U-opiod antagonists to prevent HPTA suppression/shutdown

[marcus300]

Anyone had any first hand experience on using u-opiod antagonists to prevent shutdown/supression while on AAS cycle?

Only looking for experience from someone who as used this method with success or without.

[DEE151]

never herd of it what is it? sounds interesting?

[bene7422]

this does seem very interesting,I've talked to a couple guys on some other boards that have said they've used naltrexone to prevent shutdown and have had great success with it,I'd also like to hear some peoples personal feedback

[peachfuzz]

I think Swifto may have some feedback for you. Hopefully he will chime in either way

[marcus300]

I know a couple of guys who are trying this method but i was looking for someone who as had bloodwork to back this theory up. For anyone who is interested in reading about this method here is an article by Eric M. Potratz



Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.


Suppression of the HPTA (Hypothalamus, Pituitary, Testicular Axis) is seemingly unavoidable during a steroid cycle. What I will be presenting in this article is a new idea to the world of AAS users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, I will show you how to actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (AAS).

For a moment, let’s forget the concept of “post cycle therapy ”, and embrace the idea of “on cycle therapy” – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during AAS administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use . Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to AAS.

HPTA – The basics

When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate the release of the gonadotrophins -- luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testes, to activate their respective leydig and seritoli cells. LH initiates testosterone production by stimulating the leydig cell receptor (steroidogenesis), while FSH initiates sperm production by stimulating the sertoli cell receptor (spermatogenesis).

AAS’s inhibit hormone production just as your body’s own hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary. (1) This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.

While low-dose on-cycle hCG is a good protocol to mimic LH and keep the testes from atrophy, (discussed here) it won’t help prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testes. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as time goes on. (11) This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the other hand, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.(12,13) The point here, is that only minor stimulus is required for the preservation of sensitivity in the endocrine organs. Perhaps a completely neglected and suppressed pituitary (or testes) may explain the lack of full and prompt recovery for many steroid users, despite adherence to a “tried and true” PCT regimen. So the question is – How can we prevent suppression of the testes, and better yet, how can we prevent suppression of the pituitary?



A closer look –

There are several ways that steroids can inhibit LH & FSH release from the pituitary based on the receptors they occupy, and this is important to understand if you plan on blocking AAS induced suppression. For instance, it appears that AAS which bind strictly to the AR only inhibit LH & FSH release by suppressing GnRH release from the hypothalamus (ie Primobolan , Proviron , Anavar or Masteron ). (34,37,39) However, AAS which possess estrogenic (ER) or progestogenic (PR) activity inhibit LH & FSH by directly down-regulating the GnRH receptors on the pituitary, while also reducing GnRH release from the hypothalamus. (35,38) Therefore, progestin based AAS such as trenbolone and nandrolone are “double suppressive” because they are binding to the AR and PR and suppressing LH & FSH by two different mechanisms. (36) The same can be said for steroids that aromatize, such as testosterone or methandrostenolone since they can activate both AR and ER receptors.

Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis (37), and that administration of Arimidex can greatly reduce testosterone’s suppression of LH release. (42) However, since progesterone based AAS’s such as nandrolone and trenbolone are inherently progestogenic based on their hormone structure, there is no way to prevent them from activating the PR. Therefore, it’s virtually pointless to try to block the suppression from progestin based anabolics. However, we can block suppression from the ER by using either non-aromatizing AAS’s or aromatase inhibitors. So this now leaves us with suppression of LH & FSH via the AR, but this suppression can be blocked, and that’s exactly what I’m going to show you.

When it comes to suppression of the hypothalamus, there is more than a simple on/off switch for the hypothalamus control center. Evidence suggests that there isn’t even a direct AR or ER receptor on GnRH secreting neurons. (2-6) Meaning, steroid hormones do not directly influence GnRH release from the hypothalamus, but actually communicate through an intermediary. (7)

It was well summarized here by A. J Tilbrook et al,

“It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons.”

