BBC news story about propecia?

Mens Rea

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Perhaps.

Conventional wisdom with bodybuilders etc (and seemingly the likes of Crisler and Shippen) is as ive said above.

These data demonstrate that aromatase inhibition increases
serum bioavailable and total testosterone levels to the
youthful normal range in older men with mild hypogonadism.

Im just cherry picking of course but the devil does tend to lie in the detail. Ive had the misfortune to witnesses plenty of PFS sufferers not reacting to the AI's favourably at all (despite being textbook candidates) and the reason given is usually what i've explained. Older men with border hypogonadism is different than some of the real damaged guys who have had their bodies unnaturally shutdown. A HPA "restart" tends to be more complicated.


In summary, administration of a selective aromatase antagonist
lowers (24-h mean) concentrations of estradiol by
50% and elevates LH concentrations by 100% in young and
older healthy men
. Negative-feedback adaptations to partial
estrogen withdrawal differ significantly by age. In particular,
relative estrogen depletion in older, unlike young, men fails
to evoke (further) augmentation of the following: 1) incremental
LH peak amplitude and LH pulse area; 2) daily LH
pulse frequency; 3) LH secretory-pattern irregularity; and 4)
the molar ratio of testosterone to SHBG concentrations.
These
outcomes extend concepts of aging-associated regulatory defects
in the male by hypothalmopituitary gonadal axis to
include estrogen-dependent feedback control.

As you can see in the italics it seems to imply that older men are likely to have less increases in LH. I think that's what it's saying anyway. I think you can see how im appling this to hypongondal PFS sufferers.


SERM's blocks the estrogen receptors on the HPTA (manipulating the feedback mechanism), and thereby increases the testosterone production. In our case, it would raise testosterone and estrogen - which suppresses DHT further. .

You've missed the point somewhat Enden. The point of taking a SERM concurrently with an AI is that you are already surpressing the estrogen via the AI which gives you ample opportunity to raise T levels a little with little or no consequential increase in E2, thereby tipping the ratio further in T's favour. The very fact that the AI will be working behind the scenes, if anything, will promote more DHT synthesis as the extra testosterone will be inhibited from converting to e2 thanks to our friendly AI.

Experiments shows that an AI is enough to restore the endocrine system in case of estrogen suppression, and that the HPTA is in natural control all the time

As I said that is great for HPTA's that aren't already shutdown.


And also remember what Dr Shippin said about some patients requiring much higher T/E ratios "just to feel normal".
 

Ende

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Yes, you're correct about the mix, but I would rather use hCG in addition to Arimidex, than SERM's which is prohibited by the leaflet.

HPTA shutdown is a misterm. It's suppression. Once you take care of the hormone which is causing trouble, it should correct itself. "HPTA shutdown" comes from the body building community, where they have observed that large amounts of androgenic steroids will indeed suppress your HPTA to the point where it appears as shut down, but once the serum concentration drops below a certain point, your HPTA will secrete more GnRH. Since HPTA suppression over a prolonged period of time causes testicle atrophy, and muscles atrophies at low testosterone level, they use PCT to accelerate the recovery process. This is the only purpose; to accelerate the recovery process, so they may keep as much muscle as possible, after their cycle. I've read that certain steroids, like Deca for instance, is traceable in serum for up to 18 months after use. This means that it's able to cause suppression, which in some cases leads to secondary hypogonadism. This leaves them with TRT as the only option.
 

Ende

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Colin297 said:
In summary, administration of a selective aromatase antagonist
lowers (24-h mean) concentrations of estradiol by
50% and elevates LH concentrations by 100% in young and
older healthy men
. Negative-feedback adaptations to partial
estrogen withdrawal differ significantly by age. In particular,
relative estrogen depletion in older, unlike young, men fails
to evoke (further) augmentation of the following: 1) incremental
LH peak amplitude and LH pulse area; 2) daily LH
pulse frequency; 3) LH secretory-pattern irregularity; and 4)
the molar ratio of testosterone to SHBG concentrations.
These
outcomes extend concepts of aging-associated regulatory defects
in the male by hypothalmopituitary gonadal axis to
include estrogen-dependent feedback control.

