Talk:Selective serotonin reuptake inhibitor/Archive 3

Permanent neuropsychological changes
From the article Permanent neuropsychological changes Since the early 80's scientists have used a technique called neonatal clomipramine to produce animals used in depression research. If rats are given the tricyclic antidepressant clomipramine when they are 8–21 days old they will develop behavioural changes in adulthood which resembles depression in humans.[50][51] In 1997 Lundbeck found that treatment with the SSRI LU-10-134-C, which only differs from their product citalopram by two atoms could give similar results as clomipramine.[52] Later it was found that neonatal citalopram and escitalopram makes persistent changes in the serotonergic transmission of the brain resulting in behavioral changes, [53][54] which are reversed by treatment with antidepressants.[55] By treating normal and knockout mice lacking the serotonin transporter with fluoxetine scientists showed that normal emotional reactions in adulthood, like a short latency to escape foot shocks and inclination to explore new environments were dependent on active serotonin transporters during the neonatal period.[56][57]

But when young mice were treated with the SNRI desimipramine they developed to normal adults, which suggests that serotonin and noradrenaline has different effects in the developing brain. For humans, the developmental stage sensitive to SSRI:s corresponds with the last trimester to the first years of life. A study showed that 4-year old children perinatally exposed to SSRI:s behave normally, however the young mice and rats also seems to be normal until they reach puberty and develop their behavioural disturbances.[58][59]

The mechanism is currently unknown, but it seems that early life overstimulation of the 5HT-1 receptor which acts like a thermostat for the serotonin production results in low serotonin production after puberty.[60]

Interesting, but mostly irrelevant. Why? Mice brains are different to human brains. Drugs affect mice different to human. Mice puberty is different to human puberty. Knockout mice are different to mice. I'm not entirely convinced that the fact that knockout mice, when given a rediculously high dose of a SSRI (for their weight), develop problems after puberty, is all the relevant to humans. This isn't even refering to neonatal SSRIs. This section is very long, confusing, and uncertain relevence.

Incidentally, SSRI use hasn't been shown to be associated with any real behavioural differences in those aged 4-5 and a little earlier. This link failed to be proven in quite a few studies. Naturally though the above deals with post puberty, but I thought this was a little interesting. Depression and anxiety is however associated with behavioural alternations. I had a lovely selection of articles I roughly summarised, but I forgot to save them.

I suggest axing the above quoted section, or listing the fact that SSRI use hasn't been associated with behavioural differences and *maybe* consider having 1 line on mice. 203.5.70.1 (talk) 16:58, 15 October 2009 (UTC)

You suggest that because mice brains are different to human brains, it reduces the impact of the study (which I don't necessarily disagree with), yet many of the studies of SSRIs which show their alleged benefits are done via precisely the same route. You can't have it both ways. GimpyFauxHippy (talk) 13:04, 24 January 2010 (UTC)

There is no discussion of the use of SSRI's in anxiety and panic disorder. Christinedoby (talk) 03:22, 2 April 2013 (UTC)

Pregnancy and SSRIs
Really needs referencing, and I don't really know or have enough time to figure out how to reference the articles, but I can point out the articles in question if need be.

Combined my previous edit with another editor's work, I hope it's acceptable? Evidence regarding SSRI's teratogenesis effects is a little "all over the place" due to the methodological difficulties and conflicting evidence (quite a few studies which have found nil increase). SSRIs have been found to be weakly associated in one study or another to be linked with pretty much every deformity under the sun, and yet found by most other studies to not be associated at all. Worth a slight mention in general though, but paroxitine and the septal effects has been replicated in enough studies to probably deserve special mention. Sertraline and other SSRIs in general (with the exception of paroxitine) haven't been associated with septal defects in any other studies in my knowledge.

The fact it's common to continue SSRIs in pregnancy and why I thought is also quite important, and I would like to leave it there.203.5.70.1 (talk) 16:22, 15 October 2009 (UTC)

September 2007 indicates FEWER suicides in subjects taking SSRI, not more.
In quotation from the article: "Brown found that suicide attempts were dramatically lowered once antidepressant medication began, indicating an overall benefit of these newer medications. Also, very few people who died from suicide had been taking antidepressants.

He also found consistent reductions in suicide across counties as well as across countries during the time when there was increased use of antidepressants. Now that the overall level of antidepressants have decreased since the FDA warnings, there is very early evidence of an upturn in youth suicides.

"With the FDA warnings there has been a rapid lowering of antidepressant prescriptions, and there has been a corresponding increase in youth suicides" noted Brown. "We found similar results in the Netherlands once the warning was broadcast there as well."

How did the misconception that this study shows a higher tendency sneak into the article? I'm changing that. Hugi (talk) 00:52, 29 May 2008 (UTC)


 * I've just been through the SSRI and aggresssion section and sub-sections like a blowtorch through an ice cube. I am certain there are reliable sources that discuss the relationship, Breggin is one of them, but the referencing was terrible and some references outright contradicted the statements contained in the article.  I'm sure a portion of this is a limitation of full-text versus abstract, but if the abstract says X reduced suicide, it's mis-representation to quote mine the article for only the cirtical statements without demonstrating the main conclusion.  Blech.  I would dearly love to see the links between SSRIs and suicide to appear in the article, but not based on blogs and fake sources.  WLU (talk) 19:01, 29 May 2008 (UTC)


 * Just had a look over, and I think this section needs to be redone. I think it should make more of a mention of the impact of age on the risk change (ie adolescents higher risk of suicide, anyone else lower risk), and distinguish between attempted suicide and completed suicide (very important of course). There's a lovely FDA metareview article in 2006 on the subject. I think it's also worth stressing in the article that suicide is relatively rare, and the absolute increase in risk (if any) is very low. Also, untreated depression (obviously) is a huge risk factor for suicide anyway, much more than the use of SSRIs. But in general, wikipedia is pretty lousy for this sort of stuff. POV warriors tend to cherry pick the odd study (or even a statement from a study) that stands out from the crowd and then try to make things sound as alarmist as possible /soapbox 128.250.5.247 (talk) 05:15, 12 October 2009 (UTC)

Suicidality in children
Based on the references and the discussion above, I changed "causes suicidality" to "may increase the risk of suicidality", since there seems to be significant controversy on this issue in the literature. This was reverted with a suggestion to discuss the change here. I'd say that "causes" is too strong, especially given the results of the Brown study discussed above. Klausness (talk) 13:42, 6 June 2008 (UTC)
 * First of all, both the FDA and MHRA (the UK regulatory agencies) hold that antidepressants in general, including SSRIs, cause suicidality in children (emphasis mine). These conclusions were made after the careful, case-by-case analysis of the occurrences of suicidality in double blind trials on children. I am not kidding, the FDA actually hired a group of suicidology experts from Columbia University who went, one-by-one, through the raw descriptions of all the suspicious cases of suicidality in childrens trials FDA requested fron the companies. The statistically significant increase of suicidality in double-blind trials in the antidepressant groups as compared to placebo was demonstrated beyond any doubt. If a double-blind trial demonstrates some effect it is generally hold to be causal. (Otherwise you would have to agree with such ridiculous statements as: Antibiotics are associated with improvement of acute bacterial infections, but they may not be the cause of this improvement). Thus there are warnings in the US regarding the use of antidepressants in children, and outright counterindication of such use in the UK.


 * On the other hand, the Brown study included adult patients, for whom the consensus is that antidepressants does not cause suicidality. In addition, the Brown study is not controlled but epidemiological, so it is inherently weaker. Paul Gene (talk) 14:42, 6 June 2008 (UTC)


 * I understand that these conclusions were reached after careful analysis, but many experts apparently disagree. Also, the standard way to talk about untoward side effects that occur for some, but not most, people is to say something like "may cause".  To the lay person (and wikipedia is written for the lay person), "causes suicidality" means "if you take this, you will become suicidal", and that's clearly not true.  My wording of "may increase the risk of suicidality" means "if you take this, you may become suicidal (or more suicidal)", which is exactly what the FDA and MHRA concluded.  We could also say "increases the risk of suicidality" -- that way it sounds more definitive while still making it clear that we're talking about an increased likelihood, not a certainty. Klausness (talk) 15:18, 6 June 2008 (UTC)


 * I am going to change it to "can cause" like with sexual side effects: "SSRIs can cause various types of sexual dysfunction such as...". There is about the same level of certainty. Paul Gene (talk) 16:33, 6 June 2008 (UTC)

Hmm. January 29, 2009 sees the Army reporting the highest suicide rate in history, while Paxil is one of two meds approved by FDA for PTSD. Maybe there's a connection? Ya think? Also the suicidality being acknowledged in children and young adults up to age 18 is as much of a joke as the Black Box Warnings. There is no biological mechanism that keeps maleffects of SSRIs from occurring in adults - And "FDA's strongest warning was never even used on drugs before they applied it to SSRIs - it was only used on cigarrette packaging - which is where those in FDA likely got the idea while they were smoking like expectant fathers, trying to come up with yet another way to obviate appropriate drug safety regulation - AND TAKE THE HARMFUL PRODUCTS OFF THE MARKET. Guess New Boston Tea Party strikes again. Wise up. Thanks.


 * Where have you found the data showing the SSRIs may "cause" suicidality? Most studies have only found a link between the two, so the data generally doesn't indicate a causal relationship. The FDAs publication in 2003 (which majorly covered depression trials, naturally increasing suicidality risk) found problems with SSRIs. But since then, lots of research (Gibbons, Bridge, Olfson, etc.) suggesting that there is an negative relationship between SSRIs and suicidality.  While there have been studies finding no significant benefit (especially for MDD), there is no associated risk of suicidality.  Also, you should change it to "certain" SSRIs. Prozac has been cleared multiple times and virtually all costs-benefits analysis have found that it reduces sucidiality.  —Preceding unsigned comment added by 128.42.164.188 (talk) 06:30, 5 February 2010 (UTC)

Programmed cell death by SSRI
On August 2 I added a very small note on possible neurotoxic effects of SSRI. It is about apoptosis. (Evident in vitro.) My entry as well as the references were deleted. It's a pity, I think the readers have the right to be informed....

http://www.ingentaconnect.com/content/hum/jmn/2005/00000027/00000001/art00004

Ok, I see it is now under Neuroprotection! Well, but it also shows neurotoxicity... —Preceding unsigned comment added by 62.47.180.13 (talk) 22:11, 6 August 2008 (UTC)

Can somebody put this in terms a welder (who's having antidepressants pushed upon him) can understand? —Preceding unsigned comment added by 68.17.100.179 (talk) 22:17, 14 September 2008 (UTC)

Removed Weasel Word Warning from "Criticism" section
Almost all claims in this section are well-referenced and are not empty statements in the sense of "People say they don't always work...", "Some believe that it does more harm than good...", etc. The only sentences in the section that are written in this way are: "Biopsychiatrists believe that, among other factors, the balance of neurotransmitters in the brain is a biological regulator of mental health. In this theory, emotions within a "normal" spectrum reflect a proper balance of neurochemicals, but abnormally extreme emotions, such as clinical depression, reflect an imbalance. Psychiatrists claim that medications regulate neurotransmitters, and many if not most psychiatrists also claim they treat abnormal personalities by removing a neurochemical excess or replenishing a deficit." But that's simply summing up the general point of view of modern psychiatry: restoring chemical imbalances in the brain. If there are a lot of experts that think that this is not at all what modern psychiatry is about, then maybe these sentences should be removed altogether. The sentences don't form the core of the 'criticism' section. The core is that there are a number of studies that take into account *all* available data on the efficacy of the drugs, and that the conclusions from these analyses are that the drugs are not as useful as is generally portrayed. —Preceding unsigned comment added by 82.74.127.167 (talk) 17:30, 16 December 2008 (UTC)

List of SSRIs that don't cause Tinnitus
I've heard that Tinnitus is a common side effect with SSRIs. I've been trying to find out which ones don't cause Tinnitus, I think it may be helpful to add a section listing, which SSRIs are better for people who have had Tinnitus as a side effect before, or Tinnitus in general.Violet yoshi (talk) 12:48, 23 June 2009 (UTC)

Potential source
may be a valuable source for the pharmacodynamics section, if it mentions 5-HT2A downregulation. I can't get to my university library to view the full article for several days. Jennifer500 (talk) 03:02, 1 January 2010 (UTC)
 * That particular source only includes one sentence about 5HT2. Looking at, it seems that much of the pharmacology section's unsourced paragraph about 5HT2 neurotransmission is incorrect. Yes, the stimulation of 5HT2a and 5HT1a receptors which occurs during SSRI administration downregulates 5HT2a. But this is a good thing: it occurs when the antidepressant effects of SSRIs become apparent. Also, deceased suicidal and otherwise depressed patients seem to have had more 5HT2a receptors than normal patients, suggesting that 5HT2a overactivity is involved in the pathogenesis of depression. I am modifying the paragraph to include the source, and for conformity to it. Jennifer500 (talk) 23:19, 2 January 2010 (UTC)

