Here\'s what Histogen will be forced to do -- hear me now, believe me later

Roger_that what also brought me to that observation is the fact that women react better on a treatment based on growth factors. Just look at the AAPE and Histogen studies (aside from the SGF-57, although their first study was only on women) I wondered why that is. But it became clear to me.

Women way more often than men suffer from Telogen Effluvium.

“Telogen effluvium (TE) is the most common cause of diffuse hair loss in adult females. TE, along with female pattern hair loss (FPHL) and chronic telogen effluvium (CTE), accounts for the majority of diffuse alopecia cases.”

Well it is obvious that TE isn’t related to AGA at all and is a whole other pathology. TE is marked by a shift in anagen/telogen ratio where telogen increases. So instead of the hair follicles generally being 10-15% in telogen it might shift to even 25%-30% or whatever. Women have way more problems with TE than men. Thus it is logical to me at least that they often react better to a treatment like growth factors. Because they experience a bigger shift in anagen induction…

I believe the same happens with LLLT for instance or PRP. In that sense they are just a other form of external stimuli. And no wonder again that women generally react better. Also they show around the same growth numbers. Which we know just suck. Growth factors just may be a bit better as a stimuli to these telogen hair follicles. But this is not what we need.

I’m with you that a cell based approach is by far the most realistic approach to our problem. At least this is my opinion.

[quote][postedby]Originally Posted by Swooping[/postedby]
Roger_that what also brought me to that observation is the fact that women react better on a treatment based on growth factors. Just look at the AAPE and Histogen studies (aside from the SGF-57, although their first study was only on women) I wondered why that is. But it became clear to me.

Women way more often than men suffer from Telogen Effluvium.

“Telogen effluvium (TE) is the most common cause of diffuse hair loss in adult females. TE, along with female pattern hair loss (FPHL) and chronic telogen effluvium (CTE), accounts for the majority of diffuse alopecia cases.”

Well it is obvious that TE isn’t related to AGA at all and is a whole other pathology. TE is marked by a shift in anagen/telogen ratio where telogen increases. So instead of the hair follicles generally being 10-15% in telogen it might shift to even 25%-30% or whatever. Women have way more problems with TE than men. Thus it is logical to me at least that they often react better to a treatment like growth factors. Because they experience a bigger shift in anagen induction…

I believe the same happens with LLLT for instance or PRP. In that sense they are just a other form of external stimuli. And no wonder again that women generally react better. Also they show around the same growth numbers. Which we know just suck. Growth factors just may be a bit better as a stimuli to these telogen hair follicles. But this is not what we need.

I’m with you that a cell based approach is by far the most realistic approach to our problem. At least this is my opinion.[/quote]

Our best bet (other than cloning/multiplication/etc.) is the plucking guys figuring out a molecule that triggers quromem sensing…

Of course it would take awhile for that to get through the FDA, but we don’t need the FDA. We just need to know the molecule and then people will get their hands on it one way or another…

Other than that, it’s a long long long wait (5 years minimum) until any cell-based treatment is taking actual appointments… replicel within 5 years is a pipe dream… SB follicles having their first human tests within 4-5 years is probably a pipe dream…

That leaves us with a qorem sensing molecule, laser wounding regeneration triggering, or pilox.

So, while I find these conversations intellectually stimulating… they are a poor investment of time.

Our best investment of time would be looking into laser regeneration. The lasers are widely available and we know:

  1. campfire man grew hair in two weeks

  2. dermarolling (wounding) works to some extent (but isn’t applying consistent wounding across the scalp)

  3. plucking (another type of wounding) works

Trying to figure out if we can apply consistent levels of “the right” wounding across the scalp using a laser is our best bet… Again, we already know that wounding works… it’s more about refining the application (and I believe laser is the way to do it… dermarolling just can’t compete in terms of consistency).

Wounding to hair regeneration is one of the few (probably the only) thing that we know WORKS FOR A FACT… that’s the best investment of time. I would venture to guess we’ll be seeing a lot more laser-wounding studies released over the next 6-12 months… maybe we’ll even find a entrepreneurial cosmetic surgeon starting to offer it somewhere in the US or around the world.

[quote][postedby]Originally Posted by roger_that[/postedby]
“Well I think you all get where I am heading. Perhaps these growth factors just prompt telogen hair follicles into anagen. Isn’t it ironic that a scalp has 10-15% hair in telogen and all these so called “growth factor” based treatments all give around 10-15% growth? Is that what we need though? Off course not!”

Boom. I think you’re right, Swooping. I’ve never heard this take before, but this is an excellent analysis.

Jarjar, are you paying attention to this? I think Swooping has identified something very important here, i.e. why growth factors and other “stimuli” never seem to revive more than 10-15% of follicles.

Also Swooping, I think you’re dead on about Minoxidil. Minoxidil is an antihypertensive that works in several related ways – by dilating small blood vessels, and by upregulating VEGF which results in more microscopic blood vessels being made. This is not surprising, because it’s not uncommon for related processes in the body to be mediated by similar (or the same) biochemical pathways. Dilating existing microvasculature, and creating new micro-vessels, would both tend to lower peripheral blood pressure, so it’s no coincidence that one chemical can induce both effects simultaneously.

HSC is not just reliant on VEGF, but other growth factors as well – but all these growth factors would seem to be susceptible to that 10-15% ceiling in what they can potentially accomplish.[/quote]

Yup Roger, I’m paying attention. I agree with Swooping’s point that growth factors have only been turning telogen follicles into anagen follicles so far. Yup. I think he hit the nail on the head when it comes to why growth factors have only given 15% of regrowth so far. However, I do not believe that 15% is the upper-limit of achievable regrowth from growth factors.