As you can see in the italics it seems to imply that older men are likely to have less increases in LH. I think that's what it's saying anyway. I think you can see how im appling this to hypongondal PFS sufferers.
It's normal. Your natural testosterone poduction declines as you age.
 

Ende

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Colin297 said:
And also remember what Dr Shippin said about some patients requiring much higher T/E ratios "just to feel normal".
What's the source? I've respect for Dr. Shippen, that's why I'm asking. I've only seen one comment on the subject, where he stated something like that the window for the testosterone/estrogen ratio is very narrow. In other words he's implying how difficult it's to find, adjust and maintain that ratio. When it's DHT which naturally maintains that ratio, and he's dealing with DHT deficient patients, it's going to be a very difficult task.
 

Mens Rea

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Enden said:
Colin297 said:
In summary, administration of a selective aromatase antagonist
lowers (24-h mean) concentrations of estradiol by
50% and elevates LH concentrations by 100% in young and
older healthy men
. Negative-feedback adaptations to partial
estrogen withdrawal differ significantly by age. In particular,
relative estrogen depletion in older, unlike young, men fails
to evoke (further) augmentation of the following: 1) incremental
LH peak amplitude and LH pulse area; 2) daily LH
pulse frequency; 3) LH secretory-pattern irregularity; and 4)
the molar ratio of testosterone to SHBG concentrations.
These
outcomes extend concepts of aging-associated regulatory defects
in the male by hypothalmopituitary gonadal axis to
include estrogen-dependent feedback control.

As you can see in the italics it seems to imply that older men are likely to have less increases in LH. I think that's what it's saying anyway. I think you can see how im appling this to hypongondal PFS sufferers.
It's normal. Your natural testosterone poduction declines as you age.

Yep. But these guys who have similar levels to an old man will clearly want higher T levels and they may not respond like a healthy young male hence the need to more stimulation.
 

Mens Rea

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Enden said:
Colin297 said:
And also remember what Dr Shippin said about some patients requiring much higher T/E ratios "just to feel normal".
What's the source? I've respect for Dr. Shippen, that's why I'm asking. I've only seen one comment on the subject, where he stated something like that the window for the testosterone/estrogen ratio is very narrow. In other words he's implying how difficult it's to find, adjust and maintain that ratio. When it's DHT which naturally maintains that ratio, and he's dealing with DHT deficient patients, it's going to be a very difficult task.


I'll have a look later. Basically he says that in many of his patients they have required much higher levels of testosterone than normal just to feel normal again. This is why alot of people talk about androgen resistence and all that lark i guess.
 

Ende

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Look at the graphs. The younger ones reponded significantly better in terms of testosterone production than older men. Did you read what I wrote about "HPTA shutdown"?
 

Ende

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Colin297 said:
I'll have a look later. Basically he says that in many of his patients they have required much higher levels of testosterone than normal just to feel normal again. This is why alot of people talk about androgen resistence and all that lark i guess.
Yes, I've heard that. When you overdose testosterone, you'll get a lot of conversion which might affect the ratios between testosterone, DHT and estrogen. You could use testosterone in the same amount as body builders, but it won't make you better if your ratios are bad, and just gets worse.
 

Mens Rea

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Enden said:
Look at the graphs. The younger ones reponded significantly better in terms of testosterone production than older men. Did you read what I wrote about "HPTA shutdown"?

No?
 

Mens Rea

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Enden said:
Colin297 said:
I'll have a look later. Basically he says that in many of his patients they have required much higher levels of testosterone than normal just to feel normal again. This is why alot of people talk about androgen resistence and all that lark i guess.
Yes, I've heard that. When you overdose testosterone, you'll get a lot of conversion which might affect the ratios between testosterone, DHT and estrogen. You could use testosterone in the same amount as body builders, but it won't make you better if your ratios are bad, and just gets worse.

