Opiates and Test Production/levels

[yungone501]

Hello, people. Not sure if this is the proper section for this post but some could say opiates are a "supplement" for severe/chronic pain management, LOL. Anyhow here's the scoop. About 6 months ago I ran a cycle and due to some unseen circumstances, was unable to ever really due a PCT afterwards (until recently) For those 6 solid months, I struggled daily with extremely low sex drive...really LOW. First I tried doing a PCT (finally) with Clomid, Nolvadex and HCG to no avail. I was depressed, relationship was going to hell and I figured it was time for TRT! However, one day I was doing some research and found some articles that really shed ALOT of light on the predicament. I had been prescribed Norco 10's (hydrocodones) 4/day and helped with all the pain. Curious, I begine reading these articles and decided to stop taking my prescription pain medication for a while to see what happened... My sex drive came back SOLID 100%. So to all the people that are currently taking any opoite based pain medications, hope this helps:





Clin J Pain. 2000 Sep;16(3):251-4. Links
Hypogonadism in patients treated with intrathecal morphine.

Finch PM, Roberts LJ, Price L, Hadlow NC, Pullan PT.
Perth Pain Management Centre, South Perth, Western Australia.
OBJECTIVE: The objective of this study was to investigate the hypothalamic-pituitary-gonadal response to intrathecal opioids. PATIENTS: Thirty patients receiving intrathecal morphine for chronic nonmalignant pain were studied for clinical and biochemical evidence of hypogonadism. Ten men and 10 postmenopausal women with chronic pain of similar duration but who were not receiving any form of opioid therapy acted as control subjects. RESULTS: Men and both premenopausal and postmenopausal women had evidence of hypogonadism with low levels of serum testosterone or estrogen coupled with low levels of pituitary gonadotrophins. Control subjects had hormone levels in the expected range for their sex and age. Two men demonstrated recovery after ceasing intrathecal opioid therapy. CONCLUSIONS: Hypogonadotrophic hypogonadism is a common complication of intrathecal opioid therapy in both men and women.

J Clin Endocrinol Metab. 2000 Jun;85(6):2215-22. Links
Endocrine consequences of long-term intrathecal administration of opioids.

Abs R, Verhelst J, Maeyaert J, Van Buyten JP, Opsomer F, Adriaensen H, Verlooy J, Van Havenbergh T, Smet M, Van Acker K.
Department of Endocrinology, University Hospital Antwerp, Belgium.
Intrathecal administration of opioids is a very efficient tool in the long-term control of intractable nonmalignant pain. However, despite the well known role of opioids in endocrine regulation, few data are available about possible effects on hypothalamic-pituitary function during this treatment. Seventy-three patients (29 men and 44 women; mean age, 49.2 +/- 11.7 yr) receiving opioids intrathecally for nonmalignant pain were enrolled for extensive endocrine investigation. At the time of hormonal determination, the mean duration of opioid treatment was 26.6 +/- 16.3 months; the mean daily dose of morphine was 4.8 +/- 3.2 mg. The control group consisted of 20 patients (11 men and 9 women; mean age, 54.2 +/- 14.0 yr) with a comparable pain syndrome but not treated with opioids. Decreased libido or impotency was present in 23 of 24 men receiving opioids. The serum testosterone level was below 9 nmol/L in 25 of 29 men and was significantly lower than that in the control group (P < 0.001). The free androgen index was below normal in 18 of 29 men and was significantly lower than that in the control group (P < 0.001). The serum LH level was less than 2 U/L in 20 of 29 men and was significantly lower than that in the control group (P < 0.001). Serum FSH was comparable in both groups. Decreased libido was present in 22 of 32 women receiving opioids. All 21 premenopausal females developed either amenorrhea or an irregular menstrual cycle, with ovulation in only 1. Serum LH, estradiol, and progesterone levels were lower in the opioid group. In all 18 postmenopausal females significantly decreased serum LH (P < 0.001) and FSH (P = 0.012) levels were found. The 24-h urinary free cortisol excretion was below 20 microg/day in 14 of 71 opioid patients and was significantly lower than that in the control group (P = 0.003). The peak cortisol response to insulin -induced hypoglycemia was below 180 microg/L in 9 of 61 opioid patients and was significantly lower than that in the nonopioid group (P = 0.002). The insulin-like growth factor I SD score was below -2 SD in 12 of 73 opioid patients and was significantly lower than that in the control group (P = 0.002). The peak GH response to hypoglycemia was below 3 microg/L in 9 of 62 subjects and was significantly lower than that in the control group (P = 0.010). Thyroid function tests and PRL levels were considered normal. No metabolic disturbances were recorded, apart from significantly decreased high density lipoprotein cholesterol levels (P = 0.041) and elevated total/high density lipoprotein cholesterol ratio (P = 0.008) in the opioid group compared to the control group. Supplementation with gonadal steroids improved sexual function in most patients. In conclusion, of all patients receiving intrathecal opioids, the large majority of men and all women developed hypogonadotropic hypogonadism, about 15% developed central hypocorticism, and about 15% developed GH deficiency. These findings suggest that further investigations are required to determine the need for systematic endocrine work-up in these patients and the necessity for substitutive therapy.

