Synergy Pro-active recovery therapy (PART)!!

[Dwight Schrute]

Bobo, Im sure you have read some of the articles written by the so called "guru's" pertaining to the dbol theory I mentioned as well as the theories I mentioned behind it. If their methodology is completed illogical where was it derived from, or how were these conclusions met?
Sorry, to be pissing you off with so many questions, but I have a great interest in this subject, and you seem pretty knowledgeable about this. Do you have a background in the bio-chem field or something?

It comes from a complete lack of understanding. The only "guru" that is worth mentioning is Bill Roberts who suggested the oral dosing in the morning and he will butchered for it because it made no sense at all. If you don't want to believe me, ask any endocrinologist or HRT doctor. The theory holds absolutely no water at all.

I have some formal education in the area but not a degree in that area. Once you start reading how the body reacts to hormones in a formal setting you can easily see that the theory is completely wrong and is an excuse for people to stay on longer. People will do and say anything to find some excuse that allows them to stay on longer and this is one of them. The others are the "cruising" method which makes just as little sense.

 

[Dwight Schrute]

Once your suppressed for 10 weeks of steroid use can you be further suppressed? The protocol allows natural recovery while providing small amounts of testosterone to prevent natural loss of muscle that accompanies the end of the cycle. Are you stating that clomid does nothing to help recovery?

USPLabs,

Yes you can be more suppressed in terms of "recovery time". If you stay on for 4 weeks you recover (LH pulses to testes) quicker than when you were on for 10-12 weeks.

Your protocol makes absolutely no sense at all because you seem to think the testes will respond when 150mg of test per week is administered. You are completey wrong on the subject and you can ask any HRT doc out there. It doesn't happen. If that were the case I could use low dose of just about anything and it will happen but it doesn't. Your studies don't say anything whatsoever because:

1. You haven't even posted the abstracts

2. You are basing recovery on LH when anyone who has studies this for any peroid of time knows LH recovers within 3-7 days regardless of any drug at all during PCT.

During times of exogenous administration of testosterone Clomid will do NOTHING in terms of recovery.

 

[Dwight Schrute]

Jweave23,

the references are posted. You should not reccommend unless you try it yourself first. The protocol seems to be spitting in the face of conventional wisdom. You will be a believe once you try the protocol. Are you willing to risk 3 weeks at worse you will be adding 3 additional weeks to your cycle and recovery will be much easier.

I would also like to see references from bobo that shows 150mg testosterone will raise testosterone above the 2000ng/dl in hypogonadal men.

ceosm

You references do not prove anything. They don't even help your case at all so I would stop using them.

Where did I say 150mg will raise test levels over 200ng/dl?

You seem to be missing the point and forgetting that Clomid/Nolva will not aid in recovery WHILE on. The drug does not work in that fashion at all.

You can ask Nandi the same thing (since he developed your cAMP product)

Actually I already posted his response. I also posted Swale response who works with this every single day.

 

[Dwight Schrute]

LOL..Correct I can see where you implied. I was thinking ahead of the question...My apology.

The individual who postulated this theory is working with an endocrinologist using this protocol patients on HRT. I am working on getting the creator of this protocol over to discuss the topic in depth. With his permission, I was able to spread this progressive thinking theory to the boards. I do not go out on a limb on sketchy science. The man who postulated the protocol has my deepest respect and is well versed in pharmacuetical chemistry. If comming from just a board expert( I am not expert in chemistry), I would be weary of the protocol aswell. The information is just that information. I took the information and applied it when comming off a cycle. In the past, I would lose close to 80% of LBM from a steroid cycle. Last year when I was presented this information, I applied the protocol. I ended the cycle wieghing 225 and I weigh 222 6 weeks after the cycle. I avoided the loss of libido, loss of LBM, loss of motivation and depression which accompany post ccyle. I spread the protocol to my friends and clients. The results where the same.

The purpose of presenting the information was not to portray myself as an expert in chemisty because my knowledge holds a dime to brains like Nandi, bill roberts, and cy wilson. In my time, I learned to form a great team and listen to words of the wise. You could either ditch the idea or try the idea. There is not much bad that could come from trying.

ceosm

1. Cy Wilson was torn apart by Swale. Nandi agrees with my side of the story. Bill Roberts was butchered for his oral dosing theory because it was so full of holes.

Please bring this endocrinologist and have him discuss this because I can get 2 that will refute it.


2. Of course you didn't have the loss of motivation, suppression and mass. You were still ON!

I have trained several people during PCT and have achieved those same results you have above withouth administering 150mg/week.

Even better, I have used HCG throughout the cycle and lost no gains at all (using non aromatizing hormones). I have also trained people this way and they achieved the same results.

I would simply look at what you are doing wrong when not using 150mg test then recommending people stay on and maybe cuasing further problems 3,6,9 months down the road (because that is what TRUE recovery is)

3. I also find a problem with this because why would an HRT doctor be using this protocol at all? An HRT patient is not looking for recovery. He is there for a reason and that is replace what is naturally lost, not to recover form a cycle. Clomid/Nolva use would be used as an SERM, not a recovery agent at all.


None of this makes any sense. A HRT doc wouldn't recommend any PCT theory to any patient because there is no such thing as PCT for an HRT patient.
__________________

 

[Dwight Schrute]

Bobo, a bit O/T, but I can't PM you so I'll just ask here. What are your thoughts on using DHEA while on PCT. Counterproductive or is it aiding in recovery?

Never tried it because I never needed it. I recover without losing hardly anything without it.