I think that growth factors have not been supplied to the follicles OFTEN ENOUGH so far. Keep in mind that naturally in the wild the ADSCs are supplying these growth factors to the follicles much more frequently. Let me say that again, naturally in the wild the ADSCs are supplying these growth factors to the follicles much more frequently. It’s illogical to try to compare the frequency of growth factor injections (that have been tried so far) to the frequency that nature is exposing follicles to these growth factors in the wild naturally. There is no comparison.

And I agree with Swooping that minoxidil grows hair somehow via the growth factor pathway.

And I think that the androgen pathway bleeds into the growth factor pathway insofar as hair goes.

Clinicians used to talk about how there were two ways to treat hair loss:

  1. Drugs that reduce androgen.

  2. Drugs that stimulate hair growth.

Clinicians used to say that minoxidil is one of drugs the stimulates hair growth while drugs like spironolactone and finasteride are drugs that reduce androgen. I think we are moving past that belief. I think that it is now being proved that drugs like minoxidil actually work on the same pathway as the anti-androgens, but further down that shared pathway.

When I used minoxidil, and even minoxidil plus propecia, my existing long hair started growing faster. After 2 months the increased rate of growth slowed down again. Minoxidil + Propecia petered out. I didn’t get even 1 new hair from the combo.

I later tried RU58841 and I saw new hair sprouting in 4 months. It sprouted like an explosion. It wasn’t long but it was easily visible to the naked eye. It was about a full head of hair sprouting. A few days later my breasts started to hurt/swell and I stopped the RU58841 immediately. I kept trying to tinker with different doses to make RU58841 work for me, which ultimately led to more advanced gynecomastia, and I permanently quit RU58841. Over time the gynecomastia has subsided sufficiently that it’s not visible even when my shirt is off.

At any rate, the point is that RU58841 reduces/eliminates more androgen than finasteride so I think that is why RU58841 gave me new hairs temporarily, while finasteride + minoxidil were incapable of doing this. First of all, this proved to me that DHT is NOT THE ONLY androgen causing hair loss. Secondly, this showed me that the more you affect the androgen pathway the better results you can achieve. Keep in mind that more and more it’s being demonstrated that treating hair loss via growth factors is utilizing the same pathway as treating hair loss via androgen reduction, one treatment just acts further downstream than the other.

I’m not the only person saying that RU58841 worked better than propecia + minoxidil for them. Lots of people are saying this. If YOU yourself believe that RU58841 is more effective than propecia (even with minoxidil), AND if you also accept that growth factors mediate hair growth DOWNSTREAM from the androgens, then you yourself are saying the same thing I’m saying because that is my point. Here is my point:

  1. Androgens cause hair loss in vulnerable persons by way of causing a downstream reduction of growth factors going to the follicles.

  2. Hence, reducing growth factors going to the follicles causes hair loss in vulnerable persons.

  3. A limited reduction of androgens results in a limited reversal of the androgen-dependent reduction of growth-factors, which results in limited hair health improvement.

  4. A large reduction in androgens result in a large reversal of the androgen-dependent reduction of growth factors, which results in a larger improvement of hair health.

Are you all aware that Hideo Uno proved that in macaques minoxidil does not work as well as minoxidil + finasteride, and minoxidil + finasteride does not work as well in macaques as RU58841, and RU58841 does not work as well in macaques as RU58841 + minoxidil? Doesn’t this mean that the more you reverse androgen-dependent growth factor reduction the more you improve hair health?

The advantage to using growth factors instead of anti-androgens is that the growth factor mode-of-action is closer to the end-point of the problem rather than solving the problem through middle-men.

You make a lot of good points there, Jarjar, especially about locating events upstream and downstream of androgen activity.

HOWEVER, I don’t think ANY of what you said there negates Swooping’s point about added growth factors probably having an upward limit in their effectiveness because they mainly act to revive follicles which are in telogen, by switching them over into androgen.

The empirical facts are on the table. Various compounds and drugs which activate growth factors, and these growth factors themselves, have already been in use for a number of years now, and have already been used in many different ways, at different strengths and with different application frequencies.

What we have seen empirically is that whenever any drug or compound that works this way is used, no matter how it is used, no matter the frequency of use (e.g., many people, including myself, applying Rogaine like 3-4 times per day, well above the recommended dosage), the most people have seen is about 10-15% increased visible hair growth. And that is in the very best case scenarios, which I didn’t fall into… No matter how much Rogaine is used, most people only get minimal peach fuzz.

The fact is that growth factors are definitely involved in stem cell activation, and are even secreted by stem cells, but I think to get real new growth (beyond just reactivating dormant telogen follicles), you actually need to ADD NEW LIVE CELLS.

To get guaranteed real new hair growth which can make up for the hair lost through MPB, you need to replenish inductive, trichogenic dermal papilla cells, and just adding growth factors will not accomplish that.

In short, I think that just adding growth factors, no matter how much, will not get you beyond that 10-15% barrier that Swooping cited, because all you are doing is reactivating sleeping telogen follicles – which are, remember, also subject to the MPB process and are being concurrently miniaturized by androgens anyway.

I may be wrong about this, but Swooping makes a very convincing, coherent argument. The empirical evidence of this is just too strong – it is all over the place, right under our noses – or above them, to be exact.

Sure, I would like to test this – I’d like to see if adding more growth factors can really deliver. I hope I’m wrong. But I think Swooping’s argument is compelling, and I have a hunch he will be proven right.