Talk:Mirtazapine/Archive 1

Archive 1

Psychedelic properties of Mirtazapine

I've noticed that there have been a spate of recent edits claiming that mirtazapine has psychedelic properties. From what I can gather visual hallucinations and vivid dreams are sometimes reported as side effects. There at least seems to be anecdotal evidence for this on the internet as well as some drug indication lists mentioning these as possible effects. Unfortunately I don't have academic access right now to all of the citations mentioned, but I'm not even sure there's hard evidence of these effects reported in the literature and trials. Though these effects sound plausible, this ought to be double-checked.

But even supposing that hallucinations, nightmares, etc. are a justifiably assertable side effect, I don't think that mirtazapine can be classified as a hallucinogen or psychedelic without a larger body of literature to suggest that these hallucinations/dreams/whatever are more than just a rarely-occurring secondary reaction. More strongly, I definitely don't think there is a sound basis upon which to speculate possible mechanisms by which these (not even substantiated) psychedelic effects could occur.

If I'm remembering correctly, hallucinations and vivid dreams have been noted as side effects of many other antidepressants (a cursory Google gives me this: http://www.ncbi.nlm.nih.gov/pubmed/9864082) and no one would suggest that Prozac is a hallucinogen. If you choose to include a "Psychedelia" section in the article on mirtazapine, in the name of encyclopedic equality I would suggest you include one in other articles on antidepressants.

If there is encyclopedia-worthy evidence out there to support classifying mirtazapine as a psychedelic drug, please prove me wrong and show it.

P.S. In the name of full disclosure I have been taking mirtazapine for about three months and have experienced the "vivid dream" effects, as well as an increase in incidents of sleep paralysis... but I'd like to see this phenomenon backed up with actual evidence. —Preceding unsigned comment added by 69.242.87.42 (talk) 15:00, 11 August 2009 (UTC)

I've checked around a bit on Medline and such, and as far as I can tell, there's no in-depth literature on the subject whatsoever. In fact, the only data I've actually seen are just percentages (e.g., "drowsiness (60%), hallucinations (20%), etc) in generalized side effect analyses. Nonetheless, I think there are more than enough anecdotal reports to justify mirtazapine's so-called "psychedelic" action. Besides, I doubt any studies would bother reviewing weak hallucinogenic side effects of some random antidepressant anyway. They're more a curiosity than anything else when it comes down to it. In any case, I made some slight modifications to your changes in the side effect section and put back in the Bluelight reference. Looks good to me. All that extra hallucinogen stuff was a bit over the top I'd say. Mirtazapine certainly does get interesting at higher doses and/or mixed with cannabis though, speaking from experience when I say that.. Rocknroll714 (talk) 16:45, 11 August 2009 (UTC)

I have been taking Mirtazapine for 12 months at 30mg dose, 2010/11) Almost every night i have ultra realistic story like dreams that i have not had when taking Prozac or sytraline. Conversley I have suffered from Night Terrors ( not nightmares ) all my life but strangely these have ceased since i started Mirtazapine. I have to conclude that there is some some property in the drug that is having a profound effect on my sleep architecture. (----)

Mirtazapine Mechanism of Action

"The primary mechanism of action of mirtazapine is antagonism at central pre-synaptic alpha2-receptors. Normally, these receptors are involved in a negative feedback loop and activation causes inhibition of further norepinephrine (NE) release. By blocking pre-synaptic alpha2-receptors, mirtazapine defeats negative feedback to the presynaptic nerve and causes an increase in NE release. Antagonism at central alpha2-receptors is 10-fold higher than at peripheral alpha2-receptors which results in a reduced incidence of peripheral adverse effects. Mirtazapine also antagonizes several subtypes of serotonin (5-HT) receptors. The drug is a weak antagonist at 5-HT1 receptors and a potent antagonist at 5-HT2 (particularly subtypes 2A and 2C) and 5-HT3 receptors. Blockade of these receptors may result in a lower incidence of certain adverse effects such as anxiety, insomnia, and nausea that occur with other agents like the selective serotonin reuptake inhibitors (SSRIs). Serotonergic neurons also contain alpha2-receptors, called heteroreceptors and blockade of heteroreceptors results in enhanced release of 5-HT. The increased amount of 5-HT released interacts with 5-HT1 receptors which may be relevant to the antidepressant and anxiolytic effects of mirtazapine. Mirtazapine has no effects on the reuptake of either NE or 5-HT. In addition, mirtazapine exhibits significant antagonism at H1-receptors. Histamine H1-receptor blockade is generally associated with sedation, however, the enhancement of NE release may offset the sedative potential of the drug at higher doses. Mirtazapine has minimal activity at dopaminergic and muscarinic receptors." will//defective words, defective thoughts (talk) 18:51, 4 April 2008 (UTC)

