Italian Hair Loss Lotion To Hit The Market In 2016

Swoop

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But if s-equol downregulates AR wouldn't that mean the body won't develop hyperandrogenism/trigger the feedback loop that causes finasteride to lose it's effectiveness? I also find it interesting that asian populations tend to have higher levels of s-equol. Perhaps that's why male pattern baldness has a much lower presence in these areas.

They found a association between Androgenetic Alopecia and soy consumption in Taiwanese people in this study.

I don't know if s-equol downregulates AR, maybe a little but honestly I don't think it is of significant value. It was simply a quote that I took from that company their website which has s-equol running in their clinical trials. It was based on a pre-clinical model also, so that doesn't really say that much.
 

Pray The Bald Away

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They found a association between Androgenetic Alopecia and soy consumption in Taiwanese people in this study.

I don't know if s-equol downregulates AR, maybe a little but honestly I don't think it is of significant value. It was simply a quote that I took from that company their website which has s-equol running in their clinical trials. It was based on a pre-clinical model also, so that doesn't really say that much.
It's probably because soy contains isoflavones, which mimick the function of estrogen. AFAIK DHT is an estrogen antagonist. Not sure how that affects male pattern baldness but perhaps there's some relevance here.
 

Afro_Vacancy

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It's probably because soy contains isoflavones, which mimick the function of estrogen. AFAIK DHT is an estrogen antagonist. Not sure how that affects male pattern baldness but perhaps there's some relevance here.

I think it's that soy is converted to equol by gut bacteria more common to Asian people.
 

potato87

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What are we thinking?

So to summarise for the less technical is this going to be an effective Stand Alone maintenance drug?

Many thanks,
 

Swoop

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It's probably because soy contains isoflavones, which mimick the function of estrogen. AFAIK DHT is an estrogen antagonist. Not sure how that affects male pattern baldness but perhaps there's some relevance here.

Estrogen is just also very interesting in itself. Both estrogen receptors are located in the hair follicle (ERa and ERb). And equol has affinity to ERb, still not as strong as the primarily female sex hormone 17b-estradiol though.

As I may quote Cotsarelis;

Dr. Cotsarelis: 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.

What's interesting is that when you look at occipital non balding and balding scalp of Androgenetic Alopecia men you can see that the hair follicles in occipital has less androgen receptor expression and more estrogen receptor expression of both ERa and ERb. This is totally contra to what is seen in the scalp follicles residing in the balding region namely higher AR expression and less expression of both ERa and ERb. Also aromatase is higher expressed in occipital than the frontal region.

To identify differences in the transcription of AR in defined two sites, their mRNA levels were examined. In all samples, mean mRNAs of AR were 3.4- fold higher in VERTEXDPCs than those from occipital scalp (Fig. 1A). These site-specific different expressions of AR were consistent inWestern blot (Fig. 1B). VERTEXDPCs showed 1.9-fold higher AR expression than their counterparts, consistent with the results of cultured DPCs from hair follicles from the frontal and occipital scalp [2]. Immunohistochemical study showed that AR was localized to the nuclei of the VERTEXDPCs at the anagen stage (six of eight samples), although not all the DPCs were positive (Fig. 1C). In sebaceous gland, AR immunoreactivity was mostly confined to the nuclei of the basal cells as previously described (Fig. 1D) [4].

Reversely, ERa mRNA expression levels were 2.2- fold higher in OCCIPUTDPCs than in their counterparts. ERb mRNA was consistently highly expressed by 4.2- fold in OCCIPUTDPCs versus VERTEXDPCs (Fig. 2A). ERa protein was consistently elevated in OCCIPUTDPCs by 1.8-fold higher versus vertex and ERb was also definitely increased in DPCs from non-balding scalps, with a 1.8-fold stronger intensity (Fig. 2B).

These observations are also important;




If you look at women they can have start having troubles too with hair loss due to estrogen/androgens. Women suffering from PCOS which is characterized by overproduction of androgens may also start to lose their hair on their scalp and develop hirsutism (increased body hair growth). Women can start having troubles with hair loss after the menopause period which is characterized by a decrease in estrogen production. Women who take aromatase inhibitors may start to lose their hair as seen in this study, picture here;



Also women have way more aromatase activity in their scalp than men do especially at the frontal regions. Funny if you look at the above study. Inhibit aromatase activity of women and they might suddenly start to suffer in the region where they have most aromatase activity? Coincidence? Maybe.

