Talk:Selective serotonin reuptake inhibitor/Archive 1

Archive 1

Archive 2

Archive 3

Various 2001 and 2002

Would someone familiar with the chemical action of these drugs please add this.

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Why not, Zundark? --AV

- Because it makes it look like an advertisement. --Zundark, 2001 Oct 22

- I agree with Zundark -- MarXidad, 2002-01-17 6:36 AM EST

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I was filling in a link from Multiple Sclerosis. Is that so bad? RoseParks

It was BF's contribution that I was objecting to, not yours. --Zundark, 2001 Oct 22

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Someone added ® signs to the trademarked drug names, and Zundark removed them. This information is accurate (the names really are trademarks) and is generally included in descriptive texts. If we're going to use commercial brand names (and I see no reason not to), then we should do it correctly. --LDC

Why is it only correct if you put a ® after it? We've used "Intel" and "Pentium" and numerous other registered trademarks in Wikipedia without using a ®. Are you going to go through and "correct" all these? It will look a mess. --Zundark, 2001 Oct 22

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I agree, it could get very messy (Pentium should be labelled, Intel should not). It's also hard to track down which are officially registered and which aren't. This is an editorial decision that should be made carefully, though, since it can piss of very rich people if you don't do it right. I don't have a copy of CMS with me at the moment, but I believe that in things like newspaper and magazine articles, the first use of a trademarked name is generally labelled. Larger works often just have a prologue that says "these terms...are trademarks or service marks of...". Perhaps Wikipedia could just have a statement of policy somewhere. --LDC

I think it would be best just to have such a statement. Keeping all the trademark information correct would be easier if it's all in one place, and the articles would be tidier without all those ® and ™. Perhaps this discussion should be moved to a more appropriate page. --Zundark, 2001 Oct 22

I could be mistaken, but I believe a blanket statement such as "All trademarks are the property of their respective owners" would cover us legally. Jimmy should probably check with a lawyer, though. --Stephen Gilbert

Legally, I don't think even this is necessary. (If it is, then someone needs to tell Richard Stallman -- see the GNU policy on trademarks.) I don't think LDC was talking about legal requirements, he was talking about not pissing off very rich people. --Zundark, 2001 Oct 22

Take some Prozac® if the registered symbols bother you so much and be sure to make appts. with your therapist more often *) —Preceding unsigned comment added by 130.94.122.xxx (talk • contribs) 25 February 2002

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I have to take offense to the following:

Third, the first letter of SSRI standing for "selective" indicates that not all synapses

are affected, but only selectively those that are responsible for the the mood and, thus, the depression. This gives way too much credit to the schleps who designed these drugs and their understanding of brain function as it relates to mood, which is minimal. In general this article makes the biochemists out to be some sort of gods. The reality is much closer to saying that they had some rough idea of what to do, stabbed in the near-dark, and fortuitously got it right. Depression and the brain in general is NOT well enough understood for drug design to be wholly "rational", and this article needs to reflect that. Thoughts? Graft, 26 September 2002

It was not the intention of the name SSRI to imply a selective action on certain 5-HT receptors. Rather they are "selective" in the sense that they only inhibit uptake of 5-HT, as compared to the older tricyclic antidepressants which inhibited several uptake mechanisms including 5-HT and noradrenaline. Techelf 09:28, 16 Sep 2004 (UTC)

Effexor

Someone has added

1. venlafaxine (trade name: Effexor®) Effexor is not an SSRI!

Hmm. What is it then? —Preceding unsigned comment added by The Anome (talk • contribs) 25 January 2003

Effexor inhibits reuptake of both serotonin and norepinephrine. -- Someone else 01:07 Jan 25, 2003 (UTC)

Effexor is a phenothalymine bicyclic antidepressant. It's mechanism is SNRI meaning it inhibits the reuptake of Serotonin and Norepinephrine. It also has a weak reuptake inhibiting effect on Dopamine. -- Sim

Allen J. Frances

Guys, it's late, I'm tired and pissed off, but who is this Allen Frances chap? I'm not in a mood to look him up right now.

Exactly why does he say that psychiatric conditions have no underlying physical mechanism? If they don't have one, why do psychiatric medications tend to work (not always as intended)? And what did Julius Axelrod get his Nobel on? Will he propose next that Phantom limb pain does not exist?

