opiates causing ED

[yoyo1024]

Has anyone here ever experienced Erectile Dysfunction from taking pain medication? I was prescribed oxycodone for a certain matter, and I can only get it up to maybe 80% when I'm on these meds. My pregnant girlfriend was mildly offended last night, she thought it was because of her "big baby belly". Can taking these meds result in permanent ED? Also, I am currently doing the JP90 routine, and I've been doing this routine for about 2 weeks now. I'm not sure if it's a good idea to keep doing PE while I'm on these meds. If anyone has any info on this subject, I would greatly appreciate your feedback. Thank you in advance..

[Cavalier]

I have been taking a opiate pain medicine for four years now for my back. Although I have experienced some ED problems the last two years, it was not related to the medicine. Opiate medication does not list ED as a possible side effect. It may be more related to the stress your body is in from the pain or you have been overworking your PE exercises. Take a few days off to see if your EQ comes back. If it does, back down on the intensity of your routine when you start again. There is no reason to stop PE because of this medication.

[corageon]

Has anyone here ever experienced Erectile Dysfunction from taking pain medication? I was prescribed oxycodone for a certain matter, and I can only get it up to maybe 80% when I'm on these meds. My pregnant girlfriend was mildly offended last night, she thought it was because of her "big baby belly". Can taking these meds result in permanent ED? Also, I am currently doing the JP90 routine, and I've been doing this routine for about 2 weeks now. I'm not sure if it's a good idea to keep doing PE while I'm on these meds. If anyone has any info on this subject, I would greatly appreciate your feedback. Thank you in advance..

Yes, opiates can cause E.D and destroy your libido.


Their neuro-endocrine effects are well-documented and they also decrease testosterone as well as oxytocin and other libidogenic hormones...they can cause anhedonia/emotional apathy as well...in other words, they can reduce the amount of emotions you feel.

Read em up.

Hypogonadism in men consuming sustained-action oral opioids.


Drug-induced sexual dysfunction in men and women

ED Tied to Long-Term Narcotic Use in Men


OxyContin - What effect does it have on erection and sex?

Erectile Dysfunction in Opioid Users: Lack of Association with Serum Testosterone

J Comp Neurol. 1989 Aug 1;286(1):85-95.beta-Endorphin and gonadotropin-releasing hormone synaptic input to gonadotropin-releasing hormone neurosecretory cells in the male rat.

Chen WP1, Witkin JW, Silverman AJ.
Author information



Abstract

Physiological and pharmacological evidence has suggested that both endogenous opiates and gonadotropin-releasing hormone (GnRH) itself can act centrally to exert a tonic inhibition on gonadotropin secretion via an inhibition of the neurosecretion of GnRH. To determine if the effects of these two peptides might be mediated via a direct synaptic input to the GnRH neuron, we undertook a double label ultrastructural study. We were able to localize in the same tissue section beta-endorphin and GnRH. Analysis of serial sections through GnRH perikarya and dendrites in the male rat diagonal band/preoptic area revealed that almost 10% of the synapses impinging on the GnRH neuron contained beta-endorphin; an additional 10% of the terminals contained GnRH. These data provide anatomical evidence in support of both a direct modulation of GnRH release by opiates and of the presence of an ultrashort feedback loop.


PMID:2671062[PubMed - indexed for MEDLINE]

J Pain. 2002 Oct;3(5):377-84.Hypogonadism in men consuming sustained-action oral opioids.

Daniell HW1.
Author information



Abstract

Naturally occurring opiates (endorphins) diminish testosterone levels by inhibiting both hypothalamic gonadotrophin releasing hormone production and testicular testosterone synthesis. Heroin addicts treated with a single daily dose of methadone and nonaddicts receiving continuous intrathecal opioids quickly develop low luteinizing hormone and total testosterone levels. A similar pattern was sought in men consuming commonly prescribed oral opioids. Free testosterone (FT), total testosterone (TT), estradiol (E(2)), dihydrotestosterone (DHT), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured in 54 community-dwelling outpatient men consuming oral sustained-action dosage forms of opioids several times daily for control of nonmalignant pain. Hormone levels were related to the opioid consumed, dosage and dosage form, nonopioid medication use, and several personal characteristics and were compared with the hormone analyses of 27 similar men consuming no opioids. Hormone levels averaged much lower in opioid users than in control subjects in a dose-related pattern (P < .0001 for all comparisons). FT, TT, and E(2) levels were subnormal in 56%, 74%, and 74%, respectively, of opioid consumers. Forty-eight men (89%) exhibited subnormal levels of either FT or E(2). Either TT or E(2) level was subnormal in all 28 men consuming the equivalent of 100 mg of methadone daily and in 19 of 26 (73%) consuming smaller opioid doses. Eighty-seven percent (39 of 45) of opioid-ingesting men who reported normal erectile function before opioid use reported severe erectile dysfunction or diminished libido after beginning their opioid therapy. Commonly prescribed opioids in sustained-action dosage forms usually produce subnormal sex hormone levels, which may contribute to a diminished quality of life for many patients with painful chronic illness.