And again here by FJ Hayes et al,

“It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen”

There is a network of neurogenic intermediaries in the hypothalamus governing GnRH release from steroid hormone influence. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of “suppression” to the GnRH neurons once activated by steroid hormones. (16) These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s). (7,16) The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. (8-10) For this reason, b-endorphin will be the main focus of the article (although there are other minor intermediates involved.)

When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH and consequently suppress LH & FSH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have their own AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.

This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this “antagonism” of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to hormone receptors. (15,32)

The effect of a u-opioid receptor antagonist on the HPTA is demonstrated here --



Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone , DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)

U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system. (28,29) It’s well known that strong opioid based drugs such as methadone, cocaine, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH, LH & FSH is due to the same EOP mechanisms seen with AAS induced suppression. (33) In alcoholics, cocaine and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels. (28,29) Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction. (30,31)

Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown – Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.

A word of caution: The opioid antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages; however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, cocaine, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone. Contrary to popular believe, opioid antagonists do NOT have any addictive properties.

A few point to consider -

For those who choose to embark on an opioid antagonist protocol several things should be considered.



Remember, progestin based anabolics such as trenbolone and nandrolone are “double suppressive” because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use.
As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole , or exemestane (Aromasin ) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI’s. (43-47)


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[Swifto]

Anyone had any first hand experience on using u-opiod antagonists to prevent shutdown/supression while on AAS cycle?

Only looking for experience from someone who as used this method with success or without.

After a bit of debate over this theory, I dont think its that good anymore.

If you have read my HCG thread, you'de see that the problem in starting up testosterone production again, is the testes, not the hypothalamus and pituitary. They recover fairly quickly, even during extended peroids. This is also what Dr.Crisler confirmed.

To address the main problem, testicular dysfunction, we have HCG and HMG. If one can address this problem directly, why is there a need for opiot antagonists at all?

Opoid antagonists would maintain GnRH, LH, FSH and T, but by how much is VERY debatable. Would this stop the onset of testicular dysfunction?

I have also read about more and more people coming forward with Naltrexone making them feel awful. Bad enough to not use it.

I think Naltrexone would best be used, now, at the start of PCT or a few weeks leading towards it. HCG/HMG during, then Naltrexone and a combination of SERMs is the best logical PCT and preventative measure IMHO.

[marcus300]

After a bit of debate over this theory, I dont think its that good anymore.

If you have read my HCG thread, you'de see that the problem in starting up testosterone production again, is the testes, not the hypothalamus and pituitary. They recover fairly quickly, even during extended peroids. This is also what Dr.Crisler confirmed.

To address the main problem, testicular dysfunction, we have HCG and HMG. If one can address this problem directly, why is there a need for opiot antagonists at all?

Opoid antagonists would maintain GnRH, LH, FSH and T, but by how much is VERY debatable. Would this stop the onset of testicular dysfunction?

I have also read about more and more people coming forward with Naltrexone making them feel awful. Bad enough to not use it.

I think Naltrexone would best be used, now, at the start of PCT or a few weeks leading towards it. HCG/HMG during, then Naltrexone and a combination of SERMs is the best logical PCT and preventative measure IMHO.

I understand the debate over this but I was looking for people who have tried it or using it rather than the text book theories of how it can control supression or shutdown and i was more interested in the prevention rather than the cure of supression/shutdown which some are claiming.

On paper it looks great and ive read some good results but as anyone had BW or compared it against a normal PCT protocol you know of?

I know guys who use Naltrexone for their addiction and from speaking to them, its doesnt make them feel awfull rather the oppersite but these guys are suffering from addiction and are rattling rather than being at peak health like BB's.

I think its needs first hand experiences from BB's who have ran normal PCT with BW and who have tried this theory, do you know of any?

[Swifto]

I understand the debate over this but I was looking for people who have tried it or using it rather than the text book theories of how it can control supression or shutdown and i was more interested in the prevention rather than the cure of supression/shutdown which some are claiming.

On paper it looks great and ive read some good results but as anyone had BW or compared it against a normal PCT protocol you know of?

I know guys who use Naltrexone for their addiction and from speaking to them, its doesnt make them feel awfull rather the oppersite but these guys are suffering from addiction and are rattling rather than being at peak health like BB's.

