# Opioid antagonists (Naloxone, Naltrexone, Nalmefene) use on cycle



## overlord (Apr 13, 2012)

Does anyone here have experience using any of these while on-cycle to prevent inhibition of the HPTA?? If so, how did it work? Did you have blood work done at any time to ensure it was working? Dosage protocols?

Opioid Modulation for Preventing AAS Induced HPTA Suppression. | Primordial Performance Blog


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## Standard Donkey (Apr 13, 2012)

intredasting


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## theboneman (Apr 14, 2012)

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.


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## theboneman (Apr 14, 2012)

theboneman said:


> 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 ??


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## Robalo (Apr 14, 2012)

theboneman said:


> 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


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## Digitalash (Apr 14, 2012)

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


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## overlord (Apr 14, 2012)

Digitalash said:


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



The key word here is ANTAGONIST.


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## FTW34 (Apr 14, 2012)

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


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## Digitalash (Apr 14, 2012)

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


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## ~RaZr~ (Apr 14, 2012)

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


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## overlord (Apr 14, 2012)

~RaZr~ said:


> 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


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## Digitalash (Apr 14, 2012)

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


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## ~RaZr~ (Apr 14, 2012)

Digitalash said:


> *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.


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## theboneman (Apr 15, 2012)

robalo said:


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



excellent !! Thank you.


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## Robalo (Apr 15, 2012)

~RaZr~ said:


> 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.


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## ~RaZr~ (Apr 15, 2012)

Robalo said:


> 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.


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## Robalo (Apr 15, 2012)

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)


References

1. Hypothalamic Gonadotropin-Releasing Hormone: Basic and Clinical Aspects.
Yen SSC
Raven Press, New York, pp 245-280 (1991)

2. Absence of androgen receptors in LHRH immunoreactive neurons.
Huang X, Harlan RE.
Brain Res 1993; 624:309-311

3. Augmented hypothalamic proopiomelanocortin gene expression with pubertal development in the male rat: evidence for an androgen receptor-independent action.
Kerrigan JR, et al.
Endocrinology.128:1029-1035. (1991)

4. Distribution of estrogen receptorimmunoreactive cells in the preoptic area of the ewe: co-localisation with glutamic acid decarboxylase but not luteinizing hormone-releasing hormone.
Herbison AE, et al.
Neuroendocrinology 1993; 57:751-759.

5. Unmasking the neural progesterone receptor in the preoptic area and hypothalamus of the ewe: no colocalization with gonadotropin-releasing neurons.
Skinner DC, at el.
Endocrinology 2001; 142:573-579.

6. Multimodal influences of estrogen upon gonadotropin releasing
hormone neurons.
Herbison AE.
Endocrine Reviews 1998; 19:302-330.

7. Negative Feedback Regulation of the Secretion and Actions of Gonadotropin-Releasing Hormone in Males
A.J. Tilbrook and I.J. Clarke
Biol Reprod, Mar 2001; 64: 735

8. Steroid Control of Gonadotropin-Releasing Hormone Secretion: Associated Changes in Pro-Opiomelanocortin and Preproenkephalin Messenger RNA Expression in the Ovine Hypothalamus
James A. Taylor, et al.
Biol Reprod, Mar 2007; 76: 524

9. Do gonadotropin-releasing hormone, tyrosine hydroxylase-, and *-endorphin-immunoreactive neurons contain oestrogen receptors? A double-label immunocytochemical study in the Suffolk ewe
Lehman MN, Karsch FJ.
Endocrinology 1993; 133:887-895

10. α-Endorphin blocks luteinizing hormone-releasing hormone release by inhibiting the nitricoxidergic pathway controlling its release
Alicia G. Faletti, et al.
PNAS, Feb 1999; 96: 1722.

11. The frequency of gonadotropin-releasing hormone stimulation determines the number of pituitary gonadotropin-releasing hormone receptors.
Katt JA, et al.
Endocrinology. 116:2113-2115. (1985)

12. Exogenous gonadotrophin-releasing hormone (GnRH) stimulates LH secretion in male monkeys (Macaca fascicularis) treated chronically with high doses of a GnRH-antagonist.
Weinbauer GF, et al.
J Endocrinol. 133:439-445. (1992)

13. Chronic administration of the luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix decreases gonadotrope responsiveness and pituitary LHRH receptor messenger ribonucleic acid levels in rats.
Pinski J, Lamharzi N, Halmos G, et al. 1996
Endocrinology. 137:3430-3436.

14. Acute effects of testosterone infusion and naloxone on luteinizing hormone secretion in normal men.
GB Kletter, et al.
J. Clin. Endocrinol. Metab., Nov 1992; 75: 1215 - 1219.