Yes the ratios are difficult but seemingly get even more difficult for these hypogondal PFS sufferers. This is why AI's alone are unlikely to resolve these issues for these people.
 

Ende

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Colin297 said:
Enden said:
Look at the graphs. The younger ones reponded significantly better in terms of testosterone production than older men. Did you read what I wrote about "HPTA shutdown"?

No?
Enden said:
HPTA shutdown is a misterm. It's suppression. Once you take care of the hormone which is causing trouble, it should correct itself. "HPTA shutdown" comes from the body building community, where they have observed that large amounts of androgenic steroids will indeed suppress your HPTA to the point where it appears as shut down, but once the serum concentration drops below a certain point, your HPTA will secrete more GnRH. Since HPTA suppression over a prolonged period of time causes testicle atrophy, and muscles atrophies at low testosterone level, they use PCT to accelerate the recovery process. This is the only purpose; to accelerate the recovery process, so they may keep as much muscle as possible, after their cycle. I've read that certain steroids, like Deca for instance, is traceable in serum for up to 18 months after use. This means that it's able to cause suppression, which in some cases leads to secondary hypogonadism. This leaves them with TRT as the only option.
 

Ende

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Colin297 said:
Yes the ratios are difficult but seemingly get even more difficult for these hypogondal PFS sufferers. This is why AI's alone are unlikely to resolve these issues for these people.
How so, if DHT deficiency is the problem?
 

Mens Rea

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Enden said:
Yes, you're correct about the mix, but I would rather use hCG in addition to Arimidex, than SERM's which is prohibited by the leaflet.

Yes but aromasin is a type I AI and is fine alongside SERM's...


HPTA shutdown is a misterm. It's suppression. Once you take care of the hormone which is causing trouble, it should correct itself. "HPTA shutdown" comes from the body building community, where they have observed that large amounts of androgenic steroids will indeed suppress your HPTA to the point where it appears as shut down, but once the serum concentration drops below a certain point, your HPTA will secrete more GnRH. Since HPTA suppression over a prolonged period of time causes testicle atrophy, and muscles atrophies at low testosterone level, they use PCT to accelerate the recovery process. This is the only purpose; to accelerate the recovery process, so they may keep as much muscle as possible, after their cycle. I've read that certain steroids, like Deca for instance, is traceable in serum for up to 18 months after use. This means that it's able to cause suppression, which in some cases leads to secondary hypogonadism. This leaves them with TRT as the only option.

That's rather simplistic Enden and the fact that some people's bodies fail to restart using the textbook treatments is a testament to this.

You talk about progressive problems over prolonged periods but people crash and never recover due to chain reactions that occur. You know this.
 

Mens Rea

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Enden said:
Colin297 said:
Yes the ratios are difficult but seemingly get even more difficult for these hypogondal PFS sufferers. This is why AI's alone are unlikely to resolve these issues for these people.
How so, if DHT deficiency is the problem?

Therein lies the mystery

You do realise many PFS sufferers have fine DHT levels, T/E levels etc? There is a potential malfunction in enzyme activity here, i.e. Testosterone and Dihydrotestosterone metobolism..

Distorted levels of 3-diol-G and TFT ratios etc (despite normal DHT levels!!) show this.

People may have fine DHT levels but are essentially pissing out much larger traces of DHT metabolites than they should be.....
 