 

[lifted]

Never tried it because I never needed it. I recover without losing hardly anything without it.

Lucky bastard. I always have a hard time keeping my gains no matter how conservative I approach the situation. You should offer a PCT program package in your services man, that would be awesome and something that a lot of people could use and could learn from.

 

[Jeff]

I also find a problem with this because why would an HRT doctor be using this protocol at all? An HRT patient is not looking for recovery. He is there for a reason and that is replace what is naturally lost, not to recover form a cycle. Clomid/Nolva use would be used as an SERM, not a recovery agent at all.


None of this makes any sense. A HRT doc wouldn't recommend any PCT theory to any patient because there is no such thing as PCT for an HRT patient.

Check my above post (although this is probably comparing apples to oranges), my HRT doc was making me do it. I questioned him about it, he gave me some references (which I am still trying to find). When I pressed him about it he said that running the clomid every 2 to 3 months during the HRT cycle would keep my nuts from shrinking (I know thats not the same as recovery but).

Where did I say 150mg will raise test levels over 200ng/dl?

FWIW, from the documentation I got when I started my HRT, the average male will produce about 75mg per week of test.

Really isn't what is being suggested is pyramiding off of the cycle? I know with the short cycle protocols on meso they were doing the same thing, only they were continuing past the first week of just clomid(last week from above) until their blood test showed that they were 'recovered'.

 

[Dwight Schrute]

Bobo—



I will respond to your question via reply to this email. You are welcome to cut and paste it as a post.



Simply, I do not know why anyone who knows anything about the Endocrinological system would think you can somehow “hide� androgens from the HPTA.



Estrogen blockade, ala a SERM-class drug, can occur once the serum androgen level falls, by the half-life of the particular drug(s) involved, once they are less than approximately 200 mg of testosterone per week. This does “hide� the androgens from the HPTA, for the most part. However, as the system is then being supported by the SERM, this does not qualify as “recovery�. That is to say, take away the SERM, and levels immediately begin to fall.



If one is merely trying to avoid crashing, then 150mg per week will indeed do that. However, it will maintain T levels at approximately (depending upon the particular individual) 1.5 times the top of normal range. And this definitely could not be considered “recovery�.



IOW, there is no such thing as a “bridge�. If your system is being supported by a medication, then you have not recovered. Simple as that.



I hope this clears up this prevalent, but nonsensical, misconception.



Regards,



Dr. John Crisler

 

[Dwight Schrute]

That is straight from someone who has years and years of clinical research (his OWN clinic).

Will 150mg help avoid your crash? Of course.


Will it help you recover in the long run? Absolutely not. HCG is a MUCH better alternative.

 

[chasec]

thanks for clearing that up bobo and swale. no hard feelings i hope USP labs, thanks for sharing your ideas

 

[Dwight Schrute]

Hard feelings? Bah....good discussion.

USP sponsors here so he gets to tell me to shut up

 

[size]

Will 150mg help avoid your crash? Of course.
Will it help you recover in the long run? Absolutely not. HCG is a MUCH better alternative.

I agree with that statement. This discussion seems to never die.

 

[mass_builder]

i agree with Bobo taking nolva/clomid works through blocking the negative mechanisim feedback from the hypothalamus. now when you on 150mg of test, you wont recover since the body will detect extra amount of testosterone above natural levels, and thus it will downregulates the bodies natural test productions.

using test post cycle is just an excuse to stay on, with low dose.

 

[Guest]

Progressive thought always meets resistance. Bobo will not subside his view because I advertise on his board nor would it be excpected.

ceosm

 

[Dwight Schrute]

I'm a stubborn mule.

 

[Guest]

You references do not prove anything. They don't even help your case at all so I would stop using them.

Where did I say 150mg will raise test levels over 200ng/dl?

You seem to be missing the point and forgetting that Clomid/Nolva will not aid in recovery WHILE on. The drug does not work in that fashion at all.

You can ask Nandi the same thing (since he developed your cAMP product)

Actually I already posted his response. I also posted Swale response who works with this every single day.

bobo
"You references do not prove anything. They don't even help your case at all so I would stop using them."

You can not judge a reference by the title unless you read the full text. The full text can be found in a Medical library so it would be fullish to displace the references.

Bobo I am probably confused on the whole LH thing. Why are we still suppressed even if LH is being produced? Since HCG is the only Hormone that will stimulate recovery, How does HCG work?

I anticipate your response.

thank you

 

[Meerschaum]

bobo
"You references do not prove anything. They don't even help your case at all so I would stop using them."

You can not judge a reference by the title unless you read the full text. The full text can be found in a Medical library so it would be fullish to displace the references.

Bobo I am probably confused on the whole LH thing. Why are we still suppressed even if LH is being produced? Since HCG is the only Hormone that will stimulate recovery, How does HCG work?

I anticipate your response.

thank you

I know this wasnt directed to me, but as I understand it, HCG mimics LH, like an exogenous LH, and since its given exogenous it bypasses the feedback loop, therefore preventing testiculer atrophy, as I understand it beyond that, technically you are still supressed while taking HCG (your body isnt producing LH), but it keeps away testiculer atrophy and greatly improved PCT.

 

[Guest]

I know this wasnt directed to me, but as I understand it, HCG mimics LH, like an exogenous LH, and since its given exogenous it bypasses the feedback loop, therefore preventing testiculer atrophy, as I understand it beyond that, technically you are still supressed while taking HCG (your body isnt producing LH), but it keeps away testiculer atrophy and greatly improved PCT.

