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Prolactin and Dopamine throughout orgasm?

Prolactin and Dopamine throughout orgasm?



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Dopamine is also known as a prolactin-inhibiting hormone, which keeps prolactin levels in the body in check. However, during orgasm, dopamine is released to make the experience pleasurable. I know that prolactin is released as well. Don't they counteract each other? The prolactin also has a meditative effect, which from what I know causes a refractory period where another orgasm can't be achieved. Does prolactin inhibit dopamine release too?


In this blog we’ve explored neural function during different stages of the sexual cycle: arousal and orgasm. Now we’ve reached the more mysterious and less-studied part of the cycle: post-coital resolution.

When we think about sex, we think about the approaching, the act, the fireworks of climax… and then we usually stop there. Makes sense, the sexual act in itself is over, right? However, many changes keep happening within us after we’ve rolled over and gone to sleep.

As we saw last time, when we orgasm our brain becomes flooded with dopamine in our reward pathways of in the limbic system. This feels so intensely pleasurable that it looks just like a heroin rush to the brain, producing intense feelings of well-being (Holstege et al., 2003). But the story doesn’t end there. Because orgasm activates reward pathways much in the same way as drugs, it can also produce similar experience of addiction and withdrawal. In fact, people that are treated for sex addictions tend to have other comorbid addictions, suggesting that they have addictive personalities, an inclination for overactivation in this part of the brain (Hartman et al., 2012). This is because after the rush of orgasm, dopamine levels drop below baseline, similar to what happens during withdrawal from drugs of abuse. Low dopamine levels are associated with depression, low energy, lack of ambition, social anxiety, among others (Dailly et al., 2004).

Why does dopamine drop? Well, to make sure we attend to other aspects of our life, our brains come hardwired with a neurochemical mechanism of satiety. Prolactin, another hormone, surges right after orgasm, and is considered a reliable marker of such (Kruger et al., 2003).Prolactin works as a dopamine inhibitor, curtailing our sex drives once we consummate orgasm and providing us with feelings of satiation and sexual gratification. So the happy feelings impulsed by orgasm are carried along by prolactin. These secretions are relatively long-lasting after orgasm (Kruger et al., 2012).

Orgasm also reduces androgen receptor density in the Medial Preoptic Area part of the reward circuit. Androgens regulate sexual desire by activating dopamine levels in this area, so their decreased activity could be another source of the dopamine drop (Putnam et al., 2001). While postcoital neuroendocrine changes are better documented, there is also data on postorgasm brain activation. For example, one neuroimaging study conducted immediately after orgasm in men showed activation in the amygdala, temporal lobe, and septal areas (Mallick et al., 2007). Case studies have documented hypersexuality in patients with lesions in all three of these areas, reinforcing the inhibitory evidence of what is known as the post-orgasm refractory period (Mallick et al., 2007).

This shows that the sexual cycle isn’t over when the fireworks die out. Neuroendocrine changes in our bodies orchestrate a coordinated dance to make sure that we feel content, wind down, and rest or go on with a lives for a bit. Dopamine dips from its orgasmic high and prolactin and androgen step in to produce feelings of satiety, pleasantness, and to make us want to take a break. At least for a while.

Dailly, E., Chenu, F., Renard, C. E., & Bourin, M. (2004). Dopamine, depression and antidepressants. Fundamental & clinical pharmacology, 18(6), 601-607.

Hartman, L. I., Ho, V., Arbour, S., Hambley, J. M., & Lawson, P. (2012). Sexual Addiction and Substance Addiction: Comparing Sexual Addiction Treatment Outcomes Among Clients With and Without Comorbid Substance Use Disorders. Sexual Addiction & Compulsivity, 19(4), 284-309.

Holstege, G., Georgiadis, J. R., Paans, A. M., Meiners, L. C., van der Graaf, F. H., & Reinders, A. S. (2003). Brain activation during human male ejaculation. The Journal of Neuroscience, 23(27), 9185-9193.

Kruger, T. H., Haake, P., Chereath, D., Knapp, W., Janssen, O. E., Exton, M. S., … & Hartmann, U. (2003). Specificity of the neuroendocrine response to orgasm during sexual arousal in men. Journal of Endocrinology, 177(1), 57-64.

Mallick, H. N., Tandon, S., Jagannathan, N. R., Gulia, K. K., & Kumar, V. M. (2007). Brain areas activated after ejaculation in healthy young human subjects. Indian journal of physiology and pharmacology, 51(1), 81.

