Talk:Post-SSRI sexual dysfunction
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[edit] Umm
- Umm yeah, this is total garbage--none of the sources you cite or links you post are objective in the least. Maybe this belongs in Scientology, but not Wikipedia. I also suspect that the "gene expression" sources are original research (not allowed on Wikipedia). --AJ 81.57.107.201 13:10, 30 March 2006
- As someone who suffers from this problem I can tell you there is nothing funny abou it or to be made light about. I no not understand why you simply dismiss this problem or why you suggest that it has anything to do with Scientology? Sexual side effects are one of the most common side effects when taking an SSRI, is it so hard to belive that for some people this problem does not rectify after going off them? Just becase a side effect is rare or not well known doesn't mean that it does not exist. James R. Skinner 14:35, 1 April 2006 (UTC)
I'm sorry--let me clarify. While it seems that this can happen in rare circumstances, I don't think the sources cited are objective or trustworthy enough. --AJ 81.57.107.201 12:52, 7 April 2006
- And while the problem may exist, the article is obviously written by someone with a strong bias against SSRIs, most notably in the statement about how they, "don't correct chemical imbalances, but actually CAUSE them, leading to sexual dysfunction." I don't think you'll find any scientific publication with this kind of language. 196.217.206.101 18:05, 12 April 2006
Well, here's a question for you: if you were to artificially block the serotonin transporter from taking up serotonin from the synapse for weeks, months or years at a time, would you say that it's scientifically unsound to say that that could create a neurotransmitter imbalance in some people? Because that's what SSRIs do. They selectively (hence the name) raise the serotonin neurotransmitter but do not directly effect any of the others such as dopamine, norepinephrine, epinephrine, GABA, oxytocin, nitric oxide etc.. Actually, over time the brain adapts by downregulating dopamine and norepinephrine indirectly, so if this does not constitute a chemical imbalance, I don't know what does. If you want to get your information solely from the drug companies, that's up to you, but what they and you are saying is not supported by the scientific literature. Wikipedia articles are based on the scientific literature, not on drug company propaganda. The drug comapnies realize this, so while they spout scientific nonsense about serotonin and depression on TV and pop-up ads, at the same time they are quietly developing triple reuptake inhibitors which act on all three of the major neurotransmitters. This is a much, much more complicated issue than most people realize. Your knowledge of the current literature, especially regarding neurotransmission, gene expression, chromatin remodeling and synaptic plasticity seems limited. As a start, you might want to check out the reference by Damsa et al. listed in the article Shibidee 01:48, 16 April 2006 (UTC)
There are no citations showing that sexual dysfunction can begin soon after an SSRI has been stopped, as opposed to while the medication is being taken. I'm editing out the "after" in that section. 81.159.168.57 20:22, 9 August 2006
There are no citations saying that sexual effects can begin AFTER SSRI use as opposed to DURING. But I'm guessing that you guys don't care that much about a well-cited article--you seem unwilling to believe that yes, there are only 4 case reports of this phenomenon, and that none of the sources on gene expression have anything clear link with PSSD. Furthermore, you just invented the term "PSSD"--I've never seen this in any scientific literature...but I guess a nifty, scientific-sounding acronym can inflate weak ideas pretty well. 68.214.35.93 15:11, 16 August 2006
Did you read the article? Persistent sexual arousal syndrome (PSAS) is a form of PSSD that begins AFTER quitting SSRIs. It is documented in the literature. Check papers by Goldmeier et al, referenced in the artcile.Shibidee 06:41, 25 August 2006 (UTC)
[edit] Footnotes
- How about we switch the citation method from Harvard references to Wikipeida Footnotes? I like the fact that you can easily hyperlink to the footnote with the Wikipeida style footnotes. - James R. Skinner 14:13, 18 July 2006 (UTC)
- Sure, do you want to do it? Shibidee 21:07, 18 July 2006 (UTC)
- Done. While it makes naviation easier, it certinaly seems to makes editing more difficult -James R. Skinner 00:16, 26 July 2006 (UTC)
- Sure, do you want to do it? Shibidee 21:07, 18 July 2006 (UTC)
[edit] Cases
"A growing number of cases?" Citation? There are only four case reports listed. 83.197.61.63 14:14, 19 July 2006