"based on its relatively weak actions at the α2-adrenergic receptor"

"Mirtazapine is a potent antagonist at the following receptors: H1 (~1 nM) > 5-HT2A (~10 nM) = 5-HT2C (~10 nM) = 5-HT3 (~10 nM) > α2-adrenergic (~100 nM)."

Which is it? (100nM is moderate-strong.)

Zzzzz9 (talk) 08:17, 5 July 2009 (UTC)

Excessive urinating when taken with alcohol

Does anyone know a reference to the side effect "Excessive urinating when taken with alcohol", is it proved in a scientific article or is it just a remeron user who have experienced it on their own?

Need some references

It would be nice to have references to the statements about mechanism of action involving post-synaptic 5-HT activity and the concept of low dose effecting different neurotransmitters than higher doses. I have heard of both of these ideas but never quite sure where they come from. I will attempt to research it, but added the citation needed tag until me or someone else can look this up.--Psychofarm 21:55, 29 November 2006 (UTC) 71.221.87.211 (talk) 08:04, 1 March 2008 (UTC) I was started on Mirtazapine 3 weeks ago, I'm normally a healthy 130 lbs and three weeks after taking it I now weigh 155 lbs, which is not healthy in my book. 71.221.87.211 (talk) 08:04, 1 March 2008 (UTC)

Question

My partner has been taking mitrazapine for about 2 months when treatment (admission to mental clinic for a month, followed by psychological help) started for depression, anxiety and alcoholism. The treating psychiatrist reckoned its less likely to be addictive than other previously administered drugs. There is a history of substance abuse (alcohol, cannabis, caffeine, valium, codeine) with suicidal tendencies (overdosing of antidepressant, methylated spirits). I have observed increased mood swings especially towards anger which is often self inflicted and spirals out of control. I understand agitation and aggression are known side effects. Psychological help has only just begun and has a low frequency (2 to 3 weeks. The situation has become very difficult for our family and my question is what can I do. Can I raise this issue with the treating GP for instance.Burgerman69 (talk) 00:14, 17 September 2009 (UTC)

I am wondering if Mirtazapine is used to treat any other conditions? My husband has been told he has been given this drug for a suspected heart condition. How would this drug help someone's heart? —The preceding unsigned comment was added by 58.84.113.227 (talk • contribs) .

I suppose it can only help, if the disease has a strong psychological component, so the sedative and anxiolytic properties of Mirtazapine would help your husband. Otherwise, it could even be deleterious to heart conditions, due to some cardiovascular side-effects of the drug. But you said, that the disease is only suspected? So your husband should ask for precise diagnosis of the heart condition. Perhaps Mirtazapine can then be terminated. All the best of luck. Klaus —The preceding unsigned comment was added by 84.44.132.229 (talk • contribs) .

just a thought. could stimulation of the sympathetic nervous system lower heart rate. i know Mirtazapine can increase heart rate and also make it rise more easily in response to heart rate rising events from experience. but there are also times when the heart rate drops to a fairly low 58-65 bpm. good luck. —Preceding unsigned comment added by 220.101.95.249 (talk) 08:17, 10 March 2008 (UTC)

My veterinarian prescribed Mirtazapine today for my elderly cat as an appetite enhancer. Approx. 4 mg every 3 days. First time I had heard of this drug. My cat is 18+ years old and has apathetic hyperthyroidism, had not eaten for a few days - hope this new drug works. —Preceding unsigned comment added by Rcwolfe62 (talk • contribs) 04:38, 2 September 2009 (UTC)