Why would it approve PCT? Once you stop administering HCG, whats going to bind to the receptors?

bobo states that
"The only thing that can change that and actually reverse a hypogonadic state (normal test levels) is HCG"

this is only temporary correct? Once you cease HGH, you will become hypogonadic again? HCG will suppress Natural LH.

ceosm

 

[Guest]

This is not really the same protocol as cruising in that you do eventually come off of the test, it almost looks like the tread that was floating around on short cycles where the user took 'large' doses of clomid on the first day of the cycle and then tapered down every week until you stop the androgens. I have to say that this is the way my HRT doc had me run test cyp/clomid - every two months I would start the clomid (at a lower dose then above) while still using 150 mg/wk and then after two weeks of that I would drop the test for a week and continue with the clomid. I ran that for over a year and notice no testicular shrinkage (not that they were big to begin with) without HCG. I know that no testicular atrophy is not the same as not being supressed.

Is your doctor an endocrinologist or an MD? Testicular shrinkage is due(one of the reasons) to the testicles not responding to LH.

 

[Guest]

Uh no...

There is no spike in the morning and hormones don't piggy back anything. Dbol would never prolong any testosterone spike ever. It would decrease it. Exogenous hormones suppress and there is no way to trick the body in that regard. The whole theory is so off the wall and completely wrong that any endocrinologist would cry from laughing so hard.

IRB of an oncology group is behind this concept. I would be safe to assume the doctor would stop laughing and listening.

 

[Dwight Schrute]

bobo
"You references do not prove anything. They don't even help your case at all so I would stop using them."

You can not judge a reference by the title unless you read the full text. The full text can be found in a Medical library so it would be fullish to displace the references.

Bobo I am probably confused on the whole LH thing. Why are we still suppressed even if LH is being produced? Since HCG is the only Hormone that will stimulate recovery, How does HCG work?

I anticipate your response.

thank you

I am judging the references by what you stated in thos studies and that was judging recovery based on LH levels.

As for being still suppressed while still having LH levels normal, now you are getting into the nitty gritty and what is understood is that there are mutiple feedback loops that can trigger the response of Leydig cells. HCG for some reason directly stimulates a response by the testes by mimicking LH but it also bypasses the feedback loop that would cause suppression. Why HCG works and not elevated LH while using endogenous hormones is unknown to me but there seems to be a long and a short feedback loop (one in which LH would suppress) and one in which HCG does not.

Inability to demonstrate an ultrashort loop feedback mechanism for luteinizing hormone in humans.

Kyle CV, Griffin J, Jarrett A, Odell WD.

Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.


hCG has biological properties similar to those of LH, but can be measured separately from LH by current radioimmunometric assays. To investigate the possible existence of an autoregulatory mechanism for LH in humans, we compared the basal LH concentrations and the LH response to a GnRH stimulus with and without prior administration of hCG. On two separate occasions, at least 1 week apart, six normal (eugonadal) males and six normal postmenopausal females were given, in random order, either 10,000 IU hCG or saline followed by iv injection of a 200-micrograms bolus of GnRH. Blood samples were then taken 30, 60, 90, 120, 180, 240, and 300 min after GnRH. Serum concentrations of LH and hCG were measured at each time by two monoclonal antibody sandwich assays developed in our laboratory. After exogenous hCG, serum hCG concentrations rose rapidly to 200-500 IU/L (15,000-35,000 pg/mL) in both the men and women, remaining at this high level throughout the study. In the men, sex steroid concentrations did not change in response to the hCG during the 9 study hours. Compared to saline-treated controls, hCG had no significant effect in either men or postmenopausal women on the basal LH concentration or the response to a GnRH bolus, as determined by peak response and area under the LH/time curve between 0-300 min after GnRH. We conclude that an ultrashort loop feedback mechanism for LH on its own secretion does not exist in humans, as assessed by the present protocol.


You are simply getting into an area in which all the facts are not known.

 

[Dwight Schrute]

IRB of an oncology group is behind this concept. I would be safe to assume the doctor would stop laughing and listening.

Not really, he's still laughing.

"I hope this clears up this prevalent, but nonsensical, misconception."


Dr. Crisler lectures at many seminars for various HRT clinics because this is his area of expertise. And he does find the idea of cruising and a bridge comical.

 

[Dwight Schrute]

Is your doctor an endocrinologist or an MD? Testicular shrinkage is due(one of the reasons) to the testicles not responding to LH.

Testicular atrophy is caused by a lack of stimulation of sertoli cells which make up the majority of the testes and are responsible for the production of sperm. You can have atrophied testes but still produce normal amounts of testosterone.

 

[Dwight Schrute]

IRB of an oncology group is behind this concept. I would be safe to assume the doctor would stop laughing and listening.

And no, IRB is not behind the concept of the Dbol bridge. No endocrinilogist in the world would recommend that protocol for anything.

 

[Guest]

1. Cy Wilson was torn apart by Swale. Nandi agrees with my side of the story. Bill Roberts was butchered for his oral dosing theory because it was so full of holes.

Please bring this endocrinologist and have him discuss this because I can get 2 that will refute it.


2. Of course you didn't have the loss of motivation, suppression and mass. You were still ON!

I have trained several people during PCT and have achieved those same results you have above withouth administering 150mg/week.

Even better, I have used HCG throughout the cycle and lost no gains at all (using non aromatizing hormones). I have also trained people this way and they achieved the same results.