Pilatus 22:20, 13 Jan 2005 (UTC)

Sounds like a scientology insert to me, but I guess everyone wants to keep it in as one of those "some people say..." issues. Allen J Frances is the former chairman of Duke University Medical Center and a contributing editor of the DSM-IV, I supsect he has been quoted out of context here, the EDITOR of the DSM-IV is unlikely to believe that "psychiatry’s claim that mental illnesses are brain diseases... is not true". The elipsis is highly suspect. In fact, I think this quote is so suspect I am removing it until we can get a real source. protohiro 3 July 2005 18:40 (UTC)

It is off topic in an article on a medication anyway. The whole first part of the paragraph with its discussion on whether mental diseases exist doesn't belong here.--Fenice 3 July 2005 19:00 (UTC)

I actually sent Dr Frances an email to see if this quote was even his, so we'll see. protohiro 3 July 2005 19:02 (UTC)

Suicidality

children taking SSRIs or MAOIs are 1.89 times more likely to commit suicid.

More likely than what? Children not receiving treatment? Children without depression? Children who like candy? This is important. Can you link to a study or something?

I'm removing the line until someone can clarify. --Ntg 04:06, 23 Jan 2005 (UTC)

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I think it comes from the FDA blackbox warning:

"Pooled analyses of short-term (4 to 16 weeks) placebo-controlled trials of 9 antidepressant drugs (SSRIs and others) in children and adolescents with major depressive disorder (MDD), obsessive compulsive disorder (OCD), or other psychiatric disorders (a total of 24 trials involving over 4400 patients) have revealed a greater risk of adverse events representing suicidal thinking or behavior (suicidality) during the first few months of treatment in those receiving antidepressants. The average risk of such events in patients receiving antidepressants was 4%, twice the placebo risk of 2%. No suicides occurred in these trials."

http://www.fda.gov/cder/drug/antidepressants/PI_template.pdf

http://www.fda.gov/cder/drug/antidepressants/MDD_alldruglist.pdf

Sublium, 1 July 2005

Fluoxetine Removal

Someone anonymous messily removed the list of fluoxetine SSRIs; as there was no explanation or apparent reason, I put them back. If there *was* in fact a reason, could the anonymous person please explain here. Thank you. Junkyardprince | Talk 16:43, 14 Feb 2005 (UTC)

SSRIs and IBS

Does anyone know why, or have any further information regarding SSRIs used in the treatment of irritable bowel syndrome. I just found that a little odd and I was wondering if anyone knew any further information on it.

IBS is notoriously related to stress, anxiety and panic. There are many theories, but the influence of the autonomic nervous system on the "enteric nervous system" is thought to be significant, making the patient more sensitive to peristalsis, irritation etc. Improving stress-related symptoms with tricyclics or SSRIs often improves symptoms in severe cases of IBS.

The 5HT3 inhibitor alosetron and the drug tegaserod interfere with the serotinin neurotransmission in the gut. Their role is modest, especially since alosetron has been linked to ischemic colitis. JFW | T@lk 08:48, 21 October 2005 (UTC)

Balance/NPOV

I feel that as it stands this article focuses on the critcisms of SSRIs without clearly stating why these drugs are perscribed and the benefits that the vast majority of the psychiatric professions sees in patients on the drugs. Thoughts? protohiro 17:31, 22 July 2005 (UTC)

It seems to me that the first part of the article clearly states the reasons SSRIs are prescribed. See the second paragraph. I suppose from the part "Effects not well understood" and the person on this talk page asking how this helps IBS that the benefits of SSRIs are disputed. If you would like to put in some studies that showed benefits, I'm sure that would be fine, but there were also studies that didn't show benefits and even showed harmful effects. I recall one on Prozac in particular that had been covered up that, when it came out, caused quite a scandal a few years ago and IIRC was the impetus leading to the warning labels today.

Do you have a source that, in fact, the "vast majority of the psychiatric professions" sees positive caused by SSRIs? The Royal College of Psychiatrists reports that antidepressants greatly improve depression in 50 to 65% of patients but that 25 to 35% show similar improvement on placebos. [1] It seems to me that patients who improve because of antidepressants (and not just because they are taking a pill) constitutes a minority. Perhaps a confirmation bias on the part of some in the psychiatric professions? AmyBeth 17:00:49, 2005-08-03 (UTC)

Your read of the statistics is flawed. You can't subtract the percentage that improved on placebo from those that improved on the medication (thats not how statistics work). You can only say that SSRIs where around twice as effective as placebo. I suspect most scientists and doctors would say this strongly suggests these are effective medications. protohiro 23:01, 12 June 2006 (UTC)

5-HTP section shows author bias?