Putnam, S. K., Du, J., Sato, S., & Hull, E. M. (2001). Testosterone restoration of copulatory behavior correlates with medial preoptic dopamine release in castrated male rats. Hormones and behavior, 39(3), 216-224.


Dopamine and Orgasm

Remember a few years ago, when there were all these books that tried to explain the history of everything in terms of some seemingly minor subject, like "Cod" or "Salt"? I think it's time to apply this publishing trope to neuroscience: we need a book on dopamine. That damn neurotransmitter is everywhere. Now it's even being hailed as an orgasm accelerator:

Abundant evidence points to dopamine as the key neurotransmitter involved in stimulating orgasm in humans. Thus, administration of the dopamine precursor L-dopa, dopaminergic agonists (e.g. apomorphine), dopamine releasers (e.g. amphetamine), or dopamine reuptake inhibitors (e.g. cocaine or bupropion) facilitate the expression of orgasm in men and women. Conversely, administration of antipsychotics impair orgasm, by blocking postsynaptic dopamine receptors (see Komisaruk et al., 2006).

Dopamine-synthesising neurons that originate in the lower brainstem (specifically the ventral tegmental area) are activated during ejaculation in men, as measured by PET imaging (Holstege et al., 2003).

A major projection of the dopamine neuron axon terminals is to the nucleus accumbens of the forebrain. This nucleus is activated during orgasm in women, as measured by fMRI (Komisaruk et al., 2004).

Thus, activation of the dopaminergic system of the brain evidently participates in the production of orgasm in women and men, on the basis of pharmacological functional brain imaging, and neuroanatomical studies. Consistent with this role of dopamine, hypersexuality has been reported in cases of Parkinsonism treated with dopamine precursor or agonist drugs (Bowers et al., 1971). Acute administration of drugs that increase dopaminergic activity only occasionally induces orgasm in the absence of other factors. However, intravenous injection of cocaine, which rapidly increases the release of dopamine at its neuronal terminals in the forebrain, can induce the 'cocaine rush' that individuals report as feeling similar to genital orgasm (Miller & Gold, 1988)

Serotonin, by the way, is an orgasm brake, which is why SSRI's often interfere with sex drive. But perhaps you can compensate for that neurotransmitter decrease with a little novelty (dopamine receptors love kinky new stuff). Here's the NY Times:

Using laboratory studies, real-world experiments and even brain-scan data, scientists can now offer long-married couples a simple prescription for rekindling the romantic love that brought them together in the first place. The solution? Reinventing date night.

Rather than visiting the same familiar haunts and dining with the same old friends, couples need to tailor their date nights around new and different activities that they both enjoy, says Arthur Aron, a professor of social psychology at the State University of New York at Stony Brook. The goal is to find ways to keep injecting novelty into the relationship. The activity can be as simple as trying a new restaurant or something a little more unusual or thrilling -- like taking an art class or going to an amusement park.


Changes in the responsiveness of prolactin secretion to dopaminergic blockade and TRH stimulation throughout sexual maturation in men

The pituitary prolactin (PRL) response to domperidone (DOM a dopaminergic antagonist) and TRH administration in human males during different stages of sexual maturation was investigated. Dopaminergic blockade caused an immediate and significant PRL release in all subjects, regardless of the stage of pubertal development. Even though the mean values of peak PRL levels, magnitude of PRL response (delta PRL) and areas under the PRL curve were not significantly different among the different groups, all these parameters showed a clear tendency to increase in parallel to the stage of pubertal development, as indicated by significant positive correlations between age and pubertal stage of the subjects and the magnitude of their PRL response to DOM (r = 0.661, p less than 0.01 and r = 0.536, p = 0.01, respectively). Significant positive correlations also were found between the serum sex steroid hormone concentrations and the PRL response to dopaminergic blockade (r = 0.774, p = 0.02 and r = 0.554, p = 0.01, respectively). In contrast to these findings, no significant differences or tendencies were detected in the PRL responses to TRH among the different subject groups. The different patterns of PRL response to DOM and TRH throughout male puberty might be due to differences in pituitary thresholds for sex steroids between the dopamine- and TRH-dependent intracellular pools.


Results

All control participants experienced orgasm following masturbation after 30 and 60 min. Consequently, increases of plasma prolactin concentrations were observed in each control subject. Collectively, an increase in plasma prolactin concentrations were observed following the first orgasm, with further increases following the second orgasm (Figure 1). In contrast, the case subject experienced two orgasms at 30 min, separated by 2 min, and a further orgasm at 60 min. Additionally, unaltered sexual appetence following orgasm was accompanied by unchanged concentrations of plasma prolactin in the case subject.

