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I think its' already happening with UC, no?
Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss
- Thread starter Ollie
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Minoxidil must be used indefinitely for continued support of existing hair follicles and the maintenance of any experienced hair regrowth
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You should consider what qualitative parameter is being measured . An increase in hair weight during that time period seems realistic to me . Also hair shedding shouldn’t have any impact on gains of hair weight of terminal Anagen hairs as it would on hair density
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Do you have a link by any chance? It's weird to see something like that already online.
Imagine reading the charts you're using to try and make a argument out of.
Are you seriously trying to compare the hair weight measurement's from the finasteride trials to the complete reversal of baldness from the BAY trials? You're trying to cast reasonable doubt that shedding cycles could be responsible for a multi-hundred percent rise in pure terminal hair counts? Seriously?
All you've accomplished here is shown that people shouldn't take your arguments seriously, because you basically are just showing two graphs that go upwards and trying to convince people that they could be the same because of a lack of control group lmao.
I agree that some extra data from the macaques trial would have gone a long way. Control groups, standardized percentages of hair gains normalized to a non-bald areas, etc, but this is in a different world from any previous trial on these macaques because of the sheer amount of real gains. How many hair loss trials have you seen that are so successful that they actually publish the number of new terminal hairs instead of the percentage of new hair?
And no one is disagreeing that control groups are important in general research settings, however what you're doing here is being ridiculous and trying to diminish the results of a overwhelmingly positive pre-clinical study because you think it's missing some core component.
What you're doing is the equivalent of taking a pre-clinical cancer study without a control group where all the non-human primates had no detectable cancer left in their systems but decrying that the study isn't enough to conclude that the intervention cured their cancer because of a lack of a control group. Would a control group have helped the study produce better data? Obviously. Does it diminish the result that the cancer is gone? Not at all. The same thing applies to this trial, where there is no way that these primates would have had complete reversals of baldness without the intervention.
Everyone here is aware of the points you made. We all know what a pre-clinical program is, we all know what human clinical trials are. I just don't understand why you keep rehashing these points in a section called "new research, studies and technologies". Everyone understands that human trials are needed, it doesn't mean that the discoveries from this trial didn't reveal significant insights into a link that can cure Androgenetic Alopecia.
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The graph you posted shows variation in hair WEIGHT (which I take to be thickness), rather than count. That said, I'm sure there's variation in numbers as well, however if you look at the pictures posted a few pages back, clearly that's not just seasonal variation (though I'm sure those are the best responders).
You'd have us believe that the macaque data is inconsistent with human data with your blue line, but the very study you pulled this image from says that it is consistent.
You fail to understand that the difference in hair weight here is minor, and amounts to only a few hairs. HMI-115 increased hair counts by the hundreds per cm2. That is so far above what is needed to eliminate any noise from seasonal changes that we don't have to see a control to know it worked. It is far more of an increase than seen in the finasteride or placebo group in this other trial.
Now let's look at follicular length instead of hair weights. That is a more apples to apples comparison with the HMI study which measures the number of terminal hairs instead of the weight of all hairs including vellus. In the control group the length of hairs was little changed over the course of the study, indicating no increase in terminal hair counts. "Among the 10 animals in the control group, 6 showed... progressive miniaturization of follicles.. After 6 months the pattern of the control animal showed a majority of follicles in the telogen stage, and the overall length of the follicles was less than that in the pretreatment stage". So this can not explain the results of HMI-115. There was a 7% increase in hair length in the finasteride group, which is consistent with human data and clearly inferior to HMI-115. All this study does is show that there is little change in terminal hair growth from either vehicle or finasteride, which is the same thing seen in humans as this study explicitly states.
When looking at finasteride, which has such little effect, it's possible to cherry-pick data to make statistical noise and seasonality seem more significant than they are, because you're putting them against the backdrop of finasteride results. They are not significant against the results of HMI-115. This is a laughable attempt to discredit the HMI macaque study. I will expect your resignation from trolling by morning.
I'll leave you with one more thing, the hair weights before treatment for each group were "7.3 +- 3.2 and 7.5 +- 4.1 mg hair/in2, respectively, for 2 months of growth." The control group saw an increase in hair weight of 32% vs 55% for the finasteride group. That is an increase of 2.3 and 4.13 mg/in2, respectively. That is .36 and .64 mg/cm2, respectively. An average human hair weights .2-.4mg at 6 inches length. Let's split the difference and call it .3mg/6in, and we have .05mg per in. I think it's safe to assume macaque hairs are about the same weight. They let the macaque hairs grow for 2 months before weighing them. Hair grows at a rate of about an inch per 2 months. So, one terminal hair would weigh about .05mg. Again, the increase in hair weights was .36 and .64 mg/cm2 for the v and f groups, respectively. Ignoring vellus hairs, that represents 7.2 and 12.8 terminal hairs. Of course the entire increase was not terminal hairs, and for the placebo group it was mostly vellus hairs. We can probably assume that in the finasteride group the increase in terminal hairs was no more than (12.8-7.2)=5.6 hairs/cm2. However, for argument's sake let's fantasize that the entire hair weight change was due to an increase in terminal hairs. In that case we have a terminal hair count increase of 7.2 in the control group, 12.8 in the finasteride group, and 113 in the HMI-115 group. There is no debate, HMI-115 works and is superior to finasteride. A control group in the same study would have been nice, but regardless of any problems with this trial it is clear that the drug is the most effective hair loss treatment to date. It probably is not a full blown cure, but likely as close as we are going to get to that before hair cloning. There is certainly enough evidence here that I will not get a hair transplant before trying it. You question my motives, but you are the one set on convincing people that they should get a hair transplant in the face of evidence that there will likely soon be a treatment that can greatly reduce the number of grafts they need, and prevent them from exhausting their donor supply. Do you work in the hair transplant industry?