Clin J Pain. 2002 May-Jun;18(3):144-8. Links
Sex hormone suppression by intrathecal opioids: a prospective study.

Roberts LJ, Finch PM, Pullan PT, Bhagat CI, Price LM.
Western Australian Pain Management Centre, Department of Anesthesia, Sir Charles Gairdner Hospital, Western Australia, Australia.
OBJECTIVE: Sexual dysfunction and low testosterone levels have been observed previously in males with chronic noncancer pain treated with intrathecal opioids. To investigate the hypothesis that intrathecal opioids suppress the hypothalamic-pituitary-gonadal axis, a prospective nonrandomized investigation of the function of this axis was undertaken. DESIGN: Ten males with chronic noncancer pain were evaluated for clinical and biochemical evidence of hypogonadism at baseline and during the first twelve weeks of intrathecal opioid therapy. RESULTS: Intrathecal opioid administration resulted in a significant (p <0.0001) reduction in serum testosterone, from 7.7 +/- 1.1 (mean +/- SEM) nmol/L at baseline to 2.0 +/- 0.7, 2.8 +/- 0.5, and 4.0 +/- 0.9 nmol/L at 1, 4, and 12 weeks, respectively. This was associated with a reduction in libido and potency. Luteinizing hormone and follicle-stimulating hormone levels remained within reference ranges, indicating central rather than peripheral suppression. CONCLUSIONS: Administration of intrathecal opioids may result in hypogonadotrophic hypogonadism. As part of the consent for therapy process, patients should be informed about this effect and its management. With long-term intrathecal opioid administration, the hypothalamic-pituitary-gonadal axis should be monitored. Where indicated, testosterone replacement should be undertaken to improve sexual function and prevent the potential metabolic effects of hypogonadism, in particular, osteoporosis.

Neuroscience. 2006 Jul 7;140(3):929-37. Epub 2006 Apr 3. Links
Single opioid administration modifies gonadal steroids in both the CNS and plasma of male rats.

Ceccarelli I, De Padova AM, Fiorenzani P, Massafra C, Aloisi AM.
Pain and Stress Neurophysiology Laboratory, Neuroscience and Applied Physiology Section, Department of Physiology, University of Siena, Via Aldo Moro, 2, 53100 Siena, Italy.
While morphine remains one of the most widely used opioids for the treatment of painful conditions, other opioids are also commonly employed. Because of the interactions between opioids and gonadal hormones, in particular opioid-induced hypogonadism, this study investigated the effects of widely used opioids on plasma testosterone and estradiol levels and brain testosterone levels in male rats. Animals were s.c. injected with two concentrations of morphine (5 or 10 mg/kg), fentanyl (0.05 or 0.1 mg/kg), tramadol (10 or 40 mg/kg), buprenorphine (0.05 or 0.1 mg/kg) or saline (0.7 ml/kg). Four or 24 h after treatment, the rats were deeply anesthetized to collect blood samples from the abdominal aorta and to perfuse the brains with saline. Plasma and brain hormone levels were measured by radioimmunoassay. In rats studied 4 h after treatment, all the opioids except tramadol 10 mg/kg decreased plasma testosterone in comparison with saline administration. At the same time, plasma estradiol levels were lower than control in the groups treated with the low doses of morphine, tramadol and buprenorphine, while estradiol remained at control levels in the other groups. Twenty-four hours after treatment, plasma testosterone levels were different (higher) than control in the animals treated with the low doses of morphine, fentanyl and buprenorphine. Estradiol was lower than control in the low dose groups, while the high doses did not produce any changes with respect to control. Four hours after treatment, brain testosterone was drastically decreased in all groups except buprenorphine, in which it remained at control levels. All groups returned to control levels at 24 h after treatment. In conclusion, opioids exert important effects on plasma and CNS sex hormone levels. The different magnitude and time-course of the effects of the different opiates on testosterone and estradiol levels are likely due to their different mechanism of action.

Some evidence that the decline in testosterone is related to an increased conversion of tesosterone to DHT in the CNS which would effectively tell the HPTA that the body is producing more testosterone than it actually is.

Int J Dev Neurosci. 2005 Nov;23(7):621-6. Epub 2005 Sep 6. Links
In vivo evidence for an increase in 5alpha-reductase activity in the rat central nervous system following morphine exposure.