PMID: 14622741 [PubMed]

Fed Proc. 1980 Jun;39(8):2551-4.Effects of exogenous and endogenous opiates on the hypothalamic--pituitary--gonadal axis in the male.

Cicero TJ.
Abstract

Narcotics acutely depress serum testosterone levels in the male. Three mechanisms could be involved: an enhancement of the degradation of testosterone; a direct inhibition of testicular steroidogenesis; or, finally, an inhibition of the hypothalamic-pituitary-luteinizing hormone (LH) axis resulting in a reduction in LH-dependent testicular steroidogenesis. The currently available evidence indicates that narcotics do not affect the catabolism of testosterone by the liver or testicular steroidogenesis. Rather, the data favor a direct action on the hypothalamic--pituitary--LH axis, probably by inhibiting the secretion of LH-releasing hormone (LH-RH) from the hypothalamus. The effects of narcotics on serum LH appear to be mediated via specific opioid receptors, suggesting that a naturally occurring opioid-like substance exists that normally inhibits LH. In support of this conclusion, opiate receptor blockers markedly increase serum LH levels shortly after their subcutaneous administration. In addition, endogenous opioids also seem to participate in testosterone's negative feedback control of the hypothalamic--pituitary--LH axis. Thus, it appears that opiate drugs inhibit the function of the hypothalamic-pituitary-gonadal axis by occupying opiate receptors in the hypothalamus and, moreover, that endogenous opioids exist that normally bind to these receptors and regulate activity in this axis.


PMID:6247215[PubMed - indexed for MEDLINE]

[closed224]

While true if you are using opiates for intense ongoing pain management the benefits likely out weigh the possibilities of these reactions. Also you can off set these negatives. One off set is PE, and another is meditative self speak control I g your responses. The benefits must be weighed against the possible down sides.
End all be all is ongoing intense pain sucks and can cause ED just as much.
It is a hard choice either way.

[Cavalier]

Yes, there are studies showing with long term use there is a small possibility of it lowering testosterone levels, mostly heavy users and addicts. The chance of it happening is so small that they don't even list it as a possible side effect for the drugs. I myself had my testosterone levels checked a couple moths ago and it was in the 600 range of total testosterone. But anyways, to answer the OP, two weeks use will not effect testosterone levels.

[corageon]

Yes, there are studies showing with long term use there is a small possibility of it lowering testosterone levels, mostly heavy users and addicts. The chance of it happening is so small that they don't even list it as a possible side effect for the drugs. I myself had my testosterone levels checked a couple moths ago and it was in the 600 range of total testosterone. But anyways, to answer the OP, two weeks use will not effect testosterone levels.

You make some good points - however, individuals may be more susceptible to opiate-induced sexual dysfunction if they are on anti-depressants (SSRI's), anti-psychotics and / or are under consistent stress.

http://www.ncbi.nlm.nih.gov/pmc/arti...00664-0704.pdf
Analysis of the receptor specificity of tolerance induction in stress versus opioid-related prolactin secretion in rats. - PubMed - NCBI

J Endocrinol. 1991 Feb;128(2):281-5.Analysis of the receptor specificity of tolerance induction in stress versus opioid-related prolactin secretion in rats.

