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Why Does Libido Surge During Opiate Withdrawal?

seep

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I'd like to find out what physiological mechanism causes libido to surge during opiate withdrawal. I've withdrawn from heroin or methadone dozens of times, and each time my sex drive increases approximately tenfold from my body's non-opiate-dependent norm, especially during days 2-6 of heroin w/d and days 4-12 of methadone w/d. I realize this aspect of withdrawal is well-known, but I can't find a detailed answer as to why sex drive is so acutely amplified during w/d.

To be precise, I'm not referring to the psychological desire for sex. I'm referring to the intensity and frequency of male sexual readiness, characterized by seemingly-instantaneous erection in response to even the most minimal sexual stimulus; characterized as well by the proverbial "hair-trigger orgasm," and the ability to replenish semen very rapidly and, consequently, ejaculate numerous times per day; also characterized by intensely pleasurable sensations in the penis during orgasm (enormously more pleasurable than during normal sex).

One day I'd like to look into formulating a substance which reproduces whatever physiological mechanism is responsible for this phenomenon--without, of course, any of the other symptoms of withdrawal. Has nobody attempted this already? The irony alone makes looking into it irresistible.
 
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Tsukasa

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Libido surges during SSRI withdrawal too. Serotonin mainly and opioids have the effect of decreasing the bodies primitive urges like sex, and I guess when you get off of them theirs a rebound effect.
 

eon_blue

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Your libido surges during opiate withdrawal because your body/brain is craving an endorphin release, which orgasms produce.

Ever notice how, when you have an orgasm during withdrawal, you feel 100% better for all of 3 seconds? It's like the world's shortest lasting get-well shot.

A fat shot of heroin, for example, induces a rush of endorphins, and after doing this long enough/often enough, you become physically dependent on the excess amounts in your system. Without them, you get ill. Naturally, when you start to withdrawal your body craves anything and everything that will produce endorphins: sex, drugs, good music, love, exercise, etc.

For me, "love" was actually a big one. When I was high, I couldn't give a shit less what other people thought of me. But man...when I'd start to withdrawal, I'd get super depressed and want to call my girlfriend or my mother just to be reminded that I'm cared about.
 

The Straight Dope

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I've noticed this, one thing that I wonder though, is if this might have any sort of effect on male pattern baldness if someone is prone to it.

Having a high power libido is definitely awesome, but it would be a really nasty thing to happen to someone if their hair started thinning/falling out once they quit doing heroin.

PS: During heroin usage I also get a massive reduction in desires to masturbate, so I might go on for like 10 days at a time without doing the deed, I think this might contribute to the libido rise when ceasing.
 
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seep

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Thanks.

Tsukasa, I've "withdrawn" from a few SSRI's (including paroxetine, buproprion, and sertraline), but I haven't really had a noticeable surge in libido, or (come to think of it) any other noticeable effects. I do wish all SSRI's would board a rocket and fly the fuck away.

Eon, I agree that the body, during withdrawal, is basically holding the pituitary gland at gunpoint and demanding that it secrete endorphin. But how much endorphin can these withered cells possibly secrete? Also, I think it's incorrect to assume that the heightened sensitivity present during withdrawal is a result of the body trying to milk endorphins out of itself. It makes more sense to attribute the heightened sensitivity to the sudden lack of exogenous substances that can bind to the thirsty opioid receptors, coupled with the body's poor ability to produce endogenous morphine (i.e. endorphin). Also, it's untrue that "a fat shot of heroin induces a rush of endorphins." I have to agree, though, that during withdrawal, one seems to have an enhanced ability to apprehend emotional abstractions such as love and devotion--much more so than in non-addicts. This is why I tend to say no to buprenorphine: cold turkey has serious spiritual rewards.

Nuke, wouldn't dopamine also surge in the absence of prolactin? This would shorten the sexual refractory period and also enhance sexual arousal. More interesting to me is that heroin dramatically suppresses LH, leading to a drop in spermatogenesis and decreased production of testicular fluid. LH may be the substance that most accounts (albeit indirectly) for increased libido during withdrawal, as plasma LH levels and LH production both rise after administration of naltrexone; in contrast, naltrexone doesn't cause immediate secretory bursts of testosterone. I wonder if synthetic GNRH would cause a rise in libido similar to during opiate withdrawal. I'm also slapping myself for throwing away a bottle of Revia I had a few years ago.
 

Tsukasa

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Thanks.

Nuke, wouldn't dopamine also surge in the absence of prolactin? This would shorten the sexual refractory period and also enhance sexual arousal. More interesting to me is that heroin dramatically suppresses LH, leading to a drop in spermatogenesis and decreased production of testicular fluid. LH may be the substance that most accounts (albeit indirectly) for increased libido during withdrawal, as plasma LH levels and LH production both rise after administration of naltrexone; in contrast, naltrexone doesn't cause immediate secretory bursts of testosterone. I wonder if synthetic GNRH would cause a rise in libido similar to during opiate withdrawal. I'm also slapping myself for throwing away a bottle of Revia I had a few years ago.
Testosterone and dopamine are more involved with the desire for sex, not arousal. Arousal is more attributed to acetylcholine, nitric oxide, and oxytocin.
 