The length and wording of the 5-HTP section at the end of this article seems to indicate a hidden agenda towards promoting 5-HTP and a bias against SSRIs or "medical" treatment of depression (almost to the point of recommending turkey, for example, instead of SSRIs to treat depression). Could it be shortened, revised or removed altogether? Remember, this article is about SSRIs in general, not just about their main application in medicine today. Perhaps the 5-HTP section would be more useful as an article of its own, with a one-sentence reference here for the purpose of linking?

I've moved the 5-HTP section into its own article, and changed the "newer medications" section to be inclusive of 5-HTP supplements (thus "other medications for treating depression") with a warning that 5-HTP has not been scientifically proven to treat depression (i.e.: it's not used in mainstream medicine, but some "natural healing" professionals recommend it). Personally, I think self-medication is very dangerous, especially when dealing with diseases that affect behavior and judgment, but I have refrained from stating this in the article as to avoid the appearance of bias against "natural healing" professionals.

Contradiction in text

How it works section has two contradictory statements. In 1989, the FDA made tryptophan available by prescription only, ... and Pharmaceutical grade L-tryptophan is currently available over the counter in the U.S.

Did some qualifier get deleted ? Could someone who is familiar with the situation be available to make the info correct ?

Persistent sexual dysfunction

An anonymous editor keeps on returning to push one particular point: the fact that SSRIs may affect libido and the persistence of these symptoms after discontinuation of them.

He has now finally started citing sources. The source offered for the incidence of SD in SSRI treatment cited 83%. I easily found studies with a much more conservative estimate (and the anon has been cherry picking), although these involved other drugs. It remains to be seen how much of the sexual dysfunction can actually be attributed to the SSRI, considering that people with depression are not likely to be very libidinous in the first place.

The evidence offered for persistence of SD after discontinuation is extremely thin, to the point that I've removed it all again. It's an abstract of a case report involving ONE PATIENT! As for Stuart Shipko's experience - if he could write this up into a peer-reviewed publication we would actually be able to cite him. JFW | T@lk 04:27, 17 October 2005 (UTC)

I would hardly call the animal experiments documenting the persistence of sexual side effects as "Cherry picking". As for the human data, you are right that I only cite one case report so far. However, I have written up three additional case reports with Stuart Shipko and the paper is in press due for publication early 2006. I am aware of at least 100 (yes, one hundred) additional cases, which will go into a much larger study. There is no doubt that SSRIs cause persistent sexual side effects, it has just been neglected as an area of study so far. A similar exmaple would be the recent epidemiological study by Irwin Goldsten documanting the persistence of sexual side effects in former users of the oral contraceptive pill. The pill has been on the market 40 years, but the persistent side effects are only now being documanted. In any case,I'm getting tired of this silly situation in which you keep deleting my material. You say that I have an agenda - What's yours? Shibidee

Good, you're in press. Come back when the paper is out. Or perhaps wait until the 100 cases have been analysed. For now, this is all original research. Animal models are rubbish for this kind of thing, which is why I removed the reference. People are not animals, and rat sexual behaviour is not human sexual behaviour. Who says rats are good animal models for SSRI pharmacology anyway? Do they get depressed?

My agenda is that you simply cannot denounce a whole class of generally useful and reliable medication as harmful on the basis of doubtful evidence. I fight this agenda on a large number of health-related topics on Wikipedia, and if this is undesirable to you feel free to issue a WP:RFC. JFW | T@lk 05:13, 17 October 2005 (UTC)

Oh, and my accusation of cherry picking referred to your choice of the 83% figure and its reference, not to the animal model. JFW | T@lk 05:23, 17 October 2005 (UTC)

OK, I will come back when the paper is out. You say that animal models are "rubbish"? LOL What about all of the preclinical testing in animals that is performed before drugs go to human trials? Are they "rubbish" too? Do rats get depressed? Well, there are many animal models of depression and anxiety - if you want to dispute them all, you are welcome to, but don't expect to be taken seriously by me. You are basically negating thousands of experiments. As for "denouncing" SSRIs, you said it, not me. I am merely pointing out a major, major overlooked persistent side effect of these medications that has been massively ignored. I've got more important things to do than bicker with you about this issue any more. I have plans to address this point in more democratic, impartial, and sceintifically open forums. You have got a very restrictive attitude (based on what authority, I wonder), that seems to be contrary to the very point of Wikipedia in the first place. And I question why you seem to be so *pro* these medications. Anyway, ttyl. Shibidee

Quickly now:

• Animal models are rubbish for an encyclopedia.
• Whether this is a "major, major overlooked persistent side effect of these medications" is not established until it is studied well.
• My restrictive attitude is an attempt to stop Wikipedia from degenerating from an encyclopedia into a puddle full of unsubstantiated speculation.
• I have stated my bias. I do not own stock in pharmaceutical companies, I am not on SSRIs and nor is anyone in my personal surroundings.
• I have no more authority than you on Wikipedia, but Wikipedia policy is firmly against original research.
• I have filed an RFC, as we're unlikely to achieve a solution without endless bickering. JFW | T@lk 06:21, 17 October 2005 (UTC)

[personal attack removed], if animal models are "rubbish for an encyclopedia" then I suggest you delete the entire contents of this article from Wikipedia. LOL

http://en.wikipedia.org/wiki/Animal_model

I can't be bothered to address your other points because I find them just as silly as the first one, and as I said it's time for me to abandon this nonsense. Good luck with your further censorship initiatives. LOL.Shibidee

Ah, you're losing your temper and resorting to personal attacks. Never good. I'm thrilled you're willing to leave this article alone.

Calls his friends at the Censorship WikiProject to boast of his achievement JFW | T@lk 09:14, 17 October 2005 (UTC)

Are you familiar with the term "Miereneuker"...and did you get your long-sought promotion at the Wikipolice?Shibidee

Hi there,

It seems this discussion has descended into a bit of a slanging match. However, it is important to note that there is quite an extensive literature on sexual dysfunction induced by SSRI medication. See here.

Vaughan 19:31, 17 October 2005 (UTC)

Hi. Yes, thank you. The sexual side effects of SSRIs are well established, but the persistence of these effects in quite a high percentage of former users has so far gone unnoticed. Part of the problem is the complexity of gene regulation in the human brain which is, after all, the most complex thing in the known universe. Do a Pubmed search for "antidepressant" and "gene expression" and you will find hundreds of articles. As we all know, the major effect of SSRIs is to block the reuptake of serotonin, but they have a multitude of secondary effects. When you have so many secondary effects there is no a priori reason to assume that the effects are fully reversible just by removing the initial agent. The same is true for some other drugs such as nicotine, which has lasting effects on the brain's reward system long after chronic administration has ceased (http://www.newswise.com/articles/view/514937/). Everybody has assumed so far that the effects of psychoactive substances are reversible, and they seem to be in most people, but it also appears, based on emerging data, that in a significant percentage of former users the gene expression gets "stuck". In the case of SSRIs, it then has to be nudged back to the right expression pattern using other agents - testosterone, dopamine agonists, ginkgo biloba etc. Anyway, I will address this problem in an article next year after we have more case reports, animal work, and other data. Shibidee

The Wikipolice thing was sarcasm, of course. As for "miereneuker", this is an offensive Dutch term for someone who pays a lot of attention to detail. Does not quite cover my behaviour, which has been to-the-point and open. Offense is hereby taken.

As for persistent sexual dysfunction, if you could quote a reliable mainstream clinical source, it would perhaps have been suitable for inclusion in the article. What you (Shibidee) have offered so far are preliminary animal studies, the extent of the reproductibility in humans of which is unclear, one case report, and a link to a yahoo.com self-help group. Your theories on how this would be caused (e.g. gene expression) sound very fancy, but until the extent of this problem has been documented it would be highly speculative to make such extensive mention of it in what is supposed to be a general article on SSRIs.

Due to the nature of Wikipedia, drug articles have a tendency to grow long lists of potential side-effects, and some have turned downright nasty (e.g. doctors have a stake in prescribing certain substances). I find this bias unfair, irresponsible and a potential source of legal problems for Wikipedia.

Shibidee, could you please desist from inserting your theory until reliable statistics become available? Vaughan, have you noticed the distinction between "sexual dysfunction" and "persistent" sexual dysfunction? JFW | T@lk 19:42, 19 October 2005 (UTC)

Wolff, As I said, I have no intention of putting my data and theories back in the article until they have been published in the medical literature. You are obviously far too obsessed about blocking the material and I don't have time for this. I find your authoritative tone quite preposterous, and have the distinct feeling I'm being cyber-stalked. As I already mentioned, one of these papers is already in press, and others will be submitted soon. Also, I have a lot of interest from journalists who want to cover the topic, so I can't really be bothered to engage in a petty squabble with you when I can go through the mainstream media. BTW, the Wikipolice comment was only semi-sarcastic (http://en.wikipedia.org/wiki/User_talk:84.66.181.168).Shibidee

I don't like being called "Wolff". I think my obsession in keeping your theories out more or less matches your fervor in trying to get them in. I only sound authoritative because Wikipedia policy appears to be in agreement with me.