Effect of masturbation-induced orgasm on plasma prolactin levels in males displaying normal refractoriness and the multi-orgasmic case subject. Orgasm was induced by masturbation after 30 and 60 min (orgasm of control subjects indicated by broken arrows). The case subject experienced two orgasms after the initial masturbation sequence (indicated by full arrows).


Can High Prolactin Levels Cause Erectile Dysfunction?

Erectile dysfunction is a condition in which males are unable to achieve or maintain an erection suitable for sexual intercourse. Medical research has determined that impotence in men is due in part to high prolactin levels in the blood stream.

Drugs like Viagra improve nitric oxide levels in the blood to improve a man’s erection, but does not address the high prolactin, which is also shown to be a cause of erectile dysfunction. Many men with impotence have low levels of nitric oxide in the blood and high prolactin levels produced by the pituitary gland. Ideally, a male with normal sexual function has high levels of nitric oxide and low prolactin level. The key to treat erectile dysfunction naturally is a supplement that both improves the levels of nitric oxide in the blood while reducing the prolactin levels in the blood.

What is Prolactin?

Prolactin is a peptide hormone produced in the pituitary gland that has several important functions. In women, increased levels of prolactin is required during lactation and stimulates the mammary glands to produce milk. Prolactin is also produced during sexual intercourse, and is responsible for feeling of sexual gratification after sex.

Are High Prolactin Levels a Cause of Erectile Dysfunction?

When the pituitary gland, located in the brain, over produces prolactin called Hyperprolactinemia, this condition has been shown to be a cause of erectile dysfunction, low sperm count and loss of libido in males. Production of the hormone prolactin rises sharply after intercourse. Researchers believe the increase in prolactin is the brain’s way to reduce the effects of orgasm and stimulation that happen during the sex act. Normally, the prolactin level will slowly decrease as the pleasure sensations from sex and orgasm wear off. But, when the brain does not tell the pituitary gland to stop producing prolactin or the high levels of prolactin do not diminish for several weeks, a male may be unable to achieve or maintain an erection, or may have reduced libido or sexual desire. Other symptoms of Hyperprolactinemia include headaches, mood changes, stress or anxiety.

How to Reduce Prolactin Levels Naturally

Low levels of testosterone, which can lead to erectile dysfunction, is a potential indication of high prolactin level. If a male has low testosterone levels or exhibits symptoms of erectile dysfunction, a blood test can determine if high prolactin is the cause of either male sexual dysfunction.

Changing the way you make love can impact the production of prolactin in the brain. Try including more foreplay into lovemaking, which slows the heart rate and increased stimulation that occurs during sexual intercourse and orgasm.

Unlike Viagra, which uses chemicals to trick the brain into altering the production of sex hormones, a natural male enhancement called Vimax uses all herbal ingredients known for centuries by the Chinese, Indian and Mayan cultures to heighten sexual intensity and performance, naturally increases levels of nitric oxide and reduces prolactin levels without the side effects of Viagra, reduces symptoms of sexual dysfunction, naturally reduces levels of insulin in Type 2 Diabetics and promotes emotional well-being.


Sex Is Four Times Better Than Masturbation

Why do men need a "recovery period" after orgasm? And why is sexual intercourse more satisfying than masturbation alone? Now scientists think the two phenomena might be linked.

Making abstraction of psychological arguments, scientists looked for the chemical substances released after orgasm. In order to do such a thing they turned to volunteers who agreed to masturbate or to have sexual intercourse in the lab.

Stuart Brody of the University of Paisley, UK, and Tillmann Kr?ger of the Swiss Federal Institute of Technology in Zurich, measured blood prolactin levels in male and female volunteers after orgasm. Prolactin is a hormone released after orgasm into the bloodstream in both men and women. This hormone counteracts the effects of another hormone, called dopamine, which is released during sexual arousal.

What scientists found was that, after orgasm from sexual intercourse, the increase in blood prolactin levels is 4 times higher in both sexes compared with the levels after orgasm from masturbation.

According to Brody, this explains why orgasm from intercourse is more satisfying than masturbation. This discovery also explains why men experience a "recovery period" because elevated levels of prolactin have been previously linked to erectile dysfunction. So, the increase of this hormone, needed to counteract the escalating levels of dopamine, produces the "recovery period".