I think its needs first hand experiences from BB's who have ran normal PCT with BW and who have tried this theory, do you know of any?

I dont my friend.

I know of some that use it at uk iron.net. Maxititer has threads over there about it and there is now a new Doc thats regirtered there that specialises in BB's health issues etc...He mentioned it, but didnt know much about its effectiveness.

Have a look over there mate. The Mod Psccarb (or something like that) used it.

[marcus300]

I dont my friend.

I know of some that use it at uk iron.net. Maxititer has threads over there about it and there is now a new Doc thats regirtered there that specialises in BB's health issues etc...He mentioned it, but didnt know much about its effectiveness.

Have a look over there mate. The Mod Psccarb (or something like that) used it.

Yes, I know him and will go and search for some threads over there, its does sound interesting if the claims work, it could transform the whole cycling/pct protocols

[ninesecz]

ae you ntalking about Opiate antagonist like Suboxone and Methadone or am I taking to much from your pist and it was not spelled wrong?

[marcus300]

ae you ntalking about Opiate antagonist like Suboxone and Methadone or am I taking to much from your pist and it was not spelled wrong?

Naltrexone is the product,

[Dancer]

Marcus,

How effective UO is what you are asking? There has not been anyone use it as a stand alone PCT measure and get BW to see how effective it is as a stand alone.

As Swift pointed out earlier in the first few weeks of PCT it might add/aid recovery.

The issue with the article is how effective it is as a PCT measure. The simple answer is we do not know.

[The Deuce]

He's talking of Naxolone.. the stuff the administer to you when you OVERDOSE on Opiates...

Naloxone is a drug used to counter the effects of opioid overdose, for example heroin or morphine overdose. Naloxone is specifically used to counteract life-threatening depression of the central nervous system and respiratory system. Naloxone is also experimentally used in the treatment for CIPA; an extremely rare disorder (1 in 125 million) that renders one unable to feel pain. It is marketed under various trademarks including Narcan, Nalone, and Narcanti, and has sometimes been mistakenly called "naltrexate." It is not to be confused with Naltrexone, another opioid receptor antagonist with qualitatively different effects, used for dependence treatment rather than emergency overdose treatment.



ON A SIDE NOTE:

I am on METHADONE and it is the CAUSE according to my DOCTOR as to the reason WHY my Natty Test was shut off. After being on Methadone for a length of 30 days my TOTAL TEST was 81... Yes you read that correctly.. 81!!! Methadone is and was directly responsible for the shutdown of my TEST.

My doctor considers this a "TEMPORARY SHUTDOWN" for as long as I am on Methadone. He thinks I will rebound back from it when I am off of the Methadone. We will see but for now, I am on TRT and that's the way it is.

As far as Naloxone is considered if it really does what Marcus is stating it does, it really could change the face of cycling and PCT's....

[Dancer]

ON A SIDE NOTE:

I am on METHADONE and it is the CAUSE according to my DOCTOR as to the reason WHY my Natty Test was shut off. After being on Methadone for a length of 30 days my TOTAL TEST was 81... Yes you read that correctly.. 81!!! Methadone is and was directly responsible for the shutdown of my TEST.

My doctor considers this a "TEMPORARY SHUTDOWN" for as long as I am on Methadone. He thinks I will rebound back from it when I am off of the Methadone. We will see but for now, I am on TRT and that's the way it is.

As far as Naloxone is considered if it really does what Marcus is stating it does, it really could change the face of cycling and PCT's....

WOWWOWOWOWOWOWOWOW...

When the BW was done was the only chemical in your system methandone? How long were you off cycle?

[marcus300]

Marcus,

How effective UO is what you are asking? There has not been anyone use it as a stand alone PCT measure and get BW to see how effective it is as a stand alone.

As Swift pointed out earlier in the first few weeks of PCT it might add/aid recovery.

The issue with the article is how effective it is as a PCT measure. The simple answer is we do not know.