I would simply look at what you are doing wrong when not using 150mg test then recommending people stay on and maybe cuasing further problems 3,6,9 months down the road (because that is what TRUE recovery is)

3. I also find a problem with this because why would an HRT doctor be using this protocol at all? An HRT patient is not looking for recovery. He is there for a reason and that is replace what is naturally lost, not to recover form a cycle. Clomid/Nolva use would be used as an SERM, not a recovery agent at all.


None of this makes any sense. A HRT doc wouldn't recommend any PCT theory to any patient because there is no such thing as PCT for an HRT patient.
__________________

In a debate(face to face)about hormones, chemistry, pharmakenitic, I would bet my business that cy wilson would..well to put politely, Swale would have to take a knee.

"3. I also find a problem with this because why would an HRT doctor be using this protocol at all? An HRT patient is not looking for recovery. He is there for a reason and that is replace what is naturally lost, not to recover form a cycle. Clomid/Nolva use would be used as an SERM, not a recovery agent at all.


None of this makes any sense. A HRT doc wouldn't recommend any PCT theory to any patient because there is no such thing as PCT for an HRT patient."

Are you claiming all patients on HRT would not want to keep Natural LH functioning? PCT is a fictional and only steroid user would understand so of course a Doctor would not provide PCT. As bodybuilders, we take research from studies mostly done on "sick" patients and apply it to bodybuilding. This in one instance that a bodybuilding theory has been accepted by the medical community.

Cancer patients with cachexia on testosterone replacement would want to keep natural LH functioning while taking testoterone. Of course, the study has not begun and one is yet to know the outcome. So 2-6 years down the line, One of us will be saying "I told you so."

In the meanwhile, we should all stick to the protocol that works for the individual. For those like me that lose a large percentage of LBM on a Steroid cyle using androgens, you have nothing to lose trying a "New THought" postulated on research.

In this industry, There many drugs or exagerated cyles used that would have an doctor grimising in pain. This protocol is far from jeopardizing your health. Whats the worse that can happen? It will or will not work. This is not an excuse to "stay on longer." If that where the case, I would reccomend 500mg of testosterone propionate with some winstrol and anavar not 150mg of testosterone enanthate.

Again, I am not reccomending PART just putting the information out there it's always comes down to individual choice.

Ceosm

 

[Guest]

And no, IRB is not behind the concept of the Dbol bridge. No endocrinilogist in the world would recommend that protocol for anything.

Its obvious, we are not debating the d-bol bridge.

 

[Guest]

Testicular atrophy is caused by a lack of stimulation of sertoli cells which make up the majority of the testes and are responsible for the production of sperm. You can have atrophied testes but still produce normal amounts of testosterone.

You can have atrophied testes and not produce testosterone.

 

[Dwight Schrute]

THen you can read it for yourself. CY Wilson had to resort to erasing posts and deleting threads because he was getting his ass handed to him:

Invalid Link Removed

Even Nandi agrees with Swale here:

Invalid Link Removed

That one started it all.


USPLabs,

You stated a HRT doctor came up with this protocol for PCT! There is no such thing as PCT for a HRT patient. They DON'T come off. I am going on what YOU are stating.

Once again, LH does NOT MEAN RECOVERY. Please understand this before you come up with anymore "theories"


You have nothing to lose? Sure you do. You are telling people to prolong hormone treatment without even addressing that longer cycles means LONGER SUPPRESSION. Whats the worst that can happen? They can have low testosteron levels for a very long peroid of time to to abuse of androgens. The clinics are filled with them and even the studies show it.

Pituitary-testicular responsiveness in male hypogonadotropic hypogonadism.

Weinstein RL, Reitz RE.

Clinical Investigation Center, Naval Hospital, Oakland, USA.

An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (HCG) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with HCG resulted in the return of plasma testosterone to low, pretreatment levels. That HCG therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.

Here is one in which Clomid did NOTHING.


Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.

Tan RS, Vasudevan D.

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA. [email protected]

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male. INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months. MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH. RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis. CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.


Here is one in which is took 4 months of Clomid treatment to return to noraml because of prolonged suppression.



""Hypogonadotropic hypogonadism can involve defects in the pituitary, hypothalamus, or both. That study suggests that the defect in those subjects was at the level of hypothalamic release of GnRH (or LRF as it was called at the time that early study was published), since synthetic LRF induced LH and FSH secretion. In order for clomid to stimulate LH secretion from the pituitary, the hypothalamus must be sending the appropriate GnRH pulse signal to the pituitary.



So before any theories about PCT can be made you should understand that there is PLENTY to lose.

 

[Dwight Schrute]

Its obvious, we are not debating the d-bol bridge.

A low dose protocol is the same as a...


low dosed protocol.

 

[Dwight Schrute]

You can have atrophied testes and not produce testosterone.

Yeah when you take 150mg of testosterone for a prolonged peroid of time.

 

[Guest]

I am judging the references by what you stated in thos studies and that was judging recovery based on LH levels.

As for being still suppressed while still having LH levels normal, now you are getting into the nitty gritty and what is understood is that there are mutiple feedback loops that can trigger the response of Leydig cells. HCG for some reason directly stimulates a response by the testes by mimicking LH but it also bypasses the feedback loop that would cause suppression. Why HCG works and not elevated LH while using endogenous hormones is unknown to me but there seems to be a long and a short feedback loop (one in which LH would suppress) and one in which HCG does not.

Inability to demonstrate an ultrashort loop feedback mechanism for luteinizing hormone in humans.

