Trt, hair transplants and hair loss medications.

[Grouse]

40 minutes ago, Etownone said:

Whoa...    THANKS Melvin 

I gotta look up all this stuff.    I've been Googling for months, trying to find a different approach.   Not sure what telogen effluvium,  CosmeRNA, or Pyrilutamide is,  But I'm going to look into it and schedule a visit with an endocrinologist.    Never thought about that.  An endocrinologist can do a hormone check up and maybe help me.   Thx.   

I'm a little nervous of stopping finesteride compeltely and doing only dutasteride cause I heard some people had bad experiences.   I think I'll bump it up to 3 times a week and finesteride the other 4 days.  

Do you have any side effects on your current stack? May also be worth looking into CB-03-01 and RU58841 if you're open to experimental treatments. Do your own research of course

[Etownone]

45 minutes ago, Grouse said:

Do you have any side effects on your current stack? May also be worth looking into CB-03-01 and RU58841 if you're open to experimental treatments. Do your own research of course

No sides,   but I'm also on trt so I'm sure that helps.   

I've been back to using RU58841 for the past month.    I was debating between that and cb-03-01, but I went with the RU.  

Now I have to look back nto Pyrilutamide.   I forgot all about until Melvin mentioned it.  It was still in clinical trials when I looked into it 2 years ago.  I would try that if I can get a good reliable source..  

And first I heard of CosmeRNA...  I need to lokj more into that.   

[BackFromTheBrink]

15 hours ago, GoliGoliGoli said:

 Of course absence of evidence is not evidence of absence, but when it comes to hair loss you should stay away from definitive claims like "This is not how it works". There is much we don't know, and at best you're just making an educated guess by claiming some genetic dissimilarity. 

 

It sounded like what you were saying was more DHT was carried in the blood in areas that are affected MPB.

I think it's easier to disprove that. The scalp is highly vascularised. There isn't less blood carried to the MPB areas. Similarly, DHT is carried in the blood. Not sure how you were suggesting different concentrations could be carried in different parts of the body, and in this case, areas of the scalp that are in close proximity to each other?

Edited August 18, 2023 by BackFromTheBrink

[ljpcarrera]

I tried TRT for a year, it completely whacked out my T levels at 150mg a week. Very odd my blood tests were all over the place.

Look into Eclomphenine, it’s essentially a compounded version of Clomid. Raises T naturally, so far my T levels went up from 425 to 910 in a little over a month. Free T jumped 10 points as well. No side effects to report yet. Taking a pill everyday is so much easier than injections. Good luck

[GoliGoliGoli]

10 hours ago, BackFromTheBrink said:

It sounded like what you were saying was more DHT was carried in the blood in areas that are affected MPB.

I think it's easier to disprove that. The scalp is highly vascularised. There isn't less blood carried to the MPB areas. Similarly, DHT is carried in the blood. Not sure how you were suggesting different concentrations could be carried in different parts of the body, and in this case, areas of the scalp that are in close proximity to each other?

It's possible that areas that are balding have higher concentrations of DHT. I haven't looked into it and I don't know if anyone else has either. That wasn't my point though, I'm just speculating. My only point was that 100% donor dominance doesn't seem to be true. Why that is remains a mystery.  

But yes, it's totally possible that areas that are inches apart in the scalp would have vastly different concentrations of DHT. 

[BackFromTheBrink]

30 minutes ago, GoliGoliGoli said:

It's possible that areas that are balding have higher concentrations of DHT. 

But yes, it's totally possible that areas that are inches apart in the scalp would have vastly different concentrations of DHT. 

Interesting. Could you explain how that could be the case?

[GoliGoliGoli]

20 minutes ago, BackFromTheBrink said:

Interesting. Could you explain how that could be the case?

Your body has ways of transporting molecules to very specific areas. Just because something is transported by blood doesn't mean it is going to all your tissue in the same concentration. 

[BackFromTheBrink]

1 hour ago, GoliGoliGoli said:

Your body has ways of transporting molecules to very specific areas. Just because something is transported by blood doesn't mean it is going to all your tissue in the same concentration. 

You must have studied more biology than I did (and my Dr partner sat next to me).

I thought DHT bound to the SHBG protein and the target organs have receptors which control whether or not they're 'consumed'. For receptive organs, constriction of veins control the amount of exposure. Vascularity is high in the scalp, with the veins not having significantly different diameters between the side, back and top of the head.

Am I understanding the basics, and if so, what mechanism controls the amount of DHT that follicles are exposed to?

[GoliGoliGoli]

12 minutes ago, BackFromTheBrink said:

You must have studied more biology than I did (and my Dr partner sat next to me).