I am not talking about using it in PCT but during the cycle like the article states, ive done some more research and it looks like from guys who have used it they say its stops atrophy and in some cases no need for PCT at all, these claims seem very hard to believe but it would be nice to hear from people who have used it. I know some have used it and only a slight PCT was required, i guess it all depends on the indiviual because our HPTA reacts and responds differently. I just find it very interesting and i feel more experiments are needed, at the moment i am open minded but I do like the look of how its acts in the body.

[marcus300]

He's talking of Naxolone.. the stuff the administer to you when you OVERDOSE on Opiates...

Naloxone is a drug used to counter the effects of opioid overdose, for example heroin or morphine overdose. Naloxone is specifically used to counteract life-threatening depression of the central nervous system and respiratory system. Naloxone is also experimentally used in the treatment for CIPA; an extremely rare disorder (1 in 125 million) that renders one unable to feel pain. It is marketed under various trademarks including Narcan, Nalone, and Narcanti, and has sometimes been mistakenly called "naltrexate." It is not to be confused with Naltrexone, another opioid receptor antagonist with qualitatively different effects, used for dependence treatment rather than emergency overdose treatment.



ON A SIDE NOTE:

I am on METHADONE and it is the CAUSE according to my DOCTOR as to the reason WHY my Natty Test was shut off. After being on Methadone for a length of 30 days my TOTAL TEST was 81... Yes you read that correctly.. 81!!! Methadone is and was directly responsible for the shutdown of my TEST.

My doctor considers this a "TEMPORARY SHUTDOWN" for as long as I am on Methadone. He thinks I will rebound back from it when I am off of the Methadone. We will see but for now, I am on TRT and that's the way it is.

As far as Naloxone is considered if it really does what Marcus is stating it does, it really could change the face of cycling and PCT's....

I hear the dose is very important, its nothing like you would be using if you was opiate dependant, but very small amounts are needed for the desired effect in relation to supression/shutdown.

[Swifto]

I am not talking about using it in PCT but during the cycle like the article states, ive done some more research and it looks like from guys who have used it they say its stops atrophy and in some cases no need for PCT at all, these claims seem very hard to believe but it would be nice to hear from people who have used it. I know some have used it and only a slight PCT was required, i guess it all depends on the indiviual because our HPTA reacts and responds differently. I just find it very interesting and i feel more experiments are needed, at the moment i am open minded but I do like the look of how its acts in the body.

The two ways (which we know about) in being able to maintain GnRH from the HP when technically "shutdown". Is opoid antagonists and estrogen manipulation also. There are studies done on indivuals using AI's which have maintained ganadotrophins when using exogenous androgens also. But these studies were done on very short peroids of androgen use.

[Swifto]

I hear the dose is very important, its nothing like you would be using if you was opiate dependant, but very small amounts are needed for the desired effect in relation to supression/shutdown.

This is what Maxititer states, but there is a another doctor on UKI that states 50mg+ daily is needed.

[marcus300]

The two ways (which we know about) in being able to maintain GnRH from the HP when technically "shutdown". Is opoid antagonists and estrogen manipulation also. There are studies done on indivuals using AI's which have maintained ganadotrophins when using exogenous androgens also. But these studies were done on very short peroids of androgen use.

I know Psccarb and Maxititer rate is alot from reading their threads on the subject and ive PMed him to try and find out more of an insight into it.

Swifto, as a young bodybuilder who cycles and recover's well, dont you fancy trying it as a experiement it see if it aids or stops shutdown??

[marcus300]

This is what Maxititer states, but there is a another doctor on UKI that states 50mg+ daily is needed.

No, thats not correct maxititer states 5mgs not 50mgs, at that level sides are aswfull.

[Swifto]

No, thats not correct maxititer states 5mgs not 50mgs, at that level sides are aswfull.

Thats what I meant mate.

Max states 5mg/wk or so and there is another Doc on there (UKI) that states larger doses would be needed, the same as Eric Portratz suggests.

Max suggests 5-10mg/wk with a GnRH agonist like Triptorelin Acetate at 100mcg injected ED too.

Regarding using it, I will get round to it although HCG worked verl well for me. But at the moment in my stage of development and what compounds I currently use, I'm not going to be your experiment mate!!! I havent shut myself down in over 3 years!!

