Kerastem Therapy treating hairloss from fat cells

IIRC that has been done too. Balding follicles installed into non-balding areas stay bald. It’s not the location.

The mouse thing really is significant. It has never been explained because these HM operations are trying to develop their tech into products. Solving our problem is not their #1 priority. Never has been.

[quote][postedby]Originally Posted by cal[/postedby]
IIRC that has been done too. Balding follicles installed into non-balding areas stay bald. It’s not the location.[/quote]

Balding follicles installed into non-balding areas stay bald, but is the recipient location being used just on the same person’s scalp? If so, it’d be subject to the same DHT levels. Have they tried it on a woman who has very low little testosterone or DHT, and no familial history of MPB or FPB?

Off the top of my head I’m not sure about that.

What is the relevance, though? Its not a practical treatment option. MPB is not a problem of high androgen levels, it’s a problem of excessive androgen sensitivity to normal androgen levels. We have learned that much.

The group of MPB sufferers are statistically a bit higher in DHT. But IMO that would just be a product of the way the factors work. (Albino-skinned people probably get more sunburns in warmer sunnier countries. But we still don’t call it a problem with the country having too much sunlight. The problem is still their excessive sensitivity to it.)

[quote][postedby]Originally Posted by cal[/postedby]
Off the top of my head I’m not sure about that.

What is the relevance, though? Its not a practical treatment option. MPB is not a problem of high androgen levels, it’s a problem of excessive androgen sensitivity to normal androgen levels. We have learned that much[/quote]

Exactly… and I expected you to bring that up.

However, even if DHT is the result of excessive androgen sensitivity, if a follicle with excessive androgen sensitivity (e.g., a balding follicle from a man with MPB) is placed in an environment with almost no androgens (such as the scalp of a woman who has very low serum testosterone and virtually no DHT), then the high androgen sensitivity of that follicle would be moot. I would not matter.

My working hypothesis of that mouse experiment would be simply (by Occam’s Razor), that the hair regrew into terminal size because it was removed from an environment with high androgen levels, to an environment with zero human androgen levels (mouse skin).

That, to me, is the simplest explanation for what happened. I concede that it may not be the right explanation, but I think at least it must be clearly ruled out before we consider more complicated explanations.

AFAIK no amount of androgen suppression & blocking will do anything of the sort on humans. Not to a significant degree like this.

Even sex change/chemical castration won’t do it. That combined with topical AAs (it’s been done in the transgender community) should knock the androgen levels down far enough to see some of the effect. But in practice that doesn’t give us nearly enough of the effect to explain the mouse results to my satisfaction. The reviving balded hairs don’t seem to revive in the gradual “start backing up the process” sort of way seen with human hormone manipulation. No, it’s such a full-throttle change that I think it’s beyond the scope of any action anything we have seen in live humans. I’m saying it is not just a matter of degree IMO.

Seriously, can you imagine ANY amount of cutting off androgen stimulation in live humans that wakes up totally MPB’d follicles overnight like this? (A new drug, etc) If somebody published this result from blocking androgen stimulation alone we would never believe it. Not even close. We would be looking at their results and speculating about whether there was some other factor at work.

Besides - in order to produce much MPB-reversal activity (on live humans) with hormones, a female hormone profile’s worth of Estrogens must be added to the mix as well. But if the mice are regrowing human hair because their androgens aren’t affecting the human follicles, then you are stuck answering why the mice’s Estrogens still do work on them.

IMO the more probable answer is that we don’t understand MPB as well as we think we do. The fact that lab mice are a hopelessly ineffective model for studying MPB probably has something to do with it.

I don’t know whether anyone has tried the mouse transplant thing with male facial or body hair grafts. That could be interesting because facial & body hair has basically the opposite reaction to androgens that scalp hair does.

[quote][postedby]Originally Posted by cal[/postedby]
AFAIK no amount of androgen suppression & blocking will do anything of the sort on humans. Not to a significant degree like this. [/quote]

AFAIK, that’s actually not true. Broad-spectrum anti-androgens that fully suppress all androgens have been shown to often (but not necessarily always) result in reversal of MPB. (Think of jarjarbinx’s story using RU, and many other people using that drug or similar drugs.)

The side-effects of these drugs may be unacceptable to the point of being devastating, but they often do work and do reverse MPB. Certainly not always, but enough for the phenomenon to not be considered trivial or anecdotal.