Transgenders who go from women to man also may develop hair loss on the scalp and develop body hair in return.

The other way around people who suppress the androgen/AR angle extremely hard and supplement on 17b-estradiol may regrow a considerable amount of hair as seen recently by 2 members here in the success section also.

There could be so much said about this but these observations alone should display the importance of estrogen in relation to the hair follicle. It is not far fetched to say that it seems to have a protective role for the scalp hair follicles and that androgens are more a stimulant for body hair.
 

Pray The Bald Away

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Estrogen is just also very interesting in itself. Both estrogen receptors are located in the hair follicle (ERa and ERb). And equol has affinity to ERb, still not as strong as the primarily female sex hormone 17b-estradiol though.

As I may quote Cotsarelis;



What's interesting is that when you look at occipital non balding and balding scalp of Androgenetic Alopecia men you can see that the hair follicles in occipital has less androgen receptor expression and more estrogen receptor expression of both ERa and ERb. This is totally contra to what is seen in the scalp follicles residing in the balding region namely higher AR expression and less expression of both ERa and ERb. Also aromatase is higher expressed in occipital than the frontal region.



These observations are also important;




If you look at women they can have start having troubles too with hair loss due to estrogen/androgens. Women suffering from PCOS which is characterized by overproduction of androgens may also start to lose their hair on their scalp and develop hirsutism (increased body hair growth). Women can start having troubles with hair loss after the menopause period which is characterized by a decrease in estrogen production. Women who take aromatase inhibitors may start to lose their hair as seen in this study, picture here;



Also women have way more aromatase activity in their scalp than men do especially at the frontal regions. Funny if you look at the above study. Inhibit aromatase activity of women and they might suddenly start to suffer in the region where they have most aromatase activity? Coincidence? Maybe.

Transgenders who go from women to man also may develop hair loss on the scalp and develop body hair in return.

The other way around people who suppress the androgen/AR angle extremely hard and supplement on 17b-estradiol may regrow a considerable amount of hair as seen recently by 2 members here in the success section also.

There could be so much said about this but these observations alone should display the importance of estrogen in relation to the hair follicle. It is not far fetched to say that it seems to have a protective role for the scalp hair follicles and that androgens are more a stimulant for body hair.
Hmm. So wouldn't this support the notion that hair follicles can be reawoken from their suspension in the telogen phase? From what you've shared, it seems clear that the absence of DHT does nothing to reverse hair loss other than the cessation of miniaturization. The "secret sauce" seems to be the prescence of high estrogen levels in conjunction with the inhibition of DHT, since DHT is antagonizing the estrogen. Is there any way to replicate the action of estrogen on hair follicles further down stream, so as to prevent the undesired effects of high estrogen on the male body?
 

Koga

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Also women have way more aromatase activity in their scalp than men do especially at the frontal regions. Funny if you look at the above study. Inhibit aromatase activity of women and they might suddenly start to suffer in the region where they have most aromatase activity? Coincidence? Maybe.

Transgenders who go from women to man also may develop hair loss on the scalp and develop body hair in return.

The other way around people who suppress the androgen/AR angle extremely hard and supplement on 17b-estradiol may regrow a considerable amount of hair as seen recently by 2 members here in the success section also.

There could be so much said about this but these observations alone should display the importance of estrogen in relation to the hair follicle. It is not far fetched to say that it seems to have a protective role for the scalp hair follicles and that androgens are more a stimulant for body hair.

I don't understand this. They have more aromatase activity in the frontal regions of their scalp, so that's the place they would suffer the most when inhibiting aromatase activity, that's what you imply. But isn't female hair loss characterised by widely diffuse loss? Anyway, great contribution, Swoop. I always interpreted estrogen as being purely scalp hair friendly, mainly because of the female hair loss cases after menopause (drop in estrogen) and the great succes stories from MTF transgenders or the madcaps taking oral spironolactone (increase in estrogen).
 

el_rizos

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I do not understand anything. I'm up to the balls of the pharmaceutical . I'm tired of the same story. when a drug seems to work there is always a problem. Now it seems that Dr. Brotzu lotion can work, Fidia delayed its release . Why? Why always the same ? this pathology is maddening .
I am willing to form a buying group for ingredients and try the lotion , I can not wait any longer. Here is a user who has an ultrasound machine , we could pay to him to make the lotion. Please , we have to do something.
I am from Spain. I am ready to go to Cerdeña to talk to Dr. Brotzu in person if necessary , but we have to do something dammit.
 

