optimal response to Follicept, adjusting the regimen in an iterative manner to achieve maximum benefit.
Women with AGA have a characteristic pattern of thinning hair loss that may achieve the greatest response from such an intermittent and alternating cycle regimen. Since we plan on doing a second, possibly overlapping clinical trial for women, the study design will specifically address the most effective regimen for Follicept pulse stimulation.
I have age-related thinning that is very gradual, but cumulative. A small bald spot has appeared at the vertex. I will be one of the early subjects who will start Follicept next Monday (April 27, 2015). We're all excited here at Prometheon. Hang on folks. The fireworks are about to be lit!Comment
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For me balding is like running a fever, a never ending shitty fever, you can do your stuff but you will never enjoy the day like you used before, and the treatment we have now is like curing a cold with a XVII style bloodlettingComment
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Hey guys,
This post will contain facts mainly for informational purpose for the readers of this site, not to discourage the owners of this product or what so ever. I think that it is important to stay with both feet on the ground, and stay realistic. I respect the effort put into this project, and am not sure where it went wrong. Weather it was just an over enthusiastic entrepreneur who had some connections to a professor who didn't gasp the difference between mice and human, or lack of research, but it does not matter, still respect for the try.
Follicept Quote 1:
1). No reason to find the results on a CD Hairless mice compelling. It is just confirmation of this initial study: http://www.nature.com/jid/journal/v1.../5603603a.htmlRe: the rat model/pics:
We used the CD hairless rat, which has a gene mutation that gives it kinky, wiry, wispy hair. This is ideal for transdermal testing, because it limits any follicular transport that could confound results, and the hair isn’t in the way. So basically, we are growing hair despite a gene that should be preventing it. We find that compelling. There are other rat models that are hairier or at least look it, used by other companies to show growth, about which you are all rightfully skeptical. As far as our pictures go- we are not professionals in that regard, and the inconsistency comes from user error and cropping, not from trying to find lighting or zoom that makes it look better than it is.
Let’s be clear about some facts here.Mesenchymal–epithelial signalling between the dermal papilla and the hair matrix regulates cell proliferation and differentiation in mature hair follicles. The molecular basis of these interactions is largely unexplored. According to its expression in the dermal papilla, IGF-I is likely involved in reciprocal signalling. To examine its biological function in pelage follicles further, we generated transgenic mice that express Igf-I in the inner root sheath and the medulla using an involucrin promoter fragment. We demonstrate that Igf-I affects follicular proliferation, tissue remodelling, and the hair growth cycle, as well as folliclular differentiation. Transgenic skin temporarily lacks visible adipose tissue in telogen. The onset of the second, aberrant growth phase is markedly retarded. Transgenic guard hairs are significantly elongated and a small fraction of hair follicles is severely disoriented. The microscopic appearance of most hair shafts is altered and, strikingly, Igf-I transgenic mice lack hairs with a zigzag shape due to the suppression of hair shaft bending. All transgenic effects are partially compensated by ectopic expression of Igfbp3. Finally, Pdgfr was identified as the first molecular target that is affected in Igf-I transgenic mice. In summary, our data identify IGF-I signalling as an important mitogenic and morphogenetic regulator in hair follicle biology.
- IGF1 is a mitogen, it is pro proliferation.
- CD hairless mice is mutated, which prevent the cells, from among others to proliferate, see below
Therefore, the mutation in the CR rat abrogates cell proliferation in the hair matrix and affects keratinocyte differentiation in the HF and interfollicular epidermis, a phenotype that is completely distinct from hr/hr. To test whether the CR rat harbored a mutation in the hr gene, we analyzed the coding region of this gene and consensus intron splice site sequences in mutant rats and found no mutation, further supporting phenotypic evidence that the hairless phenotype in CR rats is not allelic with hairless. Finally, using intragenic polymorphisms, we were able to exclude homozygosity at the hairless locus by use of genotypic analysis. Thus, morphologic analysis of successive stages of phenotype development in the CR hairless rat, together with definitive molecular studies, indicate that this mutation may be unique among the other hypotrichotic rat mutations.
- So you take a fresh mice, with fresh cells (not affected telomerase in contrast to AGA Calls) mice that lacks among others a strong mito genic, and feed it with a mitgogen, as results the fresh cells proliferate, and kick start the telogen phase/ matrix proliferation.