Drug-Drug Interactions

I have been taking mirtazapine (Remeron) for the past 3 years and it is the only antidepressant (out of 4 others) that works for me. However,in January 2008, I was prescribed tramadol for pain from an automobile accident, and was taking it concurrently with the mirtazapine (15mg daily). I was supposed to take 50 mg of tramadol every 4 hours as needed for pain. After the first dose I started to notice this strange side effect though. I was very tremulous (trembling). I just put some more clothes on and ignored the trembling. Then that night, my back was hurting pretty badly, so I took two of the 50 mg tramadol (Ultram). Instead of falling asleep, 30 minutes later I leapt out of bed and started cleaning the house. While I was cleaning, I started sweating profusely and had to stop because I was shaking so bad, I couldn't even stand. I was sitting on the sofa and my mother happened to come into the room and she noticed my condition. She took my temperature, and it was 104 degrees Fahrenheit. My pupils were completely dilated (mydriasis). Anyway I was rushed to the hospital, were I was diagnosed with Serotonin Syndrome. They gave me 2 mg of intravenous lorazepam , and I recovered fully. I would just like someone to add that mixing mirtazapine with other serotonin agonists (such as tramadol), and not just MAOI's, can cause a potentially fatal case of serotonin syndrome. I've researched the interaction myself and have found that I am not the only person who suffered this reaction. There are references that can be cited. Just want to save someone else from going through the serotonin syndrome ordeal through knowledge. If you have to take a medication, you should know all the "do's and don'ts associated with it, including all interactions. Dsnider1988 (talk) 09:27, 28 January 2008 (UTC)

That is very interesting because I take 45mg Remeron for 1+ years now. I also was prescribed tramadol, at 37.5mg. I went to work one morning and had taken the tramadol and had this overwhelming urge to be up and moving around (sit at desk 60% of time)...I soon made a joke to a female coworker that I knew what a hot flash felt like because I encountered a VERY rapid onset of heat and profuse sweating. I even had to go take my argyle off (and it was 69 according to them) and sit down. I felt that same tremble feeling and even felt like my stomach was seizing up or something...it was terrible. I just wrote it off as a freak incident and had the same thing the next couple of days before I related it to the tramadol. —Preceding unsigned comment added by 68.53.143.235 (talk) 17:58, 4 March 2009 (UTC)

Mirtazipine

Not too sure about using it for a heart condition. That sounds very strange to me. Read the PI sheet and get a second opinion. I wanted to post something about appetite and drowsiness. This is one of those drugs that your doctor will (or should) tell you to take immediately before getting in bed. I'm just speaking from personal experience of being on this drug for ~2 years now, but for someone who just started taking it, you will probably be asleep 10-15 minutes after taking it...whether you make it to bed or not. Absolutely do not get out of bed to eat after taking it. You will only end up falling asleep on the kitchen floor with food IN your mouth. (I am still known to do this on occasion.) The cravings and the drowsiness will level off after a while, but they have never gone away for me. On the upside, I'm bipolar and it's one of the only two drugs (the other is Effexor, also not an SSRI) that ever worked for the depression side of that. If SSRI's don't work on you, this might be something to try. I doubt anyone would offer it as a first choice for newly diagnosed depression unless they were both not eating and not sleeping. Again, this is all from my personal experience having been on it for ~2 years. I'd like to see some more content on this page about those issues. In future I may put the full PI sheet (the huge folded up paper with tiny incomprehensible print in the back of the brochure) with research results, etc. up. 65.247.225.96 01:13, 8 December 2005 (UTC)irayna

Please correct me if I am wrong, however, I am under the impression that Avanza, being a stimulant, may increase the heart rate. I am not sure how this would help a heart condition, but make what you want of it. —The preceding unsigned comment was added by 141.168.50.193 (talk • contribs) .

To the first poster: please do not put up the entire PI sheet. Such information is easily accessible on a wide variety of websites. One needs only perform a google search. To the second poster: mirtazapine is not a stimulant. --Muugokszhiion 06:08, 4 May 2006 (UTC)

First paragraph

Recent edits have turned the first paragraph into a muddy discussion: "...although there is only modest evidence from their research department to support its claimed effects. Indeed, recent work by researchers independent of Organon International has failed to replicate...". This is not encyclopedic and has no place anywhere near the top of the article. The paragraph does not describe what mirtazapine is; it only debates what it is not, or may be. This needs to be cleaned up to be clear and concise. Please discuss these issues on the talk page rather than on the article itself. --Muugokszhiion 06:47, 2 November 2006 (UTC)

I agree the first paragraph needs to be a concise overview of the article. As many people will only read the first paragraph. The independent research has raised an interesting point but it belongs lower down in the article. I will change it when I have time. --Benjaminevans82 00:57, 3 November 2006 (UTC)