Introduction

Despite the many parallels between prolactin and oxytocin in parental care and the interest in oxytocin in promoting pair bonding in monogamous biparental species [1], it is surprising that there are few papers on the role of prolactin in promoting pair-bonds. We have previously shown in the socially-monogamous, cooperatively-breeding cotton-top tamarin that peripheral oxytocin levels varied in both males and females and were correlated with sociosexual behavior (copulation, huddling and grooming) [2]. Within pairs, oxytocin levels were highly correlated between males and females. Variation in male oxytocin was explained best by variation in amount of sexual behavior observed whereas variation in female oxytocin was best explained by variation in amount of huddling and grooming behavior. In the black-penciled marmoset, a closely related species, intranasal oxytocin increased huddling with their partners whereas an oxytocin antagonist decreased proximity, huddling and food sharing [3].

As with oxytocin, prolactin appears to play an important role in the parental care of fathers as well as in mothers in species with biparental or cooperative care. Several studies in rats [4] support the role of prolactin in initiation of maternal care and, in birds, incubation, brooding and feeding of chicks appear to be related to elevations in prolactin in both sexes in species with biparental or cooperative care [5–7].

In mammals several studies have reported elevated prolactin levels in males prior to caring for infants (striped mice [8] meerkats [9] dwarf hamsters [10] cotton top tamarins [11] men [12–15]. In other species the presence of infants appears important for elevated prolactin (California mice [16] Mongolian gerbils [17] common marmosets [18] titi monkeys and Goeldi’s monkeys [19]). Studies in common marmosets have shown that prolactin levels are higher when measured immediately after infant carrying in both breeding males and non-breeding helpers [20–22].

Few studies have experimentally tested the causal effects of prolactin on infant care behavior in male mammals. When the dopamine D2 receptor agonist, bromocriptine, was administered to parentally inexperienced male and female juvenile marmosets, prolactin levels were reduced and infant retrieval and caretaking behaviors were also reduced [23]. However, another study using the dopamine D2 receptor agonist, cabergoline, which also reduced prolactin levels, reported no effect on infant carrying in paternally experienced marmosets although adult male marmosets did show an increased interest in obtaining proximity to and contact with infants [24]. In common marmosets prolactin levels were decreased through cabergoline administration and chronically elevated using an osmotic mini-pump [25]. Despite the fact that the manipulations significantly affected prolactin levels, there was no difference in infant directed behavior or infant carrying within the family group. However, there was a decrease in responsiveness to infant stimuli to both increased and decreased levels of prolactin using a test of fathers separated from the family group. Similarly there were no effects on infant care in male dwarf hamsters of reducing prolactin levels using either bromocriptine or cabergoline on infant care [26] leading researchers to question the causal role of prolactin in infant care in male mammals [27].

Although the causal role of prolactin in paternal or alloparental care is unclear, there is another possible interpretation of these results, namely that prolactin may be a consequence of infant care and may serve a potentially rewarding function to caregivers. This would explain why prolactin levels are elevated immediately after infant carrying in marmosets and other species as well as explain the lack of effect of prolactin inhibitors on direct infant care. The increased interest in being in physical contact with infants shown in fathers with cabergoline could be interpreted as male seeking greater infant contact to make up for lowered prolactin [24].

There is a relationship between prolactin and physical contact with increased grooming in rats resulting from low doses of prolactin [28–29]. It has been suggested that the continued high prolactin levels in female, but not male, red-cockaded woodpeckers is due to increased tactile stimulation with mothers spending more time in direct contact with chicks [7]. Intracerebral and intraperitoneal injections of prolactin acted centrally to increase levels of courtship behavior in newts [30]. A series of studies on hormones released at orgasm in humans [31–32] demonstrated increased prolactin at orgasm in men and women during both coital sex and masturbation. Thus prolactin appears to play a role in grooming, courtship, and sexual behavior in a variety of species.

Berridge and colleagues [33–35] have distinguished between “wanting” (the desire to obtain something) and “liking” (the positive valence of reaching a goal) with dopamine serving as a critical neurotransmitter during the “wanting” phase. However, other mechanisms must serve to provide a reward (and reduce the “wanting”). Given the reciprocal relationship between prolactin and dopamine [36], we hypothesize that prolactin might be involved in rewarding parents and alloparents for infant care and that grooming and sexual behavior may serve to increase prolactin and provide a reward for adult pair relationships as well.

In this paper we examine the relationship between prolactin and measures of contact affiliation and sexual behavior. We predicted that there would be a positive relationship between both contact affiliation and sexual behavior and chronic levels of prolactin in cotton-top tamarins. We also predicted that there would be a close correlation of prolactin levels between males and females within each pair. We completed two studies. Study 1 compared behavior and hormone levels in current mothers (no longer nursing) with former mothers and females who had never been mothers. The second study examined non-breeding male-female pairs.


