Thread: Opioid antagonists (Naloxone, Naltrexone, Nalmefene) use on cycle

intredasting

Who told you opioid derivatives prevent hpta shut down ?? Its been my experiance, seeing im on methadone, that not only wont it prevent it. It causes it !! All my test levels were comming back 86 ngdl, wich is sad !! It was the methadone and my doc prescribed 600 mgs a week (test) to compensate.

And thats the only thing that counters it, everytime i come off test my levels go down under 100, normal for my age should be 350. I hope this put a spin on it for you, excellent topic.
Later bones.

Originally Posted by theboneman

who told you opioid derivatives prevent hpta shut down ?? Its been my experiance, seeing im on methadone, that not only wont it prevent it. It causes it !! All my test levels were comming back 86 ngdl, wich is sad !! It was the methadone and my doc prescribed 600 mgs a week (test) to compensate.

And thats the only thing that counters it, everytime i come off test my levels go down under 100, normal for my age should be 350. I hope this put a spin on it for you, excellent topic.
Later bones.

edit; okay i see it, antagonist, you mean a blocker ?? Right ?? I thought words that ended with one, and fene were opiods ??

Originally Posted by theboneman

edit; okay i see it, antagonist, you mean a blocker ?? Right ?? I thought words that ended with one, and fene were opiods ??

Antagonist = chemical compound that connects to the receptors (in this case opioid receptors) without activating them

Opiates do lower test levels never heard of them preventing hpta shutdown?

Originally Posted by Digitalash

Opiates do lower test levels never heard of them preventing hpta shutdown?

The key word here is ANTAGONIST.

Intresting. Wonder how much damage i did to my natural test back in my heroin days. Oh well that was a long ass time ago

Whoops isn't taking an antagonist like naltrexone supposed to be very unpleasant or is that only in opiate addicts?

Naltrexone and Steroids...intersting....

And yes it does cause unpleasant and unwanted side effects, which includes -
"Anxiety; appetite loss; chills; constipation; delayed ejaculation; diarrhea; dizziness; drowsiness; feeling down; headache; increased energy; increased thirst; irritability; joint and muscle pain; low energy; nausea; nervousness; sleeplessness; stomach pain/cramps; vomiting." Naltrexone Side Effects | Drugs.com

Originally Posted by ~RaZr~

Naltrexone and Steroids...intersting....

And yes it does cause unpleasant and unwanted side effects, which includes -
"Anxiety; appetite loss; chills; constipation; delayed ejaculation; diarrhea; dizziness; drowsiness; feeling down; headache; increased energy; increased thirst; irritability; joint and muscle pain; low energy; nausea; nervousness; sleeplessness; stomach pain/cramps; vomiting." Naltrexone Side Effects | Drugs.com

Unpleasant side effects of aromasin:

Anxiety; back, joint, muscle, or limb pain; constipation; coughing; diarrhea; dizziness; flu-like symptoms; hair loss; headache; hot flashes; increased or decreased appetite; increased sweating; nausea; stomach pain or upset; tiredness; trouble sleeping; weight gain; vomiting. Aromasin Side Effects | Drugs.com

Diarrhea and constipation, increased energy and low energy lol how does that work. So even in a non addict blocking your bodies natural opioids will probably not be fun, if you have a habit it'll be mucho worse

Originally Posted by Digitalash

Diarrhea and constipation, increased energy and low energy lol how does that work. So even in a non addict blocking your bodies natural opioids will probably not be fun, if you have a habit it'll be mucho worse

Probably because of the receptors being "messed with". Opioids slow everything down (constipate and low energy). Once Naltrexone is added, the body bounces back. So that is why one may HYPOTHETICALLY experience the exact opposite.

Originally Posted by robalo

antagonist = chemical compound that connects to the receptors (in this case opioid receptors) without activating them

excellent !! Thank you.

Originally Posted by ~RaZr~

Naltrexone and Steroids...intersting....

And yes it does cause unpleasant and unwanted side effects, which includes -
"Anxiety; appetite loss; chills; constipation; delayed ejaculation; diarrhea; dizziness; drowsiness; feeling down; headache; increased energy; increased thirst; irritability; joint and muscle pain; low energy; nausea; nervousness; sleeplessness; stomach pain/cramps; vomiting." Naltrexone Side Effects | Drugs.com

Aspirin side effects:

irritation of the stomach or bowel, indigestion,nausea, worsening of asthma caused by narrowing of airways, allergic reactions, vomiting, inflammation (swelling) of the stomach, bleeding in the stomach, bruising, Stroke

All side effects reported by users are included in that list, that doesn't mean that you'll get them.

Originally Posted by Robalo

All side effects reported by users are included in that list, that doesn't mean that you'll get them.

Exactly and that is why I always state that the user could HYPOTHETICALLY experience any, all or none of the side effects.

Opioid Modulation for Preventing AAS Induced HPTA Suppression.


By Eric M. Potratz (Email)

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 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 suppression of LH release. (42) However, since progesterone based AAS 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 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). (7,16) The EOP 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, 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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So, i reposted the same article... NICE

For those of you that asked...Taking a Antagonist could be extremely painfull if this. Lets say a addict is trying to kick but still has opiates in his system. taking the Antagonist to early would send the addict in the worse withdrawl he's ever experianced. I mean wishing you were dead painful, I thought i was gonna die...The only way to stop that Antagonist induced withdrawl is to Take more opiates.