Kyle CV, Griffin J, Jarrett A, Odell WD.

Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.


hCG has biological properties similar to those of LH, but can be measured separately from LH by current radioimmunometric assays. To investigate the possible existence of an autoregulatory mechanism for LH in humans, we compared the basal LH concentrations and the LH response to a GnRH stimulus with and without prior administration of hCG. On two separate occasions, at least 1 week apart, six normal (eugonadal) males and six normal postmenopausal females were given, in random order, either 10,000 IU hCG or saline followed by iv injection of a 200-micrograms bolus of GnRH. Blood samples were then taken 30, 60, 90, 120, 180, 240, and 300 min after GnRH. Serum concentrations of LH and hCG were measured at each time by two monoclonal antibody sandwich assays developed in our laboratory. After exogenous hCG, serum hCG concentrations rose rapidly to 200-500 IU/L (15,000-35,000 pg/mL) in both the men and women, remaining at this high level throughout the study. In the men, sex steroid concentrations did not change in response to the hCG during the 9 study hours. Compared to saline-treated controls, hCG had no significant effect in either men or postmenopausal women on the basal LH concentration or the response to a GnRH bolus, as determined by peak response and area under the LH/time curve between 0-300 min after GnRH. We conclude that an ultrashort loop feedback mechanism for LH on its own secretion does not exist in humans, as assessed by the present protocol.


You are simply getting into an area in which all the facts are not known.

Essentially you saying, that HCG mimicks LH but LH would not stimulate testosteone production? Seems paradoxical. Bobo can you tell what the G-protein coupled receptor on the leydig cells is referred to?

 

[Guest]

A low dose protocol is the same as a...


low dosed protocol.

One can not compare testosterone and d-bol.

 

[Guest]

THen you can read it for yourself. CY Wilson had to resort to erasing posts and deleting threads because he was getting his ass handed to him:

Invalid Link Removed

Even Nandi agrees with Swale here:

Invalid Link Removed

That one started it all.


USPLabs,

You stated a HRT doctor came up with this protocol for PCT! There is no such thing as PCT for a HRT patient. They DON'T come off. I am going on what YOU are stating.

Once again, LH does NOT MEAN RECOVERY. Please understand this before you come up with anymore "theories"


You have nothing to lose? Sure you do. You are telling people to prolong hormone treatment without even addressing that longer cycles means LONGER SUPPRESSION. Whats the worst that can happen? They can have low testosteron levels for a very long peroid of time to to abuse of androgens. The clinics are filled with them and even the studies show it.

Pituitary-testicular responsiveness in male hypogonadotropic hypogonadism.

Weinstein RL, Reitz RE.

Clinical Investigation Center, Naval Hospital, Oakland, USA.

An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (HCG) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with HCG resulted in the return of plasma testosterone to low, pretreatment levels. That HCG therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.

Here is one in which Clomid did NOTHING.


Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.

Tan RS, Vasudevan D.

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA. [email protected]

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male. INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months. MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH. RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis. CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.


Here is one in which is took 4 months of Clomid treatment to return to noraml because of prolonged suppression.



""Hypogonadotropic hypogonadism can involve defects in the pituitary, hypothalamus, or both. That study suggests that the defect in those subjects was at the level of hypothalamic release of GnRH (or LRF as it was called at the time that early study was published), since synthetic LRF induced LH and FSH secretion. In order for clomid to stimulate LH secretion from the pituitary, the hypothalamus must be sending the appropriate GnRH pulse signal to the pituitary.



So before any theories about PCT can be made you should understand that there is PLENTY to lose.

I would have to see the full text of the abstact but the conclusion says "This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse."

Apparently some say it does not.

To be clear, I never stated a HRT doctor invented the protocol.

 

[Guest]

Bobo Leaving for a seminar and will return on Monday! I enjoy this debate and will resume later on the week.

Have a wonderful weekend!

 

[Dwight Schrute]

When exogneous testosterone is present, LH will not. The testes will not respond because there already is a supraphysiological dose present. This is basic physiology.

HCG however directly stimulate leydig cells to produce testosterone even when supraphysioligical doses are present.


Now can you try to twist my words around even more?

What do you want to know about G proteins? How they are activated by LH? Or how they in turn activate adenylyl cyclase?


For those who didn't read SWALES and CY, here is a little tidbit.


SWALE: "I certainly hope you are not suggesting I am not discussing this in less than a "mature manner." If such is the case, then you do yourself great disservice.

Here is the bottom line: you cannot add ANY testosterone without affecting recovery. And it absolutely is not true that you need to raise serum testosterone levels to supraphysiological levels to induce inhibition. Inhibition comes by degrees. It is not an on/off proposition. I'd invite you to see case after case from my medical files (real patients) proving this--even at 5gms of Androgel or 100mg of IM testosterone--as evidenced by decreased LH concentrations. I would consider 55-60% inhibition to be considerate, and a hindrance during post-cycle recovery.

When I said "any", I mean that NO amount of exogenous testosterone can be administered, no matter how small, without affecting LH production. I was not referring to dosages in the opposite direction. Where questions of semantics are concerned, it is often useful and appropriate to ask for clarification befire getting your dander all worked up.

It is well accepted that HCG post-cycle inhibits recovery (even though it does not generally take serum testosterone above "normal' range). Why on earth would 5gm of Androgel, or 100mg of test enanthate, be any different?

You also have forgotten the conversion of testosterone to DHT--which suppresses at the hypothalamus even moreso. So it is not just estradiol suppression we must consider. Shoot, I can block its formation if I want to.