Comparison with benzodiazepines irrelevant
Some Wikipedia authors seem not to be able to resist the temptation to insert warnings about benzo withdrawal independent of the the topic being discussed. I've lightly edited the section in this article that compares benzo and antidepressant potential withdrawal concerns. I resisted the temptation to point out that Effexor withdrawal, if one refers to withdrawal sites, appears to be more difficult that benzo withdrawal for many people and that even Heather Ashton (her opinions are well-meaning, but hopeless dated) states that about 50% of benzo users do not exhibit benzo withdrawal symptoms-making any blanket statement about benzo withdrawal invalid. Dehughes (talk) 22:45, 7 April 2010 (UTC) David Hughes

Brain-derived neurotrophic factor's role in SSRI and depression
The following comes from a paper I in progress of writing regarding PTSD and the use of SSRIs. It's directly applicable to this article as it describes one of the mechanisms of SSRIs."This is done by SSRIs acting on signal pathways such as cAMP (Cyclic AMP) on the postsynaptic cell, which leads to the release of Brain Derived Neurotrophic Factor (BDNF). BDNF enhances the growth and survival of cortical neurons and synapses. Thus, the use of SSRIs may actually help to reverse the hypoconnectivity previously described. (Kolb and Wishhaw, 2006) Source: Kolb, Bryan and Wishaw Ian. An Introduction to Brain and Behavior. New York: Worth Publishers 2006, Print." I am hoping we'll be able to add in the BDNF info to this article as I think it's missing a major facet without it. Basket of Puppies 07:00, 20 July 2010 (UTC)

Efficacy
This paper looks relevant to the discussion in the efficacy section but I can't access the full text: "In 'Initial severity and antidepressant benefits', Kirsch et al. conducted a meta-analysis of data from 35 placebo controlled trials of four newer antidepressants. They concluded that while these drugs are statistically significantly superior to placebo in acute depression, the benefits are unlikely to be clinically significant...we argue that Kirsch et al.'s is a flawed analysis which relies upon unusual statistical techniques biased against antidepressants. We present results showing that re-analysing the same data using more appropriate methods leads to substantially different conclusions."--86.23.82.164 (talk) 16:24, 1 August 2010 (UTC)

I agree the section seems too one-sided. There has been criticism on the used statistical methods, and most importantly on the use of FDA licensing trials for quantifying the benefits. Given that the FDA requires two positive trials and disregards failed ones for a drug to come on the market, a company will choose the fastest and cheapest way to meet these minimum requirements, ie short duration, no proper screening of candidates and most importantly only designed to show a statistically significant result as required by the FDA. They have no reason to optimize duration and dosage for best clinical results in these trials, yet the meta-study uses the results as such. So basically, to judge the potential efficacy of these drugs, Kirsch et al. took only data from small scale trials, some more than 20 years old, that were set up to show a mere statistical significance, and ignoring any studies that might have been more suitable for their purpose. And they mention publication bias in their meta-study... The other study that is referenced used only six FDA licensing trials with a total of 718 patients. Some replies to Kirsch's article: http://www.bmj.com/content/331/7509/155/reply 94.227.1.33 (talk) 07:24, 14 August 2011 (UTC)

In his book Bad Science,  Goldacre makes the case that SSRI's  are not effective. http://en.wikipedia.org/wiki/Bad_Science_(book)#Chapter_10:_Is_Mainstream_Medicine_Evil.3F — Preceding unsigned comment added by 209.78.20.61 (talk) 22:42, 14 August 2012 (UTC)

This section has been removed ("Efficacy") but there are still links to it within the document. Anyone want to propose either putting it back in or changing the links?

Jason A. Jensen of USA (talk) 03:47, 29 May 2013 (UTC)

Sexual side effects
"Initial studies found that such side effects occur in more than 80% of patients, but since these studies relied on unprompted reporting, the frequency was probably overestimated. In more recent studies, doctors have specifically asked about sexual difficulties, and found that they are present in between 17%[38] and 41%[39] of patients." This is incredibly unlikely (people have a known unwillingness to raise sexual issues unprompted) and I have seen books saying the exact opposite. If memory serves, under Eli Lilly's original trial it was reported infrequently, but when someone did a follow up and specifically asked if people suffered sexual side-effects, the percentage of positive responses was huge; I do have the figure of 80% in my head, though I don't know why.

Because this says the exact opposite of what it logically ought to, I suspect this is a malicious edit made at some point and not picked up. If someone could check sources and edit appropriately, that would rule. --Matthew Proctor (talk) 12:17, 11 August 2010 (UTC)

OPED in lede?
The passage ''The term SSRI is somewhat of a misnomer, invented by the pharmaceutical companies who developed these drugs. Rationally, they should be referred to as SRIs, as dopamine reuptake inhibitors and norepinephrine reuptake inhibitors are referred to as DRIs and NRIs respectively, regardless of their selectivity.'' seems to be somewhat MOS:OPED and perhaps WP:POV. Would it be better to note simply that the phrase doesn't match an existing naming pattern and move it out of the lede? Preferably with references?Autarch (talk) 21:41, 16 October 2010 (UTC)

I wouldn't call it editorialising, it is true that it was invented by the pharmaceutical companies who invented those drugs... they called them "selective" because they thought it would distinguish them from the other antidepressants available at the time, and thereby to give them more zeal. --Axxaer (talk) 05:06, 13 December 2010 (UTC)


 * It's an obvious example of editorializing, original research, and POV. As with the stuff above about "an untested hypothesis." I'm going to fix that presently. 205.211.141.188 (talk) 19:35, 1 June 2011 (UTC)

Improve the sentence: "Rationally, they should be referred to as SRIs, as dopamine ..."
The sentence in the article "Rationally, they should be referred to as SRIs, as dopamine reuptake inhibitors and norepinephrine reuptake inhibitors are referred to as DRIs and NRIs respectively, regardless of their selectivity." could be phrased more clearly.

Is what is meant: "Rationally, they should be referred to as SRIs in order to be consistent with using the term DRIs for dopamine uptake inhibitors and the term NRIs for norepinephrine uptake inhibitors." ?

Tashirosgt (talk) 22:36, 17 December 2010 (UTC)

"Selective" serotonin reuptake inhibitor is misleading as it suggests that this medication selects a specific kind(s) of serotonin. However, as long as the explanation of the name is present, there is no harm. Perhaps the explanation could be a little clearer. We can't unilaterally change the name that drug companies use. No one but us would know what an SRI is.Christinedoby (talk) 03:35, 2 April 2013 (UTC)


 * Actually, we could: Just redirect SSRI and "Serotonin Specific Reuptake Inhibitor" to SRI, then explain the series. There would be a tonne of policy wonks up in arms about verifiability, though. If it were mathematics, we could do it regarding series. With Category:Reliable sources in medicine, though, I don't think so. 75.156.178.30 (talk) 03:55, 30 July 2014 (UTC)

Possibly unnecessary weasel words re. "Post-SSRI sexual dysfunction"
This section starts with the words: "According to one source." Which sounds like weasel words to me; and IMHO, doesn't belong on Wikipedia. I'm not criticising the argument, I just think the caveat is unnecessary. Also, I've no doubt there are several reliable citations that could support the original claim. —Preceding unsigned comment added by 86.16.20.52 (talk) 00:40, 18 December 2010 (UTC)


 * I agree with your bias towards clarity. The issue goes under copyediting for redundancy, because the number of citations at the end of tested words tell readers *roughly* how many sources were consulted.75.156.178.30 (talk) 05:47, 30 July 2014 (UTC)

Also, this section is woefully lacking in references. I don't doubt that some of this is true, but how do I know which issues have good evidence behind them and which have little or none? —Preceding unsigned comment added by 86.16.20.52 (talk) 00:46, 18 December 2010 (UTC)


 * That's a difficult question that comes with skill in entering a query at toxnet pubmed, or the trip database, among the most reliable sources for peer reviewed articles and such. Sometimes, a search will hit on something good with google scholar. Since you asked the question four years ago, I certainly hope the situation haz changed. 75.156.178.30 (talk) 05:47, 30 July 2014 (UTC)

Re: SSRIs versus TCAs
I think the conclusion of this section (equality of efficacy between SSRIs and TCAs in depression) is, if not incorrect, then at least too global, and somewhat misleading. TCAs are a far too diverse group of agents in order to compare them with SSRIs who, as the name says, affect more or less serotonin only (yes, there are pharmacological differences between them, but they are minor). Amitriptyline or clomipramine are not the same as desipramine, for example. It would be hard to find a clinician who says that, say, citalopram has the same efficacy as clomipramine, particularly in severe depression. Even the one source that is referenced says in the abstract already that amitriptyline is more effective in in-patients (who are likely to present more severe forms of depression). I will try to find some more references, comparative trials and so on, but I was gonna see whether people would agree with me or not. C.d.rose (talk) 12:12, 13 January 2011 (UTC)


 * I will look this up to see if it ended up becoming an article fork, because someone might be deleting a comparison I am trying to make based upon relevance or something. 75.156.178.30 (talk) 05:52, 30 July 2014 (UTC)

I read that amitriptyline & imipramine are potent SERT inhibitors but these agents feel absolutely NOTHING like SSRIs, for example the loxamine I have here. On the other hand, the clompiramine that I have feels more similar to SSRI than it does to amitriptyline. For example it is daytime drug rather than to take as sleeping pill. I mentioned in the "similar agents" section just below the SSRI gallery clomipramine but some other user deleted it. I think clomipramine is worth mentioning, prior to SSRIs, I think it was the most potent serotonin inhibitor actually on the market.78.144.18.89 (talk) 14:05, 31 October 2015 (UTC)

SSRIs versus 5-HT-Prodrugs
The section titled like this is not at all talking about Serotonin Prodrugs but only explaining why Serotonin itself cannot be directly administered. Could a knowledgeable person update this?

If Dopamine Prodrugs + Decarboxylase inhibitor (to assure that the prodrugs are metabolized in the brain) work fine for Parkison (which is caused by a lack of Dopamine) then why shouldn't Serotonin Prodrugs + Decarboxylase inhibitor work fine for Depression, which is caused by a lack of Serotonin? —Preceding unsigned comment added by 141.53.210.36 (talk) 19:03, 12 May 2011 (UTC)

Yes, this text of this section does not relate to the title at all. richard.rankin@ieee.org — Preceding unsigned comment added by 66.188.106.93 (talk) 13:16, 5 August 2011 (UTC)

IQ and drinking water
A 16-year old reported a 30 point drop in his IQ after using the SSRI prozac.(see: "SSRI Babies") Prozac is commonly found in the drinking water of the United Kingdom and Canada.(see: "Prozac in Drinking Water? Likely So", "Drinking water contains traces of nine drugs, new study finds", "Stay calm everyone, there's Prozac in the drinking water")

Petey Parrot (talk) 03:40, 14 June 2011 (UTC)


 * The above are not reliable sources. Sorry, but it cannot be included in the article unless the sources are reliable. Basket of Puppies  10:28, 14 June 2011 (UTC)

Lawsuits
Changed the text from

The inclusion of the black box warning may have led to a decrease in prescriptions of SSRIs and a decrease in suicide. to: "..and an increase in suicide."

Because that is what the first referenced article claims (can't access the second reference) The article reads:

"Some medical professionals, including the National Mental Health Association, blame the effect of the "black box" warning that the U.S. Food and Drug Administration put on antidepressants in 2004, the year before suicide rates rose precipitously. " 94.227.1.33 (talk) 13:50, 15 August 2011 (UTC)

pov
A widely criticised study that was carried out by a guy known as a big fan of placebo effect and of the use of hypnosis in medical procedures. The studies used were carried out to meet the FDA standards for marketing of the drugs involved and they satisfied those criteria. Misusing those trials to prove things they were not designed to test is intellectually dishonest.