Now if the addict is already in full withdrawl and takes the antagonist, the antagonist will fill the receptors and the withdrawl pain will go away completely..

pretty wierd huh?

Good point FTW34

Another thing although not probable is that say you get hurt badly while on naltrexone. The opiates they would give you for pain would not work for approx 3 days it takes to clear the naltrexone from your system. I know this from my stupid days years ago when I was in early recovery and wanted to go on it to help stay clean but I had a very dangerous job and they recomended against it. Moral of story don't wreck your car- could you imagine ?!!! yeech !

Great read.

I am about to run a Tbol/MHN/Primo cut cycle. Ive got HCG for on cycle but what would be the best PCT protocol for a Progestin Receptor caused shutdown of the HPTA?

Will Nolva and Clomid still be the best?

Robolo, excellent article, im dealing with a serious shut down issue now, and i enjoyed that alot, thanks man. Very informative bro.

Suboxone + Test + Tren = Epic trifecta

Originally Posted by Little Guy

Suboxone + Test + Tren = Epic trifecta

I'd beg to differ bro, suboxone has NOT helped me in anyway during my blasts or even pct at that. I would say it has had a negative effect during my cycles with eating, sleeping, training, etc. Suboxone is buprenorphine and naloxone which is both opioid antagonists and some serious ones at that, and I wish to god I could stop and im only at a half a day, a quarter AM and another quarter PM, and my withdrawl symptoms are off the charts. So guys just leave this alone please it is not worth it trust me, one day I will be off but as of right now it is what it is, im clean and im happy so why fuck it up at the moment, but yes suboxone still sucks lmao.

By the way I've been clean for 2 1/2 years for those who care, besides my steroid usuage im a addict still there lmao.

The difference bro is buprenorphine is an opioid agonist, meaning it still feels like a damn opiate... I use them occasionally still because they're cheap and I have less trouble staying away from them than other ope's. If you don't already have a dependency issue though stay away from suboxone or you're playing with fire. I'm glad to hear you're clean though bro and that the subs help you. Just play around with decreasing dose SLOWLY until you don't need them. My dad's been taking them for years now and is more ok than in his using days so I think some people really are better off staying on them longterm, but if it's possible for you to taper down and stay off without turning to other drugs that is the best solution obviously.

Originally Posted by dav1dg90

I'd beg to differ bro, suboxone has NOT helped me in anyway during my blasts or even pct at that. I would say it has had a negative effect during my cycles with eating, sleeping, training, etc. Suboxone is buprenorphine and naloxone which is both opioid antagonists and some serious ones at that, and I wish to god I could stop and im only at a half a day, a quarter AM and another quarter PM, and my withdrawl symptoms are off the charts. So guys just leave this alone please it is not worth it trust me, one day I will be off but as of right now it is what it is, im clean and im happy so why fuck it up at the moment, but yes suboxone still sucks lma

By the way I've been clean for 2 1/2 years for those who care, besides my steroid usuage im a addict still there lmao.

i care,!!!! congrats to you brother !! 2 1/2 yrs is huge, im sure there was a time when you couldnt get a day huh, i know thats true for me, but your very honest bro, and im proud of ya, you almost was a statistic, instead your a winner now!!!, i have 4yrs 4 months, and counting, NOTHING IS WORTH LOSING THIS !!,
keep your eye on the prize. ( who aint addicted to the juice, hahaha, know what im saying)
ya dont see a gear head selling his shit like a crack head, nothing to be ashamed about,
just gotta keep things simple and not complicate em, steroids can be safe, and your smart enough to keep it that way.
keep up your awesome work, i know your proud, but also think of the people who love you,
THEY ARE PROUD OF YOU TOO, GOD BLESS.
BONES.

hey man i will tell you how to get off subs.what ever you are taking now we will say 4mg a day drop your dose by 25% which would be to 3mg a day so you would take 1.5mg twice a day for 4 or 5 days then drop again by 25 % so you would drop to 2.25mg a day then drop to i went to 2mg just to be easier to figure then drop to 1.5mg a day the 1 mg all the way douwn to .25mg a day which is just dust but still really really stroung then start skiping days so take .25mg say on monday then nothing tues then 25mg weds then start skiping 2 days then 3 days then stop.and during this weaning process if you start having w/d take a sliver which is a.25mg it will take away the wd but if you have to take a sliver you start the 3 or 4 days over.so you do not drop dose until you have went 4 or 5days with no wd.i hop this makes since and if you dont do it this way and jump off even at 1mg a day the wd will be bad and they last a long time.if you wean douwn like i say they will be a lot less you still will feel like crap but not no where near as bad. suboxone are really really stroung 1mg is as stroung as about 30mg roxi or more maybe 60mg oxy.pm me if you want to know more i am a 20 year addict and i was on subs for arroung 4 years.

See the problem is, if suboxone is taking everyday for long peroids if time you become dependant to them to, You dont have to tell me about opiod addiction, i use to shoot 10 bagz of heroin a day, for about a year, my withdrawls were insane, i used suboxone to get off... Started with 2, next day i took one, next day i took half, next day i took qaurter and stayed a qaurter for about a week than i was done. Of course i still felt a little shitty, but it was better than full on withdrawl. Doctors make big mistakes by perscribing them for long peroids of time.