There are more than ten cases listed if you include the premature ejaculation and PSAS papers.Shibidee 21:46, 26 August 2006 (UTC)
Premature ejaculation is a comlex issue and it is hard to blame it on one factor. Many SSRI users will become more sensitive and have PE. The question is how was their PE before start of SSRI and could they eventually come over the problem. I wished there were more cases of ED and other sexual difficulty after discontinuing the SSRI. -sia Fallahi 17:12, 23 November 2006
SSRIs don't make people more sensitive, quite the opposite. They are already prescribed off-label to treat PE. There is a failed SSRI called dapoxetine that Johnson and Johnson is pushing for PE, but the FDA will not approve it. Shibidee 17:26, 26 November 2006 (UTC)
What I meant was, they are more sensitive after stopping SSRI. (obviously SSRI has a calming effect) -sia Fallahi 19:35, 27 November 2006
Yes, some men obviously become more sensitive after quitting SSRIs. Isn't that the whole point about PSAS and PE? Mattlewis777 16:58, 4 December 2006 (UTC).
Speaking purely anecdotally here... a lot of men who suffer post-SSRI PE never had PE beforehand. There's also the fact that post-SSRI problems of this nature differ significantly from "normal" PE. For instance, in most cases of (non-drug-induced) PE, the latency time is significantly increased if sex is attempted again shortly afterwards, and then increases again if it's attempted a third time. This doesn't seem to be the case with post-SSRI PE. There are other differences, too: post-SSRI PE doesn't seem to be directly linked to levels of arousal or pleasure, so can't be put down to "oversensitivity". Also, in regular PE there is generally a greater latency time in masturbation, compared with intercourse, and this again does not seem to be the case post-SSRI. All this seems to point quite strongly to a physical rather than psychological explanation. By the way, it's not quite accurate to say that the delayed ejaculation experienced by people on SSRIs is down to a "calming effect" - it's entirely due to the inhibition of seratonin reuptake (seratonin reuptake is necessary to trigger orgasm). The delayed ejaculation side-effect is specifically *neurological*, and has nothing to do with decreased anxiety or lowered libido. MrBronson 02:09, 25 January 2007 (UTC)
I knew it. I have been experiencing these symptoms plus others for the last 8months. Now i realise i should have shown more concern than i initially did. After a rare yet horrific fluoxetine "discontinuation syndrome" (physical dependence with a clear cut abstinence syndrome, as obviously the targeted 5HT post synaptic receptors, DAT1 & other dopamine norepinephrine (NA)pathways fluoxetine is so "selectively" meant to target became hypersensitive when the drugs plasma levels slowly declined)i developed symptoms and signs i had never initially experienced. After substituting with a low dose of quetiapine to stabilise a state of mania, depression, apathy, akethesia, hostile behaviour, lack of impulse control, amnesia and the disinhibition this drug induced, finally i was free. Or so I thought. Ever since discontinuing fluoxetine which was prescribed for anxiety despite a lack of any clinical depression, I have developed characteristics i never had. I was never depressed before fluoxetine. I never had panic attacks before fluoxetine which are now so severe to be considered panic disorder. I am now hyperactive, over talkative, constantly in muscle tension and spasms particularly in my back muscles everyday. I have completely stuffed sleep cycles and worse insomnia that seems to only remain the same or is steadily becoming worse. I have great trouble losing weight which was never a problem despite good diet and a rigorous exercise schedule. I possess very little tolerance which used to be quite the opposite. I used to be a kind, perhaps laconic and thoughtful person but now have none of my previous personality traits and have lost my ability to reason in a logical and rational manner. I new fluoxetine was the cause of the above mentioned episodes briefly depicted, but despite my attempts to prove this through a scientifically backed unbiased way, no one believed me. Until finally I met a highly regarded specialist in this area that every specialised doctor i tried to inform had either disregarded my symptoms as a return of previous mental health ( which i never had) or simply said i new far more about the biochemical and neuropharmacological mechanisms than they did, was my theory proven to be true. A supposedly rare neurotoxic effect upon my brain caused by fluoxetine, which had