The Mayo Clinic refers to mirtazapine as a tetracyclic antidepressant and notes that it is the only antidepressant with a tetracyclic chemical structure to have FDA approval to treat depression (http://www.mayoclinic.com/health/mental-health/MH00069). As re the controversy, the link to the pubmed abstract substantiates the criticism. Nevertheless, it shouldn't headline the article. --Substantiate 23:30, 5 April 2007 (UTC)

Isn't Ludiomil also a tetracyclic? I believe it is. The first one, actually. It is older, but nonetheless, approved by the FDA for Tx of depression. It is not a NaSRI, but we must be honest and precise, so as not to mislead.--User:wgeoff00775.50.51.87 (talk) 22:56, 30 December 2007 (UTC)

I also have experienced the side effect of getting up in my sleep and eating while taking Remeron. It was a relief to become aware that this is from Remeron as I have never done this. I'm am glad to hear it will lessen and hopefully go away. —Preceding unsigned comment added by 66.91.194.88 (talk) 03:56, 2 March 2008 (UTC)

Remeron in the morning?

I have been taking Remeron 45mg for about six months now and it has seemed to resolve my depression. For the first time in a long time I feel not-depressed. Also I have an anxiety disorder and take 4-6mg of Ativan a day. Remeron is sedating and taken at bed time. I found that true for me. The idea came to me about taking Remeron in the morning to use the sedating side effects to help with my anxiety and maybe be able to take less Ativan. I could not find any information about taking Remeron in the morning. I would appreciate any feedback.

Remeron is generally taken at night because it is sedating. You will probably be more tired if you take it in the morning, but I'm no doctor. Discuss this issue with your doctor. —Preceding unsigned comment added by 67.173.19.210 (talk) 02:37, 5 June 2008 (UTC)

Dosage

I moved the following from the article to this talk page. --Ishi Gustaedr (talk) 14:46, 2 May 2008 (UTC)

Doses 90-210mg are extremely effective in alliviating major depression with predomenant symptoms of insomnia/anxiety/lethergy and loss of appetite. I submit tests with this dose should be carried out and may prove to be the fastest/safest and most tolerable antidepressant superseding all others in the treatment of the aforementioned symptoms. PLEASE HELP RESEARCH THIS FURTHER. --80.193.69.13 (talk) 11:35:42, 2008-05-01 (UTC)

NaSSA vs. SNRI

I just noticed that the link for noradrenergic and specific serotonergic antidepressant (NaSSAs) in the first paragraph actually goes to the page for serotonin-norepinephrine reuptake inhibitors (SNRIs). There doesn't appear to be a page for NaSSAs, but as far as I am aware, the two are separate classes of drugs with different actions, side effects etc. I don't know enough about this topic to edit it unfortunately. CCustard (talk) 22:56, 4 March 2009 (UTC)

Racemate

Mirtazapine is a 1:1-mixture of the (R)- and the (S)-enantiomers. I do not understand, why such information is deleted. Best regards, --Jü (talk) 15:26, 2 August 2009 (UTC)

Lots of drugs are racemic. And I mean a LOT. That doesn't mean putting up an huge ugly double image showing both enantiomers is always necessary, however. I saw that you've been putting them up all over the place, and frankly, I don't agree with it at all.. but that's just me. Personally, I like the new one a lot better, and it's even got colors! * Pets it * Rocknroll714 (talk) 18:34, 2 August 2009 (UTC)

It's nothing personal against you that your posts were edited/modified. However, I need to make it abundantly clear to you that the need to draw 2 structures in cases where the compound is a racemate is completely unjusified/uncalled for. In cases where the compound is drawn twice such as in McMurry Organic Chemistry textbook, the reason for this is where 3D glasses are worn.--Nuklear (talk) 18:36, 2 August 2009 (UTC)

It's true, lots of OLD drugs are racemic. If a drugs is used as a racemate it is recognized (in our body, a chiral enveronment) as a mixture of two different compounds, with a very limited number of exeptions. Racemic drugs may be rated as compounds with 50% impurities. [Ariëns EJ: Stereochemistry, a basis for sophisticated nonsense in pharmacokinetics and clinical pharmacology, Eur. J. Clin. Pharmacol. Volume 26 |issue=6 |pages=663–8 (1984)] This is also the view of the Food and Drug Administration (FDA). Thus, todays separate clinical studies must clearly prove the equevalence of both enantiomers of a new active ingredient of a drug before FDA approval. In >>90% of the active ingredient the pharmacology and the pharmacokinetics of the enantiomers is significantly different. Thus, almost all modern chiral drugs are only FDA-approved as single enantiomers. Drug companies marketing "old" chiral drugs as racemates try to avoid the public discussion of this topic. – Another point: If a drug is used as a racemate, the IUPAC name must reflect this. Thus, stereochemical descriptors have to be included, e. g. (±)-, (RS)-, or DL-. Best regards from Germany --Jü (talk) 20:27, 2 August 2009 (UTC)

Feel totally welcome to include the (±) sign etc for clarity. My issue was that you decided to draw 2 images.