And to quote from Meta-analysis: '''If a meta-analysis is conducted by an individual or organization with a bias or predetermined desired outcome, it should be treated as highly suspect or having a high likelihood of being "junk science". From an integrity perspective, researchers with a bias should avoid meta-analysis and use a less abuse-prone (or independent) form of research.''' 84.197.184.6 (talk) 04:01, 9 November 2011 (UTC)


 * Hi, not sure how to reply, but this is a different person. I would also like to point out that this one study being prominently featured in the first paragraph is a bit ridiculous. Why does it have more merit than any other study done? Why prominently display it? EDIT: this entire article is rife with politicization. 198.53.43.19 (talk) 03:56, 15 February 2012 (UTC)
 * Even though I added some of it, I agree that it is being given undue weight in the lede. There should be a sentence mentioning the dispute, referring to that study and others.  The details of the study should be in the section below. I'll probably make the edits in a few days if no one else does. - Maximusveritas (talk) 01:57, 16 February 2013 (UTC)

Suicidiality Original Research
The statement ending the "Suicide Warnings" section stating that concerns about increasing suicides among children were allayed by the cited CDC annual mortality survey is an original synthesis, as SSRIs are not referred to in the CDC report. Thus is is disallowed by the "no original research" policy (http://en.wikipedia.org/wiki/Wikipedia:OR ). Strictly speaking, it is not a definitive conclusion, as it is possible that increased suicides due to declining SSRI use could have been offset by other factors so that no net increase was apparent. — Preceding unsigned comment added by Alfred Bertheim (talk • contribs) 21:05, 2 March 2013 (UTC)

Neurological changes due to SSRI use in infancy
While MEDRS standards do not completely forbid the use of primary reference s or of animal studies, they do discourage both. As there is not a single citation in this section that is not both animal research and primary research, I think it may be considered to be both poorly referenced and given undue weight. I'd like to suggest either reducing it considerably or eliminating it altogether. These compounds have been around for 2 decades and have been taken by tens of millions of people. If the concerns raised in this section were representative of mainstream thought among experts, it should be possible to identify multiple secondary references of studies in humans by now. Alfred Bertheim (talk) 23:14, 2 March 2013 (UTC)

2010 review
"A 2010 review reached similar conclusions: in mild and moderate depression, specifically that the effect of SSRI is very small or none compared to placebo, while it is clinically significant in very severe depression. However, this analysis included only 6 studies out of the over 2,000 that have been done, involved just 2 medications, and did not involve studies with placebo washout periods typically used as controls."

These investigators were only able to get patient level data from 6 trials as the others they asked refused to give them the data they needed for the meta-analysis. This is an equally important point IMO. Doc James (talk · contribs · email) (if I write on your page reply on mine) 12:40, 27 March 2013 (UTC)

A vote to remove a paragraph under the "Pharmacodynamics" heading
The paragraph: "However, there is one counteracting effect: high serotonin levels will not only activate the postsynaptic receptors, but also flood presynaptic autoreceptors, which serve as a feedback sensor for the cell. Activation of the autoreceptors (by agonists like serotonin) triggers a throttling back of serotonin production. The resulting serotonin deficiency persists for some time, as the transporter inhibition occurs downstream to the cause of the deficiency and therefore, is not able to counterbalance the serotonin deficiency. The body adapts gradually to this situation by lowering (downregulating) the sensitivity of the autoreceptors.[99]"     sources a publication that states there was no effect on presynaptic autorecptors. From the abstract: "Chronic treatments had no effect on presynaptic 5-HT1B autoreceptors, functionally evaluated by measuring 5-HT1B-mediated inhibition of depolarization-induced [3H]5-HT release from cortical and hippocampal synaptosomes." although this paragraph may be true, this study does not show it — Preceding unsigned comment added by 173.206.144.178 (talk • contribs) 00:06, 6 July 2013‎
 * Hi User:173.206.144.178! I cannot judge if you are correct or not, but I put a dubious-tag at the end of the paragraph, and I hope someone comes along who knows more and decides if the paragraph should be kept or if the tag should be removed.  Lova Falk     talk   14:54, 3 January 2014 (UTC)
 * This is a bit confusing but I don't think there is actually any contradiction. When the paper says that there was no effect on autoreceptors, I take it to mean that there was no increase or decrease in the number of autoreceptors or their potency.  I don't think it is saying that there was no activation of autoreceptors. Looie496 (talk) 17:23, 3 January 2014 (UTC)

Deadly overdose
Is it true that it's impossible to take a deadly overdose? --78.156.109.166 (talk) 20:42, 15 December 2013 (UTC)
 * No, it is certainly possible. See serotonin syndrome. Looie496 (talk) 17:19, 3 January 2014 (UTC)

Okay, I get it - Looie496 is the new skinwalker... — Preceding unsigned comment added by 198.49.31.114 (talk) 21:09, 2 February 2016 (UTC)

Persistent Sexual Dysfunction
I don't object to this being mentioned, even though the sources are all pretty much non-MEDRS. But I am uncomfortable with it being presented as an clinical entity whose existence is widely accepted by mainstream medical practitioners, as it is not mentioned in any medical textbook that I am aware of, and the only "secondary" source supporting its existence is a review written by a member of the University of Iowa group that has written up the majority of the 12 case reports appearing in the literature. Furthermore, this review is published in a non-Medline indexed journal, and authored by a college psychological counselor rather than an established medical expert. Overall, its basically just another primary source. It does not serve the WP:MEDRS purpose of establishing that the subject matter is widely accepted by the mainstream medical community.

I'm also concerned about writing this up in a way that suggests that it is common, given that there are only 12 case reports in the literature from among the 100 million or so who have taken these drugs.

A hard line on this would be to say that since there are no WP:MEDRS compliant sources, this should not be mentioned in the article at all. I won't go that far. But given the lack of mainstream acceptance that this syndrome exists, and the relative rarity persons claiming to have been affected, I think more than a mention that case reports exist is over-emphasis. The language should not suggest that it is common or that the existence of they syndrome is well-established and widely accepted. Formerly 98 (talk) 19:09, 3 February 2014 (UTC)

No compliant sources? Search David Healy and PSSD Yahoo group. The article about PSSD was deleted on January, 23. So you might be happy. Now you can censor this page too and delete this part of this article. Those who are suffering with sexual dysfunction, an there is a huge number of youngsters. Instead of serving the public WeakPedia serves those who finance it. This is everywhere. Nothing new. --Justana (talk) 09:23, 12 February 2014 (UTC)


 * I'm sorry for your troubles, but advocacy is not Wikipedia's purpose. Material added to articles has to meet the requirements of notability, avoiding excess weight, and in the case of medical information, WP:MEDRS. Yahoo message boards are clearly not MEDRS compliant. Dr. Healy is an interesting minority viewpoint, but a quick look at the APA treatment guidelines will quickly show that his views are far from mainstream. Furthermore, as a paid expert witness in litigation against SSRI manufacturers, he has a very substantial financial COI.  Formerly 98 (talk) 14:01, 12 February 2014 (UTC)

"I'm sorry for your troubles." Just now I saw that. I'm a psychoanalyst and in my country, Brazil, and in Argentina psychoanalysis is still strong. You have CBT for everything and a pill for every ill as explained in UK parliament review "The Influence of Pharmaceutical Industry" APA? lol What a joke! APA, FDA... all corrupted. Take a look at the article "evergreening"; You should delete this article. I pity you. Since it is becoming personal I can say I pity you for having to work for the mainstream people. I hope you are being well payed.--Justana (talk) 21:08, 28 February 2014 (UTC)

"...but advocacy is not Wikipedia's purpose." Wikipedia is all about advocacy. It is all about the official view and advocating for the companies, politics and all of those who are... the winners. There are numerous articles with wrong information because it is the mainstream view. I wonder why PSSD had even had an article in this encyclopedia. We know quite well why the article was removed and who told you to remove it. The same people who made "Corporate Crime in the Pharmaceutical Industry" by John Braithwaite disappear from the market by the time it was published. BTW: Iatrogenesis: leading cause of death in US. Search for Dr. Kafka and you'll find your authoritative source for PSSD. We all thought that Wikipedia was a project where people would have a voice. No! It is mainstream, mainstream and once again mainstream. Ergo, no ethics and integrity in this project. Human, all too human. And, please, stop treating those who come here as a bunch of resentful few cases. This is a very serious issue and I'm sure that each of you know someone who had their sexuality altered by an antidepressant. Even among you. It is such a delicate and terrible condition that makes people ashamed of admitting they were chemically castrated. Some people never had and will never have a sexual life because they took these drugs as teenagers or even while childhood. Please, no need to answer with your famous arrogance. --Justana (talk) 00:30, 28 February 2014 (UTC)

Well, I'm sorry you're unhappy. If you want to have it reviewed by another group of people, there are multiple avenues within Wikipedia for doing that. But if you can't get people to agree with you, you can't just force your opinion on everyone else. That wouldn't be giving the people a voice, would it? Formerly 98 (talk) 04:56, 28 February 2014 (UTC)


 * You are doing consumers who wish to inform themselves a grave disservice. In my original rework, I certainly think I provided enough evidence to state that sexual side effects may persist after using these drugs.  It is not that strong of a statement, and readers were free to analyze the evidence for themselves.  Now you have removed much of it and left only the case reports.
 * No article written on the topic is admissible?
 * Despite thousands of posts by sufferers in the ssriSEX yahoo group and on pssd.forumotion.com, neither is even allowed to be mentioned?
 * What can be done to present the truth here?
 * AmiLynch (talk) 00:37, 4 February 2014 (UTC)


 * I feel quite strongly that we have to followe the MEDRS rules. We can never all agree on what the truth is, but we can agree on what is mainstream opinion. Wikipedia's rules are focused on the latter, more attainable goal.


 * Rather than further explaim my POV, I'll simply suggest compromise language. After a discussion of the well established sexual side effects that occur during SSRI treatment, I would not be opposed to something like this:


 * "Symptoms of sexual dysfunction occasionally persist after discontinuation of fluoxetine treatment. The incidence of this adverse effect is unknown. A limited series of published case reports describe loss of libido and/or genital sensation lasting for several years after cessation of therapy"


 * Can you live with this? — Preceding unsigned comment added by Formerly 98 (talk • contribs) 10:43, 4 February 2014 (UTC)

I was shocked to discover that post ssri sexual dysfunction was removed. I believe I suffer from this and I copied the references cited by Wikipedia. I now feel invalidated and extremely distressed.107.221.229.121 (talk) — Preceding undated comment added 23:54, 26 February 2014 (UTC)


 * Our articles need to be based on reputable published sources. We can't make use of people's reports of their personal experiences or our articles would degenerate into incoherence.  The fact that you feel "invalidated" is not relevant either. Looie496 (talk) 14:50, 27 February 2014 (UTC)

Would this Ph.D. thesis and the supporting docucmentation regarding PSSD be considered "relevant?" 107.221.229.121 (talk) 15:57, 11 June 2014 (UTC) Unable to post link. Please do internet search for the following Ph.D. thesis regarding PSSD published in 2013: Rebecca Diane Stanson--The Impact of Persistent Sexual Side Effects of Selective Serotonin Reuptake Inhibitors after Discontinuging Treatment: A Qualitative Study. 107.221.229.121 (talk) 16:34, 11 June 2014 (UTC)


 * I don't think this changes much. Its still primary research, and its the same University of Iowa group that has published most of the <20 case reports in the peer-reviewed literature. This does not provide meaningful support for the idea that this is a widely accepted syndrome in the mainstream medical community.  There are far more papers in the literature arguing that vaccines cause autism or that magnetic fields are the cause of Alzheimer's, and we don't discuss these hypotheses as established facts. Formerly 98 (talk) 19:06, 11 June 2014 (UTC)

"...or our articles would degenerate into incoherence." This is a joke. Mainstream views and opinions are dominated by numerous degenerate and incoherent facts, evidences and lack of ethics and integrity. "Invalidated"? You're being quite arrogant saying so but those who have the habit of "contributing" to Wikipedia know the way you mistreat any other view that is not mainstream. I don't have Wikipedia as a reference. We already know how biased this encyclopedia is. The encyclopedia done by the people. Oh, yeah.--Justana (talk) 00:41, 28 February 2014 (UTC)
 * The alternative to being based on reputable published sources is being based on people's personal opinions. Reputable published sources can be wrong, but people's personal opinions are very likely to be wronger. Looie496 (talk) 15:02, 28 February 2014 (UTC)

The article "Post SSRI Sexual Dysfunction" by Dr. Audrey S. Bahrick, Ph.D. was publishedat page 2 of the volume 7 issue 2, September, 2006 of the ASAP Tablet of by American Society for the Advancement of Pharmacotherapy (ASAP), Division 55 of the American Psychological Association. Maybe Wikipedia do not consider it to be mainstream although the there are psychiatrists who are considered as mainstream by APA - America Psychiatry Association. But Wikipedia has it's own criteria do define mainstream. Anyway, this is the article: Post SSRI Sexual Dysfunction Audrey S. Bahrick, Ph.D.

keep reading here. http://apadivision55.homestead.com/vol7no3.pdf Not good enough, we understand and we know that the word of patients and doctors are anecdotal evidence. How can a science consider the object of it's study that can communicate as an object that must be studied without it's participation will be known as something very strange if not nazi in decades to come.