induced this prefrontal lobe like syndrome within my dopaminergic system. Still no one really listened or deemed it to be of much importance because it was supposedly uncommon. Electric shock sensations had only just been accepted by the psychiatric community despite evidence of its existence three years prior. "Yes that is true and very real" he said. All this said I can move on in a more scientific approach as i am a scientists. The fact that so long ago in the 70s SSRI's showed signs of possible increase in suicidal tendencies among treated patients, they were quickly brushed off as non scientifically based observations and considered to be related to the depressive illness itself. All were convinced, as I initially was, and no follow up investigation into the matter took place for a long time. Until the numbers of reported adverse drug reactions reached a certain quota and the patents began to expire at the same time with the growing law suits, did any serious investigation seem warranted. What began to unravel was evidence of side effects, poor efficacy, bazaar reactions and aggressive behaviours of hypo manic and even mania induced reactions. The list goes on and on and finally a black bock warning was issued and closer monitoring was deemed essential. What I am getting at is that side effects were rarely reported or considered dangerous or related to SSRIs and that the patients feedback was not relevant until clinically performed studies were undertaken. The doctors dished them out with numerous repeats and no follow ups (especially at the primary care level) under the assumption that they were safe and well tolerated. Sometimes we cant afford to wait twenty years for scientific proof to support patient claims and that it is better to be cautious in contemplating the potential dangers of SSRI's based upon information not from the pharmaceutical company but of the experiences patients describe as arising when starting treatment with the drug. Whether related or not, you can no longer afford to take those risks of ignoring or not reporting something that seems out of place. It is bad medicine. As for you AJ of course you don't come to Wikipedia to read about a very newly observed phenomenon and yourself make biased opinions on whether you think it is written by anti psychotropic narrow minded individuals. It is for an overview or simplistic explanations for everyone to read. Don't get smug. Doubt you would understand any of the journal publications or have any knowledge whatsoever of the biochemical signalling pathways and genomic regulation of gene expression in this related field. If i were to drop to your low level, I might just say you belong in the church of biased opinions seeing that you yourself were so one sided on the topic with intentions to initially label it as garbage and then contradict yourself by saying "while it seems that this can happen....". As the currently accepted understanding of the role of 5HT as being a neuromodulator that can potentially make long term changes in the brain via its modifications upon multiple systems, I would be cautious. Cautious of any long term receptor down regulation, possible irreversible transcriptional modifications/polymorphisms with regard to G-proteins,cAMP and the numerous second messenger systems. In an area that we admit we know so little about, I would remain open minded of anything being possible. After all science is dynamic and forever evolving. All I can say is i have never been the same since and didn't trully need to be prescribed an atypical antidepressent. Until I can piece together all the scientific literature I have and any new studies regarding this continued sexual dysfunction long after discontinuation, I will have to wait and suffer until the time comes to expose and sue those bastards for inflicting upon me what they have. Then again. Who is to blame for adverse drug reactions? Maybe just make people aware would suffice. 203.214.90.50 22:13, 28 January 2007 (UTC)