All you needed to do was draw preferably the more active isomer and then verbally show that the commercial drug is infact racemic.

There are alternative things you can do such as drawing a wiggly line or using a star of David (∗) if it is felt that this is more appropriate.

Tramadol is a close-call because there are two chiral carbons and it is often felt that both isomers contribute equally to its therapeutic effect.

On one side there is the "morphine like" aspect, then you have the "psychostimulant" aspect of the other isomer.

If it is actually worth the financial effort of separating out the individual isomers is clearly an issue.

Citalopram I dont think is worth it, but drugs like nocaine (SS) are probably better enantiopure.

I'm sure that you agree & it is my intention that we have a mutual understanding on this issue. --Nuklear (talk) 22:18, 3 August 2009 (UTC)

Thanks for this explanation. I agree, the IUPAC name has to include the (±) sign etc for clarity, if the active ingredient is racemic. Best regards, --Jü (talk) 17:12, 4 August 2009 (UTC)

Concerning how racemic stereochemistry should be depicted in a structure drawning, see page 1968 in the IUPAC recommendations ("Graphical representation of stereochemical configuration (IUPAC Recommendations 2006)". Pure Appl.Chem. 78 (10): 1897–1970. doi:10.1351/pac200678101897. {{cite journal}}: Cite has empty unknown parameters: |1= and |month= (help)). I have redrawn the figure according to this recommendation. Cheers. Boghog (talk) 06:03, 11 September 2009 (UTC)

Trade names section

The trade names section has become very long, perhaps it should be moved to the end of the article? – Acdx (talk) 01:41, 17 September 2009 (UTC)

I will do it now. – Acdx (talk) 00:40, 20 September 2009 (UTC)

Chemistry section has a reference problem.

The section currently states: The chemical synthesis of mirtazapine has been reviewed and can be found online.

Unfortunately the supplied reference isn't to the synthesis of mirtazapine, but to that of three of the unwanted byproducts of mirtazapine synthesis. Can someone come up with a link to the synthesis of mirtazapine itself, please? --Kay Dekker (talk) 17:53, 11 November 2009 (UTC)

The key word in the text above is "reviewed". The the synthesis of mirtazapine is outlined in scheme 1 of the linked paper. In addition, references 3, 4, and 5 in the linked paper are to patent applications which describe the synthesis of mirtazapine. I have reformatted the linked paper as an in-line citation and in addition, added the US patent equivalent of reference #3 (a German patent). Cheers. Boghog (talk) 18:34, 11 November 2009 (UTC)

Thank you! --Kay Dekker (talk) 20:55, 11 November 2009 (UTC)

== Not Relevant ==

Why is the phrase "It should be noted that the withdrawal effects of antidepressants are typically nowhere near as strong as those of the benzodiazepines.[117 included in this section? The withdrawal effects of antidepressants are [sic] "nowhere as strong" as many classes of drugs, why not list pain medications, alcohol, nicotine, etc. Wikipedia seems exceptionally biased when it come to the therapeutic value of benzodiazepines. .At least omit the bias when it doesn't have anything to do with the subject being discussed. 71.125.157.232 (talk) 22:31, 12 December 2009 (UTC)Dehughes (talk) 18:48, 23 December 2009 (UTC)

I've been taking a variety of antidepressants for 25 years,

I'd say that all the effective ones are very addicting and very difficult to withdraw from.

The government doesn't focus on this because no one takes antidepressants for pleasure.

Benzodiazepines however, are abused by some people so the government reacts strongly against that.

I took the old tricyclics for 15 years, tried several times to wean myself off them,

tried to substitute Prozac & other newer drugs.

 To no avail.
It wasn't till I started taking Remeron that I could stop taking the tricyclic.