Of course journalists are licking their pens in anticipation of publishing "the horrors of mankind brought on by prescription drugs".

Your link concerning the WikiPolice is odd. I never even edited that page. Just because I'm questioning the insertion of your theories, does that make me a "censor", "cyber-stalker", "Wiki-Policeman" and all such? You seem to be taking this "petty squabble" rather a bit personal. JFW | T@lk 11:21, 20 October 2005 (UTC)

To answer your sarcastic comment about "the horrors of mankind etc." would require a detailed treatise that I don't have time to get into with you. I'd rather save it for a journal article or a book. So you don't like "wolff", huh? Would you prefer "sheep"? Till next year...Shibidee

Please do try to keep the conversation civil and amiable. If you can't manage that, then don't say anything. Thank you. -- Jitse Niesen (talk) 11:48, 22 October 2005 (UTC)

Niesen - What, like Wolff was "civil and amiable" to me from the start?? Give me a break. Shibidee

My comment was addressed to both of you, though I admit that this wasn't clear. Sorry about that. -- Jitse Niesen (talk) 00:56, 23 October 2005 (UTC)

I wasn't using quotation marks for nothing when I wrote "the horrors of mankind brought on by prescription drugs". I'm not going to address any further points by Shibidee, who is clearly very busy and has no time to present us the evidence we've been waiting for. Leaves, bleating. JFW | T@lk 01:11, 23 October 2005 (UTC)

As someone who as personally experienced the devastating persistent sexual side effects of SSRIs years after discontinuance I find it disappointing that the Wikipeida page seems state that it is not possible. From reading above the above arguments I understand the rational for not including this info but wonder if maybe we can come to a compromise that is less strong in promoting that it can't happen. Since we can't include information saying that SSRIs cause persistent sexual dysfunction becase we currently don't have proof could we at least not say that it doesn't happen? I have seen no proof that shows that there is no long term persistence. The short term proof is documented well. The reference saying that normal sexual function returns after discontinuance could be removed or at least it could be toned down to say that the majority of the time its turns to normal. I would like to find some middle ground here because as it stand I think the page makes a judgement that all sexual dysfunction gos away after the drug is stopped. I should also point out that we are not only talking about libido here but actual physical functioning. In my personal case libido mostly returned but functioning did not. -- James

I'm sorry to hear about your experiences James. The page doesn't actually say that this is impossible. The old version said "is assumed to always resolve", and now mentions "in most cases resolves". I think both are fine. My spat with Shibidee above was whether there were peer-reviewed scientific reports on the existence of this phenomenon. I felt that in the absence of such reports, it would be unreasonable to put this (admittedly rare) phenomenon in this very general article.

I hope your problem is being properly addressed by your physician. Without offering any medical opinion, this type of problems may have other causes not related to use of SSRIs, and some further tests could shed light on this. JFW | T@lk 21:50, 3 November 2005 (UTC)

I think the current wording is much better. Because its occurrence is not the norm I think it will take time to become widely known and properly researched/documented. In my case it appears the SSRIs have done something to my dopamine system and I have had some initial response with my doctor using dopamine agonists to try to correct the problem. From what I am told its not uncommon for dopamine to decrease when serotonin is boosted with SSRIs but for most people this returns to normal after discontinuance. James

I am by no means an expert on SSRIs and similar drugs, though I have read something about their effects and mechanisms. My conclusion would seem to be that no one really knows how the hell they work. however, to address the point being argued here, these drugs are specifically chosen to induce long-term permanent changes in brain chemistry. It therefore seems inconceivable to me that they would not create long term side effects in exactly the same way they create long term effects. The fact that side effects go away may in part be a measure of the long-term ineffectiveness of such drugs. Sandpiper 00:44, 4 November 2005 (UTC)

The whole idea of SSRIs is that they inhibit the reuptake of serotonin in the synaptic cleft. They are not designed to last forever, otherwise people would not be taking one tablet a day. There are not supposed to be "long-term permanent changes". It is known that cells remove receptors that are consistently blocked under certain circumstances, and this is a much more long-term process, but it is unclear whether this applies to SSRIs. The fact that you find it conceivable does not mean it actually happens. Again, I am sympathetic to James' plight and people in similar circumstances, but we need to await solid published evidence to avoid breaking the Wikipedia guideline of no original research. JFW | T@lk 08:53, 4 November 2005 (UTC)

I have to disagree. The whole idea is that you start with a depressed patient, give him something for a bit, and end up with a non-depressed patient. The whole theory of how psychoactive drugs work is that they alter brain chemistry. That depression is a consequence of faulty brain chemistry, and it is the intention of the prescriber to permanently change this. These drugs are not intended to keep the patient 'happy' while the brain sorts itself out. They are intended to actively cause changes. As I have seen this best explained, the drugs disrupt normal brain function, causing the brain to reorganise its functioning. They are required to be given for a sufficiently long period that these changes will become permanent. There effectiveness is not the direct consequence of raising serotonin, but the changes that ensue when serotonin is kept permanently raised for an extended period. They all come with warnings that they must be taken for weeks or months before any benefit will be seen, and that the patient should disregard unpleasant side effects in the short term.