_____ There is a significant problem with the frequency section. It states that sexual dysfunction is evidenced in between 83% and 98% of patients. Regarding the first figure, the source actually states that only 17% reported sexual dysfunction, and that 83% of cases persisted at the time of interview (about 3 months later). The second source refers to sexual dysfunction in depressed patients being treated with either ssri's or snri's, but does not state that 98% of people suffer from sexual dysfunction as a side effect of the drug. It is well known that depression contributes to sexual problems such as decreased libido, etc. The figure of 17% especially seems to undermine the entire paragraph. I don't know where to find better citations, but since the person who posted these appears to not even have read them, someone with expertise in the field ought to update that info. Bc88 04:25, 21 May 2007 (UTC)
It is a well known fact that statisticians are employed to manipulate clinical trial data results to create a perception in the measure of percentage values. Lets say in 1978 when fluoxetine (which wasn't the first SSRI)was put through phase 1 2 and 3 clinical trials, the sample size was n=450 participants (most didn't actually have MDD which was the drugs first indication to be prescribed for). The value is measured against say placebo in double blind randomised long term clinical trials (which didn't occur initially at all. Trials ranged from 4 weeks to 8 with a high number of participant drop outs and very small sample sizes with even fewer trial subject completion numbers). Any way lets say the placebo group is n=2400 and the incidence of genitourinary or sexual related problems etc is n=120. That equates to 5%. In the treatment group n=450 with adverse events of say 6.5% for the aforementioned problems. That means that 29 participants REPORTED the response. Drop outs are exclude and trials are design (still to this day) for maximum efficacy and the least adverse reaction profile. So the % values look pretty insignificant but what if the treated group was n=2400. That equals 156 people compared to placebo with adverse response. One fluoxetine takes really about 8 weeks to completely work especially for MDD. The trials didn't initially run long enough to really test the full efficacy of the drug nor its toxic profile. It was (and probably only recently started happening) a long time before post market follow up trials were done in lets say 10million people world wide are on Prozac and the sample say 10,000. Hardly a good study is it. Most people would be reluctant to report adverse effects especially sexual related. Any way it would take a upto twelve months to establish true steady state levels for fluoxetine due to its long half life and even longer half life of its active metabolite norfluoxetine which follows zero order pharmacokinetics and inhibits the metabolism of its active parent drug (fluoxetine) by the CYP450 isoenzyme 2D6 family (~25% of drugs metabolised by this cytochrome enzyme) and various other CYP450 enzyme families of which there are now 57 subgroups. And who knows what proportion of the sample size had SNP (single nucleotide polymorphisms) in their CYP450 enzyme genes being either poor metabolizers or ultra rapid metabolizers. 5-HT is at 15 different receptors and counting and does regulate many mediators and signalling pathways in the body, especially the NO PDE related system for erection (vasoconstriction, endothelial cell smooth muscle relaxation etc etc etc). 203.214.38.172 16:57, 23 May 2007 (UTC)
I added a cleanup tag. this article doesn't look good enough to be left on wikipedia, as far as I'm concerned, for reasons that are discussed above. 70.22.59.231 02:26, 4 June 2007 (UTC)Mary Katherine
More appropriate references have been provided for the treatment-emergent incidence of sexual dysfunction. Shibidee 22:05, 5 June 2007 (UTC)
Mary Katherine, It is unclear to me what you refer to with your statement "for reasons discussed above". Could you please briefly restate why you have tagged this article for clean-up? Please take this paper into account: Bahrick A. Post SSRI Sexual Dysfunction. American Society for the Advancement of Pharmacotherapy Tablet 2006; 7:2-10. Thank you, Dr A. Plaksel Axelplaksel 05:03, 8 June 2007 (UTC)
As someone who has suffered from Post SSRI Sexual Dysfunction since he was a teenager, I find that people's claims that "PSSD isn't real" to be offensive. Prozac caused my PSSD and other iatrogenic problems. The medical community does not want to accept that psychiatric drugs could cause this much harm to millions of people, but the damage these drugs do is very real. There is no possible way to see if SSRIs "correct" chemical imbalances, because no objective test for neurotransmitter levels exists. Psychiatric drugs have in fact been proven to cause chemical imbalances. To the ignorant person who said this belongs in "Scientology", not every person who has been harmed or dislikes psychiatric drugs is a Scientologist. I suggest that the PSSD naysayers study up on what kinds of damage these drugs do and stop learning all of their information from Zoloft commercials where the smiley face guy lies to the public and says the drug "corrects" a chemical imbalance. Wake up and realize that Post SSRI Sexual Dysfunction is very real. InfiniteWisdom 23:35, 26 June 2007 (UTC)