66.53.123.26 (talk) 03:08, 24 March 2010 (UTC)24 march 2010 jimmy

Archive 1

Removal of "opioid activity" addition

Edit: Derp. el3ctr0nika (Talk | Contribs) 00:27, 1 September 2010 (UTC)

Where does the 'common knowledge' that "the kappa-opioid receptor ... in general tends to have negative effects on mood" come from? Salvinorin seems to be the most widely used/abused kappa-opioid agonist that I'm aware of, and anecdotally, it can as easily have either a "paradoxically" positive effect on mood or little subjective effect (though it is also very short-acting, so finding out whether any positive effects on mood are directly mediated or based on a 'rebound' mechanism is of interest to me). Are there some references to other selective kappa agonists showing a clear effect, or is this one of those things being punted around from general opiate research, where kappa-mediated effects might be unpleasant when combined with (withdrawal from?) mu-mediated ones? Just curious. --64.252.204.108 (talk) 10:22, 19 November 2010 (UTC)

Overdose section somewhat misleading?

"Overdose with as much as 30 to 50 times the standard dose has shown to be relatively non-toxic. One case in which 1,200 mg was ingested proved non-fatal." seems a little misleading to me, since it sounds like 1,200 mg should be more than 50 times the standard dose, which isn't the case, unless "the standard dose" is the smallest available tablet, which seems very unlikely. Thoughts on simply removing the second sentence, and having two citations for the first? Cheyinka (talk) 22:41, 4 September 2011 (UTC)

Serotonin Syndrome

The section on serotonin syndrome is wrong, at least at the margins. For example, you can see a case of serotonin syndrome in which mirtazapine (along with olanzapine and tramadol) is partially implicated here: http://www.theannals.com/cgi/content/abstract/38/3/411

Also, I found a case study of a woman receiving only mirtazapine as a monotherapy who developed serotonin syndrome: http://www.ncbi.nlm.nih.gov/pubmed/12671522

I'd edit here, but I don't feel like I have enough expertise to get it right or to judge how rare the above kind of exception is. Does anyone know more about this, and if so would you be willing to revise this paragraph? PStrait (talk) 22:47, 5 June 2010 (UTC)

Regarding the first source, they clearly concluded that Tramadol was the likely cause of serotonin syndrome when taken alongside Venlafaxine: "An objective causality assessment revealed that the addition of Tramadol was the probable cause of the adverse reaction.". Tramadol is a serotonin releasing agent, among other things, and shouldn't be taken with SSRIs or SNRIs as far as I know. The second source cites the woman as being "an individual with risk factors for hyperserotoninemia resulting from reduced, acquired endogenous serotonin metabolism." So that looks like a rare one off. If anything these should maybe be incororated into that section stating that in very rare or exceptional cases mirtazapine has been linked to serotonin syndrome? Rather than as proof. Even then, that first case when taken alongside Tramadol and Venlafaxine proves nothing at all. For all we know, that person may have had less severe serotonin syndrome due to being on Mirtazapine as well. There's nothing conclusive either way.

The bottom line is, Mirtazapine has no effect on serotonin reuptake and actually blockades a number of serotonin receptors, so it's widely considered not to be a risk when taken with other serotonergic drugs. I take Mirtazapine and I can tell you that, on the clinical level, it isn't considered to be a risk at all. I also take Sumatriptan for Migraine alongside it and have done for years, something you'd be forbidden to do if on an SSRI. I have spoken to a couple of GPs about it and they all consider it safe. Not to mention that some Psychiatrists will prescribe Mirtazapine alongside SSRIs. So, if this perception of it being safe from a possible contributing factor to serotonin syndrome is wrong, then it's far more than just a wikipedia article that would be at fault. --Kerans (talk) 13:05, 17 September 2011 (UTC)

According to Hexal (a Mirtazapine manufacture) mirtazapine should not be taken with any MAOIs and should be used only carefully with SSRIs and venlafaxine(i.e. Effexor). Recently I started taking 15mg mirtazapine with my daily dose of effexor and after only 2 doses of mirtazapine I showed strong symptoms of Serotonin Syndrome. Do not use wikipedia as a safe source for medical information. — Preceding unsigned comment added by 212.242.226.71 (talk) 16:11, 1 July 2011 (UTC)

Side Effects - on the packaging but not in the article.

I've got the package leaflet here .. seems to date to 05/10 with Aurobindo/MilPharm/APL being behind it. A package leaflet, I presume, is less than ideal as a reference but still. In the way of the more modern leaflets of this type its fairly specific about the incidence of side effects, definging what they mean by Common/Rare etc. Reason I was motivated to post was I've just moved to this medication from an SSRI and had a fairly grotty hit of side effects, amongst other things lower back pain, joint pain and muscle pain. According to the aforementioned leaflet, this is seen in between 1 and 10 users per 100, which it describes as "common". I've added the conditions as appropriate, with a citation needed tag as I suspect it needs someone with (a) proper access to PubMed and (b) the training needed to interpret what is published.

