I have always had great results with low doses. Anytime I tried a higher dose, such as 1000mgs of test a week, the only thing that increased were the side effects.
What a lot of people don’t realize is that at a TRT dosage FSH and LH remian in the normal range. Shut down is minimal.
[quote]bushidobadboy wrote:
pickapeck wrote:
What a lot of people don’t realize is that at a TRT dosage FSH and LH remian in the normal range. Shut down is minimal.
I’m afraid you will need to provide some proof, since this goes against basic physiology. Assuming the TRT dose is enough to cause significant improvement in symptoms, it must be high enough to be ‘seen’ at the hypothalamus either as excess T or increased E. This will result in a reduction of the ‘control’ hormones, i.e. LH and FSH.
If you add in a TRT dose of test, you will experience shutdown. This has been proven in the real world time and time again.
Bushy[/quote]
In testicular failure testosterone is low and LH is high. Endo’s use the LH value, among other parameters, to adjust dosage. Hypothalmic and pituitary hypogonadism are different stories and are more likely to be congenital or result from accident or tumor.
Testicular failure is the one we are commonly referring to here. This does not go against basic physiology. In fact, a good endo uses these basic principles to “adjust” treatment. Naturally, if dosage regimen is too high LH is shut down.
If what should be there and is not is “replaced” the system is in equilibrium and LH levels (and FSH) are in the normal range. A good endocrinologist does not wish to deliver too much hormone as polycythemia, hyperlipidemia, breast tenderness, gynecomastia, increased hemaocrit… and so on will manifest. What the Bros refer to YRT is not
TRT.
[quote]bushidobadboy wrote:
pickapeck wrote:
bushidobadboy wrote:
pickapeck wrote:
What a lot of people don’t realize is that at a TRT dosage FSH and LH remian in the normal range. Shut down is minimal.
I’m afraid you will need to provide some proof, since this goes against basic physiology. Assuming the TRT dose is enough to cause significant improvement in symptoms, it must be high enough to be ‘seen’ at the hypothalamus either as excess T or increased E. This will result in a reduction of the ‘control’ hormones, i.e. LH and FSH.
If you add in a TRT dose of test, you will experience shutdown. This has been proven in the real world time and time again.
Bushy
In testicular failure testosterone is low and LH is high. Endo’s use the LH value, among other parameters, to adjust dosage. Hypothalmic and pituitary hypogonadism are different stories and are more likely to be congenital or result from accident or tumor. Testicular failure is the one we are commonly referring to here. This does not go against basic physiology.
In fact, a good endo uses these basic principles to “adjust” treatment. Naturally, if dosage regimen is too high LH is shut down. If what should be there and is not is “replaced” the system is in equilibrium and LH levels (and FSH) are in the normal range.
A good endocrinologist does not wish to deliver too much hormone as polycythemia, hyperlipidemia, breast tenderness, gynecomastia, increased hemaocrit… and so on will manifest. What the Bros refer to YRT is not
TRT.
Well OK I see your point that in primary hypogonadism, i.e. where everything BUT the testes is (or seems to be) working, it may be possible to administer T to a point whereby LH and FSH are not reduced (however, that requires a ‘good’ endo - not something I have seen much of over in the over 35 forum…).
But what would be the point?
The testes don’t ‘work’. They are never going to work. It doesn’t matter what you do to LH and FSH since they have no part to play any more.
So to qualify, your statement that “at a TRT dosage FSH and LH remian in the normal range” becomes moot. Even if you disregard the fact that most TRT doses are just given without thought to feedback assesment of LH and FSH, and are just 100 or 200mg per week (picked at random, most of the time), a healthy HPTA will probably recognise anything over about 25mg/wk as ‘excessive’ and will compensate by reducing LH and FSH.
So there may be some endos who titer the TRT dose so as not to affect LH or FSH, but they would be wasting their time, since it matters not what happens to the LH and FSH of someone who is going to use exo T for the rest of their life. All that matters is to bring T levels up to a level wherby the patient feels great, without creating unwanted sides.
Bushy[/quote]
Most of the time I think you are on the right track but this time I think you are off the mark. Using a bad endocrinologist as the standard model and justification does not inspire confidence.