Testosterone bucylate does provide a good example. It enters the blood stream as available testosterone so slowly that its inhibition can be considered instantaneous. The LH production (i.e inhibition) falls off to keep pace. That is why there is no increase in serum T levels--and why my point is made.

Finally, I would be interested in hearing what your little snipe about "ulterior motives" is supposed to mean. I have never seen comments like yours coming from the good writers at T-MAG. "


Cy: "First as I noted in my reply, that last portion was copied and pasted from this week's column and WAS NOT directed at you in any way.
I'm simply stating what the mechanisms are behind inhibition of LH and consequent endogenous testosterone. Furthermore, with the testosterone bucyclate, my point was missed as testosterone concentrations nor was LH was significantly altered.
As for your comparison to hCG, I fail to see the point. hCG is not used because of its' ability to cause down-regulation of LH/hCG receptors and it itself lowers LH secretion. Androgens on the other hand inhibit LH via the ER, AR and in some cases the PR and directly at the testicular level.
Also I did not forget the reduction of testosterone to DHT and this is again why I mentioned the AR (androgen receptor) in my last post. Again, if you don't provide enough substrate (testosterone) for reduction to DHT or aromatization to estradiol, then there I fail to see where the proposed suppression is stemming from.

Again my "ulterior motives" and such was a portion of this week's column which I'd copied and pasted and I made a note of that in my post but I apologize as I didn't make that very clear. If you check my previous post again, you'll see what I mean. "


SWALE: "Your explanation for what I interpretted as insulting language is indeed sufficient.

So, if I am understanding you, you are claiming that you can induce a 55-60% inhibition, yet not affect inhibition? Androgel at 5gms QD causes tremendous increases in serum testosterone levels (as opposed to the testosterone bucyclate example you pose). So does 100mg of testosterone IM. Also, the Androgel is not a single application--indeed grealy elevated serum T levels are rapidly acquired, and maintained, by daily applications of same. Hence, suppression is a given. Both dosages have been shown to induce complete suppression in some males--hardly what we are looking for while trying to recover from a steroid cycle.

Supression is not some magical threshold which must be violated in order to induce same. It is a sliding scale, which is why we meausre LH output concentrations within a range of values. If serum androgen goes up a little (whether from endogenous or exogenous testosterone--hence my explanation of a sentence you disagreed with), LH production is decreased. Likewise, there is not a threshold of serum testosterone concentration which must be crossed before aromatisation to estrogen and 5-alpha reduction to DHT takes place. Increasing the concentration of serum T will drive more production of estrogen and DHT, but it not correct to say none is produced when serum T concentrations are low. Therefore, any increase from exogenous testosterone will cause an increase in its metabolites as well. To be sure, both estrogen and DHT are measured in men who are severely hypogonadal.

Back to the testosterone bycyclate. Was this a single injection? That would remove it as viable analogy for the purposes of this argument. Also, I suspect if a decrease in LH was not detected (which you did not mention the first time), that was due to experimental error of the testing equipment. Adding exogenous testosterone, yet detecting no increase in serum levels, means the endogenous production was decreased to compensate. There just is no way around that. Finally, regular injections of testosterone bucyclate will indeed increase serum T levels--and therefore induce inhibition--over time. To quote a well-known author: "the pharmacokinetic properties of a the drug must be kept in mind when LH suppression is concerned."

Saying Androgel elevated serum T levels to "ONLY 462-566ng/dL", from a severely hypogonadal state (which is what it takes to actually drop below normal range) is not a very realistic way to think of inhibition and suppression. For indeed, many men find tremendous increases in health and happiness with "only" this increase in serum testosterone concentration--and, for a large percentage of men, would represent total recovery of the HPTA. I'm thinking your perspective comes from being used to dealing with serum T levels many, many times the top of normal range. The system evolved to maintain hormone levels which are compatible with life--not pack on a hundred pounds of extra muscle.

For my patients, I certainly recheck their estradiol levels after a month of Androgel at this dosage (and response) to see where their estrogens end up. It also is useful to me because it gives me an idea of how their bodies respond, an informal "receptor mapping", if you will. It is also why I do not add a SERM until after I have tuned up their serum T (by lab values AND Medical History), as doing so prevents reliable assay of estradiol.

I find no intellectual corruption in describing the Androgen Receptors of the midbrain as "sensors". Whoever thought of calling them that is providing a useful visualization tool. The AR's found there are indeed antennae, sticking out into the blood, gathering information for the HPTA to adjust itself with. Having said that, I realize I am at risk of sounding like I am offering a teleological explanation.

I think one may use Androgel in the manner you describe, as long as they understand they are merely "stepping down" their serum androgen levels, and may find some benefit from that. However, they must also know they are extending the time to complete recovery by doing so. In my experience, AAS athletes want to recover as quickly as possible (reduces their Viagra bill), and onto the next thing--or next cycle, as the case may be.