I think that cases where it doesn’t work might be in people with very prolonged hair loss which has maybe turned fibrotic or destroyed the actual follicles – which all things considered, may be just a subset of all people with MPB.

As far as a “requirement” to have a female hormonal profile with Estrogens present, I don’t think that’s true at all.

Also, remember that the mouse experiment that you cited involved the transplantation of just one or a small number of follicles into one mouse. It wasn’t a study involving a huge number of subjects. So the results could have been idiosyncratic. They showed it’s possible, but they didn’t show it would always happen.

Also remember, there is A HUGE AMOUNT of idiosyncraticity in biological systems. There’s almost no experiment you can do that will come out the same way 100% of the time in every member of a species. So, just because some miniaturized human follicles grew larger when transplanted into one mouse, doesn’t mean the same thing will always happen with every MPB follicle transplanted.

I’m just saying the simplest explanation should be tested, and ruled out, always, before moving on to more complex explanations, or before assuming that the answer must be some complex, unknown and mysterious factor that’s always hiding around the corner somewhere.

To me, it could just be that when you take DHT-sensitive MPB follicles outside of the DHT-filled environment, and grow them in an environment with zero DHT and zero Testosterone, the simplest explanation for what happened, given what we currently know about the science, is that they enlarged because they were removed from the environment containing human androgens. The murine tissue simply provided an alternative viable, living environment with a blood supply, etc.

This also assumes another thing, which is not hard to assume:

The transplanted follicles hadn’t been totally destroyed and rendered useless by the MPB. From what I know of the science, that possibly can happen, but in most cases, even when they’ve been miniaturized and there’s visible MPB, it is not the case.

I don’t think this is an unreasonable explanation. Why do we always want to believe the explanation for everything connected with MPB is some hidden, mysterious spectre that’s eternally hiding behind a corner? I think that’s a species of “magical thinking”.

There’s more research being done now than ever before. There’s more GOOD research being done now than ever before.

I agree with you that most of these companies like Kerastem with their flameout ideas touted as “cures” in the tabloid media one week, and forgotten about weeks later, are just in it to cash in on some weak “product”, but that doesn’t describe all the researchers and all the research, so you have to be very careful lumping them all together like that.

Yes, but you don’t know that this result was an anomaly or purely a hormone effect. IMO it is no less “magical thinking” to brush off potentially relevant findings like this.

I’m aware of the effects of severe hormone regimens reversing MPB. I don’t think that a thinning NW#3-4 clawing his way back to a NW#1-2 over the course of a year or two is adequate to describe the mouse results.

You’re right, hormone results do happen commonly enough to recognize that the phenomenon is factual.

The same could be said about the effects of needling & dermabrasion producing new/revived terminal hairs - but you aren’t nearly so receptive in that case.

I don’t think this mouse result is THE crucial key thing to solve the baldness riddle.

I do think it is one more provocative open question in MPB research that is frustratingly ignored. It is hard facts getting dismissed with theories because they do not reinforce other existing theories. Maybe it is just a more potent example of the sex hormone effect or maybe it isn’t. We think, we don’t know.

And when the hard facts involve fully-balded follicles springing back to full size like magic, we are being incredibly stupid by leaving it unstudied & unexplained. It’s not like we know of half a dozen other avenues for causing that kind of regrowth. If this result is representative then this effect is f**king unheard of. It could potentially redraw the boundaries of what is possible with damaged follicles.

There you go. This is exactly the mentality I’m talking about.

Oh man . . Did you really think I didn’t do that intentionally?

:rotfl:

You have such an inflated perception of your own intellect that it makes you misread other people’s communication sometimes.

Give me a break!

I’m just a regular person, no smarter than you.

But it’s the easiest thing in the world to go back and “edit” the motive for your comment like that, and even convince yourself that you meant something as a joke.

I think you just made a Freudian slip because a very emotional part of you, inside, does view these things as sort of magical. So it’s a natural word for you to use. In fact when I hit “send” on my comment above, I knew you’d go back and claim it was a joke.

I think YOU’RE the one who has an inflated sense of my intellect, not me.

You’re a very smart, well informed, and bright person but I think you’re a sloppy thinker.

For all I know you’re probably the smartest person on here. You’re even more informed than I am most of the time on new developments and even many old ones, but you’re just a sloppy, impulsive thinker driven partly or mostly by emotions, often times.

I do think you contribute a lot of good stuff to the forum, though. And good ideas to discuss.