[quote]bushidobadboy wrote:
pickapeck wrote:
bushidobadboy wrote:
pickapeck wrote:
bushidobadboy wrote:
pickapeck wrote:
What a lot of people don’t realize is that at a TRT dosage FSH and LH remian in the normal range. Shut down is minimal.
I’m afraid you will need to provide some proof, since this goes against basic physiology. Assuming the TRT dose is enough to cause significant improvement in symptoms, it must be high enough to be ‘seen’ at the hypothalamus either as excess T or increased E. This will result in a reduction of the ‘control’ hormones, i.e. LH and FSH.
If you add in a TRT dose of test, you will experience shutdown. This has been proven in the real world time and time again.
Bushy
In testicular failure testosterone is low and LH is high. Endo’s use the LH value, among other parameters, to adjust dosage. Hypothalmic and pituitary hypogonadism are different stories and are more likely to be congenital or result from accident or tumor. Testicular failure is the one we are commonly referring to here. This does not go against basic physiology.
In fact, a good endo uses these basic principles to “adjust” treatment. Naturally, if dosage regimen is too high LH is shut down. If what should be there and is not is “replaced” the system is in equilibrium and LH levels (and FSH) are in the normal range.
A good endocrinologist does not wish to deliver too much hormone as polycythemia, hyperlipidemia, breast tenderness, gynecomastia, increased hemaocrit… and so on will manifest. What the Bros refer to YRT is not
TRT.
Well OK I see your point that in primary hypogonadism, i.e. where everything BUT the testes is (or seems to be) working, it may be possible to administer T to a point whereby LH and FSH are not reduced (however, that requires a ‘good’ endo - not something I have seen much of over in the over 35 forum…).
But what would be the point?
The testes don’t ‘work’. They are never going to work. It doesn’t matter what you do to LH and FSH since they have no part to play any more.
So to qualify, your statement that “at a TRT dosage FSH and LH remian in the normal range” becomes moot. Even if you disregard the fact that most TRT doses are just given without thought to feedback assesment of LH and FSH, and are just 100 or 200mg per week (picked at random, most of the time), a healthy HPTA will probably recognise anything over about 25mg/wk as ‘excessive’ and will compensate by reducing LH and FSH.
So there may be some endos who titer the TRT dose so as not to affect LH or FSH, but they would be wasting their time, since it matters not what happens to the LH and FSH of someone who is going to use exo T for the rest of their life. All that matters is to bring T levels up to a level wherby the patient feels great, without creating unwanted sides.
Bushy
Most of the time I think you are on the right track but this time I think you are off the mark. Using a bad endocrinologist as the standard model and justification does not inspire confidence.
LOL. I’m not using bad endos as justification for poor T dosing. Rather, I see no point in titering T to precise amounts that don’t affect LH and FSH.
What would be the point (benefit to patient)? Seriously, I may be missing something here, but I don’t see how LH and FSH are in any way relevant to the patient with hypogonadism, either primary (testes) secondary (pituitary) or tertiary (hypothalamus).
If they have normal ‘control’ hormones (LH and FSH) but are lacking in T due to malfunctioning testes, then it might be ‘nice’ to preserve their natural LH and FSH levels, from some paradigm of medical science. But it’s gonna cost a lot in time and tests, and is completely non-beneficial to the patient. Except that if they stop TRT, they should still have pre-TRT LH/FSH levels - fat lot of good it did them before.
If the patient was/is secondary/tertiary hypogonadic. then their LH and /or FSH will be depressed anyway, so ‘preserving’ them is not waranted, however you look at it.
Seriously man, I think you are on the right track most of the time, so I hope we can reach a satisfactory conclusion here. I think you might be adhering to some golden theory of TRT and how it can minimally affect the HPTA, whilst I take a more pragmatic approach in this.
In other words: Sure it can be done, but what possible benefit could there be to it? If you can provide me with a valid reson for putting the patient through all that testing just to preserve LH/FSH then perhaps I will see the light 
Regards,
Bushy[/quote]
Maintenance of in range FSH and LH levels will make side effects such as polycythemia, gynecomastia, hypertension, prostate hyperplasia, acne etc. much less probable. Also, potency will be preserved. These are ample reasons to monitor LH/FSH. We are talking testicular failure here as made clear in my second post.