Swoop

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Hmm. So wouldn't this support the notion that hair follicles can be reawoken from their suspension in the telogen phase? From what you've shared, it seems clear that the absence of DHT does nothing to reverse hair loss other than the cessation of miniaturization. The "secret sauce" seems to be the prescence of high estrogen levels in conjunction with the inhibition of DHT, since DHT is antagonizing the estrogen. Is there any way to replicate the action of estrogen on hair follicles further down stream, so as to prevent the undesired effects of high estrogen on the male body?

It's indeed a important question to ask if inhibiting DHT or androgens as a whole doesn't do anything in terms of hair regrowth and repair but the shifting to a more estrogen environment is the cause of regrowth. Sort of a ying-yang relationship.

Yes, that would obviously be a very smart thing to do but there are some problems with that. First of all estrogen stimulation on hair follicles brings down a chain reaction that is broad and complex. So how are you going to differentiate exactly which factors are responsible for the pro hair growth effects? It is also probably a plethora of factors that make this happen instead of one or two factors. I mean we don't even understand how minoxidil exactly works on the hair follicle in terms of it's hair stimulating effect, so how are we going to understand this with something more broad and complex like estrogen? To underline the complexity with a example;

Male and female E2-stimulated hair follicles were analyzed by cDNA microarray. Of 1300 genes tested, more than 600 E2-responsive genes were detected in both experiments (Fig. 3.12.1). For signifcances the level was chosen for <0.5fold suppressed or > 1.5fold stimulated in at least one experiment, which decreases the number of relevant genes down to 70 genes.

With a proper model this would be way easier as you could simply do a massive trial & error and perhaps stumble on the factors that make this happen. We could do it even then as a community. But where is our proper model in this world? Nowhere to be found. We only have a terrible model; mice.

When you look at more in depth studies of estrogen and the hair follicle like this one and this one it's interesting.

The molecular mechanisms of estrogen action are relatively well investigated, but only a few target genes with consensus ERE (primary-responsive genes) are known so far, such as progesterone receptor, prolactin, lactoferrin, ovalbumin, vitellogenin, cathepsin D1, pS2, glucose-6-phosphate dehydrogenase, c-fos, c-jun, c-myc and choline acetyltransferase. There are more genes activated eventually by estrogen but without apparent ERE: EGF, EGFR, cyclin D1 and others, which can be termed the secondary E2-responsive genes

Just a few important genes regulated by ERs, which also are recognized for their involvement in hair growth control, are listed here as examples: progesterone receptor, EGFR, several growth factors like IGF-I, TGF-α and TGF-β, cathepsin D, and several protooncogenes (e.g., c-fos, c-myc, and c-jun)

Other factors mentioned are the likes of WNT, SHH, MAPK, BMP's etc, which also have a huge role in hair follicle biology but let's just look at c-myc which is a gene;

c_myc.jpg


Well if you look here at the description of function it doesn't take much to see that c-myc seems to work very stimulative for (stem)cells in almost every way possible. Hell you could even take this further and hypothesize that Androgenetic Alopecia might be simply a form of stressing of the cells in which they simply gradually stop performing the function that they were supposed to do. I made a post about this here and link to studies that underline something like that; http://hairandscience.com/possible-...r-cell-cycle-arrest-in-androgenetic-alopecia/.

Therefore if Androgenetic Alopecia is simply a form of stress of the cells in which factors respond to that stress and shut down the cells from performing their normal function, something like c-myc might simply push them to start functioning again because it might for instance oppose factors that initially made the cells stop functioning. You can also see that in the table here above in the functional class of cell cycle, in which c-myc can induce factors like cyclin D2 and oppose factors like P21.

If you take on study which look at human dermal papilla cells in vitro under stimulation of DHT;

The cell viability and cell cycle were determined, levels of ROS were examined and senescence-associated β-galactosidase assays were performed in normal human DPCs (nHDPCs). Furthermore, miRNA expression profiling was performed using an miRNA microarray to determine whether changes in the expression levels of miRNA were associated with the cellular effects of DHT. The results revealed that DHT decreased cell growth by inducing cell death and G2 cell cycle arrest, and by increasing the production of ROS and senescence in the nHDPCs. In addition, 55 miRNAs were upregulated and 6 miRNAs were downregulated in the DHT-treated nHDPCs. Bioinformatic analysis demonstrated that the putative target genes of these upregulated and downregulated miRNAs were involved in cell growth, cell cycle arrest, cell death, senescence and the production of ROS.