I also suffer from pssd. this is not a joke. this is a serious problem that was spurred by anti-depressants and it has ruined my life. i am not anti-psychiatry, people should just be a informed. i was crippled by this drug and it hurts so much, every-day, everytime i wake up, i am 20 years old and every day i just want to die because of the way this drug has impaired me. please this is a real disorder, i just want to get better :( don't even compare it to scientology we have no agenda, but to spread awareness in order to get better. 67.186.15.84 02:04, 28 June 2007 (UTC)
I also suffer from PSSD, and I will fight this attempt to silence debate on this issue. So I guess the naysayers can now count more than four people with the problem. Hey maybe we do a census on Wikipedia. But I have a sneaking suspicion those that want to change this article are not all that interested with the truth. Further I have alerted the Yahoo support group to this effort. —Preceding unsigned comment added by Jasonontko (talk • contribs) 04:09, 17 September 2007 (UTC)
I'm another case. I was prescribed Effexor for anxiety and noticed the extreme drop in libido and functionality and a general disinterest forming within the first two weeks. My doctor said these things would pass, and it would balance itself out. My five-year relationship completely faded away in the first year. I totally lost my fear of heights and any fear of socializing, but realized I had no desire to try, and nothing to say anymore. The apathy was unnatural, and the asexual nothingness I was feeling gradually became apparent to me until it was disturbing. So I let the drug go. I stopped taking Effexor in 1999, just under two years after starting. I went through "the zaps" in a horrible way while lowering the dosage to get off the drug. I don't know if this was related to the apparent permanence of my dysfunction but here it is 2008 now, almost ten years later, and I quite simply do not "work". Ten years and I think I've successfully had sex only four times. I'm 33 years old and I am horrified by the realization that this may never pass. No matter how excited I should get, no matter how much I want it, it just doesn't work. I can't function. I can't make it work, they can't make it work.. It's horrible. I don't know how to tell people. I've become totally afraid of intimacy. This is so far beyond just embarrassing or humiliating now, and so, so much worse than the anxiety I thought I was suffering when I got on the drug in the first place. 76.111.77.215 (talk) 11:04, 30 May 2008 (UTC)
[edit] External links
External links on Wikipedia are supposed to be "encyclopedic in nature" and useful to a worldwide audience. Please read the external links policy (and perhaps the specific rules for medicine-related articles) before adding more external links.
The following kinds of links are inappropriate:
- Online discussion groups or chat forums
- Personal webpages and blogs
- Multiple links to the same website
- Fundraising events or groups
- Websites that are recruiting for clinical trials
- Websites that are selling things (e.g., books or memberships)
I realize that some links are helpful to certain users, but they still do not comply with Wikipedia policy, and therefore must not be included in the article. WhatamIdoing (talk) 07:33, 17 January 2008 (UTC)
The people who dismiss PSSD are obviously unaware of the manner in which ssris work. SSRIs work by slowly desensitizing the 5ht1a receptor, at which point far more serotonin is produced in the brain. We should not need to find articles to promote this point because it is basic science.
Amongst the articles mentioned in reference to PSSD is an article from the FDA - HARDLY UNOBJECTIVE AND UNRELIALE. Their is no evidence that supports the hypothesis that the 5ht1a receptors up-regulate again after coming of SSRIs. On the other hand, the FDA have published an article demonstrating that their is a possibility that they do not.
The changes in gene expression are likely to be caused by downregulation of 5ht1a receptors. When 5ht1a receptors are downregulated, more GABA is produced. GABA is responsible for gene scilencing. This is all pretty basic stuff. I know there are lots of people out there who what to look clever by putting a pretentious link in the discussion page, but at the end of the day you guys don't know what you're talking about. —Preceding unsigned comment added by 149.170.39.33 (talk) 13:47, 2 May 2008 (UTC)
I could have missed it but is there any stated way or theory that could reverse this effect? Some medications perhaps? I know one was mentioned in passing.
—Preceding unsigned comment added by 76.116.204.247 (talk) 02:17, 6 June 2008 (UTC)