[marcus300]

Thats what I meant mate.

Max states 5mg/wk or so and there is another Doc on there (UKI) that states larger doses would be needed, the same as Eric Portratz suggests.

Max suggests 5-10mg/wk with a GnRH agonist like Triptorelin Acetate at 100mcg injected ED too.

Regarding using it, I will get round to it although HCG worked verl well for me. But at the moment in my stage of development and what compounds I currently use, I'm not going to be your experiment mate!!! I havent shut myself down in over 3 years!!

Sorry i must of read your reply wrong, my mistake.
There seems to be many different ways but at this moment in time i dont think there is a set method of dose reading all those who have used it, Pscarb likes 6.25mgs 3 x weekly which sound interesting.
I didnt know you wasnt shutting down your system at this moment in time otherwise you could of been my experiemnt lol

All this is up in the air, its a shame we dont have anyone who as treid it with results either way.

[Swifto]

Sorry i must of read your reply wrong, my mistake.
There seems to be many different ways but at this moment in time i dont think there is a set method of dose reading all those who have used it, Pscarb likes 6.25mgs 3 x weekly which sound interesting.
I didnt know you wasnt shutting down your system at this moment in time otherwise you could of been my experiemnt lol

All this is up in the air, its a shame we dont have anyone who as treid it with results either way.

I would have happilly been your guinea pig! Time isnt right though.

I'm sure there is someone that will be here though?!

[marcus300]

I would have happilly been your guinea pig! Time isnt right though.

I'm sure there is someone that will be here though?!

Where's Goose when you need him!!

[Swifto]

Where's Goose when you need him!!

Ha ha...Yeah.

He will do it.

He's probably over at RR.

[The Deuce]

WOWWOWOWOWOWOWOWOW...

When the BW was done was the only chemical in your system methandone? How long were you off cycle?

Yes THE ONLY chemical in my body, aside from Lisinopril (Blood Pressure Medication which has no adverse effects on HPTA)

According the DOC he sees this a lot in Methadone treated patients, so I am not the only one, but it would explain A LOT. When You look at people who have prescribed Methadone on a DAILY Basis. Not a recreational user but someone who doses everyday.. they lose all muscle Mass, they grow man boobs, they have a voice change to a higher pitch, they stop having sex (either because Natty Test is LOW or because the self esteem is so low because of the FAT GAIN) Whatever the reason, METHADONE is great for getting people off of their addiction to PAIN KILLERS.. especially those people that are addicted to them after A BAD MOTORCYCLE CRASH, BUT methadone is horrible for any MALE trying to perform in area that makes a man, a man.

Now, I hadn't cycled in about 2 years and upon cessation of the last cycle I did have BW done after my PCT and everything was fine.. in FACT my TOTAL TEST was at 777 I believe, I remembered because well.. 7 IS my Fave number and all 7's meant good luck !!

So inherently the Methadone, shut me down. Crazy huh?

I hear the dose is very important, its nothing like you would be using if you was opiate dependant, but very small amounts are needed for the desired effect in relation to supression/shutdown.

When referring to the naloxone it is one of the ACTIVE ingredients in SUBOXONE. A treatment that I also went through before the Methadone program. If it hadn't have been for the GOD Awful taste of the drug, I probably would have stuck with it. Less side effects. And GET THIS !! During my 6 month run with this program I have to state, I FELT LIKE I WAS ON A TESTOSTERONE CYCLE... Much so as far as LIBIDO is considered.. I was a raging HORN DOG !!!

So as far as the effects of the U-OPIOD ANTAGONIST on the HPTA, I really do not find the whole idea too far fetched at all... IN FACT I find it quite reasonable and probable...

[marcus300]

Yes THE ONLY chemical in my body, aside from Lisinopril (Blood Pressure Medication which has no adverse effects on HPTA)

According the DOC he sees this a lot in Methadone treated patients, so I am not the only one, but it would explain A LOT. When You look at people who have prescribed Methadone on a DAILY Basis. Not a recreational user but someone who doses everyday.. they lose all muscle Mass, they grow man boobs, they have a voice change to a higher pitch, they stop having sex (either because Natty Test is LOW or because the self esteem is so low because of the FAT GAIN) Whatever the reason, METHADONE is great for getting people off of their addiction to PAIN KILLERS.. especially those people that are addicted to them after A BAD MOTORCYCLE CRASH, BUT methadone is horrible for any MALE trying to perform in area that makes a man, a man.