If this is not true, then the companies selling them are nothing more than snake-oil salesmen. Now given that the drug companies claim their products make permanent changes, it seems entirely reasonable that they will also make undesireable changes. In fact, given that it is conceded by drug companies that individual patients react quite differently to the same drugs, it is pretty much inevitable. Sandpiper 21:39, 4 November 2005 (UTC)

RFC request

Comment. I am responding to the RFC request on Wikipedia:Requests for comment/Maths, natural science, and technology. Reviewing the history of edits and the above discussion, I don't think the two studies previously referenced in the article[2] [3] are enough to support the assertion that persistence of SD after discontinuation occurs in humans. Edwardian 06:03, 17 October 2005 (UTC)

Comment. I am responding to the RFC as well. Until more substantial, published, peer-reviewed research is available, we should stick to what's proven in the medical literature with regards to persistence of SD. InvictaHOG 16:16, 20 October 2005 (UTC)

healing versus dysfunction/flight versus fight

When does a victim decide to stop rationalizing abuse from an offender? Perhaps at that psychological threshold of tolerance, serotonin reuptake is inhibited rather than facilitated within the subject. Beadtot10/18/200504:51, 19 October 2005 (UTC)

5-HTP

The following note was left in the article by User:12.149.141.14:

"NOTE TO EDITORS: the Wikipedia 5-HTP page indicates that it standa for 5-Hydroxy-tryptophan and that it is USED to create Serotonin. The Serotonin page indicates it's abbreviated term is 5-HT. Also this page should reference the 5-HTP page and its use as an alternative to L-Tryptophan."

Please see serotonin and 5-HTP. -- Jitse Niesen (talk) 02:02, 5 November 2005 (UTC)

Addictive

This edit looks legitimate. However, the sentence "SSRIs meet the World Health Organization definition of 'addictive'" probably should be sourced. The closest I could find was here, which states "In the 1960s the World Health Organization recommended that both terms be abandoned in favour of dependence, which can exist in various degrees of severity." Is there a better source for the claim? --Arcadian 17:49, 13 December 2005 (UTC)

If there isn't, it should be removed as original research. JFW | T@lk 17:53, 13 December 2005 (UTC)

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It's Sim, I'm the one who re-wrote the intro then someone changed it back. First, I felt it should be very simple and brief because most readers aren't medical professionals. The reverted intro is too detailed and sometimes people just want a quick explanation in layman's terms.

As for the remark about them being called _The Wonder Drugs_, it's a reference to the face that SSRIs are the polar opposite to TCAs and MAOIs in that they have no dangerous overdose effects or drug interactions. Nothing to do with effectiveness, they just are so safe which is a wonder compared to TCAs and MAOIs which are extremely dangerous meds. —The preceding unsigned comment was added by Simman2 (talk • contribs) .

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• This class of drugs has been around for about twenty years now. They may have appeared like a wonder at first. Their safety, as you say, is only relative to the older drugs. Today many readers will have read reports about problems with SSRIs, especially paroxetine. There are cases where patients cannot get off the drug for years or they cannot get off Paxil at all. (I have not researched that yet, but a single trustworthy study was published that proves these effects.) Then a year ago or so there were all these reports that after taking SSRIs, the suicide rate suddenly rose sharply. Then there were reports that not all data from the initial studies were reported, only the ones that proved Prozac had favorable effects.--Fenice 22:25, 14 January 2006 (UTC)

• I tried to simplify the intro a little, but it probably needs to be polished. Maybe we could have a three-part-intro: 1. It is a medication, what are its effects and what is it used for. 2. para: simple discription of how it works. I thought your solution would be unintelligable, mentioning only receptor sites (if a reader knows there are receptors he will also understand a more detailed version, in a more detailed version any reader has a better chance of recognizing some word and getting a vague idea of what is going on) Better wording than the one that is in the text now is needed. 3. paragraph: comparison to the older TCAs. --Fenice 22:47, 14 January 2006 (UTC)

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Fenice, I have taken SSRIs and currently take a TCA. I suffer from Obsessive-Compulsive Disorder.