BZZZZT! Nope. Sorry. I meant it that way the first time, pure and simple!

Oh, go ahead, have it your way and don’t admit it. I’m not that invested in it the whole thing.

You could call my thinking “sloppy” or call it a good cost/benefit analysis for myself. These days I am only willing to invest conservative amounts of time & mental effort into all things MPB. Many years of membership on these forums has done little for my hair in the big picture.

My field of education and professional expertise is nowhere near medical science (which is probably obvious). It’s all an off-hours thing for me. I’m here because of MPB frustration just like everyone else.

But wasn’t there some immunosuppressant drug that when used in humans resulted in hair regrowth?

Same here, actually – I don’t keep up with the latest moves by Histogen, Follica, Kerastem, etc. Most of these companies are offering what will only prove to be very marginal treatments.

JAK inhibitors, which are all the rage in hair loss circles now (Dr. Christiano, etc.)

They are immunosuppressants -

http://www.nature.com/nri/journal/v12/n9/full/nri3292.html

Hair regrowth results can be amazing (as shown in some posts here recently), but side effects of most JAK inhibitors can be, frankly, very risky and possibly dangerous.

The JAK drugs can give impressive results in Alopecia Areata patients. The only reason we have been giving JAK’s the time of day is because current HM researchers have been acting like they know something about it working for MPB. It’s an unsettled issue as of 2016.

I remember there used to be talk about severe immune suppression via Cyclosporine causing hair regrowth. For a time during the 2000’s it almost seemed like an urban legend in the MPB community. People were familiar with the idea but I never saw a citation of a real case. At least nothing with MAJOR regrowth worthy of the legends.

Cyclosporine is used to prevent rejection of transplanted organs. It’s not something to mess around with carelessly.

A bit of evidence emerged a few years later (early 20-teens?) about a boost in the immune system actually helping hair a bit too.

This is another one of those confusing issues that might be worthy of more research (or it might not). Both immune suppression AND immune boosting have shown slight hair gains.

The Cyclosporine idea was given a boost by the mouse results that Roger & I were just discussing above. The lab mice’s immune systems are radically suppressed just to prevent rejection of transplanted human skin. The MPB community speculated that the lack of immune system in the mice may have been related to the human MPB’d follicles reviving. Not necessarily the sole reason but it could have been a component.

The hair growth effect of JAK inhibitors doesn’t have to be related to its immune-suppression activity. It can be related, or it could be a totally unrelated side effect of the drugs. Most powerful drugs like JAK inhibitors do a LOT of different things to the body, some related to their primary mode of action and some not.

An example of another class of drug that causes hair growth is Minoxidil, which was first sold as the anti-hypertensive drug Loniten. It has a wide variety of effects on body physiology. I mean VERY wide. Acutely, it dilates microscopic blood vessels. Chronically, it increases VEGF which causes more micro blood vessels to be made. It has effects on the kidneys, water retention, salt retention/excretion, etc. And those are just some of the effects. You can see that it was really hard for the researchers to figure out which, out of all the known effects of Minoxidil, was the one which causes hair growth. I believe they still don’t know for sure.

The point is, we know that some immuno-suppressant drugs can cause hair growth, and we know that a few things happen in MPB that seem related to the immune system (like increases in some kinds of T-lymphocytes in some people, I think)… On the other hand, lots of stuff that normally happens in auto-immune diseases DOES NOT happen in MPB. In fact, the major hallmarks of auto-immune disease like a known Antigen-Antibody relationship, do not even show up in MPB.

What has never been proven is that MPB is an auto-immune disorder, or that the JAK inhibitors’ immune-suppression effects are what’s causing the hair growth.

And yes, I agree with you cal, the immune suppression of the mice is a possible component in the hair growth in that experiment and should be looked into.

There is still A LOT MORE about MPB/hair that should be looked into. That’s my chronic gripe.

The MPB research world has narrowed down the targets of their efforts in the last decade as if they are that far along. They aren’t. They still are not regrowing any hair and they aren’t even explaining the condition very much better on paper.

They aren’t zeroing in on solutions. They are just neglecting more of the possibilities than they were a decade ago. This is not the path to progress.

Case closed , not worth getting excited about unless you are just starting to lose your hair.

“Kerastem is focused on the development of product solutions for women and men with early hair loss.”

From their website Innovative hair loss therapies : KERASTEM