Amini H, Ahmadiani A.
Department of Pharmacology, Neuroscience Research Center, Shaheed Beheshti University of Medical Sciences, P.O. Box 19835-355, Tehran, Iran.
In the present study, the effects of acute and chronic morphine exposure on testosterone concentrations in the central nervous system (CNS) and serum were investigated in rats. Acute morphine administration (5 mg/kg, s.c.) reduced significantly testosterone levels in serum and spinal cord but not in the brain. Following chronic morphine administration (orally for 21 days), the brain testosterone was also significantly reduced as well as serum and spinal cord. Since, the decrease in testosterone levels following morphine exposure was more obvious in the CNS than serum, we suggested that it cannot be caused by only a direct decline in testosterone levels in periphery, and an increased local metabolism of testosterone in the CNS might be attributed in these effects. This hypothesis was supported with the findings that pretreatment with finasteride, a 5alpha-reductase inhibitor (5 mg/kg, s.c.) blocked testosterone elimination from the CNS following morphine exposure. Moreover, the serum concentration of 5alpha-reduced metabolites of testosterone, dihydrotestosterone and 3alpha-diol glucuronide was increased significantly following chronic morphine exposure, but not after co-treatment with finasteride. These results suggest that morphine exposure increase the CNS activity of 5alpha-reductase, which is an important metabolizing enzyme for testosterone.

Horm Behav. 2007 May;51(5):605-10. Epub 2007 Mar 2. Links
Finasteride, a 5alpha-reductase inhibitor, potentiates antinociceptive effects of morphine, prevents the development of morphine tolerance and attenuates abstinence behavior in the rat.

Verdi J, Ahmadiani A.
Department of Physiology and Pharmacology, Kashan University of Medical Sciences, Kashan, Iran.
It has been shown that morphine increases 5alpha-reductase enzyme activity in the rat central nervous system; however importance of this finding on morphine analgesia, tolerance and dependence has not been reported. In the present study, we investigated inhibition of 5alpha-reductase enzyme on morphine effects using finasteride. To determine whether the 5alpha-reductase enzyme interact with morphine analgesia, finasteride (5 mg/kg, i.p.) was administrated with morphine (5 and 7 mg/kg, i.p.). The tail-flick test was used to assess the nociceptive threshold, before and 15, 30, 45, 60 and 90 min after drug administration. In tolerance experiments, morphine 20 mg/kg was injected i.p., twice daily for 4 days. The development and expression of dependence were assessed in the naloxone precipitation test 5 days after the morphine (20-30 mg/kg, i.p.) administration. We found that finasteride could potentiate the antinociceptive effect of morphine. In addition, chronic finasteride administration effectively blocked development of tolerance and dependence to morphine. Following chronic morphine administration, single dose injection of finasteride failed to reverse tolerance but prevented naloxone precipitate withdrawal syndrome. Therefore, it was concluded that there is a functional relationship between 5alpha-reductase enzyme and morphine.

Also, Ive read numerous places on how Opiates can hinder nutrient (protein, carb) absorbtion in the intestine and REALLY impact gains. Thanks.

[l2elapse]

I could have told you this months ago = ]

[Swifto]

I could have told you this months ago = ]

Same here...

Years ago...

But thank-you for the studies.

If you look into this subject more, opiate-antagonists (Naltrexone, Nalaxone etc..) seem to have the opposite effect. I discuss this vaguely in my PCT Article.

[yungone501]

Same here...

Years ago...

But thank-you for the studies.

If you look into this subject more, opiate-antagonists (Naltrexone, Nalaxone etc..) seem to have the opposite effect. I discuss this vaguely in my PCT Article.

Well, I figured there might be someone out there that is taking say hydrocodones while trying to PCT and is getting nowhere because of it. I NEVER would of suspected this until I accidently stumbled across one little sentence in this whole forum that said so. Just a little FYI to anyone else this hasnt happened to also.

Swifto, are you saying by taking an opiate antagonist, you can actually increase test levels?

[Swifto]

I'm saying that in theory, if you were to take opiate-anatagonists, such as Naltrexone, one may be able to maintain GnRH and endogenous LH/FSH when "shutdown" from AAS. I havent done it, but some claim to have done it. Naltrexone also notoriously makes user's feel like complete shit.

[yungone501]

I'm saying that in theory, if you were to take opiate-anatagonists, such as Naltrexone, one may be able to maintain GnRH and endogenous LH/FSH when "shutdown" from AAS. I havent done it, but some claim to have done it. Naltrexone also notoriously makes user's feel like complete shit.

Just so we're staright here, an opiate antagonist is usually whats given to users of opiates to help with desire/withdrawls?

Always a down side to PCT.

[Swifto]

Just so we're staright here, an opiate antagonist is usually whats given to users of opiates to help with desire/withdrawls?

Always a down side to PCT.

Yes. Were straight bro.