[quote]bushidobadboy wrote:
pickapeck wrote:
bushidobadboy wrote:
pickapeck wrote:
bushidobadboy wrote:
pickapeck wrote:
bushidobadboy wrote:
pickapeck wrote:
What a lot of people don’t realize is that at a TRT dosage FSH and LH remian in the normal range. Shut down is minimal.
I’m afraid you will need to provide some proof, since this goes against basic physiology. Assuming the TRT dose is enough to cause significant improvement in symptoms, it must be high enough to be ‘seen’ at the hypothalamus either as excess T or increased E. This will result in a reduction of the ‘control’ hormones, i.e. LH and FSH.
If you add in a TRT dose of test, you will experience shutdown. This has been proven in the real world time and time again.
Bushy
In testicular failure testosterone is low and LH is high. Endo’s use the LH value, among other parameters, to adjust dosage. Hypothalmic and pituitary hypogonadism are different stories and are more likely to be congenital or result from accident or tumor. Testicular failure is the one we are commonly referring to here. This does not go against basic physiology.
In fact, a good endo uses these basic principles to “adjust” treatment. Naturally, if dosage regimen is too high LH is shut down. If what should be there and is not is “replaced” the system is in equilibrium and LH levels (and FSH) are in the normal range.
A good endocrinologist does not wish to deliver too much hormone as polycythemia, hyperlipidemia, breast tenderness, gynecomastia, increased hemaocrit… and so on will manifest. What the Bros refer to YRT is not
TRT.
Well OK I see your point that in primary hypogonadism, i.e. where everything BUT the testes is (or seems to be) working, it may be possible to administer T to a point whereby LH and FSH are not reduced (however, that requires a ‘good’ endo - not something I have seen much of over in the over 35 forum…).
But what would be the point?
The testes don’t ‘work’. They are never going to work. It doesn’t matter what you do to LH and FSH since they have no part to play any more.
So to qualify, your statement that “at a TRT dosage FSH and LH remian in the normal range” becomes moot. Even if you disregard the fact that most TRT doses are just given without thought to feedback assesment of LH and FSH, and are just 100 or 200mg per week (picked at random, most of the time), a healthy HPTA will probably recognise anything over about 25mg/wk as ‘excessive’ and will compensate by reducing LH and FSH.
So there may be some endos who titer the TRT dose so as not to affect LH or FSH, but they would be wasting their time, since it matters not what happens to the LH and FSH of someone who is going to use exo T for the rest of their life. All that matters is to bring T levels up to a level wherby the patient feels great, without creating unwanted sides.
Bushy
Most of the time I think you are on the right track but this time I think you are off the mark. Using a bad endocrinologist as the standard model and justification does not inspire confidence.
LOL. I’m not using bad endos as justification for poor T dosing. Rather, I see no point in titering T to precise amounts that don’t affect LH and FSH.
What would be the point (benefit to patient)? Seriously, I may be missing something here, but I don’t see how LH and FSH are in any way relevant to the patient with hypogonadism, either primary (testes) secondary (pituitary) or tertiary (hypothalamus).
If they have normal ‘control’ hormones (LH and FSH) but are lacking in T due to malfunctioning testes, then it might be ‘nice’ to preserve their natural LH and FSH levels, from some paradigm of medical science. But it’s gonna cost a lot in time and tests, and is completely non-beneficial to the patient. Except that if they stop TRT, they should still have pre-TRT LH/FSH levels - fat lot of good it did them before.
If the patient was/is secondary/tertiary hypogonadic. then their LH and /or FSH will be depressed anyway, so ‘preserving’ them is not waranted, however you look at it.
Seriously man, I think you are on the right track most of the time, so I hope we can reach a satisfactory conclusion here. I think you might be adhering to some golden theory of TRT and how it can minimally affect the HPTA, whilst I take a more pragmatic approach in this.
In other words: Sure it can be done, but what possible benefit could there be to it? If you can provide me with a valid reson for putting the patient through all that testing just to preserve LH/FSH then perhaps I will see the light
Regards,
Bushy
Maintenance of in range FSH and LH levels will make side effects such as polycythemia, gynecomastia, hypertension, prostate hyperplasia, acne etc. much less probable. Also, potency will be preserved. These are ample reasons to monitor LH/FSH. We are talking testicular failure here as made clear in my second post.