15. Naloxone-induced increases in serum luteinizing hormone in the male: mechanisms of action
TJ Cicero, et al.
J. Pharmacol. Exp. Ther., Mar 1980; 212: 573.

16. Endogenous opioids participate in the regulation of the hypothalamic-pituitary-luteinizing hormone axis and testosterone???s negative feedback control of luteinizing hormone.
CICERO, T. J., et al.
Endocrinology 104: 1286-1291, (1979)

17. Opiatergic control of LH secretion is eliminated by gonadectomy.
BHANOT, R. et al.
Endocrinology 112: 399-401, (1983)

18. Role of endogenous opiates in the expression of negative feedback actions of androgens and estrogen on pulsatile properties of luteinizing-hormone secretion in man.
Veldhuis JD, et al..
J Clin Invest. 74:47-55 (1984)

19. Counteraction of gonadal steroid inhibition of luteinizing hormone release by naloxone.
VAN VUGT, et al.
J. Chro- naloxone. Endocrinology 34: 274-278, 1982

20. Unexpected effects of nalmefene, a new opiate antagonist, on the hypothalamic-pituitary-gonadal axis in the male rat.
P Limonta, et al.
Steroids, Dec 1985; 46(6): 955-65.

21. In vivo evidence for a direct effect of naloxone on testicular steroidogenesis in the male rat
TJ Cicero, et al.
Endocrinology, Aug 1989; 125: 957

22. Endogenous opioids participate in the regulation of the hypothalamus- pituitary-luteinizing hormone axis and testosterone's negative feedback control of luteinizing hormone
TJ Cicero, et al.
Endocrinology, May 1979; 104: 1286

23. Effect of naloxone on the plasma levels of LH, FSH, prolactin and testosterone in Beetal bucks.
Singh B, et al.
Department of Animal Production Physiology, CCS Haryana Agricultural University, 125004, Hisar, India

24. Endocrinology: The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men
G.R. Graves, et al.
Hum. Reprod., Oct 1993; 8: 1598 - 1603.

25. Effects of the novel opiate antagonist, SDZ 210-096, on luteinizing hormone secretion in the rat
RA Siegel et al.
J. Pharmacol. Exp. Ther., Apr 1989; 249: 264.

26. Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women
C.C.K. Tay, et al.
Hum. Reprod., Apr 1993; 8: 532 - 539.

27. Naltrexone administration modulates the neuroendocrine control of luteinizing hormone secretion in hypothalamic amenorrhoea
Alessandro D. et al.
Hum. Reprod., Nov 1995; 10: 2868 - 2871.

28. Heroin and naltrexone effects on pituitary-gonadal hormones in man: interaction of steroid feedback effects, tolerance and supersensitivity
JH Mendelson, et al.
J. Pharmacol. Exp. Ther., Sep 1980; 214: 503.

29. Alcohol effects on luteinizing hormone and testosterone in male macaque monkeys
NK Mello, et al.
J. Pharmacol. Exp. Ther., Jun 1985; 233: 588.

30. Erectile function and naltrexone
Goldstein JA
Ann Intern Med 105:799 (1986)

31. Opiate antagonists in erectile dysfunction: a possible new treatment option? Results of a pilot study with naltrexone
van Ahlen H, et al.
Eur Urol 28:246-250 (1995)

32. The effects of opiates on androgen binding in the forebrain of the rat.
PJ Sheridan and JM Buchanan
Int J Fertil, January 1, 1980; 25(1): 36-43.

33. Morphine exerts testosterone-like effects in the hypothalamus of the castrated
male rat.
CICERO, T. J., et al.
Brain Rae. 202: 151-164, (1980)

34. Studies of gonadotropin-releasing hormone (GnRH) action using GnRH receptor-expressing pituitary cell lines.
Kaiser UB, Conn PM, Chin WW.
Endocr Rev. 18:46-70. (1997)

35. Patterns of LH secretion in castrated bulls during intravenous infusion of androgenic and estrogenic steroids: Pituitary response to exogenous luteinizing hormone-releasing hormone
M.J. Docchio et al.
Biology of reproduction 26, 249-257 (1982)

36. Demonstration of progesterone receptor mediated gonadotrophin suppression in men.
Brady B, Anderson RA, Kinniburgh D, Baird DT 2002
J Endocrinol 3(Suppl)C37

37. The direct pituitary effect of testosterone to inhibit gonadotropin secretion in men is partially mediated by aromatization to estradiol.
Bagatell CJ, Dahl KD, Bremner WJ. 1994
J Androl. 15:15-21.

38. Studies on the role of sex steroids in the feedback control of FSH concentrations in men.
Sherins RJ, Loriaux DL. 1973
J Clin Endocrinol Metab. 36:886-893

39. Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men?
Santen RJ. 1975
J Clin Invest. 56:1555-1563

40. Influence of nandrolondecanoate on the pituitary-gonadal axis in males.
JW Bijlsma, et al.
Acta Endocrinol (Copenh), September 1, 1982; 101(1): 108-12.