But you can't just start to induce c-myc either, because that would be dangerous (cancer etc.) I mean in the past a SHH agonist was dropped before it entered clinical trials for hair loss because they found it to be too dangerous. It still hasn't been explored while in reality it might have a effect for hair growth, but yeah just way too dangerous.

When you look at these studies of estrogen and the hair follicle as a whole and the factors mentioned it does seem that estrogen can have effect on multiple factors that seem to be stimulating for the hair follicle cycle as a whole, but can also induce factors that would oppose the "bad factors" that could be induced by androgens if indeed that is true. All hypothetical but interesting nonetheless. Obviously it all might be something different too as in reality we know f*ck all including every scientist out there.

If we take this information though and understand that even castration + 17b-estradiol can't always regrow hair to great extent, we should perhaps also maybe start to understand that it's totally unrealistic to get a traditional drug that will reverse Androgenetic Alopecia. It's seems extremely unlikely for me at this point that's why I often argue hitting on the androgen/AR angle and estradiol is pretty much as good as it will get. Regenerative medicine and gene therapy seems much more realistic and practical to me.

Also we must not forget that the hair follicle is an organ and too much damage to a organ may really make it irreversible. This has really been shown too as in a certain timepoint fibrosis may set in due to Androgenetic Alopecia and this can lead to irreversible damage to the hair follicle due to infiltration of the scar tissue. Only creating a new hair follicle seems to be the answer here.

I hope this was not too difficult or overwhelming I tried to explain it as simple as I could, but just look at it from a abstract point view and just think of factors in one square that are bad and other factors in a square that are good for the hair follicle (stem) cells.

- - - Updated - - -

I don't understand this. They have more aromatase activity in the frontal regions of their scalp, so that's the place they would suffer the most when inhibiting aromatase activity, that's what you imply. But isn't female hair loss characterised by widely diffuse loss? Anyway, great contribution, Swoop. I always interpreted estrogen as being purely scalp hair friendly, mainly because of the female hair loss cases after menopause (drop in estrogen) and the great succes stories from MTF transgenders or the madcaps taking oral spironolactone (increase in estrogen).

I just gave food for thought. It's true that females indeed seem to suffer more from a diffuse pattern. That's why we need way more studies that are more in depth and focus on the site specific differences of hair follicles (patterning) on the scalp like receptor expression differences etc. That would broaden our understanding of sex hormones on the hair follicle but I guess that is even too much too ask. We have limited research to look at.
 

Alphus

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I was wrong. I have got a thing that clean with ultrasound. I thought was the same.
This is an example of what I have got: http://www.expondo.it/ulsonix-lavat...ap7-i_VQRYtYNN69HikFHiTf3RHWn_YF3wBoC7lDw_wcB

However I have an idea. We can start a topic about making that lotion. We will discuss about ingredient and where to buy. If someone can buy, will do it.
This topic will be about brotzu and fidia and nothing else.

Concerning the ultrasound, what's this "tool"? Maybe we can build an economic version with Arduino.
 

abcdefg

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Having a topical more mild version of finasteride though is a good thing. Also no script so sign me up. To bad we have to wait 1 year bare minimum probably longer. Assuming of course this even works which is a big assumption at this point.
The whole idea of finasteride still seems like trying to kill a rabbit with a cannon. Why cant this be solved topically and local to the scalp? Of course its been talked about for like a decade so guess it wont happen
Moral of the story then is take your propecia/RU because hair loss is probably not reversible.
 

Pray The Bald Away

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It's indeed a important question to ask if inhibiting DHT or androgens as a whole doesn't do anything in terms of hair regrowth and repair but the shifting to a more estrogen environment is the cause of regrowth. Sort of a ying-yang relationship.

Yes, that would obviously be a very smart thing to do but there are some problems with that. First of all estrogen stimulation on hair follicles brings down a chain reaction that is broad and complex. So how are you going to differentiate exactly which factors are responsible for the pro hair growth effects? It is also probably a plethora of factors that make this happen instead of one or two factors. I mean we don't even understand how minoxidil exactly works on the hair follicle in terms of it's hair stimulating effect, so how are we going to understand this with something more broad and complex like estrogen? To underline the complexity with a example;



With a proper model this would be way easier as you could simply do a massive trial & error and perhaps stumble on the factors that make this happen. We could do it even then as a community. But where is our proper model in this world? Nowhere to be found. We only have a terrible model; mice.