2 problems with that approach.
1. You take a mice with fresh cells, fresh telomere, which is mutated, and misses a mitogen, you give it a mitogen, and telogen phase kicks in, very logical.
2. This does not translate to human AGA cells, I will show you why.
a. In short, without running into details, aga is the result of senescenced cells. Yes it starts with excess AR in the DP in the affected area, however ROS and lack / up regulation of factors, cause senescenced (aged) cells. These cells lack the ability to proliferate, or do anything, and have basically 2 choices.
i. They destroy themselves (apoptosis)
ii. They just sit there without any faction in growth arrest. And start to affect nearby cells with negative signals.
You can’t just add igf1 to aga aged cells. IGF1 is a recognized factor in aging, refer to this study for example: http://www.ncbi.nlm.nih.gov/pubmed/22877754
With other words, you can’t just ad IGF1 only, if you want to protect your cells. Instead you start with express damaging of what is left of the DNA. Result of physically destroyed mitochondria(which is responsible for the energy metabolism within the cell.
Cellular senescence is characterized by growth arrest, enlarged and flattened cell morphology, the expression of senescence-associated β-galactosidase (SA-β-gal), and by activation of tumor suppressor networks. Insulin-like growth factor-I (IGF-I) plays a critical role in cellular growth, proliferation, tumorigenesis, and regulation of aging. In the present study, we show that IGF-I enhances cellular senescence in mouse, rat, and human primary cells in the confluent state. IGF-I induced expression of a DNA damage marker, γH2AX, the increased levels of p53 and p21 proteins, and activated SA-β-gal. In the confluent state, an altered downstream signaling of IGF-I receptor was observed. Treatment with a reactive oxygen species (ROS) scavenger, N-acetylcystein (NAC) significantly suppressed induction of these markers, indicating that ROS are involved in the induction of cellular senescence by IGF-I. In p53-null mouse embryonic fibroblasts, the IGF-I-induced augmentation of SA-β-gal and p21 was inhibited, demonstrating that p53 is required for cellular senescence induced by IGF-I. Thus, these data reveal a novel pathway whereby IGF-I enhances cellular senescence in the ROS and p53-dependent manner and may explain the underlying mechanisms of IGF-I involvement in tumorigenesis and in regulation of aging.
Let’s say or assume your “special” vehicle is as good as injection or proved nano liposomal delivery, which proved to deliver molecules/compounds bigger than 7 kda into the dermal layer, then we still have to cope with some failed human trials with IGF1, or stronger, more preferable mitogenics. See table below:
You might want to adjust your formula now and make follicept V2 with FGF2, however that is tried too, at low and high doses.
On the other forum we tried IGF1, FGF2 ,fgf7 ,fgf10 in Nano solution at 2- 25 ppm, 2 people injected IGF / FGF2 without result unfortunately about 2-3 years ago, As noobs we didn't know why back then, but now we understand why.
Some notes from my side:
Without running in to conclusion, 1. I find it worrying that some new posters pop up and start defending this hype like their life depend on it. 2. That the trial is run in-house privately, there can be some conflict of interest if the results are not as expected, and the product still need to be released.
Outsourcing the trial and preferably letting some trusted members participate is more of a hassle, but the only way to gain trust in my opinion. Perhaps this issue can be addressed by follicept.
Good luck all!Comment
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@boldy,
You are talking about fully senescent cells which is complete norwood 7 stuff. For somebody with some miniaturisation or norwood 3, the product could prove to be superior to anything available at the moment.