The Straight Dope

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I have actually experienced that buprenorphine does in fact not affect the rise in libido once quitting H.

Another thing I've noticed is that it actually becomes a lot easier to quit cigarettes if you are withdrawling, this is only true if you're not taking buprenorphine though.
 

Limpet_Chicken

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Is it just me (that notices!=D), or are there a whole lotta wankers in this thread?
 

The Straight Dope

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It's actually not uncommon for myself to be aroused and get an erection right after shooting up. I've had some good times before with the everlasting "dope dick". But I still prefer having the libido I have when not using dope.
 

nabollocks

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This has been discussed before... but does anybody have access to this paper?

Changes in estradiol and cortisol production rates in men under the influence of narcotics.
Hellman L, Fukushima DK, Roffwarg H, Fishman J.

The production rates of estradiol and cortisol in two male opiate addicts while on narcotic maintenance, were in the low normal or subnormal range. There was a sharp several-fold increase upon withdrawal with a subsequent fall to normal values after a period of abstinence. The changes in estradiol production rates were proportionally greater than those of cortisol and suggest that they were due to changes in testicular secretion of the precursor testosterone.
 

shibireru

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Nuke and Tsukasa's explanations were correct. No offense, eon blue, but that was pure nonsense and I've written some real nonsense.

Additionally, opioids suppress the sympathetic nervous system, which is why you see dyspnea, hypoxia, hypothermia, and confusion in overdose. In other words, opioids appear to antagonize the effects norepinephrine and epinephrine which are linked with libido, although apparently not very strongly or in a direct, one-to-one fashion (otherwise you'd expect more from Yohimbine). During withdrawal from opioids, the sympathetic nervous system is kicked into high gear and so you get the anxiety, hyperhidrosis, hypertension, tachycardia, insomnia, diarrhea, etc... (i.e. all the shit associated with adrenergia.)
 

permastoned

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Your libido surges during opiate withdrawal because your body/brain is craving an endorphin release, which orgasms produce.

Ever notice how, when you have an orgasm during withdrawal, you feel 100% better for all of 3 seconds? It's like the world's shortest lasting get-well shot.

A fat shot of heroin, for example, induces a rush of endorphins, and after doing this long enough/often enough, you become physically dependent on the excess amounts in your system. Without them, you get ill. Naturally, when you start to withdrawal your body craves anything and everything that will produce endorphins: sex, drugs, good music, love, exercise, etc.

For me, "love" was actually a big one. When I was high, I couldn't give a shit less what other people thought of me. But man...when I'd start to withdrawal, I'd get super depressed and want to call my girlfriend or my mother just to be reminded that I'm cared about.
What they do do is cause an activation of the endorphin, well technically, opioid system through the mu receptor.

Can people please stop saying that opioids cause a surge of endorphins... I don't know why people always get this wrong. In fact they cause a decrease in the release of endorphins.
 
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seep

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The Italians are already working on synthetizing and modulating the pharmacology of spontaneous ejaculation et al during w/d:

Pharmacol Res. 2009 Jan;59(1):13-47. Epub 2008 Oct 17.

Brain effects of melanocortins.


Bertolini A, Tacchi R, Vergoni AV.

Division of Clinical Pharmacology, Department of Diagnostic Services, University of Modena and Reggio Emilia, Policlinico of Modena, Modena, Italy. [email protected]

The melanocortins (alpha, beta and gamma-melanocyte-stimulating hormones: MSHs; adrenocorticotrophic hormone: ACTH), a family of pro-opiomelanocortin (POMC)-derived peptides having in common the tetrapeptide sequence His-Phe-Arg-Trp, have progressively revealed an incredibly wide range of extra-hormonal effects, so to become one of the most promising source of innovative drugs for many, important and widespread pathological conditions. The discovery of their effects on some brain functions, independently made by William Ferrari and David De Wied about half a century ago, led to the formulation of the term "neuropeptide" at a time when no demonstration of the actual production of peptide molecules by neurons, in the brain, was still available, and there were no receptors characterized for these molecules. In the course of the subsequent decades it came out that melanocortins, besides inducing one of the most complex and bizarre behavioural syndromes (excessive grooming, crises of stretchings and yawnings, repeated episodes of spontaneous penile erection and ejaculation, increased sexual receptivity), play a key role in functions of fundamental physiological importance as well as impressive therapeutic effects in different pathological conditions. If serendipity had been an important determinant in the discovery of the above-mentioned first-noticed extra-hormonal effects of melanocortins, many of the subsequent discoveries in the pharmacology of these peptides (feeding inhibition, shock reversal, role in opiate tolerance/withdrawal, etc.) have been the result of a planned research, aimed at testing the "pro-nociceptive/anti-nociceptive homeostatic system" hypothesis. The discovery of melanocortin receptors, and the ensuing synthesis of selective ligands with agonist or antagonist activity, is generating completely innovative drugs for the treatment of a potentially very long list of important and widespread pathological conditions: sexual impotence, frigidity, overweight/obesity, anorexia, cachexia, haemorrhagic shock, other forms of shock, myocardial infarction, ischemia/reperfusion-induced brain damage, neuropathic pain, rheumathoid arthritis, inflammatory bowel disease, nerve injury, toxic neuropathies, diabetic neuropathy, etc. This review recalls the history of these researches and outlines the pharmacology of the extra-hormonal effects of melanocortins which are produced by an action at the brain level (or mainly at the brain level). In our opinion the picture is still incomplete, in spite of being already so incredibly vast and complex. So, for example, several of their effects and preliminary animal data suggest that melanocortins might be of concrete effectiveness in one of the areas of most increasing concern, i.e., that of neurodegenerative diseases.

