Talk:Venlafaxine/Archive 2

Potential errors
First paragraph of the article In children and adolescents, venlafaxine (like other anti-depressants) has a potential to increase suicidal thoughts, attempts and events of self-harm.

Im sure this is meant to read decrease suicidal thoughts? —Preceding unsigned comment added by Fmountford (talk • contribs) 10:45, 30 March 2010 (UTC)


 * No, actually, there is a small risk of increased suicidal thoughts in some patients, but it is more likely more patients will have fewer suicidal thoughts. I don't have the citation, but one study showed that after the FDA forced most antidepressants to have the "black box warning", the overall number of prescriptions written decreased, and overall suicide rates increased, showing that overall, antidepressants reduce suicide risk.  MeekMark (talk) 16:46, 6 May 2010 (UTC)


 * Should that be moved to a different section of the page? Granted, it does have a grain of truth, but the way it comes off, it sounds like anti-medication propaganda. --174.30.2.239 (talk) 00:28, 11 February 2011 (UTC)


 * I have removed this sentence because anyone looking at the TOC will immediately notice Suicide as the first thing under Side Effects. Besides, this problem is not nearly as common as the media presents it: the difference didn't even reach statistical significance for any single drug, so they had to do a meta-analysis of many antidepressants to be able to report an increase. If you have a good reason to revert, please notify me and post here. Atxd00d (talk) 03:51, 16 February 2011 (UTC)

Side effects
If the source for the rare side effects is the same as for the side effects in the section above, I've checked it out and these were not all controlled studies. Several studies are lumped together in the pre-assessment phase. It's possible these side effects may not have all been due to Effexor. —Preceding unsigned comment added by 205.250.242.207 (talk) 04:15, 8 April 2011 (UTC)

I have now corrected this problem. 205.250.242.207 (talk) 19:11, 9 April 2011 (UTC)

Please explain the sentence: "the remission rate was significantly lower for venlafaxine"
What you wrote re: "the remission rate was significantly lower for venlafaxine" under the subject of "Depression" makes no sense, in comparing it to Wellbutrin. Everything in the surrounding sentences is implying that Effexor is more effective than Wellbutrin, but "remission rate" means the patient is relieved of all symptoms of depression. Please explain.

--Pookerella (talk) 19:01, 10 April 2011 (UTC)

These are two absolutely different facts about the pharmacokinetics (What is right?):
"In vitro studies revealed venlafaxine has virtually no affinity for opiate, ... receptors. ...[14]"

and

"Venlafaxine interacts with opioid receptors (mu-, kappa1- kappa3- and delta-opioid receptor subtypes) as well as alpha2-adrenergic receptor, and was shown to increase pain threshold in mice. When mice were tested with a hotplate analgesia meter, both venlafaxine and mirtazapine induced a dose-dependent, naloxone-reversible antinociceptive effect following ip administration. These findings suggest venlafaxine's seemingly superior efficacy in severe depression.[61]"

Has it interaction with opioid receptors like I think or hasn't it? That`s the question here. —Preceding unsigned comment added by 93.181.30.189 (talk) 19:05, 22 May 2011 (UTC)

Venlafaxine - Is it a Opioid or not?
You can find in the article first it isn't and later it is one.

"Venlafaxine interacts with opioid receptors (mu-, kappa1- kappa3- and delta-opioid receptor subtypes) as well as alpha2-adrenergic receptor, and was shown to increase pain threshold in mice. When mice were tested with a hotplate analgesia meter, both venlafaxine and mirtazapine induced a dose-dependent, naloxone-reversible antinociceptive effect following ip administration. These findings suggest venlafaxine's seemingly superior efficacy in severe depression.[61]"

61 - http://www.opioids.com/depression/antidepressants.html

What is right? —Preceding unsigned comment added by 93.181.30.189 (talk) 08:08, 23 May 2011 (UTC)

Serious problem with the side effect information
I have a problem with this article. The information about Common side effects and frequency of those side effects occurring isn't for standard dosages, it's for dosages equal to or greater than the highest recommended dose of the product. ( http://en.wikipedia.org/wiki/Venlafaxine#cite_note-pmid15260908-31 ) This information is therefore grossly misleading.Webgrunt (talk) 14:12, 9 February 2012 (UTC)

Added discussion of the role of noradrenaline and of discontinuation syndrome resulting from deprivation of neurotransmitters
Very tentative cf my reading of the literature, it would appear to be a usefully up-to-date addition, but comments and discussion invited Michael.j.lacey (talk) 10:24, 26 March 2013 (UTC)

error regarding pulmonary hypertension
In the section entitled "Heart Disease and Hypertension", a risk for "persistent pulmonary hypertension (PPHN)" is listed as a potential side-effect of this med. PPHN actually stands for "persistent pulmonary hypertension of the newborn". I believe the potential side-effect intended here is for "primary pulmonary hypertension" (PPH), as newborns are unlikely to be exposed to this drug. Also, 4 bpm increase in heart rate is listed as a side-effect under this heading, and is the only cardiac symptom listed under that heading, so I believe "heart disease" is not an appropriate heading here unless additional cardiac risk factors are added to the section. A more appropriate title heading would be for example, "Cardiopulmonary Effects and Hypertension." The section also lacks sources.

If no one objects to these changes in the next few days, I'll make these edits. O&#39;Hush (talk) 02:30, 7 July 2010 (UTC)

Suggested edits applied. Michael.j.lacey (talk) 10:33, 26 March 2013 (UTC)

Error in the "depression" section
"In a double-blind study, patients who did not respond to an SSRI were switched to venlafaxine or citalopram. Similar improvement was observed in both groups" this sentence is misleading as citalopram is an SSRI.

The article it is sourced from states "This study was designed to test the hypothesis that, after treatment failure with an SSRI, switching to venlafaxine extended release (ER) would offer advantages over switching to another SSRI, citalopram" and is therefore being misquoted. — Preceding unsigned comment added by Workforidlehands (talk • contribs) 16:00, 28 April 2013 (UTC)

Discontinuation syndrome - first sentence
"In vitro studies revealed venlafaxine has virtually no affinity for opiate, benzodiazepine, or N-methyl-D-aspartic acid (NMDA) receptors. It has no significant CNS stimulant activity in rodents. In primate drug discrimination studies, venlafaxine showed no significant stimulant or depressant abuse liability." - while interesting, these three sentences don't seem to connect in any way with the rest of the section. They just seem odd. Why are they there? Litawor (talk) 18:31, 10 July 2013 (UTC)

Weight Loss or Weight Gain?
This site (http://www.rxlist.com/effexor-side-effects-drug-center.htm) and many others list weight gain as a side effect (on this one, a common side effect), but don't mention weight loss. However, the article mentions weight loss, but not weight gain. Perhaps both could be mentioned?

199.223.21.100 (talk) 17:03, 7 March 2014 (UTC) 199.223.21.100 (talk) 17:00, 7 March 2014 (UTC)

Specific negative results interpreted as general positive results, a dubius conjecture, false assumptions.
"Some open-label and three double-blind studies have suggested the efficacy of venlafaxine in the treatment of attention deficit-hyperactivity disorder (ADHD).    ."

I think the cited studies find that venlafaxine is no more effective than placebo in the treatment of adults with ADHD. Moreover, the abstract of the first article is very vague and basically incoherent, and discloses a bias toward patients belonging to a "substance misuse population". The studies comparing venlafaxine to stimulant medications focus exclusively on children, and measure a positive response to treatment based on evaluation by parents and teachers, not scientists.

There is one (radical?) reference conjecturing that high doses of venlafaxine act as a narcotic. The claims that venlafaxine acts as a sedative or a stimulant are similarly dubious. This article's (assumptions?) that these are common experiences of people who take the drug are quite contrary to reality.

Nafindix (talk) 14:24, 16 May 2014 (UTC)

SNRI/SSNRI?
SNRI - selective norepinephrine reuptake inhibitor SSNRI - selective serotonine-norepinephrine reuptake inhibitor — Preceding unsigned comment added by Gladissk (talk • contribs) 14:06, 7 November 2015 (UTC)

Memory Loss
In previous versions of this page, there was mention (sourced) about side effects such as memory loss. The numbers found in the study seem quite profound in regards to memory loss. Why does no such information exist anywhere on the page anymore?

See this diff where it was removed: https://en.wikipedia.org/w/index.php?title=Venlafaxine&diff=next&oldid=580354405

Originally sourced: Tolerability of High-Dose Venlafaxine in Depressed Patients http://jop.sagepub.com/content/18/2/200 — Preceding unsigned comment added by 207.195.114.48 (talk) 14:07, 10 February 2016 (UTC)

Discontinuation
User:128.231.234.33 you have made the following edits:
 * diff at 06:11, 6 March 2017 via IP 2601:14a:4500:530:60fd:ea72:19e1:6ccd
 * diff at 13:18, 6 March 2017 via IP 2601:14a:4500:530:60fd:ea72:19e1:6ccd
 * diff at 18:21, 6 March 2017 via IP 2607:f220:415:611::ab
 * diff at 16:19, 14 March 2017 via IP 2601:14a:4500:530:3d89:c6a4:6554:4181
 * diff at 13:41, 16 March 2017 via IP 128.231.234.33
 * here, diff at 13:51, 16 March 2017 via IP 128.231.234.33 you finally provided 2 refs; both misformatted. The two refs are (a primary source from 1997 -- twenty years old -- and, a review that is from 2007, ten years old, but is probably OK
 * diff at 14:09, 16 March 2017 via IP 128.231.234.33 you restored that last one, fixing the formatting of the two refs and adding a third,  which is a literature review from 1997 and too old.
 * diff at 14:50, 16 March 2017 via IP 128.231.234.33 you restored it again.

The first five times you added this, it was reverted for being unsourced alone. The sixth time, it was reverted because you made a mess. The last two times, because the sources are bad and you have not come to Talk page even once to say why you think the symptoms should be listed in this article. Any number of people may have been happy to help with that. The symptoms are listed (and sourced) in the "main" article SSRI discontinuation syndrome which is linked prominently in that section. Jytdog (talk) 19:46, 16 March 2017 (UTC)

Discontinuation syndrome/Withdrawal symptoms
Dear all, I would like to propose several edits to the "discontinuation syndrome" section. For one, the term "discontinuation syndrome" term is a Wyeth/Pfizer-created term. The widely accepted term for symptoms after discontinuation of a drug is "withdrawal symptoms", so this is the title this section should have, to avoid confusion and misinterpretation by a potential patient reading the article.

Regarding the listing of symptoms in the section: While the section links to the "SSRI discontinuation syndrome", where the symptoms are stated, this is misleading, given that the prevalence and degree of symptoms is higher for venlafaxine than other SSRIs, such as e.g. fluoxetine or sertraline. (see these references: J Clin Psychiatry. 2005 Oct;66(10):1312-20. Randomized trial of sertraline versus venlafaxine XR in major depression: efficacy and discontinuation symptoms. Sir A, D'Souza RF, Uguz S, George T, Vahip S, Hopwood M, Martin AJ, Lam W, Burt T. Aust N Z J Psychiatry. 1998 Apr;32(2):291-4. Withdrawal reactions associated with venlafaxine. Parker G, Blennerhassett J. J Psychopharmacol. 2008 May;22(3):330-2. The effect of rate of antidepressant tapering on the incidence of discontinuation symptoms: a randomised study. Tint A, Haddad PM, Anderson IM.)

Therefore, linking to the general "SSRI discontinuation syndrome" is not sufficient in this case, especially since the "SSRI discontinuation syndrome" page does not list the documented rate of venlafaxine withdrawal symptoms and how it differs from other SSRIs. I would therefore like to not only add the symptoms, but also highlight that the withdrawal symptoms experienced after discontinuation of venlafaxine are of a different nature than e.g. withdrawal from fluoxetine.

Furthermore, I would like to point out that even the Wikipedia article for fluoxetine (Prozac), lists the symptoms of withdrawal, despite linking to "withdrawal syndrome" in the same paragraph: "If stopped suddenly a withdrawal syndrome may occur with anxiety, dizziness, and changes in sensation.[1]"

Additionally, I would like to add a paragraph stating that there need for a study investigating prevalence of venlafaxine withdrawal effects, as noted in the 2006 consensus ("Antidepressant Discontinuation Syndrome: Current Perspectives and Consensus Recommendations for Management," Journal of Clinical Psychiatry, 2006).

In response to some of the edits removing the references I had included: > here, diff at 13:51, 16 March 2017 via IP 128.231.234.33 you finally provided 2 refs; both misformatted. The two refs are (a primary source from 1997 -- twenty years old -- and >, a review that is from 2007, ten years old, but is probably OK > diff at 14:09, 16 March 2017 via IP 128.231.234.33 you restored that last one, fixing the formatting of the two refs and adding a third,  which is a literature review from 1997 and too > old.

Deleting a reference because it is "too old" is highly questionable. Research done in 1997 can be cited. If there is a newer study demonstrating that the 1997 study was false that reference may be included.

> The first five times you added this, it was reverted for being unsourced alone. The sixth time, it was reverted because you made a mess. The last two times, because the sources are bad and you > have not come to Talk page even once to say why you think the symptoms should be listed in this article. Any number of people may have been happy to help with that. The symptoms are listed > (and sourced) in the "main" article SSRI discontinuation syndrome which is linked prominently in that section. Jytdog (talk) 19:46, 16 March 2017 (UTC)

Again, deleting a reference because "it is bad" is questionable. If there are scientifically founded concerns with the references, I'm happy to discuss those.

Looking forward to hearing from you. — Preceding unsigned comment added by Noaanon (talk • contribs) 12:36, 20 March 2017 (UTC)
 * Thanks for talking. WP:MEDRS is a guideline that is widely accepted in the community, for very many reasons. The sources you are bringing are not OK here in WP for this kind of content.  The kind of content being proposed would be good.  The sourcing matters, as does the process.   Jytdog (talk) 23:19, 20 March 2017 (UTC)

Pharmacokinetics
The Pharmacokinetics part of this page says: "It is extensively metabolized in the liver via the CYP2D6 isoenzyme to desvenlafaxine (O-desmethylvenlafaxine), which is just as potent a SNRI as the parent compound, meaning that the differences in metabolism between extensive and poor metabolisers are not clinically important in terms of efficacy. Side effects, however, are reported to be more severe in CYP2D6 poor metabolisers."

This statement is not true.

My suggestion for this part is: "It is extensively metabolized in the liver via the CYP2D6 isoenzyme to desvenlafaxine (O-desmethylvenlafaxine),therefore, the CYP2D6 enzyme activity determines the systemic exposure (AUC and Cmax) of venlafaxine and the active moieties (venlafaxine+O-desmethylvenlafaxine), which are significantly higher in CYP2D6 poor metabolizers than in CYP2D6 extensive metabolizers . Although O-desmethylvenlafaxine is just as potent a SNRI as the parent compound, and the exposure of active moieties (venlafaxine+O-desmethylvenlafaxine)is much higher in CYP2D6 poor metabolizers, they show much lower venlafaxine efficacy and more side effects ,compared to CYP2D6 extensive metabolizers.


 * Sounds interesting. I don't suppose there is a metaanalysis on this topic? If not, per WP:MEDREV, you should include the information that these data are from just 100 / 33 / 24 patients. --ἀνυπόδητος (talk) 13:49, 22 March 2017 (UTC)

Semi-protected edit request on 18 January 2019
Venlafaxine has an opioid method of action in addition to being an SNRI. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171132/ https://www.ncbi.nlm.nih.gov/pubmed/11931344 https://www.ncbi.nlm.nih.gov/pubmed/15157989 https://www.ncbi.nlm.nih.gov/pubmed/10505622

Mwiner (talk) 03:13, 18 January 2019 (UTC)
 * The article already says that here:Venlafaxine -- Literaturegeek |  T@1k?  03:26, 18 January 2019 (UTC)
 * Very much undue weight to try to add that to the lead. Even in the body we need better references. Doc James  (talk · contribs · email) 16:18, 18 January 2019 (UTC)
 * Okay found some better refs. Doc James  (talk · contribs · email) 16:29, 18 January 2019 (UTC)

Mechanism
Ref says "Mechanisms of antidepressant and anxiolytic actions are uncertain"

Which can be summarized as "How it works is not entirely clear" Doc James  (talk · contribs · email) 04:30, 20 January 2019 (UTC)

Full quote on mechanism
Ref says "Mechanisms of antidepressant and anxiolytic actions are uncertain but appear to be associated with the potentiation of neurotransmitter activity in the CNS. Venlafaxine and ODV are potent inhibitors of neuronal serotonin and norepinephrine reuptake and weak inhibitors of dopamine reuptake"

The summary leaves out most of the statement, and oversimplifies what's left.--ScottS (talk) 17:59, 20 January 2019 (UTC)

If we compare this to the information that the same reference website provides on the mechanism of another anti-depressant, Escitalopram, a similar statement is made--that the mechanism is not fully understood. Yet the Wikipedia page for Escitalopram doesn't mention that piece of information.

As I've stated in other correspondence about inconsistent coverage on the subject of prescription medication by Wikipedia; my concern is that laymen like myself who want to compare two anti-depressants using Wikipedia might be steered in one direction or another simply because of the inconsistency of how they're summarized in Wikipedia. --ScottS (talk) 18:42, 20 January 2019 (UTC)


 * User:ScottSloe I have added "... but it is believed to involve alterations in neurotransmitters in the brain" Doc James  (talk · contribs · email) 19:54, 21 January 2019 (UTC)

Toxic levels found in deceased tramper
A coroner's report into the death of a Czech tramper in New Zealand found "toxic" (13 mg/L blood) levels of Velafaxine. The report found the death was due to hypothermia, relating to poor decisions to attempt the route while under-prepared, but I think this snippet is relevant and should be included, as depression and anti-depressants can affect decision making processes. The coroner's report includes other findings from a forensic toxicologist, and also says that such high concentrations can cause cardiac arrhythmias, which "may" have contributed to the death from hypothermia.
 * https://www.scribd.com/document/424184919/Coronial-finding-for-Ondrej-Petr
 * https://www.stuff.co.nz/national/115457620/czech-couples-decisionmaking-on-deadly-great-walk-tramp-criticised — Preceding unsigned comment added by Foobar2k20 (talk • contribs) 08:19, 3 September 2019 (UTC)

Chart showing IC50 values should also show Desvenlafaxine
The activate metabolite Desvenlafaxine contributes significantly to the activity of Venlafaxine. I think the table showing the Ki and IC50 values should show it for both Venlafaxine and Desvenlafaxine. Links to those values here and here, but I can not figure out how to correctly reformat the table. — Preceding unsigned comment added by SSyntaxin (talk • contribs) 20:20, 19 October 2019 (UTC)
 * I've added the data to Desvenlafaxine. Thanks for bringing this up! --ἀνυπόδητος (talk) 09:07, 20 October 2019 (UTC)

New Terms and Data that should be added to the article about Venlafaxine
Regarding the page for venlafaxine. I think that some terms should be added in the page.


 * Phenethylamines should be added in the category section in the bottom of the document, as well as in the body of the document (possibly in the lead) to indicate that venlafaxine is a substituted phenethylamine. In the same way that Phenethylamines appears in the page for ODV (desvenlafaxine) in the category section in the bottom of the article.


 * affinity for the dopamine transporter DAT should be added in the section pharmacology ("in numbers" as Ki and IC50) in the same way that it appears in the page for duloxetine.


 * dopamine reuptake inhibitors should be added in the category section in the same way that it appears in the page for amantadine. venlafaxine is classified as a DAT inhibitor in all chemical databases. — Preceding unsigned comment added by 79.106.215.124 (talk) 03:53, 25 January 2020 (UTC)

Proposal: Affinity for the DAT should be added in the section pharmacology ("in numbers" as Ki and/or IC50)
--79.106.215.113 (talk) 01:27, 8 February 2020 (UTC)Regarding Venlafaxine:

Affinity for the DAT should be added in the section pharmacology ("in numbers" as Ki and/or IC50) in the same way that it appears in the page for duloxetine [].

It appears that binding profiles have been added in this page [] Therefore there is no reason not to add it in the separate page for venlafaxine (as IC50)

79.106.215.113 (talk) 01:27, 8 February 2020 (UTC)

Proposal: New information about cardiovascular toxicity of Venlafaxine should be added in a new section
Proposal: New information about cardiovascular toxicity of Venlafaxine should be added in a new section because there appears to be many case reports of venlafaxine abuse in very high doses. In these very high doses venlafaxine prolongs the QT interval potentially causing fatal cardiac arrhythmia. There should be more transparence so that patients become more aware of the dangers of abusing this drug.
 * https://www.psychiatrictimes.com/article/qt-prolongation-and-antidepressants
 * https://www.uspharmacist.com/article/qtc-prolongation-with-antidepressants-and-antipsychotics
 * https://www.sciencedirect.com/science/article/abs/pii/S1876201815001409
 * https://crediblemeds.org/healthcare-providers/


 * https://www.empr.com/home/news/drug-news/qt-prolongation-risk-assessed-for-non-ssri-antidepressants/
 * https://www.ncbi.nlm.nih.gov/pubmed/16574528
 * https://www.practicalpainmanagement.com/treatments/pharmacological/non-opioids/qt-intervals-antidepressants


 * https://www.medsafe.govt.nz/profs/PUArticles/Dec2012AntidepressantsQTProlongation.htm
 * https://www.medsafe.govt.nz/profs/adverse/Minutes151.htm#3.2.1
 * https://www.bmj.com/content/361/bmj.k1415/rr-4
 * https://www.pfizermedicalinformation.ca/en-ca/effexor-xr/warnings-and-precautions#

— Preceding unsigned comment added by 79.106.215.52 (talk) 03:57, 26 January 2020 (UTC) 79.106.215.113 (talk) 02:04, 8 February 2020 (UTC)

Possibility of venlafaxine being a TAAR1 agonist?
I stumbled across this article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733524/ which suggests that venlafaxine may reverse monoamine transporters. Since venlafaxine is a PEA derivative this is very plausible because many PEA derivatives are TAAR1 agonists and cause reversal of transporters leading to monoamine release.

... ''Venlafaxine’s affinity for norepinephrine transporter (K[i] = 2,984 nM) is 10^3-fold lower than that of atomoxetine (K[i] = 5 nM), yet venlafaxine causes an increase (242%) in synaptic norepinephrine levels comparable to that by atomoxetine (290% ± 33%) Curiously, chronic treatment with venlafaxine does not reduce norepinephrine transporter binding sites. These facts point to the possibility that increases in synaptic norepinephrine are due to norepinephrine transporter reversal, akin to dopamine transporter reversal associated with amphetamine''

Please somebody check for further verification.

79.106.215.52 (talk) 09:46, 18 June 2020 (UTC)

"Complete ineffectiveness"
This has now been added and removed four times. Why is it needed here? Thanks. Martinevans123 (talk) 15:55, 5 March 2021 (UTC)


 * Well, it's research about antidepressants, and venlafaxine is commonly classified as an antidepressant, so why shouldn't it be here? 93.71.254.113 (talk) 13:08, 6 March 2021 (UTC).


 * Because it's not specifically about venlafaxine. We have dedicated articles for Antidepressant and for Serotonin–norepinephrine reuptake inhibitor, so that's where it should be, if anywhere. Martinevans123 (talk) 13:30, 6 March 2021 (UTC)
 * To go further, Serotonin–norepinephrine reuptake inhibitor is still not the right place for the "complete ineffectiveness" claim since the claim is about antidepressants in general. Antidepressant article is probably the best place to discuss it. But please be sure to post in Talk first, as the claim of "complete ineffectiveness" flies in the face of the existing consensus and, arguably, does not need to be reflected in Wikipedia as a WP:FRINGE view. The Sceptical Chymist (talk) 14:58, 6 March 2021 (UTC)


 * But the page WP:FRINGE doesn't say, of course, that minority views shouldn't be in Wikipedia. That would be totally unscientific, because scientific consensus doesn't build by majority vote, but by quality of research; and it happened many times in the history of science that a minority view was later accepted as the correct one and became consensus. WP:FRINGE just says that "a Wikipedia article should not make a fringe theory appear more notable or more widely accepted than it is". So, even if that line of research was "fringe", and it's not because many different researchers support it, that would definitely not justify censoring it. Why are you so afraid of a small paragraph? 93.71.254.113 (talk) 10:38, 7 March 2021 (UTC).
 * We can discuss it at Talk:Antidepressant The Sceptical Chymist (talk) 13:53, 7 March 2021 (UTC)

Dosage
Hello! I have edited the Dosage section as it contained incorrect information about the efficacy of Venlafaxine, according to the source, which states (relevant text bolded):

The efficacy of venlafaxine increased fairly steeply up to around 75–150 mg and more modestly with higher doses (ie, 151–375 mg), whereas the efficacy of mirtazapine increased up to a dose of 30 mg and then decreased. Dropouts due to adverse effects increased steeply with increasing doses for both drugs, resulting in a dose-acceptability curve that was convex at the lower licensed range, which approximately corresponded with 20–40 mg of fluoxetine equivalents in both cases. However, studies for each individual drug were few, and the 95% CIs of the spline curves remained wide.

Bennycat (talk) 06:05, 6 January 2023 (UTC)

Recreational abuse section
Are there better sources for the phenomenon of venlafaxine being abused recreationally? I've never ever heard of this happening, and the reference looks like it's a single case study. Given the class of the drug, it seems like you'd need a larger burden of proof than one or even a handful of cases to show it's a phenomenon warranting its own section on the page. If it's just something a very small number have attempted I would think it's more misleading than not to include it as a section. 66.235.168.196 (talk) 06:05, 23 February 2023 (UTC)
 * This drug actually addicted me, I need a new dose of quick release venlafaxine every three times a day. It also appears to be contraindicated for people with pulmonary hypertension. I could never have imagined any SSRI or SNRI to be addictive. --0dorkmann (talk) 07:44, 1 April 2023 (UTC)

TAAR-activity missing
Can you check it out --0dorkmann (talk) 07:45, 1 April 2023 (UTC)

Brain Zaps
In the past I had been prescribes Effexor XR for about 10 years for Bipolar Depression. I frequenly got what I can only call, "Brain Zaps". And I wasn't the only one. A few years after I had started Effexor XR my Mother was presiced the same. About a week afer my Mother started taking her prescribed Effexor XR she said to me, 'Oh wow! Now I know what you mean by brain zaps.' BrainZap (talk) 00:51, 24 May 2023 (UTC)