Yeah they might do that, I suppose, but I’m still not convinced that just monitoring T and keeping it at a high mormal wouldn’t be just as effective and safe. Also, easier to get to grips with, for the TRT prescribing non-endos out there.
Personally, I am in favour of treating the symptoms in this case (since the cause can’t be rectified). Treating ‘ranges’ only is often what gets valid TRT candidates refused treatment, because their ‘low normal’ radings should be more than adequate (according to the doc).
When you say “potency will be preserved” are you referring to fertility?
Bushy[/quote]
That’s the idea. Look into it. If I have some time later I will post some references. But you are a grad student so if you are curious enough you know how to find the references.
[quote]pickapeck wrote:
Maintenance of in range FSH and LH levels will make side effects such as polycythemia, gynecomastia, hypertension, prostate hyperplasia, acne etc. much less probable. Also, potency will be preserved. These are ample reasons to monitor LH/FSH. We are talking testicular failure here as made clear in my second post.[/quote]
When I was on HCG, my RBC increased 4 points, so in my single experience it definitely didn’t prevent polycythemia. I matched the top of the range. That’s a sample size of one though which doesn’t count for much.
Since HCG increases testosterone, and testosterone increases RBC levels I don’t see how HCG could protect against polycythemia.
HCG is known for increasing estradiol levels so I don’t see how it would protect against gyno either. My estradiol levels doubled on 100IU per day.
Increased estradiol from HCG can cause hypertension as well as prostrate hypertrophy.
Since acne is more a function of cortisol and DHT I would think HCG would be neutral in this case, unless there is some other mechanism I’m missing.
If you have the research backing your statements I would like to see it. I’m not as familiar with HMG’s effects other that it being a FSH agonist. I can’t see it would reverse all these side effects.
[quote]Dopamineloveaffa wrote:
pickapeck wrote:
Maintenance of in range FSH and LH levels will make side effects such as polycythemia, gynecomastia, hypertension, prostate hyperplasia, acne etc. much less probable. Also, potency will be preserved. These are ample reasons to monitor LH/FSH. We are talking testicular failure here as made clear in my second post.
When I was on HCG, my RBC increased 4 points, so in my single experience it definitely didn’t prevent polycythemia. I matched the top of the range. That’s a sample size of one though which doesn’t count for much.
Since HCG increases testosterone, and testosterone increases RBC levels I don’t see how HCG could protect against polycythemia.
HCG is known for increasing estradiol levels so I don’t see how it would protect against gyno either. My estradiol levels doubled on 100IU per day.
Increased estradiol from HCG can cause hypertension as well as prostrate hypertrophy.
Since acne is more a function of cortisol and DHT I would think HCG would be neutral in this case, unless there is some other mechanism I’m missing.
If you have the research backing your statements I would like to see it. I’m not as familiar with HMG’s effects other that it being a FSH agonist. I can’t see it would reverse all these side effects.[/quote]
I am not talking about HCG. I am talking about a good endo titrating TRT test dosage in testicular failure patients to bring FSH and LH into normal range. You are out in left fiend with HCG.
[quote]pickapeck wrote:
I am not talking about HCG. I am talking about a good endo titrating TRT test dosage in testicular failure patients to bring FSH and LH into normal range. You are out in left fiend with HCG.[/quote]
I reread all your posts. I must’ve misread some of it.
So what you’re saying is with people that are Primary, you would titrate your dose to what the testes would be capable of if they were healthy I’m imagining.
An example being; based on your LH if your testes were healthy you would have a blood level of 800ng/dl. If you titrate to that dose and not higher, your LH and FSH numbers wouldn’t go down.
I would think your body’s negative feedback loop would treat a steady state testosterone level from injections differantly as opposed to natural pulses. The steady state levels would cause more suppression.
I understand where you’re coming from but all the bloodwork I’ve seen from all the popular HRT forums, everyone’s LH and FSH levels approach 0 whether they are secondary or primary, with IM’s or gels/creams. Your idea may work in theory but I’ve never seen it in practice.
Prove me wrong though. My mind is open, and I’m willing to learn if there is some data or at least anecdotal evidence that supports it. It’s possible it may have slipped through the cracks during my researching.
I’m a bit confused about this protocol. Are we saying that a very low weekly dose of testosterone would not suppress natural production, but instead be added on to what the body is naturally putting out?