• Researchers/doctors make a distinction between "safety" and "tolerance". What they mean by "safety" is does it cause damage or even death (including provoking suicide.) By "tolerance" they mean how well can the person put up with the side effects or withdrawal effects. Therefore, side effects and withdrawal effects are not dangerous as they do not cause the person to die or suffer any kind of damage, although they may find them intolerable as in unpleasant. When it comes to safety, it's pretty hard to get anymore safer than SSRIs! I know this from firsthand experience!

• Yes, Paxil can cause nasty withdrawal effects. It's because it has a short half-life, hence, the med level drops quickly causing serotonin levels to drop quickly, ergo, nasty withdrawal effects. All the SSRIs except for Prozac have short half-lives so it's just not Paxil. Paxil has the shortes which is why it has the worst withdrawal effects.

I'll write more about SSRI safety for you later, go to run right now.

-- Sim

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Suicide

Why isn't the stuff on suicidal ideation in the section on side effects? It is a side effect (and a serious one, too) yet that section doesn't even mention it. 24.4.248.59 22:30, 19 February 2006 (UTC)

• Short answer: the article does even better than this and devotes a whole section of its own ("Criticism of SSRIs") and the current Side effects section does list "increased feelings of depression and anxiety" (which are more common than any rate of increased suicidal ideation).
• The current side effect section is currently written to discuss the most likely common (? 1 in 3 patients) mild symptoms (eg bowel disturbance) that are often transitory, rather than listing rare but serious problems (eg severe allergic reaction, bone marrow effects etc). For those who do experience "increased feelings of depression and anxiety", these are usually relatively mild.
• The issue as to whether more severe initial disturbance occurs (suicidal ideation or even less-common carrying out of suicidal intent) is currently contentious, with the existance or precise significance of such effect unclear.
  • The issue is how much of the suicide rates seen (which are of course "real") reflect in part just the underlying disease (e.g. those being started on medication are likely to have worse disease than those whose condition is not thought to warrant starting medication), whether there is a genuine initial increase in suicidal tendence in some patients and if so then by how much, and finally how many suicides might be prevented in the long term from patients taking SSRIs beyond the initial 4 weeks.
  • I think most doctors would accept there is a small risk of initial increase in suicides, which is offset by a greater prevention of suicides in patients left untreated, and also for the majority of those treated the improvement in the equality of life. Of course anyone is free to suggest that doctors are wrongly informed or misguided in their assessment, but it is (de facto) the overwhelming current medical consensus. Also it is felt (hoped) that suicidal tendency can be reduced by prior counselling of patients, starting at low dosages and then building up and close monitoring of patients.
  • There clearly are many points above that are contested by supporter/detractors of SSRIs, and even the data itself is not always consistant (eg recent a single study suggesting SSRIs reduced the suicide rate, which I think surprised many). Wikipedia, being an encyclopedia, will not be the place to debate in the finest possible detail the current ongoing research (both inappropriate level of detail and WP:NOR policy), but rather highlight the nature of uncertainty and the notable debate.
• Of course in recent years this issue of increased suicidal tendency has become more widely spread: newspaper articles, regulatory bodies have issued advice to doctors, doctors (should) be cautioning their patients about this possible effect and be monitoring their patients rather more carefully. This in itself makes the issue of suicidal ideation notable, quite separately from whatever the final conclusion as to the size of any such effect.
• I think therefore the subject of suicides is therefore already reasonably covered in the current "Criticism of SSRIs" section. David Ruben ^Talk 01:20, 20 February 2006 (UTC)

deleted block

As the production error responsible for the contamination would have been easily correctable, some critics have suggested that this appears to have been done to make money for the manufacturers of SSRIs. This bureaucratic action neglecting the most important fact established regarding the biochemistry of tryptophan: that it is an essential amino acid that humans cannot live without eating, led to renewed questioning as to whether the FDA was a science based or political agency.

This section was recently deleted from the article. Any comments? Kim Bruning 13:46, 21 February 2006 (UTC)

Neurotoxicity? Where's the proof?