Now, I hadn't cycled in about 2 years and upon cessation of the last cycle I did have BW done after my PCT and everything was fine.. in FACT my TOTAL TEST was at 777 I believe, I remembered because well.. 7 IS my Fave number and all 7's meant good luck !!

So inherently the Methadone, shut me down. Crazy huh?



When referring to the naloxone it is one of the ACTIVE ingredients in SUBOXONE. A treatment that I also went through before the Methadone program. If it hadn't have been for the GOD Awful taste of the drug, I probably would have stuck with it. Less side effects. And GET THIS !! During my 6 month run with this program I have to state, I FELT LIKE I WAS ON A TESTOSTERONE CYCLE... Much so as far as LIBIDO is considered.. I was a raging HORN DOG !!!

So as far as the effects of the U-OPIOD ANTAGONIST on the HPTA, I really do not find the whole idea too far fetched at all... IN FACT I find it quite reasonable and probable...

I am speaking to some now who use's it all the time for the effcets on the HPTA and he as bloodwork to back it up with, looks like a very interesting product and could be very usefull to bodybuilders.

Interesting you felt like you was on a test cycle,

[The Deuce]

Interesting you felt like you was on a test cycle,

Only... ONLY... The Libido Increase and the ENERGY that is usually associated with a TEST CYCLE..

I felt GREAT.. I was CLEAN.. because of the goddamned TASTE of the Medication I had to switch from that to Methadone to continue my TREATMENT from Drug Addiction.. It's a lifelong illness and I am very happy to be clean, I have done a complete turn around in my life.. NOT ONLY THAT but because of all of this I was able to focus on switching gears to be able to follow my dream to become a BODYBUILDER. It's GREAT!! I have never been happier... the downfall.. apparently METHADONE shuts down my natty test..

SO NOW.. I don't know how this is going to effect my body but I need to inject TEST every week. I haven't gone a week since February 14th,2009 without injecting at least 200mgs EW.. I mean.. how is that going to effect me in the long run?? I have cycled twice... since then, 700mgs per week... 1st one I ran 14 weeks... Now this one I am 6 weeks deep... and when I end this one.. at 12 weeks I will be returning to my TRT dose of 200mgs EW. So that's 36 weeks NON-STOP so far on Test... I mean it must be safe right??

Obviously when I started I was an OVERWEIGHT BASTARD... I weighed 260lbs. 36% BF when I injected my First Cypionate Dose.. when I started my First Cycle.. I was 235lbs. 26%... Half way through I was down to 215lbs. 21% When I finished the cycle.. I was at 18% Bf and 220lbs. So... The start of this cycle I was 225lbs. 15.5% and Now I am halfway through this cycle and at 14.5% Bf and 227lbs.

So I mean... it was a bad thing to USE AAS at a HIGH BF% but I Dieted appropriately and did what was necessary to make the best of it all.. YES I KNOW I AM

But I am going over the basis... of How I was able to take a Methadone Opiate Addiction program and have a total shutdown of Natty Test and be supplemented with TRT and use that to transform my Body to what it is now... But I am thinking LONG TERM... I probably should have started my own thread on this.. and I probably will since this is a total discussion on U-OPIOID ANTAGONIST... I should be deleting and copy and pasting into my own thread.. but hey too late... I'M .

What do you think?? I don't plan to stop cycling.. it's what I do now.. and I am on TRT so obviously on the cessation of my CYCLES I will be returning to my TRT... I know there are no long term studies, but unlike 90 percent of everyone on here.. I can't PCT and regain my Natty levels.. I have to use synthetic Test. If I cycle.. even MODERATELY for let's say the next 20 some odd years.. that's 1000 more WEEKS of injecting TEST Non-stop... Is this a safe practice as long as my BW comes back stylin' each and every time??