Cabergoline – the latest in libido enhancement

Cabergoline increases the levels of dopamine through its action of stimulating D2 receptor sites, it is officially approved to assist in the treatment of Parkinson’s disease, as well as treat states of prolactinoma (i.e. prevent breast development in men and reduce excess milk secretion in women).

However, cabergoline (brand name Dostinex has been described as being able to do everything that Viagra can’t! This is because rather than induce an erection (as Viagra can) cabergoline has been shown to improve libido, orgasm and ejaculation (which Viagra has not).

Cabergoline is from the dopaminergic family of drugs that increase the level of dopamine and also decreases the levels of the hormone prolactin. Prolactin is the hormone secreted in women after giving birth and to enhance their lactation for breast feeding. However, prolactin has recently been shown to be an inhibitor to a healthy libido, this may help explain why many women have a low sex drive after giving birth- whilst they are breast feeding. But men can also suffer from prolactinoma (high levels of prolactin) leading to a lack of sex drive- as well as developing breasts, particularly as prolactin levels tend to increase for most men with age.

Recently it has been discovered that prolactin is released immediately after an ejaculation and may be part of the reason men like to go sleep after sex with no will for further love making.

Cabergoline has been proven to significantly decrease prolactin and in so doing increase the sex drive (libido) substantially. There have been reports of enhanced and multiple orgasms as well as stronger ejaculations.

To date, bromocriptine has been the main drug of choice to reduce prolactin levels, however clinical studies have confirmed that cabergoline is much more effective in this regard. For example in 450 tested subjects over 8-weeks 77% of the subjects had their prolactin levels returned to normal using 0.5mg of cabergoline twice a week, compared to 59% of subjects using bromocriptine at 2.5mg twice a day. Furthermore, side effects were far fewer in the cabergoline group, recorded at 2% of incidences compared with 60% of those taking broinocriptine.

One fascinating trial on 60 healthy males, between the ages of 22 and 31 discovered that they needed a break of 19 minutes between love making. However, after taking cabergoline, they were able to have several orgasms within a few minutes!

Dr. Schedlowski went on to say “We interviewed the subjects and found they were able to have multiple orgasms in very rapid succession. This is sitting very nicely with our hypothesis that orgasms and sexual drive are steered by prolactin and dopamine in the brain.”

Furthermore, cabergoline had no side effects on men during the tests this was reported in an article for the International Journal of Impotence Research. The researchers now plan to carry out trials to investigate whether cabergoline will have the same effect on women.

Another medical study by the Federico University, in Naples, Italy published in the European Journal of Endocrinology showed cabergoline to be very potent in increasing libido and sexual potency. The study examined cabergoline vs. bromocriptine (Par

odelâ) and proved that cabergoline was superior in all respects to bromocriptine.

17 males with prolactinoma were treated with cabergoline or bromocriptine for 6 months. All patients initially suffered from libido impairment, with 10 suffering from reduced sexual potency and 6 were infertile. Before treatment all patients suffered from low number of erections and had a low sperm count. After 1 month of treatment prolactin levels were significantly reduced in both groups of patients. A notable increase in the number of erections during the first 3 months was recorded and continued throughout the 6 months of treatment. However the improvements in seminal fluid parameters and sexual function were more evident and rapid in patients treated with cabergoline. A significant increase in the serum levels of testosterone and dihydrotestosterone were also recorded. At the beginning of treatment, mild side-effects were recorded in 2 patients using cabergoline compared to 5 in the bromocriptine patients.

Conclusion:
It is now recognised that the stimulation of dopamine can enhance sexual arousal and this has been shown to occur with drugs such as bromocriptine, deprenyl and Sinemet®. Now that prolactin is being recognised as an inhibitor of sexual function and desire, a drug such as cabergoline that enhances dopamine levels and reduces prolactin levels is being heralded as a significant libido enhancer- despite the fact that it has not yet been approved for this purpose.

Dosage:
Take 0.25mg or 0.5mg no more than twice per week, unless treating a serious medical disorder whereupon the dosage may differ according to your physician’s guidance, usually built up slowly to no more than 1mg twice weekly.


Epilogue

The involvement of peripheral DA and SAL in the systemic disorders discussed above are still poorly understood. Clearly, much remains to be done. There is no doubt that both peripheral and central DA systems are sensitive to environmental effects [68]. Concomitant changes in the peripheral DA and SAL system must make a significant contribution to these homeostatic events. Given a possible future use of such compounds, it is clear that better understanding of the integrated role of DA and SAL is a critical aspect in respect of the whole organism.