41. Endocrine approaches to male fertility control.
UA Knuth et al.
Baillieres Clin Endocrinol Metab, February 1, 1987; 1(1): 113-31.

42. Aromatization Mediates Testosterone's Short-Term Feedback Restraint of 24-Hour Endogenously Driven and Acute Exogenous Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone and Follicle-Stimulating Hormone Secretion in Young Men
J. A. Schnorr, et al.
J. Clin. Endocrinol. Metab., June 1, 2001; 86(6): 2600 - 2606.

43. Short-Term Aromatase-Enzyme Blockade Unmasks Impaired Feedback Adaptations in Luteinizing Hormone and Testosterone Secretion in Older Men
Johannes D. Veldhuis et al.
J. Clin. Endocrinol. Metab., Jan 2005; 90: 211 - 218

44. Effects of Aromatase Inhibition in Elderly Men with Low or Borderline-Low Serum Testosterone Levels
Benjamin Z. Leder, et al.
J. Clin. Endocrinol. Metab., Mar 2004; 89: 1174 - 1180.

45. Comparative Assessment in Young and Elderly Men of the Gonadotropin Response to Aromatase Inhibition
Guy G. TSjoen, et al
J. Clin. Endocrinol. Metab., Oct 2005; 90: 5717 - 5722.

46. Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males
Nelly Mauras, et al.
J. Clin. Endocrinol. Metab., Dec 2003; 88: 5951 - 5956.

47. Differential Regulation of Gonadotropin Secretion by Testosterone in the Human Male: Absence of a Negative Feedback Effect of Testosterone on Follicle-Stimulating Hormone Secretion
Frances J. Hayes, et al
J. Clin. Endocrinol. Metab., Jan 2001; 86: 53 - 58


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## Robalo (Apr 15, 2012)

So, i reposted the same article... NICE


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## FTW34 (Apr 15, 2012)

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?


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## ~RaZr~ (Apr 15, 2012)

Good point FTW34


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## l69lou (Apr 15, 2012)

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 !


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## AugustWest (Apr 15, 2012)

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?


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## theboneman (Apr 16, 2012)

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


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## _LG_ (Apr 16, 2012)

Suboxone + Test + Tren = Epic trifecta


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## dav1dg90 (Apr 16, 2012)

Little Guy said:


> 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.


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## Digitalash (Apr 16, 2012)

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.


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## theboneman (Apr 16, 2012)

dav1dg90 said:


> 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.


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## BIGBEN2011 (Apr 16, 2012)

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.


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## FTW34 (Apr 16, 2012)

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.


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## overlord (Apr 16, 2012)

So, nobody here has experience using opioid antagonists while on cycle then...?


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## theboneman (Apr 17, 2012)

overlord said:


> So, nobody here has experience using opioid antagonists while on cycle then...?



ha,ha,ha,ha,lmfao !!!! i guess not bro, we went off the deep end, you just made me laugh, that was funny.


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## PSYCHOPATH. (Apr 17, 2012)

You don't take that shit to prevent HPTA shutdown, you take it because AAS dramatically raise dopamine levels. A dopamine antagonist, for lack of better words, helps prevent long term dopamine receptor shut-down/desensitization. 


This was recommended to me by a doctor who juices himself when he found out that i was blasting and cursing for life. Needless to say, i didn't follow through with his advice....


...FYI, i'm open to being corrected, i don't claim to know this shit inside out.


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## theboneman (Apr 17, 2012)

PSYCHOPATH. said:


> You don't take that shit to prevent HPTA shutdown, you take it because AAS dramatically raise dopamine levels. A dopamine antagonist, for lack of better words, helps prevent long term dopamine receptor shut-down/desensitization.
> 
> 
> This was recommended to me by a doctor who juices himself when he found out that i was blasting and cursing for life. Needless to say, i didn't follow through with his advice....
> ...



no way bro, you put a spin on this for us, and your opinion is just fine, the more the better, you just gave us another way to look at it, that some of us didnt know .
thank you, you also got me thinking when you said you didnt take ya docs advice, hahahaha, most of us dont, i know i didnt....
peace bro
bones.


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## BIGBEN2011 (Apr 17, 2012)

overlord said:


> So, nobody here has experience using opioid antagonists while on cycle then...?


yes i have taken suboxone while on many times i have all so taken every opioid known to man while on.and i have cycled while on none i did not notice any diff.


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## overlord (Apr 17, 2012)

theboneman said:


> no way bro, you put a spin on this for us, and your opinion is just fine, the more the better, you just gave us another way to look at it, that some of us didnt know .
> thank you, you also got me thinking when you said you didnt take ya docs advice, hahahaha, most of us dont, i know i didnt....
> peace bro
> bones.