If need be, and it would be more beneficial.. I am obviously not going to be part of the Methadone program forever... I am actually beginning the process of medically weening down... but if this Naxolone is actually a good thing and does what this thread is discussing.. would it be in my better interest to try switching back to the Suboxone treatment while I go through my drug counseling and abandon the methadone which is inhibiting my HPTA...

IT'S A WHOLE LOT TO DIGEST, I have a lot to think of.. and HOW to be successful in the BB-ing world but I also don't want to endanger my health in any way shape or form... YES I KNOW THE RISKS *Possible* OF USING AAS. That's not what I am speaking of... I am talking about the possibility of the next 1000+ weeks injecting a synthetic form of Testosterone ... WHAT DO YOU GUYS THINK???

Or maybe MY ANXIETY is just getting the better of me right now and I am reading WAAAAAY to into this... lol... GOD I AM HYPOCHONDRIAC !!!

Oh and sorry about being kinda

[Mooseman33]

i had a course with subaxone and was on nothing else. bloodwork had doctor worried cause liver value/enzmes were high.
and Duece is right Marcus, the overall feeling is amazing, only cause u are clean, have ur life back and it feels great to be clean..no effects lphtsical effects of cycle, libido goes up cause the narcotics/dope/vice are out of system..

[JiGGaMaN]

i am investigating the use of mu-receptor agonists.

[Narkissos]

Thats what I meant mate.

Max states 5mg/wk or so and there is another Doc on there (UKI) that states larger doses would be needed, the same as Eric Portratz suggests.

Max suggests 5-10mg/wk with a GnRH agonist like Triptorelin Acetate at 100mcg injected ED too.

Regarding using it, I will get round to it although HCG worked verl well for me. But at the moment in my stage of development and what compounds I currently use, I'm not going to be your experiment mate!!! I havent shut myself down in over 3 years!!

I've read most of what Max has written on uki, and I've been researching Naltrexone for over a year now.

I think I'll take the plunge later this year to see how it works.

I just put in an order for Naltrexone... so 'later this year' may actually be a lot sooner than i let on.

I'm going to order enough to try both methods outlined... Max's and the other guy.

The other guy comes highly regarded, and so does Max... so it's a toss up really.

I know Max better, so I'll go with his protocol.

[marcus300]

I've read most of what Max has written on uki, and I've been researching Naltrexone for over a year now.

I think I'll take the plunge later this year to see how it works.

I just put in an order for Naltrexone... so 'later this year' may actually be a lot sooner than i let on.

I'm going to order enough to try both methods outlined... Max's and the other guy.

The other guy comes highly regarded, and so does Max... so it's a toss up really.

I know Max better, so I'll go with his protocol.

Lets us know how you get on, thanks Nark

[Narkissos]

Will do mate.

[BJJ]

Any update?

[anabolic1979]

i am on suboxone and i have found it to slightly hurt muscle growth and strength gains. I have been on for 4 years now and i dont make quite the same gains as i did in the years before i started taking it. also i find my energy levels are way down compared to before. personally i wouldnt mess with any of these drugs, i wish i didnt have to take them but i did it to myself and i have to just make the best of it now.

[BJJ]

bump for Nark

[Narkissos]

I haven't been able to acquire it to be honest :|

[Captain Insane]

Hey guys, sorry for bumping an old topic (a really interesting one, though). I've got a question concerning the article by Eric M. Potratz. He states nandrolones and trenbolones are "double supressors" because of their progesterone activity and thus should be avoided if u are going for a "little or no supression" cycle with naltrexone and an AI to avoid AR and ER supression. But why not just use Stan or any drug to combat elevated progesterone levels? And some caber to combat prolactin.
Thx for your help in advance!


Also wanna say I benefited a great deal from the materials provided on these forums (have been reading the site for almost a year). A hell lot of great info here. So, wanna thank everyone for that.

[BJJ]

Finally able to put my hands on Naltrexone.
I am going to use it on my next cycle.

[2jz_calgary]

i have aquired some as well and will use it this fall in my next cycle.