I was prescribed with this medication in March 2011 and has stopped few weeks after. As a sideeffect, I lost my emotions and have trouble with my regular bowel movement. As if, every nerve connected to my brain has been disconnected. I felt there was like a feeling of numbness all over my body, it was like a place where gradually water is flowing which means, losing my feelings all over my body one at a time. And fr then on, i always feel cold whereever i am... I always have goosebumps where ever I am. — Preceding unsigned comment added by 99.234.203.160 (talk) 19:18, 18 September 2011 (UTC)

There's probably other discrepancies, but I don't want to rewrite that bit of the article unless someone Pharmy-ish wants to help! — Preceding unsigned comment added by 94.8.124.250 (talk) 17:54, 1 September 2011 (UTC)

Adverse Effects

This section is written very poorly. Half the points have no citation and some claims reference sources which say nothing about the point in question. Take this line from the second paragraph: "This is probably due to the loss of efficacy of the drug over time, as tolerance develops with long-term use. [28][37][38][39]". Correct me if I'm wrong, but I see nothing in any of those four sources that state the drug's efficacy decreases over time or that people "develop a tolerance". In fact, that is a ridiculously bold and, I would argue, fictitious, claim. It's also not clear whether they mean the drug's general efficacy or just relating to those side effects mentioned before. It's a sloppy sentence and should be rewritten or removed. --Kerans (talk) 12:37, 17 September 2011 (UTC)

Done. This section mixes invention and fact, unattributable adverse events with confirmed adverse drug reactions. Needs to be changed into "side effects" and sourced to appropriate MEDRS source, rather than conjectured from the raw data, due to synthesis. Have removed a few which have been added over time and seem not to be supported by refs. 70.137.148.24 (talk) 06:29, 23 September 2011 (UTC)

Mirtazapine is not a Tetracyclic

Mirtazapine is classed as an atypical antidepressant, but more specifically as an Alpha 2 antagonist; NaSSA (noradrenaline and specfic serotonergic agent); dual serotonin and norepinephrine agent; antidepressant. This needs to be changed in the first paragraph talking about Mirtazapine's class.

Reference: Stahl, Stephen M. MD, PhD. "Essential Psychopharmacology: The Prescriber's Guide". Cambridge University Press, 2006. On Page 325. —Preceding unsigned comment added by 69.133.155.151 (talk) 23:38, 5 February 2011 (UTC)

What?-of course mirtazapine is a tetracyclic-it can, of course be described in other ways-but it has four ring systems, therefore, it is chemically a tetracyclic. Being "tetracyclic" does not infer any specific mode of biological activity, it is just a chemical classification. Dehughes (talk) 01:11, 26 October 2011 (UTC)

Ineed, it is both a TeCA and a "NaSSA", the former describing its chemical structure, and the latter describing its pharmacological profile. el3ctr0nika (Talk | Contribs) 03:18, 27 October 2011 (UTC)

Factual error in Interactions section:

Interactions paragraph states: "As a serotonin receptor antagonist, mirtazapine will not cause serotonin syndrome at any dose"

I am taking Mirtazapine and the inbox leaflet for "Mirtazapine 15, 30 and 45mg Orodispersible tablets" produced bt Teva UK ltd (leaflet last approved feb 2009) clearly states: (copied exactly as written in leaflet) If you experience a high temperature, muscle stiffness or twitching, confusion, irritabilty and extreme agitation, you must contact your doctor immediately as these symptoms may be an indication of so called seretonin syndrome. Although this syndrome only occurs very rarely, it can be life-threatening.

Forgive me if I've done something in error but I thought a life-threatening consequence needs correcting. 94.10.21.251 (talk) 12:17, 17 March 2010 (UTC)

I believe that is a standard boilerplate warning that goes with all anti-depressants. Sort of like how with Vyvanse, a sustained release amphetamine, there are instructions not to chew or crush the pills, something that makes no sense b/c vyvanse is already a powder and it is a pro-drug so crushing it doesn't cause it to be released into your bloodstream any faster. Pharmacists are stupid -- anyone with an eighth grade education could do their job. Pharmacists tend to have blind faith re: the package insert, not knowing enough about the underlying science to challenge something that is obviously wrong. Once I had a pharmacist try to not dispense seroquel until checking with my doctor b/c of a supposed risk of serotonin syndrome. I was able to browbeat him into just giving it to me without checking, because the concern was silly and unfounded, but the guy was just following the written instructions like a mindless robot.