PMID: 18996199 [PubMed - indexed for MEDLINE]
 

Roujaxian

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In the midst of the physical withdrawal symptoms I noticed my libido significantly increase. Now that that is over however my libido seems to have gone to back to opiate-using levels.
 

seep

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Almost everything I'm reading on this seems to (unwittingly) connect the topic of this thread to the putative effects of bremelanotide.

Bremelanotide. The substance purported to be the first real aphrodisiac.

I could be just jumping to conclusions, or naive, but where am I erring here? I could cite so many voices that seem to be converging. Like the Neuropsychopharmacology text:

When administered on
a chronic basis in humans or in rodents, short-acting opiates
such as heroin and morphine cause suppression of the HPA
axis and with no sustained activation in rodents. During
either spontaneous or naloxone-precipitated withdrawal,
one sees activation of the hormones of the HPA axis in all
species studied.
And a 2008 Chinese study:

The function of the Hypothalamic-Pituitary-Adrenal (HPA) axis during opioid dependence has been inconsistent. We compared HPA axis measures between subjects during methadone stabilization and drug-free detoxification with healthy controls. METHODS: Sixty heroin dependent patients received either non-opiate treatment (NOT) with benzodiazepines and clonidine (n = 30) or methadone stabilization treatment (MT, n = 30), and their serum levels of corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol (COR) were measured and compared to those of healthy, nondependent controls. RESULTS: Compared with healthy controls, CRH was significantly lower (p < .001) while COR was higher (p < .001) during acute withdrawal in the NOT group. CRH and COR was lower (p < .001), while ACTH was normal in the MT group compared to healthy controls. CONCLUSIONS: Our findings suggest that chronic opioid dependence may cause reduced function of the HPA axis, while opioid withdrawal may decrease the response of the pituitary to CRH and increase the adrenal response to ACTH.
And the following, from the developer of of bremelanotide herself:

Melanocortins are a group of small protein molecules that share the same precursor molecule, POMC (proopiomelanocortin). (25) These peptides include ACTH (adrenocorticotropic hormone), the melanocyte-stimulating hormones ([alpha]-MSH, [beta]-MSH and [gamma]-MSH), [beta]- and [gamma]-lipotropin, and [beta]-endorphin. In the CNS, melanocortins may act as neurohormones or neurotransmitters, regulating numerous functions within the neuronal systems in which they are synthesized and secreted. (26) It has been proposed that melanocortins, oxytocin and dopamine use a common pathway in the CNS that involves activation of NO to control erection. (27)

Five melanocortin receptors have been identified that are associated with such diverse biological functions as skin pigmentation, food intake, the sleep-wake cycle and sexual response. Investigations into the role of the melanocortin system on sexual response has focused on the melanocortin 3 (MC3R) and melanocortin 4 (MC4R) receptors in the CNS. There is abundant expression of both MC3R and MC4R in the brain and in peripheral genital sensory outputs (Figure 2). (27) However, MC4R has been shown to modulate erectile function and sexual behavior, whereas MC3R has not been shown to have a pro-erectile effect. (28) MC4R is expressed in the rat and human penis, as well as in rat spinal cord, hypothalamus, brainstem and pelvic ganglion, but not in rat corpus cavernosal smooth muscle cells. In mice, administration of an MC4R agonist increased copulation, whereas knockout mice lacking the gene encoding for the receptor showed decreased copulatory behavior.

Melanocortins and erection

Preclinical work conducted indicate that melanocortins promote erection primarily through activity in the CNS. Both ACTH and [alpha]-MSH injected into the hypothalamic periventricular region of the third ventricle of male rats resulted in increased levels of penile erection, as well as stretching, yawning and grooming. (29) However, neither caused those effects when injected into the preoptic area, the caudate nucleus or the CA1 field of the hippocampus.

In a different rat model, 10 min after intracerebroventricular administration of [alpha]-MSH, there was a 10-fold increase in the frequency of penile erections. (30) Increases in erection frequencies were seen by injecting both ACTH and [alpha]-MSH directly into PVN of the hypothalamus. Blocking the MC4R with HS014, a non-selective MC4R antagonist, did not alter these responses...
 

CitioKid

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I can jack off six times in a row during suboxone withdrawals. I'm talking pedicures on our toes, toes..

God I hate that song.

I'm talking like within 20 seconds of jacking off the previous time I am ready to go again. Even by the sixth time, when my dick is a giant, wed noodle, i can still have an orgasm.
 
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