Sarms Should Have Been The Cure To male pattern baldness For A Long Time Now

[hemingway_the_mercenary]

FIrst of all its a disgrace how imcompetent hair loss research has been when compared to almost any other disease research. We all know its due to androgens that male pattern baldness begins and somehow these big companies don't seem to get this and invest in an application of anti androgens in such a way that side effects don't occur. Ayways,

SARMS are selective androgen receptor modulators. They have the ability to be androgenic in certain cells but be anti androgenic in other cells. Many SARMS out now are being used in bodybuilding are androgenic in muscle cells but seem to have a very low androgenic effect in hair/skin.

A great example for the potential of SARMS is actually SERMS. In women with breast cancer, Novaldex (a SERM) is used because it is selectively estrogenic in bones and a host of other cells, but anti estrogenic in breast tissue. This makes a great treatment for breast cancer because it doesnt contribute to osteoporosis

WHY can't this be made for men already. There are already numerous sarms that have an anti DHT effect and sarms that dont have an androgenic effect in hair. Such a shame that no research is being invested into the production of a SARM that is antiandrogenic in hair tissue only.

Has this topic been discussed here already?

 

[hemingway_the_mercenary]

Hairloss is not a disease, no matter how much you try to convince yourself.

I don't think it is either, do we really have to talk about how I worded that tho instead of the info I talked about in my post?

 

[Endmymisery]

Hairloss is not a disease, no matter how much you try to convince yourself.

Hairloss is a disease of the soul

 

[SamFT]

Hairloss is not a disease, no matter how much you try to convince yourself.

Wow how ignorant lol this right here goes to show how people that are not knowledgeable in a specific field will still try to convince people things. YES male pattern baldness can be considered a disease. A disease is considered a particular quality (our hair) that is dysfunctional or abnormal (hair loss) that can adversely affect a person or group of people (hair loss sufferers). Many uninformed people believe a “disease” is something like cancer or multiple sclerosis. A disease is a more broad definition than you think

 

[jamesbooker1975]

FIrst of all its a disgrace how imcompetent hair loss research has been when compared to almost any other disease research. We all know its due to androgens that male pattern baldness begins and somehow these big companies don't seem to get this and invest in an application of anti androgens in such a way that side effects don't occur. Ayways,

SARMS are selective androgen receptor modulators. They have the ability to be androgenic in certain cells but be anti androgenic in other cells. Many SARMS out now are being used in bodybuilding are androgenic in muscle cells but seem to have a very low androgenic effect in hair/skin.

A great example for the potential of SARMS is actually SERMS. In women with breast cancer, Novaldex (a SERM) is used because it is selectively estrogenic in bones and a host of other cells, but anti estrogenic in breast tissue. This makes a great treatment for breast cancer because it doesnt contribute to osteoporosis

WHY can't this be made for men already. There are already numerous sarms that have an anti DHT effect and sarms that dont have an androgenic effect in hair. Such a shame that no research is being invested into the production of a SARM that is antiandrogenic in hair tissue only.

Has this topic been discussed here already?

It is not that simply, you can't take a drug , have all the benefits of DHT but don't have any of the side effects of DHT . THat simple don't exist.
First, your body will sense the lack of DHT, so it will drive it crazy, will drop the progesterone to almost zero , will increase the estrogens, etc.

 

[hemingway_the_mercenary]

It is not that simply, you can't take a drug , have all the benefits of DHT but don't have any of the side effects of DHT . THat simple don't exist.
First, your body will sense the lack of DHT, so it will drive it crazy, will drop the progesterone to almost zero , will increase the estrogens, etc.

what are you talking about? You clearly don't understand the subject. Read up on SARMS please, no disrespect.

 

[whatevr]

Bunch of retards in this thread FML.

 

[d3nt3dsh0v3l]

FIrst of all its a disgrace how imcompetent hair loss research has been when compared to almost any other disease research. We all know its due to androgens that male pattern baldness begins and somehow these big companies don't seem to get this and invest in an application of anti androgens in such a way that side effects don't occur. Ayways,

SARMS are selective androgen receptor modulators. They have the ability to be androgenic in certain cells but be anti androgenic in other cells. Many SARMS out now are being used in bodybuilding are androgenic in muscle cells but seem to have a very low androgenic effect in hair/skin.