So a declaration of 'nice try' is inappropriate. We may rule out full baldness reversal but that does not mean this will not be a game changer. If I want to get a hair transplant to recover hairline I can maintain with follicept instead of fin, and that's the difference between hair and no hair.Comment
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Why are people still questioning the legitimacy of Follicept's design? This isn't some philosophical debate; trials begin on Monday and will reveal whether or not it's effective. If not, the skeptics can yell "I told you so!" while the real scientists (e.g. those behind Follicept) continue doing research. There's no sense in going back and forth when we'll have answers in several weeks. I think most people here would love for follicept to work but very few sincerely believe it will be a game changer (myself included).Comment
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I particularly believe this could be a game changer too. But, I am being careful with getting my expectations high. And this is only cause I lack the technical knowledge that goes into all this science, meaning I am not an expert in this domain. Monday is fast approaching! Can't wait! Devon, I am praying that it does work... Just went for a trip with a bunch of friends, and trust me.. the balding jokes were just off the charts. hahaha... Gets to me sometimes, despite telling myself not to worry about it.Comment
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I won't lie, Boldy's argument is powerful. Now, I don't know if there is an argument against this or not, and maybe we will only get a real answer to this after the Follicept trial results, but his argument definitely made me think and was really well put together. Really eager to hear what Follicept has to say about what he said, from a scientific point of view.Originally posted by ArashiComment
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I would have to agree with Boldy though. And basically the only problem I have with all of this is:
.2. That the trial is run in-house privately, there can be some conflict of interest if the results are not as expected, and the product still need to be released.
As for the senescent cells in our scalp, no one can tell with certainty that NW3 doesn't have senescent cells. Basically all of the areas on the scalp that are completely bald could have senescent cells.
However if follicept is completely transparent about the results or lack thereof it is still nice someone is actually trying.
I guess this could be closed in a matter of month or two unlike waiting for something for a year to see if it actually does something as it is the case with Bimatoprost.Comment
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Hey guys,
This post will contain facts mainly for informational purpose for the readers of this site, not to discourage the owners of this product or what so ever. I think that it is important to stay with both feet on the ground, and stay realistic. I respect the effort put into this project, and am not sure where it went wrong. Weather it was just an over enthusiastic entrepreneur who had some connections to a professor who didn't gasp the difference between mice and human, or lack of research, but it does not matter, still respect for the try.
Follicept Quote 1:
1). No reason to find the results on a CD Hairless mice compelling. It is just confirmation of this initial study: http://www.nature.com/jid/journal/v1.../5603603a.html
Let’s be clear about some facts here.
- IGF1 is a mitogen, it is pro proliferation.
- CD hairless mice is mutated, which prevent the cells, from among others to proliferate, see below
Therefore, the mutation in the CR rat abrogates cell proliferation in the hair matrix and affects keratinocyte differentiation in the HF and interfollicular epidermis, a phenotype that is completely distinct from hr/hr. To test whether the CR rat harbored a mutation in the hr gene, we analyzed the coding region of this gene and consensus intron splice site sequences in mutant rats and found no mutation, further supporting phenotypic evidence that the hairless phenotype in CR rats is not allelic with hairless. Finally, using intragenic polymorphisms, we were able to exclude homozygosity at the hairless locus by use of genotypic analysis. Thus, morphologic analysis of successive stages of phenotype development in the CR hairless rat, together with definitive molecular studies, indicate that this mutation may be unique among the other hypotrichotic rat mutations.
- So you take a fresh mice, with fresh cells (not affected telomerase in contrast to AGA Calls) mice that lacks among others a strong mito genic, and feed it with a mitgogen, as results the fresh cells proliferate, and kick start the telogen phase/ matrix proliferation.
2 problems with that approach.
1. You take a mice with fresh cells, fresh telomere, which is mutated, and misses a mitogen, you give it a mitogen, and telogen phase kicks in, very logical.
2. This does not translate to human AGA cells, I will show you why.
a. In short, without running into details, aga is the result of senescenced cells. Yes it starts with excess AR in the DP in the affected area, however ROS and lack / up regulation of factors, cause senescenced (aged) cells. These cells lack the ability to proliferate, or do anything, and have basically 2 choices.
i. They destroy themselves (apoptosis)
ii. They just sit there without any faction in growth arrest. And start to affect nearby cells with negative signals.
You can’t just add igf1 to aga aged cells. IGF1 is a recognized factor in aging, refer to this study for example: http://www.ncbi.nlm.nih.gov/pubmed/22877754
With other words, you can’t just ad IGF1 only, if you want to protect your cells. Instead you start with express damaging of what is left of the DNA. Result of physically destroyed mitochondria(which is responsible for the energy metabolism within the cell.
Let’s say or assume your “special” vehicle is as good as injection or proved nano liposomal delivery, which proved to deliver molecules/compounds bigger than 7 kda into the dermal layer, then we still have to cope with some failed human trials with IGF1, or stronger, more preferable mitogenics. See table below:
You might want to adjust your formula now and make follicept V2 with FGF2, however that is tried too, at low and high doses.