I thought DHT bound to the SHBG protein and the target organs have receptors which control whether or not they're 'consumed'. For receptive organs, constriction of veins control the amount of exposure. Vascularity is high in the scalp, with the veins not having significantly different diameters between the side, back and top of the head.

Am I understanding the basics, and if so, what mechanism controls the amount of DHT that follicles are exposed to?

Think of it this way: DHT is converted from T via the 5AR enzyme. It's well known that the 5AR enzyme is more active in some tissue of the body than others. So if the top of the scalp has more 5AR than the donor, the hair on the scalp is going to be exposed to more DHT regardless of how much is circulating in the blood. Testosterone circulates in the blood at MUCH higher concentrations than DHT, so whether a specific tissue is exposed to DHT is more about the 5AR enzyme concentration in the tissue than the DHT concentration in the blood. Enzymes themselves really do not circulate in the blood, they stay put in the tissue. 

Furthermore, DHT by itself inside your cell does basically nothing. It's only when it binds and combines to the androgen receptor inside the cytoplasm and then moves into the cell nucleus that it causes the effects we associate with DHT (Muscle growth, body hair growth, scalp hair loss). So if the cytoplasm of the cells on the top of your scalp have much more androgen receptors than the cytoplasm of the cells in your donor, the hair on the scalp is going to be exposed to more of the effects of the combined DHT/AR complex. 

You'll notice in my post I first said "DHT activity" not "DHT". Then I got lazy and just started saying DHT as kind of a short hand, but what I'm really referring to is the DHT/AR complex because for this discussion its all that really matters. DHT is lipid-soluble so it freely moves in and out of the cell based on a concentration gradient (Just like with water and osmosis), and it's only when it combines with the AR and turns into the DHT/AR complex that it works it's magic. So you can have a huge amount of DHT in your blood, but if you don't have the AR it's not going to do anything to the hair follicle. 

My undergrad degree is in microbiology, but that really doesn't matter much in terms of understanding this stuff on a deeper level. I'm not a huge fan of credentialism, and most medical professionals have a very rudimentary understanding of molecular biology. 

 

[GoliGoliGoli]

1 minute ago, GoliGoliGoli said:

Think of it this way: DHT is converted from T via the 5AR enzyme. It's well known that the 5AR enzyme is more active in some tissue of the body than others. So if the top of the scalp has more 5AR than the donor, the hair on the scalp is going to be exposed to more DHT regardless of how much is circulating in the blood. Testosterone circulates in the blood at MUCH higher concentrations than DHT, so whether a specific tissue is exposed to DHT is more about the 5AR enzyme concentration in the tissue than the DHT concentration in the blood. Enzymes themselves really do not circulate in the blood, they stay put in the tissue. 

Furthermore, DHT by itself inside your cell does basically nothing. It's only when it binds and combines to the androgen receptor inside the cytoplasm and then moves into the cell nucleus that it causes the effects we associate with DHT (Muscle growth, body hair growth, scalp hair loss). So if the cytoplasm of the cells on the top of your scalp have much more androgen receptors than the cytoplasm of the cells in your donor, the hair on the scalp is going to be exposed to more of the effects of the combined DHT/AR complex. 

You'll notice in my post I first said "DHT activity" not "DHT". Then I got lazy and just started saying DHT as kind of a short hand, but what I'm really referring to is the DHT/AR complex because for this discussion its all that really matters. DHT is lipid-soluble so it freely moves in and out of the cell based on a concentration gradient (Just like with water and osmosis), and it's only when it combines with the AR and turns into the DHT/AR complex that it works it's magic. So you can have a huge amount of DHT in your blood, but if you don't have the AR it's not going to do anything to the hair follicle. 

My undergrad degree is in microbiology, but that really doesn't matter much in terms of understanding this stuff on a deeper level. I'm not a huge fan of credentialism, and most medical professionals have a very rudimentary understanding of molecular biology. 

 

I tend to be long winded so here is the TLDR: Your donor tissue and scalp tissue can have the same amounts of DHT circulating in the blood supply, but that means nothing in regards to the levels of balding in each area. What matters is the concentrations of 5AR in each area, and the concentrations of androgen receptors in each area. 

[BackFromTheBrink]

The very long winded explanation of lots of irrelevant information seems to get back to the original point you were arguing against.

It's the receptors (or lack thereof) in the hair follicles that impact their succeptibility, not differing levels of DHT across the scalp.