What the fuck is this bullshit you spew? Everything you write is incoherent and sounds stupid as shit.


BIGBEN2011 said:


> yes i have taken suboxone while on many times i have all so taken every opioid known to man while on.and i have cycled while on none i did not notice any diff.


Suboxone is a combination agonist and antagonist. The effects of suboxone are going to be different than an antagonist alone.


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## dirtbiker666 (Apr 17, 2012)

You can litterly get away with takin a little ass piece of a suboxene (the pill though) not the strip an be good to go all day. Subutex and the strips suck ass in my opinion though. So it's safe to run a cycle and take subs ? As long as your not abusing correct ?


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## theboneman (Apr 18, 2012)

i would think so !?? ive been on methadone for 4 1/2 yrs and ive cycled with good gains and actually i think it helps to repair, i read somewhere a while ago bout guys doing pain killers etc. and it keeps ya from feeling sore, i could be wrong> just saying. anti catabolic or something to that effect.
BIGBEN said the same thing, that he didnt notice any difference.
i will say this though in full confidence, once you start playing with the opiates, theres a good chance youll be doing more and more, untill its a problem, and i can only speak on my behalf, but there are alot of guys RUINED from that addiction, it can get out of control,
i actually went from one to the other, (CROSS ADDICTION ) from drugs to roids, an addict is an addict is an addict.
best thing is we can be a nonactive addict, once one gets a grip on his lifestyle anything is possible.
roids helped me to get away from the heavyshit, actually all the shit,hahaha. it put me in the gym, and then the snowball effect, no not the 8-ball effect,hahaha,
i started eating better, training, stopped smoking, and got good rest, at 45 thats a way better life than where i was at,
ive been grateful for it all and for you guys that are there when we all need ya.
thanks,
bones.


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## _LG_ (Apr 18, 2012)

Suboxone is supposed to be used for a few days to make wd from opiates somewhat bearable.  If you use it longer under a doctor recommendation then you need a new doctor.  Because yours is either an uneducated fucktard, or a scamming piece of shit.  That being said, suboxone is one of my favorite recreational drugs.  I'm just glad my access to it is severely limited.  Also using these as an hpta shutdown inhibitor is a stupid idea.


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## Digitalash (Apr 18, 2012)

Using suboxone as a opioid ANTAGONIST is completely backwards. As far as I know the naloxone is included in them only so people don't inject them, it's far too little to have an effect orally but when injected it will put you into withdrawal. 

If anything using an opioid AGONIST like suboxone or other "real" opiates will have the exact opposite effect and shut you down harder. Not sure how we got on to this topic as it's not the same at all


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## Diesel618 (Apr 18, 2012)

Damn there's a lot of ignorance in this thread. I took an antagonist called naltrexone for months while I was trying to get clean. Happened to also be on cycle. I didn't have bloodwork done so I can't say how much it prevented shutdown, I don't think you're gonna find anyone who experimented on how an opiate antagonist would prevent shutdown. It's kind of ignorant to even ask. No one around here has used them for that purpose I can assure you.


To ol boy that is "2 1/2 years clean", you're not clean, sorry. As long as you stay on suboxone, you are not clean. Whether or not you get high off of it, I certainly didn't, even at 16 mg's, it is still a narcotic and a scheduled drug. Man up and taper down and get through the week of withdrawals and pick up another white keytag. Then you will be clean.


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## dirtbiker666 (Apr 20, 2012)

True story So many people always say I am clean I have not takin anything but subos in a week or a month bla bla..THE TURTH IS ALL SUBS DO ARE PROLONG WITHDRAWL UNTILL YOUR READY TO QUIT.NOT ONLY THAT WITHDRAWL LAST 5X LONGER AN IS MORE HARSH THEN REGULAR OPIATE WITHDRAW.
It is like saying hey bro I quit smokin but I dip now. Granted it still takes will power to stop an just take what your prescribed it is a life long addiction. 



Diesel618 said:


> Damn there's a lot of ignorance in this thread. I took an antagonist called naltrexone for months while I was trying to get clean. Happened to also be on cycle. I didn't have bloodwork done so I can't say how much it prevented shutdown, I don't think you're gonna find anyone who experimented on how an opiate antagonist would prevent shutdown. It's kind of ignorant to even ask. No one around here has used them for that purpose I can assure you.
> 
> 
> To ol boy that is "2 1/2 years clean", you're not clean, sorry. As long as you stay on suboxone, you are not clean. Whether or not you get high off of it, I certainly didn't, even at 16 mg's, it is still a narcotic and a scheduled drug. Man up and taper down and get through the week of withdrawals and pick up another white keytag. Then you will be clean.


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