Ende

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Colin297 said:
Enden said:
HPTA shutdown is a misterm. It's suppression. Once you take care of the hormone which is causing trouble, it should correct itself. "HPTA shutdown" comes from the body building community, where they have observed that large amounts of androgenic steroids will indeed suppress your HPTA to the point where it appears as shut down, but once the serum concentration drops below a certain point, your HPTA will secrete more GnRH. Since HPTA suppression over a prolonged period of time causes testicle atrophy, and muscles atrophies at low testosterone level, they use PCT to accelerate the recovery process. This is the only purpose; to accelerate the recovery process, so they may keep as much muscle as possible, after their cycle. I've read that certain steroids, like Deca for instance, is traceable in serum for up to 18 months after use. This means that it's able to cause suppression, which in some cases leads to secondary hypogonadism. This leaves them with TRT as the only option.

That's rather simplistic Enden and the fact that some people's bodies fail to restart using the textbook treatments is a testament to this.

You talk about progressive problems over prolonged periods but people crash and never recover due to chain reactions that occur. You know this.
Chain reactions are reversible. Some people fail to recover in this case, becuase most doctors doesn't know the significance of the testosterone/estrogen ratio, and that DHT is what maintains the ratio. What I wrote about HPTA suppression, is a fact. It's basicly how it works.
 

Ende

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Colin297 said:
Therein lies the mystery

You do realise many PFS sufferers have fine DHT levels, T/E levels etc? There is a potential malfunction in enzyme activity here, i.e. Testosterone and Dihydrotestosterone metobolism..

Distorted levels of 3-diol-G and TFT ratios etc (despite normal DHT levels!!) show this.

People may have fine DHT levels but are essentially pissing out much larger traces of DHT metabolites than they should be.....
Pissing out metabolites? If I'm not mistaken, traces indicates activity. More metabolites equals more activity. It doesn't matter if the DHT level appears normal. What does matter is the DHT/estrogen ratio. Ratios are more important than levels. 3-Adiol-G, isn't that some sort of depot for DHT? I think I read that somewhere. I haven't put much research into that, but I know that serum tests come back low. Way too low. It makes sense if DHT is under suppression.
 

TEDDYRUXPIN

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Not surprised this has hit this website.

Please remember, no matter what drug (medicine) you take, someone will have side effects.

So people who have side effects taking antibiotics? Should these drugs be banned? They save so many people?

I've been on this drug up to 9 years, and I mean propecia merck, not generic and it has worked for me without any side effects.

No... my penis has not shrunk, I don't suffer from impotence, and no I have not mutated in some way or form. And no... I don't have DD breasts.
 

Ende

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TEDDYRUXPIN said:
Please remember, no matter what drug (medicine) you take, someone will have side effects.
Yes, but in this case, some people get a severe health condition which wasn't reported during the drug trial, and the worse part is, all hormone levels appear normal according to standards - which in most cases means that you won't get help. In cases where they can prove secondary hypogonadism with baseline values - and therefore provide treatment, they're struggling to reverse the condition, and most professionals doesn't know why. People need to be aware of this, so they can make a choice based on the true risk. I'm not for banning Propecia, even though I'm one of those who're suffering.
 

Mens Rea

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Enden said:
Colin297 said:
Therein lies the mystery

You do realise many PFS sufferers have fine DHT levels, T/E levels etc? There is a potential malfunction in enzyme activity here, i.e. Testosterone and Dihydrotestosterone metobolism..

Distorted levels of 3-diol-G and TFT ratios etc (despite normal DHT levels!!) show this.

People may have fine DHT levels but are essentially pissing out much larger traces of DHT metabolites than they should be.....

Pissing out metabolites? If I'm not mistaken, traces indicates activity. More metabolites equals more activity. It doesn't matter if the DHT level appears normal. What does matter is the DHT/estrogen ratio. Ratios are more important than levels. 3-Adiol-G, isn't that some sort of depot for DHT? I think I read that somewhere. I haven't put much research into that, but I know that serum tests come back low. Way too low. It makes sense if DHT is under suppression.


DHT converts into 3-adiol-G.

Yeah some people have overactive metabolism of T or DHT. Some have low. Its crazy and if this is induced by finasteride finding ratios can be a tough task (if possible..)
 
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