When you look at more in depth studies of estrogen and the hair follicle like this one and this one it's interesting.





Other factors mentioned are the likes of WNT, SHH, MAPK, BMP's etc, which also have a huge role in hair follicle biology but let's just look at c-myc which is a gene;

c_myc.jpg


Well if you look here at the description of function it doesn't take much to see that c-myc seems to work very stimulative for (stem)cells in almost every way possible. Hell you could even take this further and hypothesize that Androgenetic Alopecia might be simply a form of stressing of the cells in which they simply gradually stop performing the function that they were supposed to do. I made a post about this here and link to studies that underline something like that; http://hairandscience.com/possible-...r-cell-cycle-arrest-in-androgenetic-alopecia/.

Therefore if Androgenetic Alopecia is simply a form of stress of the cells in which factors respond to that stress and shut down the cells from performing their normal function, something like c-myc might simply push them to start functioning again because it might for instance oppose factors that initially made the cells stop functioning. You can also see that in the table here above in the functional class of cell cycle, in which c-myc can induce factors like cyclin D2 and oppose factors like P21.

If you take on study which look at human dermal papilla cells in vitro under stimulation of DHT;



But you can't just start to induce c-myc either, because that would be dangerous (cancer etc.) I mean in the past a SHH agonist was dropped before it entered clinical trials for hair loss because they found it to be too dangerous. It still hasn't been explored while in reality it might have a effect for hair growth, but yeah just way too dangerous.

When you look at these studies of estrogen and the hair follicle as a whole and the factors mentioned it does seem that estrogen can have effect on multiple factors that seem to be stimulating for the hair follicle cycle as a whole, but can also induce factors that would oppose the "bad factors" that could be induced by androgens if indeed that is true. All hypothetical but interesting nonetheless. Obviously it all might be something different too as in reality we know f*ck all including every scientist out there.

If we take this information though and understand that even castration + 17b-estradiol can't always regrow hair to great extent, we should perhaps also maybe start to understand that it's totally unrealistic to get a traditional drug that will reverse Androgenetic Alopecia. It's seems extremely unlikely for me at this point that's why I often argue hitting on the androgen/AR angle and estradiol is pretty much as good as it will get. Regenerative medicine and gene therapy seems much more realistic and practical to me.

Also we must not forget that the hair follicle is an organ and too much damage to a organ may really make it irreversible. This has really been shown too as in a certain timepoint fibrosis may set in due to Androgenetic Alopecia and this can lead to irreversible damage to the hair follicle due to infiltration of the scar tissue. Only creating a new hair follicle seems to be the answer here.

I hope this was not too difficult or overwhelming I tried to explain it as simple as I could, but just look at it from a abstract point view and just think of factors in one square that are bad and other factors in a square that are good for the hair follicle (stem) cells.

- - - Updated - - -



I just gave food for thought. It's true that females indeed seem to suffer more from a diffuse pattern. That's why we need way more studies that are more in depth and focus on the site specific differences of hair follicles (patterning) on the scalp like receptor expression differences etc. That would broaden our understanding of sex hormones on the hair follicle but I guess that is even too much too ask. We have limited research to look at.
Wow! That's some knockout research you've put together. Admittedly a bit of it went over my head, but I'm able to digest most of it. The main takeaway seems to be that a "cure" will likely come by side-stepping this giant web of interwoven feedback loops that traditional medicine acts upon and opting for the replication of occipital hair. Thanks for laying it out for me, I'll definitely be looking further into all this.
 

opti

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I don't understand this. They have more aromatase activity in the frontal regions of their scalp, so that's the place they would suffer the most when inhibiting aromatase activity, that's what you imply. But isn't female hair loss characterised by widely diffuse loss? Anyway, great contribution, Swoop. I always interpreted estrogen as being purely scalp hair friendly, mainly because of the female hair loss cases after menopause (drop in estrogen) and the great succes stories from MTF transgenders or the madcaps taking oral spironolactone (increase in estrogen).
let me try to explain it to you :
Women have more Estrogen receptors on their temples/hair line then on the top of the head/vertex. If they suffer low estrogen levels (trough aromtase inhibitors etc.) they will most likely develop hair loss on the top of the head while they will rarely lose their hair in the temple area/hair line.They will have perfect hair lines most of the time.

ludwig-scale.jpg

if you look at that picture it might help you to understand that their hair line doesnt recede.