Matton A1, Buydens P, Finné E, Govaerts J, Vanhaelst L.
Author information



Abstract

The effects of restraint stress and opiates on prolactin secretion in male rats have been measured. Both induced a short-lived increase in prolactinaemia. Experimental evidence indicates that both opioids and restraint stress bring about their actions by the activation of opioid receptors. When restraint stress was followed by administration of the specific kappa-agonist bremazocine, a second prolactin peak was observed. In contrast, morphine (predominantly a mu-agonist) lost its prolactin-stimulating capacity when given after a period of restraint stress. This indicates cross-tolerance between restraint stress and morphine. Tolerance was overcome when the dose of morphine was doubled, and an increase in prolactin secretion could again be obtained. The cross-tolerance phenomenon argues that a common opioid receptor is involved in morphine- and restraint stress-stimulated prolactin release. In another set of experiments, in which morphine administration replaced restraint stress as a means of inducing tolerance, a second rise in prolactinaemia was seen only with bremazocine and not with a further administration of morphine. This suggests a morphine (mu) receptor-specific development of tolerance. Two consecutive administrations of bremazocine also produced tolerance, in this case for the kappa-receptor. This illustrates the rapid and receptor-specific development of tolerance for the prolactin-releasing capacity of opioid compounds.


PMID:1848587[PubMed - indexed for MEDLINE]

J Pharmacol Exp Ther. 1987 Mar;240(3):831-6.
Role of serotonin in opiate-induced prolactin secretion and antinociception in the developing rat.

Bero LA, Kuhn CM.
Abstract

Our laboratory has demonstrated previously that the ability of opiates to stimulate prolactin (PRL) release during ontogeny precedes the appearance of a PRL response to serotonergic drugs. The present study tests the hypothesis that opiates stimulate PRL secretion through a serotonergic mechanism in adult rats, but a nonserotonergic mechanism in neonatal rats. Morphine stimulated PRL secretion in adult and neonatal (10-day-old) rats and this increase was blocked with the opiate antagonist naloxone. Ten-day-old or adult rats were pretreated with the serotonin antagonist, cyproheptadine (CYPRO), or the neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). Both CYPRO and 5,7-DHT attenuated the PRL response to morphine in adult but not neonatal rats. 5,7-DHT decreased serotonin and 5-hydroxyindoleacetic acid substantially in the hypothalamus. When rats were pretreated with 5,7-DHT several weeks before morphine challenge, serotonin depletion was more pronounced, but the PRL response to morphine was not decreased. In addition, the PRL response to 5-hydroxytryptophan was greatly potentiated, suggesting that functional supersensitivity developed in the 5,7-DHT-treated animals. The ability of CYPRO and 5,7-DHT to block the serotonergic component of a different morphine-induced behavior in the neonate was tested using the tail immersion test for analgesia. Morphine produced profound antinociception in the rat pup which was attenuated markedly by 5,7-DHT and CYPRO. These studies demonstrate that opiates mediate their stimulatory effects on PRL release, at least in part, through a serotonergic mechanism in adult rats.(ABSTRACT TRUNCATED AT 250 WORDS)


PMID: 2435887 [PubMed - indexed for MEDLINE]

[corageon]

Brain Res. 1987 Dec 15;465(1-2):189-96.
Early ontogeny of kappa-opioid receptor regulation of prolactin secretion in the rat.

Bero LA1, Lurie SN, Kuhn CM.
Author information


Abstract

Although both mu- and kappa-opioid components of prolactin (PRL) secretion have been identified in the adult rat, the neural pathways through which these multiple receptor subtypes modulate PRL secretion have not been thoroughly investigated. The present study utilizes the differential ontogeny of opioid systems which alter PRL release to examine the mechanisms by which mu- and kappa-receptors regulate prolactin. The responses of PRL, corticosterone and growth hormone to opioid receptor subtype-specific agonists were studied in neonatal rats. The PRL response to the kappa-agonist, U50488, preceded the response to the mu-agonist, morphiceptin. Like adults, neonates demonstrated a growth hormone, but not a PRL, response to the delta agonist, [D-pen2,pen5]enkephalin. U50488-induced PRL secretion was not attenuated by cyproheptadine in adults or neonates, suggesting that the kappa-opioid mechanism operates independently of serotonin. In contrast, the PRL response to morphine was attenuated in adult rats. In addition, U50488 decreased median eminence dopamine synthesis in both adults and neonates. These findings suggest that the early developing, serotonin-independent opioid regulation of PRL is mediated through kappa-receptors, while the later-developing mechanism which requires intact serotonergic transmission works through mu-receptors. kappa-Receptors appear to regulate PRL secretion by directly inhibiting the activity of tuberoinfundibular dopamine neurons, while mu-receptors might regulate the tonic dopaminergic inhibition of PRL through a serotonergic pathway.


PMID: 2894234 [PubMed - indexed for MEDLINE]