A great example for the potential of SARMS is actually SERMS. In women with breast cancer, Novaldex (a SERM) is used because it is selectively estrogenic in bones and a host of other cells, but anti estrogenic in breast tissue. This makes a great treatment for breast cancer because it doesnt contribute to osteoporosis

WHY can't this be made for men already. There are already numerous sarms that have an anti DHT effect and sarms that dont have an androgenic effect in hair. Such a shame that no research is being invested into the production of a SARM that is antiandrogenic in hair tissue only.

Mentioning tamoxifen and alluding to an experimental SARM or two still being investigated is like asking, "I see here that there are a handful of obscure superconducting materials that happen to work near -130 °C; why don't we have room temperature superconductors already? It's 2018"

For a receptor modulator to be selective, it has be become activated or inactivated in some tissues but not others; one may be able to achieve this by utilizing enzymes or other metabolic pathways within the tissues of interest; this means part of the work has to be done by the body and therefore suitable architecture must be available within the body.

Then in order for the compound to agonize or antagonize the receptor, it has to satisfy the structure-function relation required, which it appears can be beyond the simple "lock-and-key" cartoon used to describe receptors.

Here is tamoxifen's structure (left), and that of its active metabolite, 4-hydroxytamoxifen (right); I've circled the only difference.

The former is a weak estrogen receptor agonist and the latter is a strong antagonist.

Here is a cartoon from Wikipedia showing how within the estrogen receptor, the participation of coactivators control the activity of the complex as well.

Compound the intricacies of the structure-function relationships with the difficulty of developing a drug that the body can metabolize in a favorable, selective manner, and one that has favorable pharmacokinetics and pharmacodynamics, and the heroic efforts required to clinically investigate a drug and perhaps eventually commercialize it, and I think you will find a very sobering answer to your question of why we don't have SARMS at our disposal - it's pretty HARD to design and test them.

It's probably easier to try to confine a regular old AA to within the scalp region by choosing a delivery route more involved than a simple small molecule vehicle.

The simplicity of describing what a SARM is in abstract belies basically the entire complexity involved in actually realizing the technology.

You can add this to the list of other humanity's "shortcomings" like cold fusion, warp drive, time travel (into the future, not the past, obviously), the perfect nootropic, "the cure" for cancer, etc.

 

[hemingway_the_mercenary]

Mentioning tamoxifen and alluding to an experimental SARM or two still being investigated is like asking, "I see here that there are a handful of obscure superconducting materials that happen to work near -130 °C; why don't we have room temperature superconductors already? It's 2018"

For a receptor modulator to be selective, it has be become activated or inactivated in some tissues but not others; one may be able to achieve this by utilizing enzymes or other metabolic pathways within the tissues of interest; this means part of the work has to be done by the body and therefore suitable architecture must be available within the body.

Then in order for the compound to agonize or antagonize the receptor, it has to satisfy the structure-function relation required, which it appears can be beyond the simple "lock-and-key" cartoon used to describe receptors.

Here is tamoxifen's structure (left), and that of its active metabolite, 4-hydroxytamoxifen (right); I've circled the only difference.
View attachment 83183

The former is a weak estrogen receptor agonist and the latter is a strong antagonist.

Here is a cartoon from Wikipedia showing how within the estrogen receptor, the participation of coactivators control the activity of the complex as well.

View attachment 83184

Compound the intricacies of the structure-function relationships with the difficulty of developing a drug that the body can metabolize in a favorable, selective manner, and one that has favorable pharmacokinetics and pharmacodynamics, and the heroic efforts required to clinically investigate a drug and perhaps eventually commercialize it, and I think you will find a very sobering answer to your question of why we don't have SARMS at our disposal - it's pretty HARD to design and test them.

It's probably easier to try to confine a regular old AA to within the scalp region by choosing a delivery route more involved than a simple small molecule vehicle.

The simplicity of describing what a SARM is in abstract belies basically the entire complexity involved in actually realizing the technology.

You can add this to the list of other humanity's "shortcomings" like cold fusion, warp drive, time travel (into the future, not the past, obviously), the perfect nootropic, "the cure" for cancer, etc.

whats your point? Tamoxifen breaks down to its active metabolite and is still anti-estrogenic mainly only in breast tissue. Also they have been able to make SARMS that target muscle and bone cells but have significantly weaker androgenic expression in hair follicles. I'm saying they have been able to selectively target breast tissue for women with cancer but there has been no push for men with male pattern baldness

you resort to saying its complicated, well thats a given, but there are working on many other hair loss treatments that are also complicated, but have less potential to work

 

[Jimm]

Hairloss is not a disease, no matter how much you try to convince yourself.

I don't think it is either, do we really have to talk about how I worded that tho instead of the info I talked about in my post?

You both are a bunch of dumb c****, ain't ya? You can define 'disease' for yourself, if you'd like. I prefer to stick to Webster or Oxford definitions.

Disease: "a disorder of structure or function in a human, animal, or plant, especially one that produces specific signs or symptoms or that affects a specific location and is not simply a direct result of physical injury."

Disease: "a particular quality, habit, or disposition regarded as adversely affecting a person or group of people."

 

[Jimm]

Bunch of dumbasses.

 

[hemingway_the_mercenary]

You both are a bunch of dumb c****, ain't ya? You can define 'disease' for yourself, if you'd like. I prefer to stick to Webster or Oxford definitions.

Disease: "a disorder of structure or function in a human, animal, or plant, especially one that produces specific signs or symptoms or that affects a specific location and is not simply a direct result of physical injury."

Disease: "a particular quality, habit, or disposition regarded as adversely affecting a person or group of people."

how does the medical community define male pattern balding? Aren't you the one trying to assign a definition onto something for yourself.


Who cares what its called!

 

[Jimm]

how does the medical community define male pattern balding? Aren't you the one trying to assign a definition onto something for yourself.


Who cares what its called!

If the medical view male pattern baldness against simple definitions of 'disease', they would be right to consider it one, rather than as the simple inconvenience they view it as currently.

 

[d3nt3dsh0v3l]

whats your point? Tamoxifen breaks down to its active metabolite and is still anti-estrogenic mainly only in breast tissue. Also they have been able to make SARMS that target muscle and bone cells but have significantly weaker androgenic expression in hair follicles. I'm saying they have been able to selectively target breast tissue for women with cancer but there has been no push for men with male pattern baldness

you resort to saying its complicated, well thats a given, but there are working on many other hair loss treatments that are also complicated, but have less potential to work

Well what's YOUR point, besides, "Waaahh, we don't have SARMs!"?

And I didn't say NO SARMs existed. I said they are all experimental. I said SARM design is harder than the design of non-selective drugs - I think that much is clear.

The list of approved anti-androgens far outnumbers the list of SARMs under investigation, and the AA list is quite short.

My problem with your post is that just because we don't have what you want, you appear to think that 1) somehow this means that the research on the topic is non-existent and 2) somehow SARMs are a low resistance path to the baldness cure amd 3) we have a SERM or SARM that works in one area, so somehow this means it is straightforward to make a SARM or SERM that can work in another area.

1) is wrong because SARMs would solve a broad range of problems besides hair loss and there obviously is research in this field, especially considering that sports industries are enormous; you yourself mentioned bodybuilding
2) is wrong because the design of a non-selective anti-androgen acting at the receptor for male pattern baldness has also proven difficult; the most successful candidate is RU-58841, which as we all know was never even officially released.
3) may or may not be possible; again, as I mentioned in the previous post, part of the mechanism of action relies on there being a favorable (i.e. one we can safely use) metabolic contrast between the region of interest and all other regions of the body. You have to work with what's there.

I'm not going to reply to you again if after taking the time to make a detailed post, I return to find that you have seemingly reflexively retorted, "What's your point?," all the while replying with trivia such as "tamoxifen exists." My points were in my previous post and I have just iterated them here.

Again if you want to look at tamoxifen, the textbook SERM, the very few other SERMs available, and point to an experimental SARM or two and say, "Hey look, the concept works - why can't I pick up my SARM for Androgenetic Alopecia at the local drugstore?" Then what I am saying is that you are totally glossing over what making a working SARM entails and are instead enamoured by the concept.

I'll make it very simple:
If you want to tell me that you disagree with me, why don't you go ahead and reply with answers to some of my questions -

Why do you think SARM development should be much farther along than it is now, given our current capacity to design drugs?

Why would the development of a SARM for male pattern baldness make technological and economic sense over using a traditional AA with a delivery route to locking the AA into the scalp? What makes you think the former is less of a challenge than the latter?

Why do you think shutting down the androgen receptor alone will be sufficient for curing male pattern baldness? Do you not see that even dutasteride does not give regrowth in a significant number of cases?