Men have less ER on the temple/hairline than on the vertex/oppicital region.I think the reason why finasteride might give you hair growth is due to the fact that it increases aromastase and thus increases Estrogen ( it s the estrogen which probably give you bitc* tits on finasteride and not low dht levels). RU doesnt increase aromastase and in most cases RU wont give you any regrow and just a hair loss stop.
This chinese guy who used diane lotion regrow his temples completely but became feminine.

I still think that high estrogen levels on temples and hair line can regrow all of your bald scalp, but however noone ever managed to get such a increase in scalp estrogen without an increase in system estrogen levels.
 

Follisket

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I'd like to send an email as well.
What are you guys writing in yours?


I just told them how excited I was about it and inquired about the trials; when they're starting and how long they'll be, when we can expect the product to actually hit the market, etc. (stressing the importantance of time for those of us suffering from male pattern baldness).

Got a kind and prompt reply saying they won't know enough about its exact effectiveness and tolerability until trials start so no exact launch plans have been made yet. Pretty much what I expected to hear but I was mainly just hoping to show them it's generating interest. Because - you know, I'm not taking any chances.
 

cocohot

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Ok, this is a huge thread and I haven't been following it so if someone could answer this question I'd be hugely grateful:

Does this work and when is it coming out?
 

Pray The Bald Away

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Ok, this is a huge thread and I haven't been following it so if someone could answer this question I'd be hugely grateful:

Does this work and when is it coming out?
We don't know and we don't know.
 

abcdefg

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We don't know and we don't know.

Yeah this entire thread can be summarized with we dont know. There is almost no actual info on whether it works, or anything. Something is being looked at that may or may not ever be anything.
Its safe to say a lot of people want a finasteride alternative like a topical that is a little safer to use more preemptively
 

el_rizos

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Hi. I want to ask the Italian forero who said a user of an Italian forum had spoken with Dr. Brotzu and said his lotion worked in 100% of the Androgenetic Alopecia .
Can you ask that Italian user if there is a chance to talk again with Dr. Brotzu and to see pictures of the results in people ? I guess if Dr. Brotzu has spent years studying his aftershave , he will have many pictures where you can see the results not ??? ,
please , I turn to Italian users . try to contact Dr. Brotzu for more information and ask if he has pictures of the results .
 

StartingToLose

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Hello All. I was lurking on this thread yesterday as I've been recently diagnosed with male pattern baldness and have been shedding since November. My dermatologist prescribed me Finasteride, and I have a bottle right here, but after a bit of Googling, I can't bring myself to take it. My sympathies to all who have and who are experiencing the sides or continue to after discontinuing. Anyhow, someone here I believe mentioned that more of us should write the pharmaceutical company inquiring about this drug to maybe help speed them up. So, I did. Not a lot to add here except that it seems the trial still has not begun--so anyone who was thinking it'd be a 1-year trial, well, that clock hasn't started yet. =\
Thank you for contacting us regarding Prof. Brotzu’s hair loss remedy. We provide you here with some information on the project, that you may find useful.

Professor Brotzu has been working on an innovative hair loss therapy, in collaboration with his research team at the University of Cagliari (Italy), as far as the development of the most appropriate formulation is concerned. Fidia farmaceutici has considered this achievement a scientific breakthrough, with a very high potential, and has decided to acquire the intellectual property rights of the technology, to offer all patients who are affected by the problem, a real treatment option.

Fidia will soon begin a clinical trial, with a defined protocol, focusing on a specific formulation suitable for industrial scaling-up.

Regretfully, we are not able to figure out in advance the formulation’s effectiveness and tolerability, that shall be demonstrated during the trial, with statistical significance and clinical relevance.

For this reason, neither exact launch plans nor time-to-market priorities have been defined for the product yet.

We will keep you abreast of the company’s future steps in this concern.

Please, do not hesitate to contact us if you have any further questions on the subject.

Cordially yours.


Elena Fedeli
Responsabile Comunicazione
Tel (+39) 049 8232359
Cellulare (+39) 342 0704040

Finding a safe way to stem the loss is my newfound addiction, so I'm sure you guys will hear more from me in time. For now, I'm following you guys on this one and am also stalking the Hasson&Wong and Polichem topical fins that should be out well before this Brotzu cream. So many threads on so many forums on the web, it's hard to know what to try--but I'm starting to get the impression that only the future holds the safe solution to our problems. Best of luck to all.
 
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