[GoliGoliGoli]

It seems you are illiterate both in the classical sense and also in the scientific sense, but I will still try my best to explain my original point to you in another very long winded post. The TLDR is that you're misunderstanding what I'm saying by focusing on the follicle, whereas I'm talking about the entire scalp region and how it's health is impacted by DHT (and other factors not including DHT), and how the health of this entire scalp region (and not just the follicle) affects ones ability to permanently take hairs from the donor and plant them in the recipient. 

You'll notice how in the first very long winded post I use the world "scalp" 5 times and the word "tissue" 4 times, but used the word "follicle" only once. There is a reason for this as I'm very careful with my words. Hair health is directly influenced by the tissue the follicle is planted into and by using "scalp" and "tissue" I'm including both the follicle and the surrounding scalp tissue, whereas if I use the word follicle alone like you did that changes the entire point. The exact mechanism by which DHT causes hair miniaturization is completely unknown and at best people have different theories, but it seems  that it's a combination of factors going on that affect both the hair follicle itself and the scalp tissue the follicle sits in. As I said there are competing theories on why DHT causes hair loss. There is the theory that DHT could be causing genetic changes in the hair follicle that cause it to shrink (This is very odd though given it has opposite effect in all other hair follicles in humans and all other mammals); there is the theory that DHT could be causing inflammation and slowly damaging the area; there is the theory that DHT is negatively impacting blood flow to the area. No one really knows and it's likely a combination of many different things, some of which have nothing to even do with DHT. 

So to circle aaaaall the way back to my original point: If you agree that the health of the scalp tissue plays a role in  hair health, then it stands to reason that if you take hairs from the back of the scalp (donor) and put them on the top of the scalp (recipient), the newly transplanted hairs could fall victim to the same factors in the scalp that killed off the original inhabitants. They may be of "hardier" stock than the original inhabitants, but it doesn't mean they're invincible either. Basically, maybe "donor dominance" is 80% true but 20% false. 

Do you understand what I'm saying now? Were you even familiar with the term donor dominance before reading my posts? If not you're welcome for the free education. Wish your "Dr partner" (Whatever that means) well for me. 

 

 

Edited August 18, 2023 by GoliGoliGoli

[mustang]

On 8/17/2023 at 5:26 PM, Etownone said:

Pretty similar to mine.   Expect no top prog. 

I dropped the test down to 120 last week,   I hope that makes a difference.    I'm pretty sure my continued hair loss is related to the high test.   

 So why did you stop?  So many benifits being on trt.   

use seventeen alfa estradiol with topical fin or dut. That will prevent further hair loss from Test, not DHT.

[Etownone]

9 hours ago, mustang said:

use seventeen alfa estradiol with topical fin or dut. That will prevent further hair loss from Test, not DHT.

Never heard of alfa estradiol.  

Thx Mustang...  Will look into it.    🫶

[mustang]

It basically stimulates aromatase in your scalp so it converts your free test to a weak form of estrogen and also acts as a local 5AR inhibitor.

People who lose ground on dutasteride and have miniaturization despite having almost zero DHT have this issue. It's almost always resolved by addressing free testosterone 

There is a reason it's called androgenic alopecia and not DHT alopecia.

[Etownone]

21 hours ago, mustang said:

It basically stimulates aromatase in your scalp so it converts your free test to a weak form of estrogen and also acts as a local 5AR inhibitor.

People who lose ground on dutasteride and have miniaturization despite having almost zero DHT have this issue. It's almost always resolved by addressing free testosterone 

There is a reason it's called androgenic alopecia and not DHT alopecia.

I'm looking into 17 alpha-estradiol,    I can't find much info.   Lots of trans women take it from what I can find. 

Would my urologist prescribe this,  or is this something on the black market?    Is it Pills or some topical solution?  

 

I dont know how you come across this stuff Mustang but you are on another level with your info.   

[Etownone]

So I found a very very informative video.   

 

It seems lowering my dosage of trt to 120mg a week has made a significant change for the better for me.   

 

 

 

[Portugal]

On 8/18/2023 at 2:19 AM, Etownone said:

Whoa...    THANKS Melvin 

I gotta look up all this stuff.    I've been Googling for months, trying to find a different approach.   Not sure what telogen effluvium,  CosmeRNA, or Pyrilutamide is,  But I'm going to look into it and schedule a visit with an endocrinologist.    Never thought about that.  An endocrinologist can do a hormone check up and maybe help me.   Thx.   

I'm a little nervous of stopping finesteride compeltely and doing only dutasteride cause I heard some people had bad experiences.   I think I'll bump it up to 3 times a week and finesteride the other 4 days.  

How are you getting on now? What have you changed since these messages? Have you had thyroid bloods done? Under active thyroid can cause hairloss