Why do you think that the existence of successful SARMs or SERMs that work in one type of tissue imply that it should be within reach to design SARMs or SERMs that work in other tissues, given that the selectivity is not conferred by the drug itself, but by the contrast in metabolisms of the tissues themselves? In other words, how do you know that "metabolized here, but not there" can be done with the skin? Specifically the skin on the scalp, but not the skin elsewhere, much less any other tissues?

 

[Ollie]

What is the defining difference between androgen receptors in skin vs muscle ? I've come across Sarms a lot but have never been convinced over the idea that they are exclusively impactful on JUST muscle and skeletal receptors - how do we know they don't affect skin/hair receptors?

 

[hemingway_the_mercenary]

Well what's YOUR point, besides, "Waaahh, we don't have SARMs!"?

Well first of all SARMS would be better to research for male pattern baldness than other treatments because it is known that the cause of hair loss is for sure starting with androgens. So you can work on stopping it at the source rather than investigating some other way of treating it.

As for your posts regarding how difficult it would be to get selectivity in SARMS, you don't seem to get it. There are already sarms that are anti-androgenic in hair and skin but androgenic in muscle. THIS ALREADY EXISTS. I can't remember the compound name but if you do your research on sarms you will see that they have already been made.

Also even if this wasn't done, my logic for why it would be possible is that if you can targer muscle and bone cells, but exclude prostate/skin/hair cells for androgenic activity than its possible you can do the opposite as well. I don't think I have to keep explaining this to you because such sarms already exist

 

[d3nt3dsh0v3l]

Well first of all SARMS would be better to research for male pattern baldness than other treatments because it is known that the cause of hair loss is for sure starting with androgens. So you can work on stopping it at the source rather than investigating some other way of treating it.

As for your posts regarding how difficult it would be to get selectivity in SARMS, you don't seem to get it. There are already sarms that are anti-androgenic in hair and skin but androgenic in muscle. THIS ALREADY EXISTS. I can't remember the compound name but if you do your research on sarms you will see that they have already been made.

Also even if this wasn't done, my logic for why it would be possible is that if you can targer muscle and bone cells, but exclude prostate/skin/hair cells for androgenic activity than its possible you can do the opposite as well. I don't think I have to keep explaining this to you because such sarms already exist

Ok now you are just not reading my posts. Like at all. Here, let me just copy and paste.

If you think "exists" is the same as "working and safe" then that's where we can disagree.




And you totally didn't answer this basic question:

Given that AAs alone won't address the full scope of Androgenetic Alopecia, I think autologous cell/organoid transplants are a safer, more effective, "one time" treatment as compared to bringing a hair loss SARM to market just for maintainence therapy via long term drug use.

 

[Johnt1997]

Is it possible to get your hands on sarms created for a different purpose and just use them on your scalp? I've never heard of them before so I'm curious if this has been tried before?

 

[Hate da Bt]

Given that AAs alone won't address the full scope of Androgenetic Alopecia, I think autologous cell/organoid transplants are a safer, more effective, "one time" treatment as compared to bringing a hair loss SARM to market just for maintainence therapy via long term drug use.

You are clever, but the above statement is rather contradictory.
Hair loss happens gradually, so organ germ transplants can't be a "one time" thing.
Maintenance via drug administration without frightening side effects ain't a bad alternative, amigo.

 

[d3nt3dsh0v3l]

You are clever, but the above statement is rather contradictory.
Hair loss happens gradually, so organ germ transplants can't be a "one time" thing.
Maintenance via drug administration without frightening side effects ain't a bad alternative, amigo.

Actually, all of the autologous treatments aim at a one time solution; Tsuji has stated that there is a strategy for those who are in the process of balding - it involved depilation of dying hair and either replacement with the immune organoids or in some way conferring immunity to existing follicles, I imagine in a manner similar to that of rch-01.

Tsuji has definitely been asked what the plan is if hairloss has not yet stabilized.

Last I checked, Shiseido is also trialing various doses for rch-01s but not multiple treatments within their pivotal study; this implies that they too are aiming for a one-and-done treatment.

I think it makes sense. Taking a biopsy for each treatment and over multiple treatments makes the procedure more invasive than it needs to be and potentially affects the aesthetics of the outcome; storing the biopsies for a long time/years for each person is not a very viable strategy either.