That is where the HCG example becomes useful. My current HCG protocols recommend intermittent, but regular, application of smaller amounts of the hormone, in order to stave off testicular atrophy. This is for both AAS athletes and gentlemen on HRT. It has been shown that maintaining the testicles during the cycle shortens the time to recovery at the end. I seriously doubt there is LH receptor downregulation of any import when employing this protocol. Even if there is, sometimes we must content ourselves that we are doing the best we can. The point you have missed is precisely that the testosterone HCG induces causes downregulation of LH (hope that clears that up for you), via the AR, and the ER (from increased aromatisation of same). Again, there is no free lunch--if you increase serum T levels exogenously, you induce inhibition. I was not aware LH directly suppresses its own production at the HP (do you have time to provide a reference?). That would not surprise me, though, as LH has effect much further upstream than that. Also, since the cross-reactivity of HCG and LH is so high, I'd predict it would be the same for HCG. Some think that aromatase is actually toxic to the Leydig cells. Therefore we would be causing permanent primary hypogonadism to go along with the temporary secondary hypogonadism induced by the steroid cycle, IF we use too much of it. It's a fine line we walk. "




Also, is there a reason why you are using 2 different fonts for a lot of the more technical questions?

 

[Dwight Schrute]

One can not compare testosterone and d-bol.

When you comparing how the body reacts to exogenous hormones, yes you can. They both suppress, peroid.

 

[Dwight Schrute]

I would have to see the full text of the abstact but the conclusion says "This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse."

Apparently some say it does not.

To be clear, I never stated a HRT doctor invented the protocol.

If you are saying that the axis is not shut off I suggest you tell that to the number of HRT patients that have to inject for the rest of their life due to abuse.

Its a fact.

 

[Dwight Schrute]

Bobo Leaving for a seminar and will return on Monday! I enjoy this debate and will resume later on the week.

Have a wonderful weekend!

This really isn't a debate.

Its fact vs. myth.


.....but you have a nice weekend as well.

 

[mass_builder]

you guys were talking about short loop negative mechanisim feedback, well my college physiology book says it dose exist in humans. i hope this graph helps:

 

[Dwight Schrute]

Inability to demonstrate an ultrashort loop feedback mechanism for luteinizing hormone in humans.

Kyle CV, Griffin J, Jarrett A, Odell WD.

Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.


hCG has biological properties similar to those of LH, but can be measured separately from LH by current radioimmunometric assays. To investigate the possible existence of an autoregulatory mechanism for LH in humans, we compared the basal LH concentrations and the LH response to a GnRH stimulus with and without prior administration of hCG. On two separate occasions, at least 1 week apart, six normal (eugonadal) males and six normal postmenopausal females were given, in random order, either 10,000 IU hCG or saline followed by iv injection of a 200-micrograms bolus of GnRH. Blood samples were then taken 30, 60, 90, 120, 180, 240, and 300 min after GnRH. Serum concentrations of LH and hCG were measured at each time by two monoclonal antibody sandwich assays developed in our laboratory. After exogenous hCG, serum hCG concentrations rose rapidly to 200-500 IU/L (15,000-35,000 pg/mL) in both the men and women, remaining at this high level throughout the study. In the men, sex steroid concentrations did not change in response to the hCG during the 9 study hours. Compared to saline-treated controls, hCG had no significant effect in either men or postmenopausal women on the basal LH concentration or the response to a GnRH bolus, as determined by peak response and area under the LH/time curve between 0-300 min after GnRH. We conclude that an ultrashort loop feedback mechanism for LH on its own secretion does not exist in humans, as assessed by the present protocol.



Endogenous luteinizing hormone surges following administration of human chorionic gonadotropin: further evidence for lack of loop feedback in humans.

Nader S, Berkowitz AS.

Department of Obstetrics, Gynecology and Reproductive Sciences, University of Texas Medical School, Houston 77030.

The existence of inhibitory short- and ultrashort-loop feedback mechanisms for luteinizing hormone (LH), while documented in animals, has been questioned in humans. Since human chorionic gonadotropin (hCG) binds to LH receptors but can be distinguished from LH in immunoassays, it is possible to identify LH surges in the face of exogenously administered hCG. The present study demonstrates LH surges at midcycle in normal volunteers and in women undergoing controlled ovarian hyperstimulation, given hCG. This provides further evidence for lack of loop feedback control of LH secretion in humans.


Science evolves


My old physiology book said a lot of things that just arne't true anymore, especially in this area.

 

[Meerschaum]

Bobo on a seperate note, I've heard all sorts of crazy doses of hCG, I think it was Swale he said 250 to 500iu is sufficient, and I've heard good reports from people using this low dosage, others say 'no way man 2500iu' then you hear people saying as much as 10000iu... now, from what I gather the higher the dose, the easier it is to become LH desensitized, so if 250iu is sufficient, why not stick with it?... I'm just wondering what you think, do you think lower doses like 250-500 iu given 2x a week are okay, or do you lean toward requiring more to get the same effect in your expierence ?

 

[Rogue Drone]

[/color]

Essentially you saying, that HCG mimicks LH but LH would not stimulate testosteone production? Seems paradoxical. Bobo can you tell what the G-protein coupled receptor on the leydig cells is referred to?

HCG can stimulate the Androgen desensitized Leydig Cells because it's a more powerful activator of cAMP by the G Proteins than LH is.

Invalid Link Removed

" The hCGß protein is larger than the LHß protein, containing a C-terminal extension of 29 amino acids, with four additional O-linked glycosylation sites not present in LHß. This structural difference explains the longer circulating half-life and higher biopotency of hCG over LH."

 

[bioman]

I've had fairly good luck dosing 250 iu HCg 2 x a week. Testicle size and test levels definitely respond nicely at these doses however it seems to take longer to regain libido than without HCG (just my own observation).

IMO, mego-dosing HCG is bad idea as the resulting suppression will far outweigh any possible temporary benefit of having big, fat nuts.

