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SIED Moderators: Genetic Freak | Serotonin101
Do muscle relaxing drugs enhance recovery/growth?
- Thread starter ranunky
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No, they do not. Benzodiazepines have shown to reduce muscle mass with continued use. They could be used on occasion to treat specific pains without detriment...
GHB increases growth hormone levels (it does definitively, but I am not sure if this translates into muscle growth)...
GHB increases growth hormone levels (it does definitively, but I am not sure if this translates into muscle growth)...
djsim
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NSAIDs should technically also inhibit growth.
Dinoprost (synthetic prostaglandin F2) has been shown to act as a highly anabolic substance, and prostaglandins are inhibited by NSAIDs, so even aspirin could be detrimental. But it's hard to know b/c the effects of this specific prostaglandin are highly localised (ie where you inject it is where it acts)
Also, GHB is beneficial for BBing only in that it inhibits dopamine release, which is indirectly linked to INCREASED GH (growth hormone) levels. But BBers figured out many years ago that addiction is too risky for what can be much better sourced directly from sleep, or even from GH itself
Dinoprost (synthetic prostaglandin F2) has been shown to act as a highly anabolic substance, and prostaglandins are inhibited by NSAIDs, so even aspirin could be detrimental. But it's hard to know b/c the effects of this specific prostaglandin are highly localised (ie where you inject it is where it acts)
Also, GHB is beneficial for BBing only in that it inhibits dopamine release, which is indirectly linked to INCREASED GH (growth hormone) levels. But BBers figured out many years ago that addiction is too risky for what can be much better sourced directly from sleep, or even from GH itself
bighooter
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i never got addicted to ghb and used to do it a couple times a week for about a year.
definatly good for sleep and relaxing after a good session, but the only reason i dont do it anymore is because it is a drug and most drugs tend to fcuk you up.
definatly good for sleep and relaxing after a good session, but the only reason i dont do it anymore is because it is a drug and most drugs tend to fcuk you up.
p-mo
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Use of GHB has also been linked to rises in prolactin and cortsiol (as well as GH). These would probably overpower the anabolic effects of the GH release. That being said GHB is a pretty easy on the body substance. It is almost certainly less harmful than using alcohol for relaxation (which is why it became popular in bbing circles, much in the same way as nubain, evryone needs a vice 
)
)
theartofwar
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LucidDream
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^ alcohol can ruin training. not a good idea to drink heavy when ur trying to bulk up
PARooolller
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illegal drugs and alcohol NEVER have a positive effect on muscle gain
ranunky
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PARooolller
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It's funny you should say this in a steroid discussion forum
i jsut consider steroids, hormones...also, they're performance enhancing...big different from taking dianabol and working out to taking oxy and working out
Crook county
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ghb is just like booze, so idk what you are getting at? If your talking about drinking a 12pk of beer 3x a week & diet suks & going to da gym, yea your body will suk. But if you drink on weekends your cooL. a lil booze never hurt
I take benzo's b4 bed 2 get a good nights sleep. I also take Hydrocode 10/325 for muscle soreness 3x a week & it does help & all this relaxes my muscles to grow grow grow, you only grow when resting
MY 2 CENTS
PARooolller
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Taking hydrocodone 3x a week will inhibit muscle growth...I know there's a study out there linking lower t levels with opiate use...
Crook county
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lower test levals b/c of opiate use? or did I read it wrong
PARooolller
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that's what I've heard...there has even been threads on this
VictorZ06
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Some medical articles on the issue...
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.
Researchers recognized that both heroin and methadone were associated with decreased serum testosterone levels in men.
[Brown and
Zueldorf 2007; Cicero et al. 1975; Hanbury et al. 1977; Mendelson et al. 1975a, 1975b].
http://74.125.93.132/search?q=cache...ioid-Induced+Androgen+Deficie.pdf&hl=en&gl=us
/V
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.
Researchers recognized that both heroin and methadone were associated with decreased serum testosterone levels in men.
[Brown and
Zueldorf 2007; Cicero et al. 1975; Hanbury et al. 1977; Mendelson et al. 1975a, 1975b].
http://74.125.93.132/search?q=cache...ioid-Induced+Androgen+Deficie.pdf&hl=en&gl=us
/V
Last edited:
Show me the study where benzos reduce muscle growth? Do reasearch before you spout off.
PARooolller
Bluelighter
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Benzos DEFINATELY cause muscle weakness in my experience with them...I don't have any studies to back this up but daily use of benzos will cause muscle weakness---not too sure about loss of muscle...
When I detoxed off of benzos my joints were on fucking fire...benzos are the one drug that NEEDS to be used sparingly for any benefits...daily use or random abuse just leads to negative sides...
When I detoxed off of benzos my joints were on fucking fire...benzos are the one drug that NEEDS to be used sparingly for any benefits...daily use or random abuse just leads to negative sides...
Crook county
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i use them b4 bed to relax & sleep all night, but u gotta know that gabba is produced naturally in your body & that is what benzo's are, not 2 recommend to take benzos b4 the gym b/c yea u will feel like jello.