You fail to understand that the difference in hair weight here is minor, and amounts to only a few hairs. HMI-115 increased hair counts by the hundreds per cm2. That is so far above what is needed to eliminate any noise from seasonal changes that we don't have to see a control to know it worked. It is far more of an increase than seen in the finasteride or placebo group in this other trial.
Now let's look at follicular length instead of hair weights. That is a more apples to apples comparison with the HMI study which measures the number of terminal hairs instead of the weight of all hairs including vellus. In the control group the length of hairs was little changed over the course of the study, indicating no increase in terminal hair counts. "Among the 10 animals in the control group, 6 showed... progressive miniaturization of follicles.. After 6 months the pattern of the control animal showed a majority of follicles in the telogen stage, and the overall length of the follicles was less than that in the pretreatment stage". So this can not explain the results of HMI-115. There was a 7% increase in hair length in the finasteride group, which is consistent with human data and clearly inferior to HMI-115. All this study does is show that there is little change in terminal hair growth from either vehicle or finasteride, which is the same thing seen in humans as this study explicitly states.
When looking at finasteride, which has such little effect, it's possible to cherry-pick data to make statistical noise and seasonality seem more significant than they are, because you're putting them against the backdrop of finasteride results. They are not significant against the results of HMI-115. This is a laughable attempt to discredit the HMI macaque study. I will expect your resignation from trolling by morning.
I'll leave you with one more thing, the hair weights before treatment for each group were "7.3 +- 3.2 and 7.5 +- 4.1 mg hair/in2, respectively, for 2 months of growth." The control group saw an increase in hair weight of 32% vs 55% for the finasteride group. That is an increase of 2.3 and 4.13 mg/in2, respectively. That is .36 and .64 mg/cm2, respectively. An average human hair weights .2-.4mg at 6 inches length. Let's split the difference and call it .3mg/6in, and we have .05mg per in. I think it's safe to assume macaque hairs are about the same weight. They let the macaque hairs grow for 2 months before weighing them. Hair grows at a rate of about an inch per 2 months. So, one terminal hair would weigh about .05mg. Again, the increase in hair weights was .36 and .64 mg/cm2 for the v and f groups, respectively. Ignoring vellus hairs, that represents 7.2 and 12.8 terminal hairs. Of course the entire increase was not terminal hairs, and for the placebo group it was mostly vellus hairs. We can probably assume that in the finasteride group the increase in terminal hairs was no more than (12.8-7.2)=5.6 hairs/cm2. However, for argument's sake let's fantasize that the entire hair weight change was due to an increase in terminal hairs. In that case we have a terminal hair count increase of 7.2 in the control group, 12.8 in the finasteride group, and 113 in the HMI-115 group. There is no debate, HMI-115 works and is superior to finasteride. A control group in the same study would have been nice, but regardless of any problems with this trial it is clear that the drug is the most effective hair loss treatment to date. It probably is not a full blown cure, but likely as close as we are going to get to that before hair cloning. There is certainly enough evidence here that I will not get a hair transplant before trying it. You question my motives, but you are the one set on convincing people that they should get a hair transplant in the face of evidence that there will likely soon be a treatment that can greatly reduce the number of grafts they need, and prevent them from exhausting their donor supply. Do you work in the hair transplant industry?
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One more thing, that line I drew was not a projection. I think everyone understands that but you. I put that there to illustrate that during the 6 month study they did not reach the top of the curve, making it impossible to project results, but indicating clearly that results would continue to increase beyond 6 months. How much we can't know, but the trend is clearly beyond the bounds of seasonality and statistical noise.
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thomps1523
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I think it’s clear what is being suggested. If you can wait then there may be hope. Try to bridge it with needling, minoxidil, and finasteride. If you can’t then don’t. This may save how many grafts you need substantially but everyone is in a different position.
I think @pegasus2 has helpful insight and that is his intention. Too many seem to ask him for definitive answers only to have other posters attack him for trying to answer them according to his opinion.
If people read this thread they have an idea of what is possible. From there the choice is yours to decide how you want to move forward.
I think @pegasus2 has helpful insight and that is his intention. Too many seem to ask him for definitive answers only to have other posters attack him for trying to answer them according to his opinion.
If people read this thread they have an idea of what is possible. From there the choice is yours to decide how you want to move forward.
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I am wondering which was the result n Dr Phill,...., Near one year using it plus microneedling.
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You have been on it for one year?
Using what ?
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Wonder when they'll test this on the first human male. Imagine being that person, would feel so amazing tbh
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That piece of sh*t will never understand how lucky he is. Shame they probably won't get the dose right for everyone, always the case when dose ranging hasn't quite been established
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A med related to prolactin receptors, but I am not sure what exactly. A group in Discord
Project PDRN
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