 

[crazydoc1]

Why are you expressing concentration of the T esters instead of total dosage?...... Are you presuming
to argue that an aliquot at 150 mg/mL @ 1cc vs. 0.75cc @ 200 mg/mL produce a profoundly altered pattern of
absorption?>...... Again, its hard to maintain the confidence of a group that includes individuals who are no clinically and/or scientifically lay with confusion such as this.

You are also indicate that is 'increases' things such as TSH. TSH is an indirect mechanism. TSH would increase in
response to lowered FT3, FT4 and or lowered bound T3,T4 ... Adding Levothyroxine or Levothyroid will reduce TSH i

Your statement offers that TSH will increase... so are you trapping or presuming to lower T3/T4... why? and by what mechanism? do the concept involve making the patient subclinically or clinically hypothyroid? or was this just another example of how the author and product develop are medically and scientifically lay and can offer a plan and product to people as though it was subjected to medical rigor when the authors cannot comprehend the simple feedback mechanisms of the thyroid regulation............

This is what a person is left to presume from the style of course of the writing...

No sir, I am not taking on testers. This method has been tested by my clients and many others.

Correct, You could even go to 200mg/ml of testosterone and recover, but an estrogen antagonist must be used in combination. I would stay on the safe side at 150mg/ml. You will not be dissappointed on the results...absolutely no crash!

You will have to reduce training volume.

ceosm

 

[crazydoc1]

An interesting way of testing these possibilities might involve
the use of very expensive synthetic recombinant LH usually relegated to
fertility clinic use in combination with clomid with several PCT patients on several
low doses of short acting T-esters.

I don't understand why this guy keeps expressing concentration instead of dosage and why given
their rationalization, they are not favoring very short acting proprionate or a compounded transdermal
done with prop to split out the low dose througout the week.

I see a vendor striving to push product..............

Could you please provide scanned copies of these? They were in the early and late 70's and the information is not on Pubmed.

From every account that I have seen Clomid/Nolva will not reverse a hypogonadic state while still administering exogenous hormones, especially 150mg of testosterone. Clomid/Nolva will not bypass the feedback loop like HCG will. The only thing that can reverse atrophy and a hypogonadic state while still taking exogneous hormones is HCG. This has been well documentd in many HRT clinics.

 

[crazydoc1]

morning erections can occur in fully suppressed patients still.....

there is generally the LH--- ghrh--- test spiking deemed related... but you
can't make a judgement call on the morning erection alone.

I ran it during my PCT, I was not using it as bridge, as i like to take breaks in between cycles. It definately helped avoid a crash and helped keep gains. However, I was not fully recovering.

Bobo, can you post a link or study showing this please? Most things I have read indicate that there is a natural testosterone spike approximately around the time we wake up. I know many people say morning erections are proof of this; I dont know if I would take it that far though.

 

[crazydoc1]

True........ the spematogenesis relates to the volume side moreso and that functions form the FSH resumption while
the LH spike relates more principally to GNRHs... Notwithstanding HCG mimicking (and by many arguments densensitizing) the leydig cells to LH response, there is clearly some volume relationship related to the LH/GNRH side inasmuch as there are countless sums of our own anecdotal and empirical observations of FSH-0, LH-0 persons increasing total testicular volume via HCG dosing.

I share your frustration with USP labs based on what I've read here..

Testicular atrophy is caused by a lack of stimulation of sertoli cells which make up the majority of the testes and are responsible for the production of sperm. You can have atrophied testes but still produce normal amounts of testosterone.

 

[Guest]

An interesting way of testing these possibilities might involve
the use of very expensive synthetic recombinant LH usually relegated to
fertility clinic use in combination with clomid with several PCT patients on several
low doses of short acting T-esters.

I don't understand why this guy keeps expressing concentration instead of dosage and why given
their rationalization, they are not favoring very short acting proprionate or a compounded transdermal
done with prop to split out the low dose througout the week.

I see a vendor striving to push product..............

The product is supported by literature based on research. this is not a sly attempt to market. I would not attach marketing to such a controversial topic. Marketing gomes from paid advertisment, gifted products, and members log. The market on this board is not a novice consumer.

Dosage is listed.

ceosm

 

[crazydoc1]

Lets have a refresher..

A concentration is a quantity of an arbitrary item over the volume in which it is contained..
example..... 150 mg/mL

A dosage or quantitiy of an arbitrary product would be a mass, mole, or other related absolute quantity
function.... example 150 mg..

If your trying to say that your premise involves a dosage of 150mg BID.... then just say it...... as opposed
to expressing concentration which is not logical.

I've read all these threads and they all express concentration and not dosage.

You've not adequately responded to the questioning of the methdology put forth and citing peripherally related
studies doesn't constitute actual trials of validity of your concept.

Sometimes those who are not medically (clinically) or scientifically lay, and there are several on this board, who normally pride themselves on educating those around them irrespective of those persons' backgrounds (even though sometimes it is very frustrating) retain to right to fed up from time to time of those persons such as yourself who put forth uncorroborated concepts and never rebut with legitimate scientific rigor or even a forensically worded statement of position. People such as yourself who fail to provide answers to direct legitimate questions and defer the question to avoid it as a red herring frustrate individuals who help out with professional commentary on this site...

Thats my two cents.......

The product is supported by literature based on research. this is not a sly attempt to market. I would not attach marketing to such a controversial topic. Marketing gomes from paid advertisment, gifted products, and members log. The market on this board is not a novice consumer.

Dosage is listed.

ceosm

 

[Jeff]

damn swale, I wish you were still taking on people for TRT :thumbsup: