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Archive 1Archive 2

Exercise

Just dropping these refs here for now since I don't have time to add them here for another article for which I was doing this lit. search.

Refs+reflist

Not really surprising to me since it's also markedly anti-addictive too. Seppi333 (Insert 2¢ | Maintained) 06:40, 3 February 2015 (UTC)

References

  1. ^ Cooney GM, Dwan K, Greig CA, Lawlor DA, Rimer J, Waugh FR, McMurdo M, Mead GE (2013). "Exercise for depression". Cochrane Database Syst Rev. 9: CD004366. doi:10.1002/14651858.CD004366.pub6. PMID 24026850. Authors' conclusions
    Exercise is moderately more effective than a control intervention for reducing symptoms of depression, but analysis of methodologically robust trials only shows a smaller effect in favour of exercise. When compared to psychological or pharmacological therapies, exercise appears to be no more effective, though this conclusion is based on a few small trials.
  2. ^ Mura G, Moro MF, Patten SB, Carta MG (2014). "Exercise as an add-on strategy for the treatment of major depressive disorder: a systematic review". CNS Spectr. 19 (6): 496–508. doi:10.1017/S1092852913000953. PMID 24589012. Considered overall, the studies included in the present review showed a strong effectiveness of exercise combined with antidepressants. ...
    Conclusions
    This is the first review to have focused on exercise as an add-on strategy in the treatment of MDD. Our findings corroborate some previous observations that were based on few studies and which were difficult to generalize.41,51,73,92,93 Given the results of the present article, it seems that exercise might be an effective strategy to enhance the antidepressant effect of medication treatments. Moreover, we hypothesize that the main role of exercise on treatment-resistant depression is in inducing neurogenesis by increasing BDNF expression, as was demonstrated by several recent studies.
  3. ^ Josefsson T, Lindwall M, Archer T (2014). "Physical exercise intervention in depressive disorders: meta-analysis and systematic review". Scand J Med Sci Sports. 24 (2): 259–272. doi:10.1111/sms.12050. PMID 23362828. Physical activity has also become increasingly and firmly associated with improvements in mental health and psychological well-being (Mutrie, 2000; Landers & Arent, 2007). In particular, exercise is believed to be effective in preventing depression and also to significantly reduce depressive symptoms in clinical as well as in nonclinical populations (O'Neal et al., 2000; Landers & Arent, 2007). Several correlational studies show that exercise is negatively related to depressive symptoms (e.g., Galper et al., 2006; Hassmén et al., 2000). Moreover, a considerably large number of intervention studies have by now investigated the effect of various exercise programs on depression and the vast majority of them indicate that exercise significantly reduces depression (e.g., Blumenthal et al., 2007; Martinsen et al., 1985; Singh et al., 1997).
  4. ^ Rosenbaum S, Tiedemann A, Sherrington C, Curtis J, Ward PB (2014). "Physical activity interventions for people with mental illness: a systematic review and meta-analysis". J Clin Psychiatry. 75 (9): 964–974. doi:10.4088/JCP.13r08765. PMID 24813261. Discussion
    This systematic review and meta-analysis found that physical activity reduced depressive symptoms among people with a psychiatric illness. The current meta-analysis differs from previous studies, as it included participants with depressive symptoms with a variety of psychiatric diagnoses (except dysthymia and eating disorders). ... This review provides strong evidence for the antidepressant effect of physical activity; however, the optimal exercise modality, volume, and intensity remain to be determined. ...
    Conclusion
    Few interventions exist whereby patients can hope to achieve improvements in both psychiatric symptoms and physical health simultaneously without significant risks of adverse effects. Physical activity offers substantial promise for improving outcomes for people living with mental illness, and the inclusion of physical activity and exercise programs within treatment facilities is warranted given the results of this review.

Will probably add something on its efficacy as a sole/adjunct treatment for depression under "Systematic reviews" using these 4 papers sometime tomorrow. Seppi333 (Insert 2¢ | Maintained) 04:53, 5 February 2015 (UTC)

Antidepressant

hi jeatdog (sorry for my english) yes my "source" was french.

http://apps.who.int/medicinedocs/fr/d/Js4896e/9.html "To avoid the association with dependence, an increasing number of researchers have used a different term, discontinuation syndrome, instead of withdrawal syndrome. The number of hits for discontinuation syndrome in searches of the international medical literature began to increase, relative to the occurrence of withdrawal syndrome, in 1997 after a symposium on antidepressant discontinuation syndrome held in 1996."

  • ok it is not written elli lily or pfizer. because it was a sentence i found in this version.

https://en.wikipedia.org/w/index.php?title=Physical_dependence&oldid=647840566 "SSRI drugs, which have an important use as antidepressants, are considered to cause physical dependence, although it is considered mild compared to drugs like opioids and GABA modulators, but they engender a discontinuation syndrome, which was originally called "SSRI withdrawal" until a 1997 symposium sponsored by Pfizer and Eli Lilly (the producers of several anti-depressants including Prozac and Effexor) was held, with the drug representative attendees concluding that "discontinuation syndrome" sounded less threatening than "withdrawal"

and steppi333 had revert this because no source. (and perhaps because the end of the sentence:"with the drug representative attendees concluding that "discontinuation syndrome" sounded less threatening than "withdrawal". i have a source, and i have revert the problematic end of the sentence. what the problem? Vatadoshu (talk) 20:41, 26 February 2015 (UTC)

Thanks for talking! sounds like you understand what was wrong with your initial edit - it was not true, was based on a french source, and bizarrely cited a diff of unsourced being removed from another article. Based on the WHO document it seems that you could write new and accurate content. please go ahead. Jytdog (talk) 21:34, 26 February 2015 (UTC)
@Jytdog: it is not my language. i can't reformulate, i will do spelling mistakes. please do it for me. it is not in my competence to write from zero just with a document. that's why i keep the english sentence.(i cited the diff unsourced because it correspond). (french source can be true). i don't know how to do a correct link. the wikicode is not the same than french wiki. i tried here and it is bad, really. perhaps you have bot that traduct the french wikicode link?. (this document is interesting, there are 31 pages,-the table of content is at the top of the document)Vatadoshu (talk) 09:52, 27 February 2015 (UTC)
I added the source as a reference. Jytdog (talk) 12:18, 27 February 2015 (UTC)
@Jytdog:
yep it's ok.
(i find the original source, it was that http://www.cochrane.dk/research/theses/Nielsen%20PhD.pdf that say"1996Authorities describe SSRI withdrawal reactions as rare and relatively mild.Closed symposium on “Antidepressant discontinuation events” sponsored by Eli Lilly.UK authorities published a review of SSRI withdrawal reactions with the conclusion that there was no evidence of a physical dependence problem with the SSRIs and that withdrawal reactions were rare and “relatively mild”A supplement to the Journal of Clinical Psychiatry was published with several proceedings from the symposium in 1996. The supplement was sponsored by Eli Lilly.1998At a meeting in the Committee on Safety of Medicines (UK) an Eli Lilly representative expressed concern of the use of the term “withdrawal reaction” when referring to the symptoms occurring on withdrawing treatment due to the fact that the term “withdrawal”has a specific meaning and implies that the drug is addictive. Lilly suggested the term “discontinuation reactions”."
->yep neither pfizer, neither "sounded less threatening than" , but the remaining was correct. just needed to be reformulate.).
the modification you made is ok for me.Vatadoshu (talk) 18:03, 27 February 2015 (UTC)

Autism in pregancy, reason for reverting

I am about to revert the addition of a subsection titled "Increase in autism risk" and would like to explain why. The first cited source is a primary research study and therefore not compatible with the guidelines in WP:MEDRS. Moreover there are serious reasons for doubting the validity of the conclusions, as the cited commentary explains. (By the way, it comes from Science magazine, not Science News as the citation states.) We should not use this material until it can be referenced to reputable secondary sources. Currently the only secondary source is the Science commentary, which certainly does not back up the statements. Looie496 (talk) 14:29, 16 December 2015 (UTC)

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Why a 'Categories' section?

What is the point of including

Categories

Antidepressants
Drug classes defined by psychological effects
Drugs by psychological effects
Psychoactive drugs

… when the categories are also listed at the bottom of the page? —Tamfang (talk) 17:31, 27 September 2016 (UTC)

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Antidepressant drug trials, etc

User:Nils nilsen - it is clear that you are a fan of the book, but the content you are trying to add here and here and here is not OK.

A problem with using scales like this is that they do not measure quality of life or end points that really matters such as better relationships or being able to get back to work.[1]Peter Gotzsche, professor of research methodology and co founder of the Cochrane collaboration has pointed out that all research on antidepressants is done by withdrawing patients from their previous drug cold turkey, and after a week puting half of them back on a similar drug, and letting the rest, the placebo group, continue in cold turkey withdrawal. With this biased design, the drug group scores 3 points better on the HAM-D scale. However, a few days later, the placebo group reaches the same level, despite being in cold turkey withdrawal. The smallest change that patients or doctors can perceive on the HAM-D scale is 6.

References

  1. ^ Gotzsche, Peter (2014). DEADLY PSYCHIATRY AND ORGANISED DENIAL. People's Press.

Respected though the author may be in some ways, please see WP:ONEWAY. Jytdog (talk) 09:15, 18 March 2017 (UTC)

Antidepressants and the Placebo Effect

Antidepressants and the Placebo Effect

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172306/

Benjamin (talk) 01:34, 6 May 2017 (UTC)

Effect of antidepressants exaggerated due to buried data

I came across this article [1] and found the graph very interesting. The graph is from an article in the The Wall Street Journal and is sourced to the New England Journal of Medicine. What I find particularly interesting is that the second medicine on the list, Zoloft, is the most prescribed Antidepressant in the US, and the third one on the list, Remeron, is considered one of the most efficacious Antidepressants according to a meta-analysis published in 2009. I'd like to get thoughts on how this info can be incorporated and where. -- Somedifferentstuff (talk) 18:21, 16 May 2017 (UTC)

WP content about health is based on sources that comply with WP:MEDRS. Please actually read the article associated with this talk page: at the MDD section, which is up to date with reviews published since 2012. Jytdog (talk) 23:57, 16 May 2017 (UTC)

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comparative efficacy and tolerability table

this is a gobsmacking work of WP:OR; the refs are horribly out of date as well.

Comparative efficacy and tolerability
Comparative efficacy and tolerability table
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
[1][2][3][4][unreliable medical source?][5] [1][4][5][6] [2][3][7]
[1][4][5][6] 		[1][4][5][7][8] [1][3][4][5][7] [1][3][4][5][7][9] [1][3][4][5][7][9] [1][3][4][5][7] [3][7]
[1][4][5][9] 		[1][3][4][5][7] [1][3][4][5][7] [1][3][4][5][7]
Tricyclic antidepressants (TCAs)
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
Amitriptyline 3 1 3 4 3 4 v 4 3 1 4/3
Amoxapine 2 2 4 2 2 2 2 2 2 v ND
Clomipramine 3 2/1 2 2 2 4/3 v 4 2 1 4
Desipramine 2 2/1 3 1 1 1/v 1 1 2 1/v ND
Dosulepin (Dothiepin) 2 1 4 ? 3/2 3/2 v 3/2 2 v 3/2
Doxepin 2 2/1 3 3 4 3 v 3 3 v 3
Imipramine 3 1 3 4 4/3 3 1 3 3 1 3
Lofepramine 2 3 1 1 1 1 1 2 1 ? ?
Maprotiline 2 2/1 4 2 2 3 v 2 3 v ND
Nortriptyline 2 2 2 1 2 1 v 1 2 v ND
Protriptyline 2 2/1 2 1 2 1 1 2 3 1 4/3
Tianeptine 2 4 ? ? ? ? ? ? ? ? ?
Trimipramine 2 1 2 4 3 4 1 4 2 2 v
Monoamine oxidase inhibitors (MAOIs)
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI toxicity SD
Isocarboxazid 2 1 3 1 2 1 2 1 v 1 4
Moclobemide 2 3 1 v v v ? v v v 1/v
Phenelzine 2 1 3 2 3 1 1 1 v 1 4
Seligiline ? 3 2 v 1 v 1 1 v v v
Tranylcypromine 2 1 3 1 2 v 2 1 v 1 4
Selective serotonin reuptake inhibitors (SSRIs)
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
Citalopram 2 3 2 1 1 v 1 v 2 1 3
Escitalopram 3 3 1 1 1 v 1 v 1 1 3
Fluoxetine 2 3 1 1 1 v 2 v 1 1 3
Fluvoxamine 2 3 2 1 1 1 1 v 1/v 2 3
Paroxetine 2 3 1 2 2 1 1 1 1/v 1 4
Sertraline 3 3 1 1 1 v 2 v 1/v 2 3
Serotonin–norepinephrine reuptake inhibitors (SNRIs)
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
Desvenlafaxine 2 3/2 1/2 v v v 2 v v 2/1 3
Duloxetine 2 3 1 v v v 2 v v 2 3
Milnacipran 2 3 ? v v v 2 1 v 2 v
Venlafaxine 3 2 2 v v v 2 v 1 2 (IR)
1 (XR) 		3
Noradrenergic and specific serotonergic antidepressants (NaSSAs)
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
Mianserin 2 3 ? 4 v 4 v 1 1 v 1
Mirtazapine 3 3 1 4 v 4 v 1 1 v 1
Serotonin antagonist and reuptake inhibitors (SARIs)
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
Nefazodone 2 3 2/1 v 1 2 v 1 v 2 v
Trazodone 2 [10] 3 1 1 3 4 v v 2 3 1
Serotonin modulator and stimulators (SMSs)
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
Vilazodone 2 3/2 ? v v v 2 v v 4 2
Vortioxetine 2 3 ? v v v 1/v v v 3 1
Other
Drug Relative efficacy Tolerability Danger
in overdose 		Weight gain Ortho hypot Inactivating effects Activating effects Anti-ACh QTc i. p. GI
toxicity 		SD
Agomelatine 2 3 1 v v 1 1 v v 1 1/v
Bupropion 2 3 3/2 v v v 2/1 v 1 1 v
Reboxetine 1 3 1 v v v 2 v v 1 1
St John's wort 3/2 4 1 1/v 1/v 1/v 1/v 1/v 1/v 1/v 1/v

Where:

For adverse effects/overdose toxicity

4 means very strong effect/extreme toxicity.

3 strong effect; efficacious/high toxicity.

2 moderate effect/moderately toxic.

1 weak effect/weakly toxic.

v very weak/negligible effect

For tolerability

4 extremely tolerable. These drugs have proven to be better tolerated than the SSRIs.

3 very tolerable ? few, mild and transient side effects. These are drugs such as the SSRIs.

2 moderately tolerable. Some of the more tolerable of TCAs.

1 poor tolerability. TCAs and MAOIs mostly.

For efficacy

3 Superior efficacy drug, according to at least one review article.

2 Ordinary efficacy drug. Maybe some primary sources indicate superior efficacy relative to superior efficacy agents (e.g. agomelatine has shown superior efficacy to venlafaxine in one clinical trial) but insufficient data to say with much confidence.

1 Inferior efficacy compared to ordinary efficacy drugs, according to at least one review article.

Acronyms/terms used in the above table:

Activating effects – adverse effects such as agitation, anxiety, insomnia and tremor.

AMH – Australian Medicines Handbook.[9]

GI – Gastrointestinal.

Inactivating effects – sedating effects such as drowsiness, somnolence and sedation.

IR – Immediate release tablets.

ND – No data.

Ortho hypot – Orthostatic hypotension

QTc i. p. – QTc interval prolongation

SD – Sexual dysfunction.

XR – Extended release tablets.

PER DRUG NOTES: [2][3][4][6][7][8][9]

Tricyclic antidepressants (TCAs)

Amitriptyline: Preferentially (8x over norepinephrine) inhibits the reuptake of serotonin but norepinephrine reuptake inhibition is clinically significant.[2] Listed as a more hepatotoxic antidepressant in a recent review article.[11]

Amoxapine: Sometimes classed with the tetracyclic antidepressants. Has atypical antipsychotic actions too. Not available in Australia, Canada or the UK but available in the US. May be faster acting. Antidopaminergic, which means that it can cause extrapyramidal side effects, tardive dyskinesia and neuroleptic malignant syndrome.[12] Causes kidney failure and seizures in overdose, although it usually does not cause cardiotoxic effects in overdose.[13]

Clomipramine: Highly selective (~120x) for serotonin reuptake inhibition. More epileptogenic than other TCAs.[2]

Desipramine: Preferentially inhibits the reuptake of norepinephrine (22x over serotonin).[2]

Dosulepin (Dothiepin): Not available in the US. Available in Australia (where it is still commonly referred to as dothiepin) and the UK.
Weight gain: probably 2
Danger in overdose: 4 [9]

Doxepin: Somewhat selective for inhibiting norepinephrine reuptake (2.3x over serotonin).

Imipramine: First marketed TCA. Somewhat selective for serotonin reuptake (26x over norepinephrine).
Relative efficacy: 3[14][15] More hepatotoxic than most other antidepressants.[11]

Lofepramine: Not licensed in Australia, US or Canada. Licensed in the UK and other European countries.
QTc i. p.: 1 (dose-dependent)

Maprotiline: Fairly selective (~90x over dopamine) norepinephrine reuptake inhibitor.[2]

Nortriptyline: Active metabolite of amitriptyline. Somewhat selective (4.2x) for norepinephrine reuptake inhibition.

Protriptyline: Relatively (14x over serotonin) selective norepinephrine reuptake inhibition.

Tianeptine: Enhances the reuptake of serotonin and increases dopaminergic and glutamatergic neurotransmission. Not approved for clinical use in Australia, Canada, the UK, the US and Ireland. More hepatotoxic than most other antidepressants.[11]

Trimipramine: Has antidopaminergic effects and hence can cause extrapyramidal side effects, tardive dyskinesia and neuroleptic malignant syndrome.

Monoamine oxidase inhibitors (MAOIs)

Isocarboxazid: Not licensed for use in Australia.

Moclobemide: Only clinically utilized reversible inhibitor of monoamine oxidase A (RIMA). Not approved for use in the US. Approved for clinical use in Australia, Canada, most European countries (including the Czech Republic, Finland and Ireland), New Zealand, Singapore, South Africa and the UK.
Activating effects: ? (insomnia common according to the AMH)

Phenelzine: Phenelzine is more prone than tranylcypromine and most other antidepressant to causing liver damage.[11]

Seligiline: Originally used a treatment for Parkinson's disease due to its selective, irreversible inhibition of MAO-B but at higher doses MAO-A inhibition occurs.

Tranylcypromine: Metabolized into amphetamine analogues in vivo. Can cause liver damage.[9]

Selective serotonin reuptake inhibitors (SSRIs)

Citalopram: Most likely of the SSRIs to prolong the QT interval. Also the most toxic SSRI in overdose. Less hepatotoxic than most other antidepressants.[11]
QTc i. p.: 2 (dose dependent; doses >40 mg/day are particularly dangerous)

Escitalopram: The more active S-enantiomer of citalopram. May be the most efficacious of the SSRIs (although no statistically significant difference between the efficacy of sertraline and escitalopram have been teased out to date). Based on the available evidence it is less toxic than its racemic counterpart, (R,S)-citalopram, in overdose. Less hepatotoxic than most other antidepressants.[11]

Fluoxetine: First SSRI to receive FDA approval in 1987. Some studies have shown slight (often statistically insignificant) weight reductions in those on fluoxetine. Has the longest net half-life (taking into account the effects of its active metabolite, norfluoxetine) of any antidepressant clinically used, and consequently, when abruptly stopped, withdrawal effects are usually mild and rare. Dermatologic reactions are more common than with sertraline.[4]

Fluvoxamine: Not FDA approved for major depression; FDA approved for OCD. Has the highest affinity of any SSRI towards the sigma-1 receptor at which it serves as an agonist.[16][17] Less hepatotoxic than most other antidepressants.[11]

Paroxetine: Only SSRI that's not Australian pregnancy category C but is rather category D due to an increased risk of Persistent Pulmonary Hypertension of the Newborn. The FDA of the US has placed it in category D. It is associated with a higher risk of sexual dysfunction, weight gain, anticholinergic side effects and drowsiness than the other SSRIs. Has a short half life compared to other SSRIs and hence is the most prone to causing withdrawal effects whenever a dose is missed. Paroxetine has the lowest affinity for the sigma-1 receptors of all the SSRIs.[16] It also possesses the highest propensity of any SSRI for causing extrapyramidal symptoms.[13] Less hepatotoxic than most other antidepressants.[11]

Sertraline: Highest risk of psychiatric side effects (e.g. mania, suicidal behavior/ideation, psychosis, etc.)[4] Has slight (but clinically significant) inhibitory effects on dopamine reuptake.[18][19] Has the second highest affinity of the SSRIs towards the sigma-1 receptor where it may serve as a sigma-1 receptor antagonist.[17]
GI toxicity: 2 (mostly diarrhoea)[7]

Serotonin–norepinephrine reuptake inhibitors (SNRIs)

Desvenlafaxine: Active metabolite of venlafaxine.

Duloxetine: Unlike the other SNRIs listed here duloxetine does not cause dose-dependent hypertension as a common adverse effect. Used to relieve neuropathic pain too. More hepatotoxic than most other antidepressants.[11]

Milnacipran: Primarily used as a treatment for neuropathic pain.
Danger in overdose: ? (No single-drug fatal overdoses reported yet)

Venlafaxine: Relatively selective (116x) for serotonin reuptake inhibition over norepinephrine.
GI toxicity: 2 (IR) / 1 (XR)

Noradrenergic and specific serotonergic antidepressants (NaSSAs)

Mianserin: Not licensed for use in the US and Canada. Licensed for use in Australia and the UK. Can cause blood dyscrasias (including agranulocytosis) and consequently both the BNF and AMH recommend regular complete blood count monitoring.[9][20]

Mirtazapine: Licensed for use in the US, UK, Australia and Canada. Mianserin's successor and analogue.

Serotonin antagonist and reuptake inhibitors (SARIs)

Nefazodone: Risk of hepatotoxicity. Available in the US but not in Canada, Australia or Europe.

Trazodone: Not available in Australia. More hepatotoxic than other antidepressants.[11]
Relative efficacy: 2 [10]

Serotonin modulator and stimulators (SMSs)

Vilazodone: Potential for serotonin syndrome as an adverse effect.
Danger in overdose: ? (probably low aside from an increased risk of serotonin syndrome)

Vortioxetine: Introduced to the US market in September 2013 and hence data on its adverse effects may be lagging behind. Serotonin syndrome is a possible (rare) adverse effect.

Other

Agomelatine: Not licensed in the US or Canada. Licensed in Australia and the UK.
Relative efficacy: 2 [21]

Bupropion: Only licensed in the UK and Australia as a smoking cessation aid, but in the US it is licensed for the treatment of major depressive disorder. More hepatotoxic than most other antidepressants.[11]

Reboxetine: Not licensed in the US or Canada. Licensed in Australia and the UK.

St John's wort: Not a prescription drug in most countries; available as an over-the-counter herbal supplement.

References

  1. ^ a b c d e f g h i j k l Cite error: The named reference SJW Cochrane review was invoked but never defined (see the help page).
  2. ^ a b c d e f g Brunton LL, Chabner B, Knollmann BC, eds. (2011). Goodman and Gilman's The Pharmacological Basis of Therapeutics (12th ed.). New York: McGraw-Hill Professional. ISBN 978-0-07-162442-8.
  3. ^ a b c d e f g h i j k "Side effects of antidepressant medications". UpToDate. Wolters Kluwer Health. Archived from the original on 2 November 2013. Retrieved 24 October 2013. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  4. ^ a b c d e f g h i j k l m n o Royal Pharmaceutical Society of Great Britain. MARTINDALE – The Complete Drug Reference. Pharmaceutical Press. Archived from the original on 26 July 2013. Retrieved 31 October 2013. {{cite book}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  5. ^ a b c d e f g h i j k l Ernst E; Rand JI; Barnes J; Stevinson C (1998). "Adverse effects profile of the herbal antidepressant St. John's wort (Hypericum perforatum L.)". European Journal of Clinical Pharmacology. 54 (8): 589–94. doi:10.1007/s002280050519. PMID 9860144. Collectively, the data suggest that hypericum is well tolerated, with an incidence of adverse reactions similar to that of placebo.
  6. ^ a b c Cipriani A, Furukawa TA, Salanti G, Geddes JR, Higgins JP, Churchill R, Watanabe N, Nakagawa A, Omori IM, McGuire H, Tansella M, Barbui C (2009). "Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis". Lancet. 373 (9665): 746–58. doi:10.1016/S0140-6736(09)60046-5. PMID 19185342.
  7. ^ a b c d e f g h i j k l Taylor D, Paton C, Shitij K (2012). The Maudsley prescribing guidelines in psychiatry. West Sussex: Wiley-Blackwell. ISBN 978-0-470-97948-8.
  8. ^ a b White N, Litovitz T, Clancy C (2008). "Suicidal antidepressant overdoses: a comparative analysis by antidepressant type". J Med Toxicol. 4 (4): 238–50. doi:10.1007/BF03161207. PMC 3550116. PMID 19031375.
  9. ^ a b c d e f g h Rossi, S, ed. (2013). Australian Medicines Handbook (2013 ed.). Adelaide: The Australian Medicines Handbook Unit Trust. ISBN 978-0-9805790-9-3.
  10. ^ a b van Moffaert M, de Wilde J, Vereecken A, Dierick M, Evrard JL, Wilmotte J, Mendlewicz J (March 1995). "Mirtazapine is more effective than trazodone: a double-blind controlled study in hospitalized patients with major depression". Int Clin Psychopharmacol. 10 (1): 3–9. doi:10.1097/00004850-199503000-00001. PMID 7622801.
  11. ^ a b c d e f g h i j k Voican, CS; Corruble, E; Naveau, S; Perlemuter, G (April 2014). "Antidepressant-induced liver injury: a review for clinicians". The American Journal of Psychiatry. 171 (4): 404–15. doi:10.1176/appi.ajp.2013.13050709. PMID 24362450.
  12. ^ "AMOXAPINE tablet [Watson Laboratories, Inc.]". DailyMed. Watson Laboratories, Inc. August 2010. Archived from the original on 2 November 2013. Retrieved 30 October 2013.
  13. ^ a b Walker, R; Whittlesea, C, eds. (2007) [1994]. Clinical Pharmacy and Therapeutics (4th ed.). Edinburgh: Churchill Livingstone Elsevier. ISBN 978-0-7020-4293-5.
  14. ^ Bruijn JA, Moleman P, Mulder PG, van den Broek WW, van Hulst AM, van der Mast RC, van de Wetering BJ (1996). "A double-blind, fixed blood-level study comparing mirtazapine with imipramine in depressed in-patients" (PDF). Psychopharmacology. 127 (3): 231–7. doi:10.1007/BF02246131. PMID 8912401. Archived from the original (PDF) on 18 August 2017. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  15. ^ Bruijn JA, Moleman P, Mulder PG, van den Broek WW (1999). "Depressed in-patients respond differently to imipramine and mirtazapine". Pharmacopsychiatry. 32 (3): 87–92. doi:10.1055/s-2007-979200. PMID 10463374.
  16. ^ a b Fishback JA, Robson MJ, Xu YT, Matsumoto RR (2010). "Sigma receptors: potential targets for a new class of antidepressant drug". Pharmacol. Ther. 127 (3): 271–82. doi:10.1016/j.pharmthera.2010.04.003. PMC 3993947. PMID 20438757.
  17. ^ a b Kishimoto A, Todani A, Miura J, Kitagaki T, Hashimoto K (2010). "The opposite effects of fluvoxamine and sertraline in the treatment of psychotic major depression: a case report". Ann Gen Psychiatry. 9: 23. doi:10.1186/1744-859X-9-23. PMC 2881105. PMID 20492642.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  18. ^ Borkowska A, Pilaczyńska E, Araszkiewicz A, Rybakowski J (2002). "[The effect of sertraline on cognitive functions in patients with obsessive-compulsive disorder]". Psychiatr. Pol. (in Polish). 36 (6 Suppl): 289–95. PMID 12647451.
  19. ^ Schmitt JA, Ramaekers JG, Kruizinga MJ, van Boxtel MP, Vuurman EF, Riedel WJ (2002). "Additional dopamine reuptake inhibition attenuates vigilance impairment induced by serotonin reuptake inhibition in man". J. Psychopharmacol. 16 (3): 207–14. doi:10.1177/026988110201600303. PMID 12236626.
  20. ^ Joint Formulary Committee (2013). British National Formulary (BNF) (65 ed.). London, UK: Pharmaceutical Press. ISBN 978-0-85711-084-8.
  21. ^ Goodwin GM (2009). "Clinical studies on the efficacy of agomelatine on depressive symptoms". CNS Drugs. 23 Suppl 2: 35–9. doi:10.2165/11318650-000000000-00000. PMID 19708724.

-- Jytdog (talk) 20:50, 23 January 2018 (UTC)

Discussion

Help me understand how these uniform rankings culled from all these sources is not a completely inappropriate work of WP:OR. Jytdog (talk) 21:02, 23 January 2018 (UTC)

I would really like someone who knows a thing or two about antidepressants to step in here. To me, the table contains useful and important information that you don't get anywhere else in the article. I know that Jytdog deleted the subpage "Comparative efficacy and tolerability of antidepressants" created by Doc James and I do not agree with his reasoning. 87.78.39.203 (talk) 23:43, 10 February 2018 (UTC)
Well, the userpage of the (still active) editor that made this in 2013 is fully supportive of using reliable sourcing...should we get his input or not?Petergstrom (talk) 00:06, 11 February 2018 (UTC)
I say go ahead and get Fuse809's input. 87.78.39.120 (talk) 03:02, 12 February 2018 (UTC)
It was a summary of the sources. Thought it was a good deed, but if you's dislike it and think of it as inappropriate feel free to delete it. I think this deletion would reduce the quality of this article, but alas I may be bias as it was the product of my several hours of work. Fuse809 (contribs · email · talk · uploads) 07:17, 12 February 2018 (UTC)
Fits best as a separate article as articles should not generally have hidden text. I have no strong feels one way or the other. Doc James (talk · contribs · email) 08:20, 12 February 2018 (UTC)

The subpage link for comparative efficacy and tolerability leads straight back to the main page on antidepressants, can someone please fix this as I need that chart — Preceding unsigned comment added by 101.185.8.119 (talk) 09:33, 4 February 2018 (UTC)

Prior content is here[2] Doc James (talk · contribs · email) 23:57, 10 February 2018 (UTC)
Are you going to fight to get that subpage reinstated, Doc James? 87.78.39.120 (talk) 03:02, 12 February 2018 (UTC)
Not planning too right now. If there is consensus to keep it happy to restore. Doc James (talk · contribs · email) 08:34, 12 February 2018 (UTC)

Adding a section on antidepressant adherence

I plan on adding a sub-section on antidepressant adherence to the article. I will be adding this sub-section under the "society and culture" section of the article after sub-section 7.2 "most commonly prescribed." Anthonyb9798 (talk) 17:34, 1 March 2018 (UTC)

Clarified initial paragraph about efficacy

I changed the last few sentences in the opening paragraph to clarify that the debate about antidepressant efficacy is about how much of the observed effect is due to placebo, not if all observed effects is due to placebo.I added an additional reference to that claim compared with what was already there. I also added in a sentence with six references that clarifies that the bulk of the scientific research shows that the efficacy of antidepressants is superior to placebo, as the initial paragraph had a clear anti-psychiatry bias since the only reference on efficacy was a review paper by Irving Kirsch (noted opponent to antidepressants), no primary research papers and no balanced treatment of the issue. EmilKarlsson (talk) 18:28, 3 August 2019 (UTC)

Antidepressant withdrawal symptoms

This seems relevant for the section on discontinuation syndrome:

A new systematic review reports that about half of the patients discontinuing anti-depressants experience withdrawal symptoms. About half of those who experiencing withdrawal symptoms consider them severe.

<redact likely WP:COPYLINK violation>

http://prescribeddrug.org/millions-at-risk-from-antidepressant-withdrawal-new-review-concludes/

While most data is on SSRI/SNRI, the review also includes some studies on tricyclics and MAOIs. Another question that this review raises is whether 'discontinuation syndrome' should actually be replaced by 'withdrawal'. The article argues in favour of the latter on the basis of incidence, severity and duration of the withdrawal effects.Lucleon (talk) 20:03, 2 October 2018 (UTC)

I've removed what appears to be a WP:COPYLINK violation. See also here - the paper has been temporarily retracted for some reason. (prior link is archiveurl for today; here is the live sciencedirect link, which may change) Jytdog (talk) 20:12, 2 October 2018 (UTC)
Thanks for the immediate feedback. Interesting... well then let's wait until this is clarified. The PDF of the paper is still linked at the end of the press release from appg on prescribeddrug.org (link above). Lucleon (talk) 20:21, 2 October 2018 (UTC)

The paper is online now: https://www.sciencedirect.com/science/article/abs/pii/S0306460318308347 including the following main claims:

"-More than half (56%) of people who attempt to come off antidepressants experience withdrawal effects.

-Nearly half (46%) of people experiencing withdrawal effects describe them as severe.

-It is not uncommon for the withdrawal effects to last for several weeks or months. ". I'd be happy to draft a short summary if this considered sufficient support for including it in the section discontinuation syndrome here and probably as well in the respective section for SSRI. Lucleon (talk) 12:49, 3 October 2018 (UTC)

@Lucleon: I would be happy to see that summary if you are still interested in writing it. I know that many object to the term "discontinuation syndrome" on the basis that it is just a euphemism for withdraw. This viewpoint deserves to be heard.
I've added this information a while a go to Antidepressant discontinuation syndrome Lucleon (talk) 09:15, 4 May 2019 (UTC)

Content

[3]

It seems quite a bit of good content was removed. Benjamin (talk) 12:10, 28 April 2019 (UTC)

yes, and that doesn't make the article better. for example, the section effectiveness still describes the more than a decade old star*d trial in complete detail while the most comprehensive systematic review from 2018 and other systematic reviews from the last years have been removed.Lucleon (talk) 16:47, 1 May 2019 (UTC)
An encyclopedia should first be readable and second verifiable. We should strive for summaries rather than complete detail. I agree that most of the STAR*D section should be deleted. Wikiman2718 (talk) 23:45, 1 May 2019 (UTC)
I'd rank verifiability over readability, at leat readable but not verifiable seems problematic to me, but anyway I agree that the section on effectiveness can be improved, so let's try to do that.Lucleon (talk) 21:22, 2 May 2019 (UTC)
@Lucleon: Great. I'll try to add in some of those studies from earlier as time allows. I plan to clear out a lot more material in the future. If I delete something you think is important, just leave me a message about it.

Wiki Education Foundation-supported course assignment

This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Anthonyb9798.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 14:28, 16 January 2022 (UTC)

Cognitive performance and SSRIs

Serotonin is an inhibitory neurotransmitter and thus, has been using to calm down hypersensitive lymbic systems of patients with depression and anxiety disorders. However, due to its inhibitory function, the serotonin may also supresses the function of dopamine, a neurotransmitter that affects memory and learning in a positive way. There are some studies confirming SSRIs' adverse effects on cognitive functions. There are also studies arguing the vica versa. As far as I can see, the article has no info regarding SSRIs-cognitive functions/performance connection. I can create a subsection discussing the connection, but I am not sure if this would be UNDUE. Puduḫepa (talk) 08:25, 22 June 2019 (UTC)

Serotonin can have excitatory or inhibitory effects depending on the postsynaptic receptor type. For example, the 5-HT1 receptor is inhibitory while 5-HT2 is excitatory. There is no simple relationship between serotonin and dopamine. Having said that substantial results on cognitive function during SSRI treatment would of course be interesting.Lucleon (talk) 10:05, 22 June 2019 (UTC)
@Lucleon:, I am going to create a subsection discussing the topic—mentioning postsynaptic receptor stuff would also be informative for the readers. But as far as I know, it is the SNRIs that have excitatory effect on dopamine. Puduḫepa (talk) 10:14, 22 June 2019 (UTC)
I don't know how it should be phrased, but it seems like it's worth at least a mention. Benjamin (talk) 10:20, 26 June 2019 (UTC)

Eating disorders

would adding the cochrane common mental disorder's systematic review on treatment of anorexia nervosa with antidepressants [1] be useful? Edieg02 (talk) 13:55, 10 July 2019 (UTC)

References

  1. ^ Link text

Edits regarding references to the Management of depression article

Hi @Doc James: I made another edit to that sentence in the lede. Please let me know what you think.

I'm curious about why you removed the link from the "see also" section to the Management of depression article. I think that the link is good to include there. ↠Pine (✉) 01:40, 24 April 2020 (UTC)

Hey User:Pine hope all is well. Since we link to management of depression in the lead IMO we do not need to put that in the see also section aswell. Doc James (talk · contribs · email) 01:47, 24 April 2020 (UTC)
Hi @Doc James: I think that the link is good to include there for the benefit of readers who go take time to read the entire article and may want to read related pages after they get to the bottom of the article. Also, I use the "see also" section to find related articles in a way that is similar to how I use categories, and from my admittedly non-expert perspective the article Management of depression is closely related to the topic of antidepressants, so I think that including the link in the "see also" section is preferable. ↠Pine (✉) 01:57, 24 April 2020 (UTC)
Yah. We have WP:See also "As a general rule, the "See also" section should not repeat links that appear in the article's body". I am easy either way if you want to return it. Doc James (talk · contribs · email) 02:56, 24 April 2020 (UTC)
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