The article claims that antidepressants have been shown to be neurotoxic. Nothing could be farther from the truth. Numerous studies have indicated that SSRIs may actually promote neurogenesis, quite the opposite effect. If no one can supply evidence of purported neurotoxicity, I am going to remove the claims, as they are currently devoid of any scientific basis, and in the light of new research suggesting an effect to the contrary, ridiculous. --Muugokszhiion 05:18, 10 May 2006 (UTC)

I totaly agree. SSRI promote neurogenesis protect against stress and depression related volume (maybe neuron) loss in the hippocampus. even for very high doses no proof of neurotoxicity. particular SSRI may even be neuroprotective in stroke yet needs more proof.

Should be deleted. Neurobio 01:41, 18 May 2006 (UTC)

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More and more the science will see, that many depressions are not coming by a lack of serotonin. Some are the result of lack of noradrenalin and also a surplus of stress.hormones, such like cortisol. This of course only, if the depression is endogenous, which is a small minority of d. The many side.effects of SSRI (selective serotinon reuptake inhibitors) make this therapy dangerous! --Fackel 21:35, 30 May 2006 (UTC)

Merge proposal

The following discussion is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.

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See also Wikipedia:Articles for deletion/Post-SSRI sexual dysfunction ψ Result: Redirect to Selective serotonin reuptake inhibitor#Sexual_dysfunction

Listed at Proposed mergers

I propose merging Post-SSRI sexual dysfunction into Selective serotonin reuptake inhibitor. This idea has already been floated at WT:MED. The principal reason for the merger is that PSSD is purported to be a medical diagnosis. I don't think publishing a limited number of primary studies is sufficient to establish a diagnosis, no matter how many reviews are published thereafter, especially if the conclusions are summarily rejected by field experts. Rather, a reasonable standard for inclusion would be if the condition is (A) a recognized medical diagnosis OR (B) a widely disseminated fringe/alternative diagnosis, this is clearly neither. The "endorsement" by the EMA does not count towards A, because it is based on a misunderstanding of the limited authority of a medical products agency.

I suggest a limited merger, and it has to be a limited merger with respect to DUE in order to not unbalance the target. Lets keep the historical context, the statement by the EMA and decision concerning the labels, and most importantly be very careful in describing to what extent knowledge about the condition is frought with uncertainty. I'm aware there's already plenty here at the intended target. Essentially this merger is not about adding more, but rather establishing formal consensus for converting PSSD into a redirect for the time being and undertaking a clean up here. Draken Bowser (talk) 11:35, 29 July 2023 (UTC)

Noting also that there has been WP:ADVOCACY and SPA editing fed by at least two internet fora noted at the WT:MED discussion and on Talk:Post-SSRI sexual dysfunction (some of those posts have been removed from the internet fora, but I have kept archive.org copies). SandyGeorgia (Talk) 12:47, 29 July 2023 (UTC)

Merge. What is left after cleaning out the advocacy editing from the PSSD article says it all in terms of whether Wikipedia should be recognizing it as a separate article:

• The status of PSSD as a legitimate and distinct pathology is contentious; several researchers have proposed that it should be recognized as a separate phenomenon from more common SSRI side effects.[7]
• A 2023 review stated that ongoing sexual dysfunction after SSRI discontinuation was possible, but that cause and effect were undetermined.[3]
• Diagnostic criteria were proposed in 2022,[4] but as of 2023, there is no agreement on standards for diagnosis.[3]
• There is no standard treatment as of 2023, and no evidence that any individual approach is effective.[3]
• As of 2023, prevalence is unknown.[3]
• The biological mechanism underlying the reported symptoms of PSSD is unclear.[6]

The European Medicines Agency was seriously misconstrued and misrepresented in earlier versions of the PSSD article (which also included SYNTH and non-WP:MEDRS sourcing), and there are reviews that indicate PSSD is not yet defined as a thing separate from the sexual dysfunction already reported for SSRIs, for which there is already a section here at Sexual dysfunction.

The article has been heavily edited since late 2022 by at least eight SPAs coming from internet fora, and should go back to the redirect it was before that, until/unless anything about PSSD as a separate condition is established (cause, treatment, diagnosis, prevalence, etc). SandyGeorgia (Talk) 13:02, 29 July 2023 (UTC)

Merge. Adding on what has been said, the content kept in the PSSD article after removal of original research and primary sources is a short text that is necessarily inserted into the current context of sexual dysfunction as a side effect of SSRIs, so that's where it should be located for now. Sto0pinismo^0_o 14:01, 29 July 2023 (UTC)

Merge. Per WP:NOPAGE. The previous consensus not to have a standalone article is sound. Bon courage (talk) 16:35, 31 July 2023 (UTC)

Merge. We can't go around letting patients diagnose themselves! --RudolfoMD (talk) 06:39, 3 August 2023 (UTC)

The discussion above is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.