On the other forum we tried IGF1, FGF2 ,fgf7 ,fgf10 in Nano solution at 2- 25 ppm, 2 people injected IGF / FGF2 without result unfortunately about 2-3 years ago, As noobs we didn't know why back then, but now we understand why.
Some notes from my side:
Without running in to conclusion, 1. I find it worrying that some new posters pop up and start defending this hype like their life depend on it. 2. That the trial is run in-house privately, there can be some conflict of interest if the results are not as expected, and the product still need to be released.
Outsourcing the trial and preferably letting some trusted members participate is more of a hassle, but the only way to gain trust in my opinion. Perhaps this issue can be addressed by follicept.
Good luck all!
Although some of this might make sense, lot of this is also pretty off base or very loosely tied together. don't have time right now to explain all of it, but ill address more later. I have read some of Boldy's posts in the past, and although like swooping you have some understanding of AGA and are good at linking lots of articles and information, I don't find your ability to make sense of it all to be all that insightful. Most of the stuff on cell senescence makes no sense as a counter argument to why this might work. Cells go senescent (die) because of a lack of the proper proteins and growth factors. IGF-1 is unlikely to completely revive dead hair cells, as there is scarring involved and many channels have been broken, but delivering the proper factor at the proper intervals for people with thinning hair can probably prevent cells from senescing or turn around cells that are halfway there. rogaine is used on cells that are dying as well, and the ways it releases certain chemicals turns this process around. same with fin, some regrowth happens because cutting off the negative chemicals lets the cells be nourished and stop dying. In this sense Im not sure what boldy's argument is.
True, the IGF-1 could be a less potent on human follicles than on mice, but that has not been proven yet. you say that hairless mice are missing a mitogenic factor, and that human cells are not. this is exactly what follicept is addressing. androgens are setting off a chain of reactions in people that cuts off the mitogenic factors in the follicle. it's the same problem, except the mice are genetically programmed NOT to ever grow hair, while balding humans can sort of grow hair but some of the mitogenic factors are being hampered. Cell senescence is the end product of all aging and diseases really, but it is not "the cause" of AGA. AGA is caused by genetic constructs that lead the androgen receptor to set off a chain of chemicals that in turn cause cells to die. The point of follicept and other treatments is to halt this dying.
b) As far as injections are concerned I'm really not sure that injecting growth factors into the scalp is the same as using follicept's vehicle. I pretty sure Dr. Hsu has addressed this in the past. While I definitely harbor some skepticism about just how important IGF-1 is to balding until it is used in humans, I'm not sure that even an injected study has ever been carried out for balding. The fact that there are anecdotes of forum people indiscriminately injecting this stuff into the bloodstream and were unsuccessful,does not guarantee that follicept won't work. If anything the graph you posted shows that all these growth factors did indeed have an effect on hair growth. I myself have a hunch that there might be better factors to use than IGF-1, or maybe a mix would be best, but this is definitely a good start, especially as related to inducing anagen (something that has been shown very clearly as something that IGF-1 does). Dr. Hsu wants to start simple and see what happens. He understands the science of this much better than I do and certainly much better than anyone else on here, and if he thinks its worth a shot then Im very interested.
c) as far as the in house trials, this is all nonsense. what company do you really expect to outsource their trials? They can trial this effectively and as simply/cheaply as possible, and involving a mass of crazy forum users is of no value in the initial stages. No one owes you guys anything, and demanding follicept to do this or do that is not only unrealistic, but also indicative of an entitled attitude that belies the young age or psychological malfunction of a lot of forum users. If their trials were to be botched it would not be hard to tell, and there has been no indication that these guys are anything but an upstanding crew. And even if these guys were scammers,which they aren't, you can always NOT BUY. If you know so much about hair loss or are so skeptical, you still have control of your own mind/pocketbook. all follicept is on here to do is get some useful feedback and hopefully start building a customer base should their product work. If they are a scam then so is every other company that sells anything to anyone. everyone wants to build a good product and market it effectively. but not all are as open and generous with their info as follicept has been, which is why its cool that there is a hair loss startup. if you'd rather have only huge universities and big pharmas working on this, with all the interests that they have to represent, all the hurdles they have to jump through, etc, then you are all pretty dumb. this grassroots action is good whether it works or not.Comment
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