I’m not very knowledgeable, but wouldn’t some sort of feedback mechanism “see” this exogenous test and correspondingly decrease natural production? Not necessarily shut down, but at least decrease output to match the body’s natural level, leaving no net gain? To qualify I’m talking about someone healthy without any kind of failure.
OK, After reading the AACE Hypogonadism Guidelines, Endocr Pract. 2002;8(No. 6)I can not find reference to the use of FSH and LH values in primary hypogonadism treatment. My original assertion was based on a conversation with an endocrinologist, who may have been among the minority in his use of these values for treatment of certain cases.
[quote]BIGZEUS wrote:
I’m a bit confused about this protocol. Are we saying that a very low weekly dose of testosterone would not suppress natural production, but instead be added on to what the body is naturally putting out?
I’m not very knowledgeable, but wouldn’t some sort of feedback mechanism “see” this exogenous test and correspondingly decrease natural production? Not necessarily shut down, but at least decrease output to match the body’s natural level, leaving no net gain? To qualify I’m talking about someone healthy without any kind of failure. [/quote]
Feedback mechanism definitely comes into play depending upon the quantity of exogenouse test put into the body. However, ALL feedback control systems, be they mechanical, electrical, chemical, AND biological have tolerances built in. This means there is a level of exogenous test that can be added to the system without disrupting the natural feedback control system. If you exceed this tolerance, then feedback comes into play and a reduction in LH occurs. The trick and premise to the protocol is to determine what that tolerance level is.
This tolerance level will be an individual level; no two people will have exactly the same tolerance levels, and I strongly believe that if a study was set up the researcher would find that the range of this tolerance will be a statistical wide band.
I believe all of our natural testosterone producing control system is operating at a level that is below what it could run at. I believe if each of us can increase our test in our system to a level that our individual feedback control system will tolerate there WILL be positive benefits.
[quote]buffd_samurai wrote:
BIGZEUS wrote:
I’m a bit confused about this protocol. Are we saying that a very low weekly dose of testosterone would not suppress natural production, but instead be added on to what the body is naturally putting out?
I’m not very knowledgeable, but wouldn’t some sort of feedback mechanism “see” this exogenous test and correspondingly decrease natural production? Not necessarily shut down, but at least decrease output to match the body’s natural level, leaving no net gain? To qualify I’m talking about someone healthy without any kind of failure.
Feedback mechanism definitely comes into play depending upon the quantity of exogenouse test put into the body. However, ALL feedback control systems, be they mechanical, electrical, chemical, AND biological have tolerances built in.
This means there is a level of exogenous test that can be added to the system without disrupting the natural feedback control system. If you exceed this tolerance, then feedback comes into play and a reduction in LH occurs. The trick and premise to the protocol is to determine what that tolerance level is.
This tolerance level will be an individual level; no two people will have exactly the same tolerance levels, and I strongly believe that if a study was set up the researcher would find that the range of this tolerance will be a statistical wide band.
I believe all of our natural testosterone producing control system is operating at a level that is below what it could run at. I believe if each of us can increase our test in our system to a level that our individual feedback control system will tolerate there WILL be positive benefits.
[/quote]
Great post!
[quote]buffd_samurai wrote:
Feedback mechanism definitely comes into play depending upon the quantity of exogenouse test put into the body. However, ALL feedback control systems, be they mechanical, electrical, chemical, AND biological have tolerances built in. This means there is a level of exogenous test that can be added to the system without disrupting the natural feedback control system. If you exceed this tolerance, then feedback comes into play and a reduction in LH occurs. The trick and premise to the protocol is to determine what that tolerance level is.
This tolerance level will be an individual level; no two people will have exactly the same tolerance levels, and I strongly believe that if a study was set up the researcher would find that the range of this tolerance will be a statistical wide band.
I believe all of our natural testosterone producing control system is operating at a level that is below what it could run at. I believe if each of us can increase our test in our system to a level that our individual feedback control system will tolerate there WILL be positive benefits.
[/quote]
Good Post. I think allot of people that are used to ‘normal’ AAS cycles don’t understand, or want to understand this. And as someone previously said, most Body-builder’s today just want the fastest results possible within the boundary of sides they are willing to put up with.
Hello by the way, this is my first post 