Discussion in 'Men's Health Forum' started by AlexanderDenmark, Jun 11, 2009.

  1. AlexanderDenmark

    AlexanderDenmark Junior Member

    I was wondering whether any smart people in here could elaborate on the phenomenon Post-SSRI-Sexual-Dysfunction. Unfortunately this isn't a condition made up by the guys in the yahoo group, it's real, I know since I have it myself and it sucks. As if people who feel bad enough to try antidepressants in the first place won't feel any worse when the outcome is chronic sexual dysfunction.

    Any who since we have so many smart people here and actual doctors and pdocs perhaps you could explain the possible causes of PSSD and possible treatments. Because it aint a condition your local doctor can fix, so your basicly on your own. Also i'm sure the people over at the yahoo group would be absolutely delighted and filled with hope if they read an article by smart pdoc who could elaborate on it since that group is just a gathering of desperate and sad souls looking for answers.
  2. xray9

    xray9 Junior Member

    One theory: SSRI's can raise prolactin which is associated with a loss of libido and decreased sexual performance. cabergoline, a dopamine receptor agonist, lowers prolactin, increasing libido, sexual performance and reducing refractory time between orgasms. I have taken 20 mg of fluoxetine daily for over ten years now and had two blood tests, six months apart, showing elevated levels of prolactin. MRI ruled out pituitary adenoma. I recently added cabergoline, .25 mg twice a week, to my HRT. My prolactin levels are now in normal range and sexual functioning has improved. Beware that there are extreme claims of increased sexual prowess supposedly obtained throught he use of cabergoline which I believe are highly exaggerated. And cabergoline is a very powerful drug with very long half life. That said, it has been safely used for Parkinson's patients in dosages upwards of 10 mg a day.

    Also important to sexual function are proper levels of testosterone and the ratio of T to E2. These levels may be affected by SSRI's:

    "chronic treatment with fluoxetine (Prozac) has been shown to cause persistent desensitization of 5HT1A receptors even after removal of the SSRI in rats.[26] These long-term adaptive changes in 5-HT receptors, as well as more complex, global changes, are likely to be mediated through alterations of gene expression.[27][28][29][30][31] Some of these gene expression changes are a result of altered DNA structure caused by chromatin remodeling,[32][33] specifically epigenetic modification of histones[34] and gene silencing by DNA methylation due to increased expression of the methyl binding proteins MeCP2 and MBD1.[35] Altered gene expression and chromatin remodeling are also involved in the mechanism of action of electroconvulsive therapy (ECT).[36][37]

    Because described gene expression changes are complex, and can involve persistent modifications of chromatin structure, it has been suggested that SSRI use can result in persistently altered cerebral gene expression leading to compromised catecholaminergic neurotransmission and neuroendocrine disturbances,[11] such as decreased testosterone levels[38], reduced sperm counts[39], and reduced semen quality with damaged sperm DNA[40]. However, without detailed neuropsychopharmacological, pharmacogenomic and toxicogenomic[41] research, the definitive cause remains unknown."

    Low T and E2 levels can be corrected through proper HRT.

    Every individual is different and should try to find a physician qualified and willing to find and treat the underlying cause of their condition. IMO a urologist should make sure there are no physical problems with the "plumbing" and psychological causes should be considered.
    Last edited: Jun 11, 2009
  3. AlexanderDenmark

    AlexanderDenmark Junior Member

    Shouldn't prolactin levels return to normal once the SSRI has been discountinued? Some poor people has had the problem for like 10 years? Or can SSRI's in other words create a chronic imbalance of neurotransmitters in brain?
  4. tedda

    tedda Junior Member

    I have suffered from PSSD for 10 years, I'm pretty livid that not only did ssri's worsen my depression I am now permanently impotent. I am incredibly sceptical about taking more medications for it
  5. 1erCru

    1erCru Member

    Ive been on SSRI for 8 years. The drugs actually restored sexual sensation and helped to correct a pretty horrible delayed ejaculation problem. So Ive experienced the opposite of what you hear most people complain about. Orgasms are much more powerful when Im on medication. Sex drive and testosterone took a hit though, although I doubt the test was there in the first place.
    Ive always taken very small doses i.e. Zoloft 25 mg, prozac 5 mg etc. The higher doses will get ya in trouble from my experience.
  6. saru

    saru Member

    Depression is thought of as a symptom and not a disease. Symptoms of depression can result due to varied reasons.

    Bth a dopamine deficient individual and a serotonin deficient individual can land up with depression. If a dopamine deficient individual is (wrongly) treated with SSRI, it further lowers his/her dopamine and aggrevates the symptoms. What more, first casualty of reduced dopamine levels is loss of libido (and, subsequently, erectile disfunction). This blunder happens too very often in a psychiatrist's office.

    These patients do well on bupropion (Welpbutrin), which increases the nor-epinephrine and subsequently dopamine.

    If you have not tried this drug alredy, please consult with your doctor. There is a chance that both your problems will be addressed in a single shot!
  7. sade

    sade Banned

    I've heard Trazodone works but it can cause priapism. A urologist cured himself of impotence using this drug.
  8. HeadDoc

    HeadDoc Psychologist

  9. zkt

    zkt Member


    Mechanism of action
    Bupropion is a dopamine and norepinephrine reuptake inhibitor.[122] It is about twice as potent an inhibitor of dopamine reuptake than of norepinephrine reuptake.[123] As bupropion is rapidly converted in the body into several metabolites with differing activity, its action cannot be understood without reference to its metabolism. The occupancy of dopamine transporter (DAT) by bupropion and its metabolites in the human brain as measured by positron emission tomography was 6–22% in an independent study[124] and 12–35% according to GlaxoSmithKline researchers.[125] Based on analogy with serotonin reuptake inhibitors, higher than 50% inhibition of DAT would be needed for the dopamine reuptake mechanism to be a major mechanism of the drug's action. By contrast, approximately 65% occupancy or greater of DAT is required to achieve euphoria and reach abuse potential.[126] However recent research indicates that dopamine is inactivated by norepinephrine reuptake in the frontal cortex, which largely lacks dopamine transporters, therefore bupropion can increase dopamine neurotransmission in this part of the brain, and this may be one possible explanation for any additional dopaminergic effects.[127] Bupropion does not inhibit monoamine oxidase or serotonin reuptake. However, it has been shown to indirectly enhance the firing of serotonergic neurons, via activation of downstream norepinephrine flow. Bupropion has also been shown to act as a noncompetitive ?3?4 nicotinic antagonist.[128] The degree of inhibition of ?3?4 receptors correlates well with the decrease in self-administration of morphine and methamphetamine in rats,[129] and may be relevant to the effect of bupropion on nicotine addiction. The drug is supplied as a racemic mixture, and the activities of the individual enantiomers were not found to differ.[130]
  10. Fowl

    Fowl Junior Member

    I've been on Trazadone for sleep for 10 years and I can say that I have seen no impacts on libido one way or the other from it.
  11. tedda

    tedda Junior Member

    We should all get together and file suit - seriously, they make millions and leave us holding the bag - literally