So, how will the fourth phase of clinical trials will be done? Double-bind, oops Double-blind studies? Great! Hilarious! --Justana (talk) 21:59, 20 April 2014 (UTC)

You are being repetitive but I understand that there is no other argument. It is not about people's personal opinions. It is about those scientists, doctors, journalists, lawyers, social scientists, psychologists all these serious people with M.D or PhD who are working hard and with no help, no money to fund their researches because science is in the hands of... guess who? Does Wikipedia has an article about the way science is used? Keep doing what you're already doing: copy from all mainstream sources and censor dissent and the work of those professionals who are fighting for awareness, I'm happy i'm on the side of the solution, not the problem. You on the contrary: help intervention in countries that leads to tortures, genocides, people dying because of iatrogenesis - leading case of death in US -; suicides, homicides. crimes against humanity in general. It would be impossible for me to sleep if I did the kind of work you're doing. I even have a book by mainstream psychiatrist that I could leave here but I'll not do so because it can disappear and it is where people can read and have information. Have a great life and sweet dreams!--Justana (talk) 20:57, 28 February 2014 (UTC)

"Furthermore, as a paid expert witness in litigation against SSRI manufacturers, he has a very substantial financial COI." (about Dr. David Healy) Could you please provide the evidences for such accusation? This is serious and puts Dr. Healy's ethics in question, so, please, produce your evidences. Thank you.--Justana (talk) 15:24, 12 April 2014 (UTC)

How serious of Wikipedia! Put someone's integrity in question without proving. --Justana (talk) 21:59, 20 April 2014 (UTC)

http://www.davidhealy.org.php53-23.dfw1-1.websitetestlink.com/wp-content/uploads/2012/05/2009-Healy-Adolescent-suicide-Canadian-J-Psychiatry1.pdf. See the COI disclosures at the end of the paper. Pointing out a conflict of interest is not an accusation nor is it questioning their integrity. Suggesting that they were writing on behalf of undisclosed third parties, that they are aiding and abetting human rights violations, and fighting to "bury the truth" as you have in multiple places in this thread would be examples of such behavior. Formerly 98 (talk) 20:17, 22 April 2014 (UTC)

People are being castrated en masses by these drugs, it's ruining lives, do you know what it's like to be castrated in your brain and know that you will never feel horny, sexually aroused or any sexual feelings ever again, the pleasure centers of your brain ruined? I'm sure it's rare that a person is not consumed with suicidal thought after castration. These "happy drugs" are causing castration suicides I'm sure. And you don't want to save lives by adding at least this little sentence? Why? Because there are no good studies? Well, and there won't be because studies are funded by big pharma and they don't want it to get out that their blockbuster drugs sometimes act as the perfect lifelong castration agent instead. Whoever deletes that sentence will have blood and suffering on their hands. Broomattack (talk) 17:44, 24 August 2015 (UTC)
 * Please read WP:NOTADVOCACY and WP:NPOV. There are some issues with sexual side effects but if the problem were as drastic as you describe it things would be different in the real world. Do not use Wikipedia as a lever to try to change the world.   Thanks Jytdog (talk) 19:09, 24 August 2015 (UTC)


 * But why can't case reports be mentioned? Like "However, there are case reports[38][39] which suggest that sexual dysfunction may persist after discontinuing SSRIs. The frequency with which this happens is unknown but believed to be rare." Which policy does that violate? Because I'm starting to think this page has a pro-drug agenda. Broomattack (talk) 23:01, 24 August 2015 (UTC)

Aside from numerous case report series (see             ), published in MEDLINE-Index journals there are various non-primary sources like press articles (http://psychcentral.com/lib/sexual-dysfunction-persists-after-discontinuing-antidepressants/  and  http://www.oncns.com/content/some-drugs-not-much-rock-and-roll  )  paragraph from Handbook of clinical neurology ( ISBN 9780444632470 ) written by Waldinger MD and prozac label ( http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/018936s091lbl.pdf ). Summarising, there is no good reason other than censorship to not mention that, sexual dysfunction can last beyond drug withdrawal in some individuals.GPUmaniac (talk) 17:47, 30 August 2015 (UTC)

removal of sourced content
Regarding the edit summary of this removal of sourced content, please note the paragraph that was removed does not say these 3 critics of SSRI oppose antidepressants. The paragraph that was removed says these critics oppose the view of antidepressants as correcting chemical imbalance because that view is not supported by the evidence. IjonTichy (talk) 01:12, 28 May 2014 (UTC)

Good to meet you. I see your point, but if you're going to put this in here, could you at least include some discussion of what they think causes depression? My concerns are:


 * Ultimately, depression has to be related to a "chemical imbalance" of some sort, as there are not obvious macroscale structural changes in depression.  Either that, or one believes that the brain and the mind are not related to one another. That seems like a stretch to me, but maybe you can fill me in on the theory.


 * You can affect your mood directly with changes in your facial expression. Forcing a smile on your face and getting some eksersize will affect your mood. There are also cognitive-behavioural therapies, like reading P.G. Wodehouse, Bill Waterson, or watching Robin Williams. There are actually lots of drugs that work with varying degreez of persistence.75.156.178.30 (talk) 13:09, 27 July 2014 (UTC)


 * There is no discussion of WHY they think that the prevailing theory is incorrect. These folks are not such household names that simply saying they disagree with mainstream thought is a very meaningful remark.  Could you get a sentence in there at least explaining their reasoning?


 * First on my list of to-dos regarding this article is actually to cut down content from their argument, because it seems to be redundant.75.156.178.30 (talk) 13:09, 27 July 2014 (UTC)


 * Finally, I think these books and news articles are really primary sources, and not WP:MEDRS compliant.

Let me know what you think. Formerly 98 (talk) 02:04, 28 May 2014 (UTC)


 * If they are not needed to support facts, then go ahead, and be careful with the one from JAMA, especially, because it's in a trade journal. 75.156.178.30 (talk) 13:16, 27 July 2014 (UTC)

Avoiding Discussion of Causation with Evasion
Evasion versus WP:discussion for those who want to vote. Optimally, finding a courageous source, and I really do not know what to search for. Does anybody want to discuss whether Tricyclic Anti-depressants increase rates of heart attack? It's like you can't do anything but observational studies, because an interventional experiment would cause death. And, if I evade, then I warn less, so I do not consider weasel words to be ethical. If you will fuck up, then do a good job of it. 75.156.178.30 (talk) 13:38, 27 July 2014 (UTC)
 * I have no idea what you are talking about. Jytdog (talk) 16:42, 27 July 2014 (UTC)
 * OK, the key dispute seems to be whether to have a pretty complex statement about correlation of heart attack with antidepressant like 75 would have it or have a more general summary statement as DocJames would have it.    75 thinks DocJames' version is weasel wording.   I reckon DocJames would say (as he often does) that his edit emphasizes MEDMOS' directive to summarize and write for a general audience.  DocJames and 75 appear to agree that you have to be careful with interpreting the results of observational studies so I am not sure what the acrimony in the above comment is about.  As for me, I find 75's version to be too technical for the average reader. I would go for something in middle, like, "People who take SSRIs appear to be a bit less likely to have a heart attack than (what? healthy people or untreated depressed people?  need to check source)  and this apparent "protective" effect is much stronger among smokers. This is in contrast to people who take TCAs, who are more likely to have a heart attack.  These results are based on epidemiological studies so it is not possible to say that SSRIs actually protect the heart or that TCAs actually cause heart attacks."  something like that.  Jytdog (talk) 17:05, 27 July 2014 (UTC)


 * 👍 I am glad you understand the question. It's not between me and Doctor Heilman, though: Both versions are mine. I predict that he would prefer the foggy version that does not imply causation. He can determine otherwise. 75.156.178.30 (talk) 17:21, 27 July 2014 (UTC)


 * Actually, it is possible to infer causation. That's why I am pointing to confounding. Statisticians hav shot bull about causation for ages, and it does not go anywhere without specific examples. You hav to think about some of them for quite a while to understand them. For example, there's a .8 correlation between the population of Storks nesting in Britain, and the birth rate in India. I shit you not! Storks bring babies to India. :) If you think about it long enough, then you will realize that Stork nesting and human reproduction are periodic, because they are both related to reproduction, and genetics contributes to periodicity. So duz the weather. Ultimately, it's a coincidence, and you make that conclusion from common knowledge (if such a thing really exists). If you can't think of a third variable that affects the variables you are testing, then you ask around, or you do an intervention. To repeat myself, we can't do an intervention with TCAs, because that would *probably* cause death. I inferred causation in an elaborate way, here, from somebody's assertions against causation. 75.156.178.30 (talk) 05:21, 29 July 2014 (UTC)

Lets actually look at the conclusions of the study "This meta-analysis of observational studies in subjects with no history of CHD suggests that neither SSRI nor TCA use is associated with an increased risk of CHD." Than lets look at the results "There was no association between SSRI use and the risk of CHD overall (OR, 0.93; 95% CI, 0.65-1.33)" Check out those confidence intervals. They vary from 0.65 to 1.33, the middle point is 0.93. This does not mean that SSRI decrease the risk of heart disease. It however does mean that "evidence does not support an increased risk". The ref is of observational studies and thus does not support causation. Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:11, 28 July 2014 (UTC)


 * I was hoping to resolve this dispute on the simple terms of readability. I would like to be terse, and it seems that I will need to point out about five documents, heavy on WP:AGF, confounding, and confidence intervals. We are looking at a Gausian distribution (bell curve) {to refresh your memory}. I need you to understand that the document you are pointing to has contrasting terms between numbers and words. This is explicable in the implications of a document that effectively considers whether all people on earth should be given an SSRI prescription. Does citalopram benefit all people? According to a ninety-five percent probability of significance, SSRIs benefit our population as used: Doctors are not causing harm with SSRIs. According to a nearly normal 93% risk ratio (normally relating to one), this data is insignificant, so consult stratified data. 75.156.178.30 (talk) 12:51, 28 July 2014 (UTC)

Clarity

 * These changes are horrible and are not supported by the sources in question.  Doc James  (talk · contribs · email) (if I write on your page reply on mine) 02:51, 29 July 2014 (UTC)


 * All experiments are conclusive without evidence against them in citations. Start there, and eliminate evasion to get where I got. Ultimately, I do not know what you are talking about. My version iz more readable. 75.156.178.30 (talk) 05:00, 29 July 2014 (UTC)


 * Additionally we are to write in plane English. Doc James  (talk · contribs · email) (if I write on your page reply on mine) 02:52, 29 July 2014 (UTC)


 * Ingglish, I teL yuu. Pleez riit in Ingglish! Either that or stop enforcing rules that you do not understand, like preferring one primary source over another. They are both meta-analytical, so according to WP:MEDRS, they are both acceptable. 75.156.178.30 (talk) 05:00, 29 July 2014 (UTC)
 * You are talking about that 13 year old source? Doc James  (talk · contribs · email) (if I write on your page reply on mine) 20:18, 29 July 2014 (UTC)


 * 90/5=18. No wonder I flunked enjineering! :) User:Jmh649 identified a sentence az a question, so I am inclined to flunk him in Ingglish. Please see recentism. Overturning an old conclusion attacks your own conclusions in some cases. It's called Biting the hand that feeds you. If you fail my assignments, then I do not need to do yours. I am not reading through all of the sources on this page to find which is thirteen years old, assuming that it is only one. Which source do you mean to attack? Daman Hongren (talk) 12:54, 31 July 2014 (UTC)

Summary
So it appears that 75 wishes to summarize the meta-analysis as:
 * "According to a ninety-five percent probability of significance, SSRIs benefit our population as used: Doctors are causing an average benefit with SSRI prescriptions. According to a nearly normal risk ratio, this data is insignificant, so consult stratified data."

I propose summarizing as:
 * "SSRIs do not appear to affect the risk of coronary heart disease."


 * ...except in stratified data. Dose distinguishes drug from poison. When a study or analysis intentionally restricts their population, then they often see stronger correlations. For example, if you stratify coffee drinkers to those who drink one or two cups per day, then their death rate goes down. If you stratify to (select) wimin under fifty-five who drink four or more cups per day, then their death rate doubles. Dose distinguishes drug from poison. 75.156.178.30 (talk) 05:00, 29 July 2014 (UTC)

Ref conclusion is: "This meta-analysis of observational studies in subjects with no history of CHD suggests that neither SSRI nor TCA use is associated with an increased risk of CHD." What are peoples thoughts? Doc James (talk · contribs · email) (if I write on your page reply on mine) 03:01, 29 July 2014 (UTC)
 * To reflect the findings more accurately, I would summarize it as "SSRIs do not appear to affect the risk of coronary heart disease among healthy people with no history of CHD".-A1candidate (talk)
 * Came here from posting on WT:MED. Would prefer ""SSRIs do not appear to affect the risk of coronary heart disease in those without a history of CHD." I would avoid mentioning "healthy" people as that may suggest someone without any history of any medical problems. Yobol (talk) 17:43, 29 July 2014 (UTC)
 * Am happy with Yobol's suggestion. Doc James  (talk · contribs · email) (if I write on your page reply on mine) 20:17, 29 July 2014 (UTC)
 * That abstract haz me lost.75.156.178.30 (talk) 05:31, 29 July 2014 (UTC)

Also agree with 's suggestion, as it is accurate and accessible to our general reader. It is vastly better than any of the semi-literate comments of the 75... IP editor. 03:39, 30 July 2014 (UTC)

Accurate and Terse, please expand.
According to a ninety-five percent probability of significance, Serotonin-specific reuptake inhibitors (SSRIs) benefit our population as used: Doctors are causing an average benefit with SSRI prescriptions. According to a nearly normal .93 risk ratio, this data is insignificant, so consult stratified data. In data stratified for smokers, TCAs contrast in effect on heart attack rates with SSRIs: TCAs increase the rate of Coronary heart disease to one hundred fifty-one percent of normal, while SSRIs protect smokers from myocardial infarction with a thirty-five percent of normal risk after adjustment for Aspirin use and other known confounding factors.

New paper claims that 5-HT depleted mice do not show depressive symptoms
Some of you have probably seen this new study that's been doing the rounds on scientific news sites recently. I'm hesitant to add this to the article since I don't have the time to read the paper properly, and think it's probably better to discuss it first anyway, but I think it probably deserves a mention either here or over at monoamine hypothesis. Opinions? -Mojace (talk) 02:58, 3 September 2014 (UTC)
 * Its a really interesting paper but WP:MEDRS limits the use of this kind of paper (primary research, animal research) to draw conclusions about human health issues. A couple of the questions I would have would be
 * How does the neurochemistry of a serotoin knockout mouse compare to that of a regular mouse? There are known examples of people who can't synthesize norepinephrine.  But since they didnt have it during development their physiology has adjusted to use dopamine in place of norepinephrine for all its usual functions. So they aren't the same as a person who suddenly becomes devoid of norepinephrine in adult life.
 * The animal models of depression are very crude. The activity of SSRIs in these assays in the knockout mice might be telling us  more about the assays than about the mechanism of SSRIs.
 * About half of published preclinical research isn't reproducible.


 * So I'd keep an eye on the area, but wait for additional work in the area and expert commentary in secondary sources.Formerly 98 (talk) 03:20, 3 September 2014 (UTC)


 * I'm inclined to agree. Obviously extrapolating preliminary research on mice to make bold claims about effects on humans is a Bad Idea (I'd argue that even with reliable secondary sources this is dubious, for the reason you touch upon in your second point; animal testing in psychiatry is not reliable, barely standardised and difficult to draw any meaningful conclusion about humans from, since it involves trying to guess what's going on in the animal's brain from behaviours that could have a multitude of different possible causes.


 * As a primary source, someone could still add a description of the researchers' observations and findings on the mice without making iny inferences about its significance for humans, but I hesitate to assume that it meets the standard for WP:N.


 * As for your first point, that's a very interesting thought. I remember reading something similar a while back about MAO-B knockout mice being virtually unaffected by it compared to wild type mice, through compensating with increased MAO-A production. What makes the situation with serotonin somewhat different to the example you cite about (nor)epinephrine however is that AFAIK serotonin is the only hydroxytryptamine neurotransmitter, whereas dopamine and norepinephrine are both catecholamines that differ only by the β-hydroxy substituant, so I can't think of any endogenous compound (that's roughly equally abundant, so ruling out trace amines) that's similar enough to be used in its place. I definitely agree that more research is needed, starting with determining what differences 5-HT KO mice do exhibit, rather than what they don't. -Mojace (talk) 16:18, 3 September 2014 (UTC)

Semi-protected edit request on 27 September 2014 - some adverse effects
Please add the following sections in the adverse effects.

Infertility SSRIs significantly affect the main sperm parameters, including reduction in concentration, poor morphology and increased DNA fragmentation. Sources: http://www.goldjournal.net/article/S0090-4295(13)01536-7/abstract http://www.ncbi.nlm.nih.gov/pubmed/24529582 http://www.ncbi.nlm.nih.gov/pubmed/20565446 http://www.jurology.com/article/S0022-5347(08)01837-5/abstract http://www.fertstert.org/article/S0015-0282(09)01007-3/abstract http://rsx.sagepub.com/content/18/4/391.short

Endocrine disruption: Disturbs FSH, LH and testosterone in rats Sources: http://www.fasebj.org/cgi/content/meeting_abstract/24/1_MeetingAbstracts/761.5 http://journals.lww.com/psychopharmacology/Abstract/2008/08000/Evaluation_of_Endocrine_Profile_and.9.aspx http://link.springer.com/article/10.1007/s002130050406

Pregnancy: Miscarriage, preterm birth and long-term neurobehavioral abnormalities in offspring Source: http://www.ncbi.nlm.nih.gov/pubmed/23117129 http://hms.harvard.edu/news/study-links-pregnancy-risks-antidepressants-10-31-12 http://humrep.oxfordjournals.org/content/early/2012/10/31/humrep.des383.short

Fabrisiq (talk) 01:23, 27 September 2014 (UTC)


 * The infertility refs are all primary research studies either using small numbers of patients or studies performed in animals. Per WP:MEDRS we use secondary sources, such as review articles and meta analyses. Ditto the endocrine disruptor material.


 * There is one WP:MEDRS compliant reference among the pregnancy refs, but my impression is that we have already covered this subject using better quality references than the one cited in the request. Formerly 98 (talk) 01:39, 27 September 2014 (UTC)

Hi Formerly 98. Thanks for the quick response and clarifications. Please see links below for literature reviews about SSRI links with infertility: http://www.nature.com/ijir/journal/v24/n5/abs/ijir201212a.html http://www.medscape.com/viewarticle/771138_4 — Preceding unsigned comment added by Fabrisiq (talk • contribs) 07:52, 27 September 2014 (UTC)
 * Red information icon with gradient background.svg Not done: please establish a consensus for this alteration before using the template. &mdash;  LeoFrank   Talk 06:21, 2 October 2014 (UTC)

Controversy
Search 'SSRI active shooter', and you will see a long list of controversies. I'm not sure if SSRI's have a link to homicidal ideation and suicidal ideation, but I'm sure theres probably a medical publication that supports the notion.

--JT2958 (talk) 07:59, 4 December 2014 (UTC)

Not so much. The idea that people take an SSRI and suddenly go out and shoot up a schoolyard has been popularized by anti-psychiatry groups and discussed in the popular media, but there is little if any support for this idea in the academic literature. Violence is not discussed as a possible side effect of SSRIs in treatment guidelines issued by major medical organizations; there is no trial data supporting this hypothesis; and a pubmed search for SSRI's and violence turns up mainly studies of the use of SSRIs to treat PTSD, along with a handful of small clinical trials in which SSRIs were found to reduce violence in convicted spouse abusers and the like.

The apparent correlation of SSRIs with violence likely falls in the same category with the observation that people in the hospital are morel likely to die than people who are not hospitalized. It reflects the fact that you wouldn't be in the hospital if you were not sick, not that hospitals increase mortality. Formerly 98 (talk) 12:31, 4 December 2014 (UTC)

http://psychrights.org/research/Digest/SSRIs/kauffman2009.pdf JT2958 (talk) 00:30, 6 December 2014 (UTC)


 * That's not a serious journal. It's published by the Association of American Physicians and Surgeons, a political group which has filed a lawsuit to overturn Obamacare.  The articles in the journal are all basically political essays and editorials rather than scientific publications.  The first article in this month's issue claims that there is no relationship between healthcare coverage and mortality.  The second is an anti-Obamacare article.  The third accuses Democrats of wanting to leave the elderly to die without care.  The SSRI article you refer to claims "all SSRI's have long half lives" but this is not true for the vast majority.  It contains demonstrable factual errors in about every third paragraph.  The common thread throughout this "journal" is political ranting with no research and a casual disregard for facts that conflict with the author's point of view.  Formerly 98 (talk) 05:52, 6 December 2014 (UTC)
 * You know what's funny, I had never heard of Journal of American Physicians and Surgeons before tonight and this is the second time I've seen it, here and also at Talk:Fluoride toxicity. It isn't MEDLINE-indexed and it's clearly not reporting well-accepted, mainstream thinking.   05:04, 7 December 2014 (UTC)

Scientific NPOV regarding Consumerized Summary of SSRIs
I'm not sure how a "best buy" rating from a popular consumer products magazine qualifies as encyclopedic information for a class of chemical compounds. — Preceding unsigned comment added by 66.244.75.98 (talk) 22:57, 27 January 2015 (UTC)

definition of "slight" increase
About 1 to 2 babies per 1000 babies born in the U.S. develop PPHN shortly after birth, and often they need intensive medical care. It is associated with about a 25% risk of significant long-term neurological deficits.[91] A 2014 meta analysis found no increased risk of persistent pulmonary hypertension associated with exposure to SSRI's in early pregnancy and a slight increase in risk associates with exposure late in pregnancy; "an estimated 286 to 351 women would need to be treated with an SSRI in late pregnancy to result in an average of one additional case of persistent pulmonary hypertension of the newborn.".


 * a slight increase of 150% or more, isn't that a contradictio in terminis? Ssscienccce  (talk) 02:37, 24 September 2015 (UTC)

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Why so many refs
User:User931 please explain why so many refs are needed here and after I reverted, citing WP:CITEOVERKILL, why you ignored that and restored them. Thanks. Jytdog (talk) 15:10, 4 April 2016 (UTC)
 * I imagine part of it is that you're reverting more than just references; you've removed content as well.  Seppi  333  (Insert 2¢) 15:16, 4 April 2016 (UTC)
 * Hi, please discuss in a non-confrontive way. I thought your revert was because of the bare-url references and i therfore fixed the references and added back the content. All references aren't needed, i just wanted to highlight the high number of review articles coming to similar conclusion. I can add back the content with less references if that's better. User:User931 16:01, 4 April 2016 (UTC)
 * Please do not edit war. My first edit note was very clear about WP:CITEOVERKILL. You are not adding any information to the article - what is your goal here? Jytdog (talk) 16:08, 4 April 2016 (UTC) Jytdog (talk) 16:08, 4 April 2016 (UTC)
 * please answer the question. All you need is one recent review to state something in WIkipedia's voice.  Why are you adding six sources?  Again, what is your point?  Your content edits are outside the norms here, and your behavior is one step away from being blockable.  So please stop and Talk.  What is the purpose of adding all these citations?  Please answer. Jytdog (talk) 16:20, 4 April 2016 (UTC)
 * Hmm, I have to ask you the same, what is your goal about this... How can you say i'm not adding information? I'm adding both content and references that support the content. There are many other bits of content in this article that have 3-4 references so I can't see the problem?User:User931 16:26, 4 April 2016 (UTC)
 * Look i am happy to collaborate but adding 11 refs and then 6 (and doing the WP:OR of actually saying you are adding 11 refs, in the content)  is really over the top pointy editing in Wikipedia.  You don't seem to be aware of it, but this is the equivalent of walking up to someone at a bar and jabbing your finger in their chest and yelling at them.   it isn't normal and is very aggressive.  So I am asking you what are you so upset about, that you have to add content with a sledge hammer like this?   What is your point?  I am really asking. Jytdog (talk) 16:32, 4 April 2016 (UTC)
 * I'm not aggressive or upset or anything. I explained before why I added many references, see my first comment in this thread. Can I add back the content with 1 review and 3 meta-analysis then? Since several other bits of content in this article is backed up by 4 references. User:User931 16:40, 4 April 2016 (UTC)

Ok so you are unwilling to deal with the fact that the WP:CITEOVERKILL is alarming. Now let's talk about the content. if we take out the clutter, it is this: We get rid of the first, "meta"/ WP:OR bit and are left with:
 * "Since 2005, many review articles and three meta-analysis have concluded that significant evidence suggest that SSRIs may decrease bone mineral density and increase incidence of osteoporosis and fracture risk. Serotonin have been shown to have a direct action on bone metabolism through serotonin receptors on both osteoclasts, osteoblasts and osteocytes. Suggestions include monitoring of patients BMD and prevention and control of osteoporosis in patients taking SSRI."
 * "Significant evidence suggest that SSRIs may decrease bone mineral density and increase incidence of osteoporosis and fracture risk. Serotonin have been shown to have a direct action on bone metabolism through serotonin receptors on both osteoclasts, osteoblasts and osteocytes. Suggestions include monitoring of patients BMD and prevention and control of osteoporosis in patients taking SSRI."
 * And I am right there stuck a bit. The evidence is much more mixed than what you are expressing there.  (note, am going to pause and sign here as you seem to be in some god awful hurry and if you insert it again before we are done working this over, you will get blocked. so i am trying to save us drama... I will sign and then finish my comment.  Please wait till we finish talking before re-inserting yet again.  this will take me a bit of time, so be patient.  Jytdog (talk) 16:50, 4 April 2016 (UTC)

Just looking at the meta-analyses to stay focused on evidence: may play a role in bone metabolism and that medications that affect these transporter systems may also affect bone metabolism." They also bring up the confounder of the association between depression and decreased BMD and increased falls.  And they raise a bunch of other confournders as well.
 * - the existing source - meta-analysis from 2012, submitted April 2011 with 13 studies "Overall, our meta-analysis showed a 72% increased relative risk of fracture for SSRI users compared to non-SSRI users..... However, SSRI use was not significantly associated with bone loss (P=0.29). Furthermore, adjusting for BMD had no effect on the strength of association between SSRI use and risk of fracture. These results suggest that SSRIs may exert an increased risk of fracture independent of BMD. Previous reviews have summarized the association between SSRIs and fracture and have tried to address the inconsistent findings regarding this association". ( Right - so the inconsistency has been in the literature for a long time.  )   These results suggest that SSRIs may exert an increased risk of fracture independent of BMD reduction. Other pathways, such as impaired bone architecture by SSRIs leading to decreased bone strength, cannot be excluded. Previous studies have identified antidepressant use as a risk factor for falls in elderly patients. (and that goes on; they also mention "Our previous meta-analyses showed that depression is a risk factor for fracture and bone loss" and they talk about that as a confounder.
 * - systematic review from 2012, submitted Oct 2011. 12 studies (!).  They found a "1.69-fold increase in the risk of fracture owing to SSRIs". They say "The increased fracture risk may be explained through cardiovascular effects such as syncope and orthostatic hypotension. One explanation is that increased fracture risk is mediated simply by falling. The likelihood of the effect, however, is much less than with TCAs" (they emphasize the latter a lot.  Then they bring up this: "Recent research reveals a potentially important role for the serotonergic system in bone physiology. Functional serotonin receptors and transporter systems have been found in osteoblasts, osteoclasts, and osteocytes in animal models. Thus, increased serotonergic activity may directly affect bone metabolism, causing excessive bone loss" (note that they don't actually look at bone loss in their meta-analysis, while the study above did).  Then they also the depression/bone loss + fracture thing as a possible confounder.  That's it.  So the SSRIs cause bone-loss thing here is a hypothesis, and the study above actually looked at bone loss and found no difference.
 * published in 2012, submitted November 2011 (!) They ended up 34 studies (!!)  Wow.  dramatically more than the other two, and not that much separated in time.  They found: "a moderate and clinically significant increase in the risk of fractures of any type. ...The exact mechanism by which antidepressant drugs increase the risk of fracture in the elderly has not yet been  elucidated, and the mechanism may differ across the classes of antidepressants... SSRIs have also been associated with an increased risk of fractures, due to an increased tendency to falls. In addition, the recent description of functional serotonin transporters in osteoblasts, osteoclasts, and osteocytes raises the possibility' that serotonin transporters

So your content doesn't reflect the sources. SSRI uses clearly does increase the risk of fracture (not maybe, as you wrote). And there is no evidence that SSRIs actually decrease BMD; two of these meta-analyses hypothesize that they might, but the first meta-analysis actually looked at that, and found no difference. So in my view the "may decrease BMD" part of your proposed content, and content on the mechanism for the hypothesized (!) loss of BMD, and the strong warning to monitor BMD... none of that comports with the evidence. (I'll note here that this would make interesting content for the research section, but that is different from this, which is meant to be actual side effects)

So again I ask you, what's up? Jytdog (talk) 17:18, 4 April 2016 (UTC)


 * I don't know why you're coming at this so hard, i'm just trying to reflect the scientific litterature in content here on wiki. I'm sorry I used too many references, didn't know that was not allowed or bad behaviour. Your way of arguing in this last post has nothing to do with the original topic of too many references and could be applied to more or less all references in this article because there is always uncertainty in research and there's often confounding factors. However, the references i included points in one direction and there's also a causal relationship mentioned with osteoblats, osteoclasts and oceocytes directly being affected by serotonin through expression of serotonin receptors, something that is mentioned in several of the review articles. Something smells wrong if someone use this much effort as you do to defend their stance and argue against the scientific litterature. Best regards. User:User931 17:45, 4 April 2016 (UTC)


 * It is only possible to deal with one thing at a time. The first and overwhelming issue, was the bludgeoning with references.  You have backed down from 11 to 6 and now just four; that is the right direction.  As I said, all you need is one.  Because you seem oblivious to your bludgeoning, I moved on to deal with the second thing.  i wrote: "Ok so you are unwilling to deal with the fact that the WP:CITEOVERKILL is alarming.  Now let's talk about the content.".  now let's talk about the content.   Do you see that up there?  So I started talking about the content.
 * The content you wanted to add is the second problem; it doesn't reflect the literature, as I just laid out very carefully above. Your content said SSRI's may increase the risk of fracture, but there is no "may" about it - they do increase the risk.  You also load up the content with speculation about possible loss of BMD as a side effect and (speculation on top of speculation) discuss a possible mechanism for speculated side effect, and then you included advice on top of speculation, saying that doctors should monitor BMD.  But as i wrote above, only one of the three meta-analyses actually deals with BMD, and it found no difference.  Would you please respond to what the sources actually say?  Thanks. Everything here in the world of medicine in Wikipedia is decided by what the strongest sources say - and only one meta-analysis (the strongest kind of source here) gives us clinical evidence about that.    Jytdog (talk) 18:32, 4 April 2016 (UTC)

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Pharmacogenetics
Further information: Pharmacogenetics

Increasing research demonstrates the pharmacogenetic mechanisms underlying the therapeutic effects of SSRIs. Pharmacogenetics investigates metabolic pathways and genetic markers to predict whether patients will respond to SSRIs (and additional antidepressant medications) or have side effects that will cause their discontinuation, although these tests are not yet ready for widespread clinical use. Therapeutic effects of SSRI medications are not seen until at least 2 weeks after the onset of treatment, although the blockade of serotonin transporters happens before this period. This suggests downstream effects of these medications which may more accurately explain how these medications work at treating depression and mood disorders, as well as serve as markers for treatment outcome. In addition, antidepressants such as SSRIs have low rates of treatment success, largely due to patient compliance and numerous side effects. Identifying genetic markers, and their role in patients’ physiological response, will improve patient treatment outcomes.

Through computational methodology, epigenetics has been found to play a critical role in mood disorder susceptibility and development, and has also been shown to mediate treatment response to SSRI medications. Several epigenetic factors are related to mood dysfunction, particularly in major depressive disorders, which are frequently treated by SSRI medications. Methylated DNA for example is known to attract methyl CpG brining proteins, which aid in the formation of repressor complexes at promoter sites, resulting in inactive chromatin states and subsequent repression of genes related to depression and mood disorders. Brain derived neurotrophic factor (BDNF), which has shown been shown to be downregulated in patients with major depressive disorder, has been associated with histone-methylation and a pro-depressive phenotype. In addition, various signaling pathways result in recruitment of CREB binding proteins, which have intrinsic histone acetyltransferase activity, which loosen chromatin structure, and result in increased transcriptional activation of c-fos and BDNF which play a role in depressive disorders. SSRI medications including fluoxetine, paroxetine, and escitalopram reduce gene expression and enzymatic activity related to methylation and acetylation pathways in numerous brain regions implicated in patients with major depression.

Pharmacogenetic research has focused on epigenetic factors related to BDNF, which has been a biomarker for neuropsychiatric diseases. BDNF has been shown to be sensitive to the prolonged effects of stress (a common risk factor of depressive phenotypes), with epigenetic modifications (primarily histone methylation) at BDNF promoters and splice variants. Such variation in gene splicing and repressed hippocampal BDNF expression is associated with major depressive disorder while increased expression in this region is associated with successful antidepressant treatment. Patients suffering from major depression and bipolar disorder show increased methylation at BDNF promoters and reduced BDNF mRNA levels in the brain and in blood monocytes while SSRI treatment in patients with depression results in decreased histone methylation and increased BDNF levels. Assessing such biomarkers in patients provides information on the pathophysiology of underlying neuropsychiatric disorders and treatment with SSRI medications.

In addition to the BDNF gene, micro RNAs (miRNAs) play a role in mood disorders, and transcript levels are suggested in SSRI treatment efficacy. Post-mortem work in patients with major depressive disorder, as well as other psychiatric diseases, show that miRNAs play a critical role in regulating brain structure via synaptic plasticity and neurogenesis. Increased hippocampal neural development plays a role in the efficacy of antidepressant treatment, while reductions in such development is related to neuropsychiatric disorders. In particular, the miRNA MIR-16 plays a critical role in regulating these processes in individuals with mood disorders. Increased hippocampal MIR-16 inhibits proteins which promote neurogenesis including the serotonin transporter (SERT), which is the target of SSRI therapeutics. MIR-16 downregulates SERT expression in humans, which decreases the number of serotonin transporters. Inhibition of MIR-16 therefore promotes SERT production and serves as a target for SSRI therapeutics. SSRI medications increase neurogenesis in the hippocampus by reductions in MIR-16, thereby restoring hippocampal neuronal activity following treatment in patients suffering from neuropsychiatric disorders. In patients with major depressive disorder, treatment with SSRI medications results in differential expression of 30 miRNAs, half of which play a role in modulating neuronal structure and/or are implicated in psychiatric disorders.

Understanding epigenetic profiles of patients suffering from neuropsychiatric disorders in key brain regions has led to more knowledge of patient outcome following SSRI treatment. Genome wide association studies seek to assess individual polymorphisms in genes which are implicated in depressive phenotypes, and aid in the efficacy of pharmacogenetic studies. Single-nucleotide polymorphisms of the 5-HT(2A) gene correlated with paroxetine discontinuation due to side effects in a group of elderly patients with major depression, but not mirtazapine (a non-SSRI antidepressant) discontinuation.In addition, hypomethylation of the SERT promoter was correlated with poor patient outcomes and treatment success following 6 weeks of escitalopram treatment. Such work addressing methylation patterns in the periphery has been shown to be comparable to methylation patterns in brain tissue, and provides information allowing for tailored pharmacogenetic approaches.

Not only does pharmocogenetic work provide information related to better treatment outcomes, but it provides additional information related to the mechanisms underlying depressive and neuropsychiatric pathophysiology and mechanisms underlying the therapeutic effects of SSRI medications.


 * My previous post was removed. However, due to use of pharmacogenetics in SSRI treatment, this page should include clinical work related to SSRI efficacy.

Mgemmel (talk) 23:04, 28 November 2016 (UTC)
 * This is almost identical to what you originally addded. I'll copy with modifications the response I gave you at my talk page here:


 * The source is kind of OK. If you look at worldcat, the book is available in only 12 libraries worldwide --- not great.... and edited book chapters are not as rigorous as our preferred sources which are literature reviews published in good journals. See WP:MEDDEF and WP:MEDRS generally.  But if you are going to use it, please at least provide page numbers - and by this I mean the actual page number where the content here is supported.    But the book is not a great choice, as it is difficult to verify based on an obscure book.


 * But the bigger issue is the content. First, you put this in a clinical section but the content is all research -- there are no PGX/theranostic tests to guide SSRI prescribing.  The content also mushes together the biology of depression with putative mechanisms of actions for SSRIs and ends up being WP:SYN. If you want to take another shot at this, please post on the article's talk page so that folks who watch the article can review it.  The last sentence is unsourced editorializing and WP:PROMO to boot.  PGX is not used clinically and this imagines that it is.  It isn't used because it hasn't been shown to actually be robust enough to be actually be useful on an individual patient level.


 * Where do you propose this be added in the article? If you still want to add this to the pharmacogenomics section that is not OK, as none of this is in clinical use.  Jytdog (talk) 00:29, 29 November 2016 (UTC)

I can certainly add in specific page numbers for each citation. Would you recommend that I add this piece in an additional section? I am confused by the discussion of a "clinical" section. It appears that research related to SSRI medication is on the page elsewhere, and I included only information relating to patients suffering from depression/mood disorders and its relation to SSRI efficacy. Just trying to understand further where my errors are. Thank you. Mgemmel (talk) 03:18, 29 November 2016 (UTC)
 * As the article stands, every thing in it is clinical - how the drugs are actually used, what their actual side effects are, etc . Everything in your proposed content above is research.  There are no theranostic tests for SSRIs. Jytdog (talk) 03:38, 29 November 2016 (UTC)

"The efficacy of SSRIs in mild or moderate cases of depression has been disputed"
I have actually externally seen, on multiple occasions, people misreading the last sentence of the header to mean that the overall effectiveness of SSRIs is suspect. Now if you actually read citations [4][6] they say something very different, to the tune of the effectiveness of SSRIs scaling with the severity of the depression. So while it's certainly true that they can be ineffective against low-level depression, the ambiguity of that qualifier seems to lead some readers to believe that the page says that SSRIs are ineffective as a whole.

Is anything to be done about this? — Preceding unsigned comment added by 128.151.150.1 (talk) 17:25, 17 January 2017 (UTC)


 * This Systematic Review and metanalysis finds that "SSRIs might have statistically significant effects on depressive symptoms, but all trials were at high risk of bias and the clinical significance seems questionable. SSRIs significantly increase the risk of both serious and non-serious adverse events. The potential small beneficial effects seem to be outweighed by harmful effects."·maunus · snunɐɯ· 11:55, 10 February 2017 (UTC)

Edit War: The persistence of Sexual side effects after SSRI discontinuation
Dear All,

I am currently having a dispute with one of the editors in regards to a contribution I have tried to make under the sexual dysfunction section.

I would like to alter:

Occasionally symptoms of sexual dysfunction may persist after discontinuation of SSRIs.

to:

Occasionally, symptoms of sexual dysfunction may persist months, years or indefinitely after the discontinuation of SSRI treatment.

I understand how WP:Weight is distributed in wikipedia articles but I have only added a few extra words. Also, my edit not only agrees with the current statement but also expands on it and tells you the reported time scale of the persistence of these sexual side effects. The reference I have used is:

Kauffman RP, Murdock A (2007). ″Prolonged Post-Treatment Genital Anesthesia and Sexual Dysfunction Following Discontinuation of Citalopram and the Atypical Antidepressant Nefazodone.″. The Open Women's Health Journal. 1: 1-3.

I would also like to add:

There have also been reports that withdrawal from SSRIs can cause persistent premature ejaculation (in patients with no history of premature ejaculation).

Backed up by the references:

Adson DE, Kotlyar M (2003). ″Premature Ejaculation Associated with Citalopram Withdrawal.″. Annals of Pharmacotherapy. 37: 1804-1806.

Csoka A, Bahrick A, Mehtonen O (2008). ″Persistent Sexual Dysfunction after Discontinuation of Selective Serotonin Reuptake Inhibitors.″. The Journal of Sexual Medicine. 5: 227-233.

To tell you a bit about myself, I have read numerous papers on the persistence of sexual dysfunction post-SSRI treatment and have already written a literature review on the subject. I am currently in the process of writing a research paper on the same topic.

Below are some of the papers I have read on Post-SSRI Sexual Dysfunction:

Csoka, A., Bahrick, A., Mehtonen, O. Persisent Sexual Dysfunction after Discontinuation of Selective Serotonin Reuptake Inhibitors. Psychother. Psychosom., 2006, 75, 187-188

Bolton, J. M., Sareen J., Reiss, J. P. Genital Anaesthesia Persisting Six Years after Sertraline Discontinuation. Journal of Sex & Marital Therapy, 2006, 32, 327-330

Csoka, A., Persisent Sexual Side Effects after SSRI Discontinuation. J. Sex. Med., 2008, 5, 227-233

Hu, X.H., Bull, S.A., Hunkeler, E.M., Ming, E., Lee, J.Y., Fireman, B., Markson, L.E. Incidence and duration of side effects and those rated as bothersome with selective serotonin reuptake inhibitor treatment for depression: patient report versus physician estimate. J. Clin. Psychiatry, 2004, 65(7), 959-965

Ben-Sheetrit, J., Aizenberg, D., Csoka, A. B., Weizman, A., Hermesh, H. Post-SSRI Sexual Dsyfunction: Clinical Characterization and Preliminiary Assessment of Contributory Factors and Dose-Response Relationship. J. Clin. Psychopharmacol., 2015, 35(3), 273-278

Adson, D. E., Kotlyar M. Premature Ejaculation Associated with Citalopram Withdrawal. Ann. Pharmacother., 2003, 37, 1804-1806

Waldinger, M. D. The Neurobiological Approach to Premature Ejaculation. J. Urol., 2002, 168, 2359-2367

Waldinger, M. D., Berendsen, H. H., Blok, B. F., Olivier B., Holstege, G. Premature ejaculation and serotonergic antidepressants-induced delayed ejaculation: the involvement of the serotonergic system, Behav. Brain. Res., 1998, 92(2), 111-118

Deisenhammer, E. E., Trawoger, R. Penile anesthesia associated with sertraline use. J. Clin. Psychiatry, 1999, 60(12), 869-870

Bahrick, A. S. Persistence of Sexual Dysfunction Side Effects after Discontinuation of Antidepressant Medications: Emerging Evidence. The Open Psychology Journal, 2008, 1, 42-50

Bahrick, A. Post SSRI sexual dysfunctions. ASAP Tablet, 2006, 7, 2-3

Maciag, D., Simpson, K. L., Coppinger, D., Lu, Y., Wang, Y., Lin, R.C., Paul, I. A. Neonatal antidepressant exposure has lasting effects on behaviour and serotonin circuitry. Neuropsychopharmacology, 2006, 31, 47-57

De Jong, T. R., Snaphaan, L. J., Pattij, T., Veening, J. G., Waldinger, M. D., Cools, A. R., Olivier, B. Effects of chronic treatment with fluvoxamine and paroxetine during adolescence on serotonin-related behaviour in adult male rats. Eur. Neuripsychopharmacol., 2006, 16(1), 39-48

Keltner, N. L., McAfee, K. M., Taylor, C. L. Mechanisms and treatments of SSRI-induced sexual dysfunction. Perspect Psychiatr. Care, 2002, 38, 111-116

Damsa, C., Bumb, A., Bianchi-Demicheli, F., Vidailhet, P., Sterck, R., Anreoli, A., Beyenburg, S. “Dopamine Dependent” side effects of selective serotonin reuptake inhibitors: A clinical review. J. Clin. Psychiatry, 2004, 65(8), 1064-1068

Frohlich, P. F., Meston, C. M. Evidence that serotonin affects female sexual functioning via peripheral mechanisms. Physiol. Behav. 2000, 71, 383-389

Frohlich, P. F., Meston, C. M. Fluoxetine-induced changes in tactile and sexual functioning among clinically depressed women. J. Sex. Marital. Ther., 2005, 31, 113-28

Stahl, S. M. Eessential Pharmacology. Cambridge University Press, 2000

Clayton, A. H., Montejo, A. L. Major depressive disorder, antidepressants, and sexual dysfunction. J. Clin. Psychiat., 2006, 67, 33-37

Woodrum, S. T., Brown, C. S. Management of SSRI-induced Sexual Dysfunction. Ann. Pharmacother., 1998, 32, 1209-1215 — Preceding unsigned comment added by Tpconroy (talk • contribs) 20:39, 27 March 2017 (UTC)

Tpconroy (talk) 20:41, 27 March 2017 (UTC)TPConroy


 * This

Kauffman RP, Murdock A (2007). ″Prolonged Post-Treatment Genital Anesthesia and Sexual Dysfunction Following Discontinuation of Citalopram and the Atypical Antidepressant Nefazodone.″. The Open Women's Health Journal. 1: 1-3.


 * Does not appear to be pubmed indexed. It is also a case study. So not a suitable source.
 * Please read and follow WP:MEDRS Doc James  (talk · contribs · email) 06:13, 28 March 2017 (UTC)

Okay, but the following two papers do appear on PubMed:

Adson, D. E., Kotlyar M. Premature Ejaculation Associated with Citalopram Withdrawal. ''Ann. Pharmacother''., 2003, 37, 1804-1806

Csoka, A., Persisent Sexual Side Effects after SSRI Discontinuation. ''J. Sex. Med''., 2008, 5, 227-233

so I would still like the following sentence added to the sexual dysfunction section:

There have also been reports that withdrawal from SSRIs can cause persistent premature ejaculation (in patients with no history of premature ejaculation).

Tpconroy (talk) 00:00, 29 March 2017 (UTC)


 * Two things.
 * First, please always cite the pmid. In this case the articles are  and.
 * Second, both of these are case reports, and are much older than 5 years old. They both fail WP:MEDRS.  Please read MEDRS, and if you don't understand it, please ask about it.
 * There are more recent and stronger sources already in the article. Please see your talk page for a note about formatting citations.  Jytdog (talk) 00:44, 29 March 2017 (UTC)

Add "Anti-Inflammatory Effects" to "Mechanisms of Action" Section
I want to add a section on the anti-inflammatory effects of SSRIs that have been shown in various studies, meta analyses and reviews. An outline of points I want to add follows:

Anti-Inflammatory effects of SSRIs
The role of inflammation and the immune system in depression has been extensively studied. The evidence supporting this link has been showed in numerous studies over the past ten years. Nationwide studies and meta-analyses of smaller cohort studies have uncovered a correlation between pre-existing inflammatory conditions such as type 1 diabetes, rheumatoid arthritis (RA), or hepatitis, and an increased risk of depression. Data also shows that using pro-inflammatory agents in the treatment of diseases like melanoma can lead to depression. Several meta-analytical studies have found increased levels of proinflammatory cytokines and chemokines in depressed patients. This link has led scientists to investigate the effects of antidepressants on the immune system.

SSRIs were originally invented with the goal of increasing levels of available serotonin in the extracellular spaces. However, the delayed response between when patients first begin SSRI treatment to when they see effects has led scientists to believe that other molecules are involved in the efficacy of these drugs. To investigate the apparent anti-inflammatory effects of SSRIs, both Kohler et al. and Więdłocha et al. conducted meta-analyses which have shown that after antidepressant treatment the levels of cytokines associated with inflammation are decreased. A large cohort study conducted by researchers in the Netherlands investigated the association between depressive disorders, symptoms, and antidepressants with inflammation. The study showed decreased levels of interleukin (IL)-6, a cytokine that has proinflammatory effects, in patients taking SSRIs compared to non-medicated patients.

Treatment with SSRIs has shown reduced production of inflammatory cytokines such as IL-1β, tumor necrosis factor (TNF)-α, IL-6, and interferon (IFN)-γ, which leads to a decrease in inflammation levels and subsequently a decrease in the activation level of the immune response. These inflammatory cytokines have been shown to activate microglia which are specialized macrophages that reside in the brain. Macrophages are a subset of immune cells responsible for host defense in the innate immune system. Macrophages can release cytokines and other chemicals to cause an inflammatory response. Peripheral inflammation can induce an inflammatory response in microglia and can cause neuroinflammation. SSRIs inhibit proinflammatory cytokine production which leads to less activation of microglia and peripheral macrophages. SSRIs not only inhibit the production of these proinflammatory cytokines, they also have been shown to upregulate anti-inflammatory cytokines such as IL-10. Taken together, this reduces the overall inflammatory immune response.

In addition to affecting cytokine production, there is evidence that treatment with SSRIs has effects on the proliferation and viability of immune system cells involved in both innate and adaptive immunity. Evidence shows that SSRIs can inhibit proliferation in T-cells, which are important cells for adaptive immunity and can induce inflammation. SSRIs can also induce apoptosis, programmed cell death, in T-cells. The full mechanism of action for the anti-inflammatory effects of SSRIs is not fully known. However, there is evidence for various pathways to have a hand in the mechanism. One such possible mechanism is the increased levels of cyclic adenosine monophosphate (cAMP) as a result of interference with activation of protein kinase A (PKA), a cAMP dependent protein. Other possible pathways include interference with calcium ion channels, or inducing cell death pathways like MAPK.

The anti-inflammatory effects of SSRIs have prompted studies of the efficacy of SSRIs in the treatment of autoimmune diseases such as multiple sclerosis, RA, inflammatory bowel diseases, and septic shock. These studies have been performed in animal models but have shown consistent immune regulatory effects. Fluoxetine, an SSRI, has also shown efficacy in animal models of graft vs. host disease. SSRIs have also been used successfully as pain relievers in patients undergoing oncology treatment. The effectiveness of this has been hypothesized to be at least in part due to the anti-inflammatory effects of SSRIs. Alexandracassano (talk) 22:00, 27 July 2017 (UTC)

Blunted emotions
This text was added based on the Guardian

"Many SSRI users report blunted emotions, even long after they have ceased taking pills. "

Removed it as it is unclear whether or not the reported rates differ from baseline or before they took the medications. And we need a better source. Doc James (talk · contribs · email) 14:34, 5 August 2017 (UTC)
 * Based on a primary source. Still not appropriate. Doc James  (talk · contribs · email) 03:28, 6 August 2017 (UTC)

Date of Availability
I do not seem to see any mention in this article when SSRIs were first developed and became available on prescription to the general public. Could somebody with access to this information please add this glaring omission ? Thanks.  अनाम गुमनाम  22:57, 26 July 2017 (UTC)
 * We just need to find a way to incorporate at least a summary of Development and discovery of SSRI drugs into this article, that should cover this issue adequately while solving the broader issue of this article failing to even mention the history. I might try tackling this later but I'm not feeling up to summarizing that article at the moment. Maybe there's something that can be reused in Antidepressant or Management of depression... Garzfoth (talk) 03:51, 6 August 2017 (UTC)

anti-inflammatory effects
User:Alexandracassano - about this edit... i am doing something unusual here, and commenting on it.


 * in general, this is really good. Good sources, well summarized, with decent writing.  Most students cannot do this.  So kudos.
 * Two WP:MEDHOW issues
 * none of the refs cite the pmid. please add that
 * we do not use the word "patients". We say "people" or "people with X" or the like.  This is described in WP:MEDMOS.  Please fix this.


 * issues of WP:WEIGHT and placing content in appropriate places
 * Please look at the article overall. Now look at the content you added - how big it is relative to the rest of the article.  Is this reasonable WEIGHT (space) for this MoA compared to everything else in the article?
 * content sorting - like many students, you created a block of content and plunked into the article in one piece. Students generally think in a "here is my homework" framework of doing schoolwork, and tend to do this.  But there is content in that has nothing to do with mechanism of action but rather should be in the Research section, right?

Otherwise -- again, really great work, in my view. I hope you stick around and do more! Jytdog (talk) 07:06, 10 August 2017 (UTC)

Irrelevant
What is "A number of (non-SSRI) drugs are not associated with sexual side effects (such as bupropion, mirtazapine, tianeptine, agomelatine and moclobemide.[45][46])" doing in the section on sexual side effects of SSRI's? 81.155.219.212 (talk) 06:03, 24 August 2017 (UTC)

Comment ref
User:82.196.109.14/User:130.241.202.29 -- about:


 * diff at 16:49, 24 January 2018
 * diff at 18:42, 25 January 2018
 * diff at 00:26, 15 February 2018
 * diff at 20:31, 15 February 2018

As we have mentioned, we don't use primary sources to "over-rule" secondary ones. Please see WP:MEDRS which explicitly discusses this. Jytdog (talk) 20:58, 15 February 2018 (UTC)

Selective serotonin reuptake inhibitor Re: questioning
Jytdog and Doc James, I would like a clarification why I am not allowed to post peer-reviewed commentary for the 2017 systematic review regarding efficacy and side effects of SSRIs. The conclusions that appear on the page are merely a result of methodological inaccuracies and blatant errors, as pointed out by the commentary. The reasons I have heard from you and other editors so far are i) The criticism wasn't heavy enough and/or this is not notable. I could not agree less - such lengthy commentary is exceptional and the result is that none of the main conclusions of the original paper are supported ii) Single comments shouldn't be used to refute reviews. Other authors have also criticised the paper, see for example here or discussion here (in Danish). If one source of criticism isn't enough, I'm happy to post both letters and/or the news article. The debate about SSRI efficacy and side effects is a complex one and both critics and their critics should be allowed. Thank you.

-- — Preceding unsigned comment added by 82.196.109.14 (talk) 23:39, 19 February 2018 (UTC)
 * We have pointed you to WP:MEDREV several times and you have given no indication - none - that you have read it. Jytdog (talk) 23:53, 19 February 2018 (UTC)

What? Was that what you were waiting for? There are several points in the article that support including the commentary, or excluding the review: i) The impact factor of BMC Psych is merely 2.6. The guidelines state that "Even when an article is one of the most useful types and recently published, it can be helpful to check the journal's impact factor if it makes extraordinary claims." Yes, it is an extraordinary claim that SSRIs are toxic and do not work. ii) "An integral part of finding high quality sources is avoiding articles from journals without a reputation for fact-checking and accuracy." The publisher has retracted 43 articles because of fake peer review. iii) A big part of the quote from the article consists merely of opinions, and the guidelines do not favour such. "The clinical significance of these effects seems questionable" is based on old NICE criteria that have since been abandoned, and "the harmful effects of SSRIs versus placebo for major depressive disorder seem to outweigh any potentially small beneficial effects" is not the conclusion psychiatrists make from looking at the same data, as you see for example in the Danish article.

-- — Preceding unsigned comment added by 82.196.109.14 (talk) 00:41, 20 February 2018 (UTC)
 * You have entirely missed the point of MEDRS. Jytdog (talk) 01:50, 20 February 2018 (UTC)

Again, what? Please explain instead of being arrogant. — Preceding unsigned comment added by 82.196.109.14 (talk) 02:43, 20 February 2018 (UTC)

To add to my comments, please explain why you consider the commentary a primary source. It fulfils none of the criteria in WP:MEDREV. It is also a summary of primary sources, in fact the same primary sources as the review, see the supplementary file. — Preceding unsigned comment added by 82.196.109.14 (talk) 18:23, 20 February 2018 (UTC)
 * If you are talking about this; it is called by the journal a "letter to the editor". a letter to the editor is not a full blown literature review that is classified as such and reviewed as such during the pre-publication peer review, nor do we treat it as such, per MEDRS. Jytdog (talk) 19:16, 20 February 2018 (UTC)

No, I'm talking about this. It contains the same synthesis of previous studies as the original meta-analysis. Also, see here "All articles published in Acta Neuropsychiatrica undergo peer review". — Preceding unsigned comment added by 82.196.109.14 (talk) 21:54, 20 February 2018 (UTC)
 * You are still not understanding the issue. Peer review is not the point. I have brought this to WT:MED for wider discussion. See Wikipedia_talk:WikiProject_Medicine. Please don't batter the discussion there - I have tried to ask the question in a neutral manner. Let's see what folks say. Perhaps they will agree that this can be used as you are suggesting. The question is more interesting than i originally thought now that i see what a "commentary" is at that journal. Jytdog (talk) 22:14, 20 February 2018 (UTC)

Good, thank you. If you would like to, you can clarify about the peer review, and that this commentary contains an actual re-analysis of the same studies as the original meta-analysis.

I also feel the need to bring up another study that could be considered for this section. Cipriani et al. published yesterday in The Lancet a meta-analysis of all currently available antidepressants, in total 522 trials or 116 000 patients. I think this is the biggest meta-analysis in this field so far, even though I'm not entirely sure. Their conclusion is that "All antidepressants were more efficacious than placebo in adults with major depressive disorder".82.196.109.14 (talk) 14:36, 22 February 2018 (UTC)

Inaccuracy in "Interactions" subsection?
In the last paragraph of the "Interactions" subsection is the text: "The CYP2D6 enzyme is entirely responsible for the metabolism of hydrocodone, codeine[125] and dihydrocodeine to their active metabolites..."

However, looking at the respective Wiki pages for "hydrocodone" and "codeine", one can see in the infobox at the top right of the hydrocodone article that CYP3A4 is listed as the enzyme most involved with its metabolism (with CYP2D6 listed as playing a lesser role), and CYP3A4 is listed in the codeine article as playing a minor role in its metabolism as well.

As such, either the word "entirely" in the text in question or the information listed in the other two articles is inaccurate. — Preceding unsigned comment added by KajHansen (talk • contribs) 05:30, 11 January 2019 (UTC)

Unsupported/unclear statement in "Side effects" section?
The second paragraph of the "Sexual dysfunction" subsection, under "Side effects", states that "In some cases, symptoms of sexual dysfunction may persist after discontinuation of SSRIs", followed by several (generally problematic) citations. This statement could be construed to mean either some as in 'a small number' or some as in 'an unknown number'. If the intended meaning is the first, than the statement is unsupported, if the later is meant, it is unclear and should be changed.

The first citation (in the order cited), Bahrick AS (2008), states "Most individuals probably do return to their previous level of sexual functioning", which is clearly an unsupported assumption, and goes on to say in the full text that "The present article presents available evidence indicating that SSRI and SNRI-emergent sexual dysfunctions, for an unknown number of patients, may not resolve upon cessation of medication.".

The second citation, Waldinger MD (2015), states "Very rarely, their sexual side-effects persist after SSRI discontinuation" but is problematic for several reasons: It is comparatively out of date, as there has been a lot of activity in this particular area since 2017; it does not seem to support this claim anywhere in the text; and neither the full text nor references are freely available to be checked. (Further, though not an expert, even the provided page seems to, in numerous instances, clash with recent papers I've been reading on this subject.)

The third citation, "Prozac Highlights of Prescribing Information", does not discuss persistant effects at all, and is also a terrible source as it is produced by the drug manufacturer. For instance the stated incidence of sexual dysfunction is 2% where it has recently been measured to likely be greater than 54% (even the DSM puts the lower bound at 25%).

The fourth citation, Reisman Y (October 2017), makes no claim regarding the rate of incidence and thus is not a source.

The fifth citation, the DSM 5th edition, states "In some cases, serotonin reuptake inhibitor-induced sexual dysfunction may persist after the agent is discontinued" but as above, this is very out of date, unsupported and given the context, likely means "in an unknown number of cases".

There may also have been an intended citation of Gibbons RD, Hur K, Brown CH, Davis JM, Mann JJ (June 2012), however this also does not discuss incidence.

Compare the above to a more current and relevant source such as Areeg, Bala MD et al (2018) (https://doi.org/10.1016/j.sxmr.2017.07.002) which states "The prevalence of persistent sexual side effects after discontinuing SSRIs is not well known" (which is actually supported by the first citation mentioned above.) It is thus clear that the current state of research and only supportable statement is that an unknown number of individuals will experience this side effect. — Preceding unsigned comment added by Naturalnumber (talk • contribs) 03:12, 31 August 2019 (UTC)

Comment: "The prevalence of persistent sexual side effects after discontinuing SSRIs is not well known" means in laymans terms: "There are spurious reports and we are not sure whether the effect exists at all." - It certainly does NOT mean "It's a major effect and we just don't know if its 10% or 50%." I'm pointing this out as a patient who took Serotin blockers for a while, experienced the temporary side effect and found them to go away quickly. Many people are worried about those side effects. It is important to point out that the improvement gained from Serotine blockers outweigh the temporary loss of sexual activity and should not dissuade anybody from starting to take this medication. — Preceding unsigned comment added by 93.218.97.242 (talk) 10:31, 2 December 2019 (UTC)

I know several people who have experienced permanent impairment in sexual function from taking SSRIs, and you're going to find them in any community with high rates of antidepressant use. It doesn't matter if the risk is 1% or 5% or 10%, people deserve to know about it. And the fact that a review article says the equivalent of "there isn't enough data to know the actual prevalence" doesn't simply invalidate the fact that the actual studies report relatively high numbers. There's pages about vaccine hesitancy in spite of the movement's lack of credibility of, but mentions of an extremely serious side effects of a medication that alternatives to exist, gets nuked just because the exact incidence rate is uncertain? Not changed to say "but the actual incidence rate is uncertain", but outright removed? The actual paper you bring up to justify the removal states "All patients need to be educated about the possibility of persistent impairment of sexual dysfunction with SSRI usage" 178.235.185.238 (talk) 11:37, 20 April 2020 (UTC)

Risk of death increased by 33% ??
Side effects/Risk of death That sound like a very strong statement.. maybe some more evidence/citations/sources needed? 2A01:CB1D:655:AA00:1031:1107:1AE7:C183 (talk) 05:59, 13 June 2022 (UTC)