In any event, if you see my post below, I think that the section on serotonin syndrome is inaccurate... but probably only at the margins, and certainly not based on "evidence" provided by the package insert...PStrait (talk) 22:52, 5 June 2010 (UTC)

According to Hexal (a Mirtazapine manufacture) mirtazapine should not be taken with any MAOIs and should be used only carefully with SSRIs and venlafaxine(i.e. Effexor). Recently I started taking 15mg mirtazapine with my daily dose of effexor and after only 2 doses of mirtazapine I showed strong symptoms of Serotonin Syndrome. Do not use wikipedia as a safe source for medical information and always the package insert. It is NOT just standard BS as some might have you believe — Preceding unsigned comment added by 212.242.226.71 (talk) 16:17, 1 July 2011 (UTC)

To the poster above, you shouldn't crush Vyvanse because it can make you nauseous. — Preceding unsigned comment added by Astrohoundy (talk • contribs) 09:29, 5 December 2011 (UTC)

Pharmacology contradiction?

In the pharmacodynamics table, the drug is listed as a NET blocker in the micromolar range, but the same section then goes on to state "Unlike most conventional antidepressants, however, mirtazapine is not a reuptake inhibitor and has no appreciable affinity for the serotonin, norepinephrine, or dopamine transporters...". I notice that the NET affinity is an order of magnitude at least lower than the receptor affinties listed. I haven't changed anything though because this isn't my subject and that K_i value may well be insignificant at the drug's normal dosage, but it still sounded like a possible mistake to me. Psymun (talk) 19:14, 22 March 2011 (UTC)

I originally put that in just for exclusiveness's sake, despite it being much low to be significant. In any case, I've removed it. el3ctr0nika (Talk | Contribs) 17:26, 16 April 2012 (UTC)

Also pharmacodynamics "Mirtazapine is an antagonist/inverse agonist..." then the following paragraphs proceed to only mention antagonism. its either an antagonist or an inverse agonist it cant be both — Preceding unsigned comment added by Dimesnake (talk • contribs) 22:47, 11 September 2011 (UTC)

Actually it can be and in fact is. Mirtazapine is an inverse agonist at certain receptors such as H₁ while it is an antagonist at others like α₂-adrenergic and 5-HT₃. el3ctr0nika (Talk | Contribs) 17:26, 16 April 2012 (UTC)

Primary research

This article like all others should be based on review articles not primary research. Doc James (talk · contribs · email) 14:32, 11 July 2011 (UTC)

We have issues with the POV of this article for example we say it is useful for itching yet support this only with primary research (one study looked at only 4 patients, the other was a pilot). One cannot draw this conclusion based on the evidence provided. Thus the POV tag.--Doc James (talk · contribs · email) 05:33, 21 July 2011 (UTC)

I think that parts of this must have been written by drug reps or something. The sentence about mirtazapine not causing serotonin syndrome is pure rubbish; if you type the words "mirtazapine" and "serotonin syndrome" into Pubmed or the like, you will find many incidences of serotonin syndrome caused by mirtazapine monotherapy and in combination with other drugs. Hopefully PStrait from above reconsiders what (s)he says, and perhaps does some research into exactly how mirtazapine works before offering dangerous advice. Chairman Xi (talk) 12:18, 24 August 2011 (UTC)

"Any (over)dose, no serotonin syndrome" has been removed as unsourced wikiality. Alessandra Napolitano (talk) 04:48, 17 November 2011 (UTC)

I'm a bit wary of claims that relatively recent drugs have no longer term adverse effects or withdrawal issue, have to be pragmatic, we don't really know but there's no obvious reason to suspect a big problem. That said it was over ten years after SSRI medication became available before the discontinuation issue was acknowledged, and I've got personal experience of the dependency/withdrawal problems Tramadol can deliver, that being another drug that was supposed to be free of such things until it turned out not to be. Got to be very careful about confidently asserting something is safe or free of a problem, especially if even the drug company/pharmacist/GP is being cautious. Well, more importantly, as someone above said, don't get your medical advice from wikipedia! — Preceding unsigned comment added by 94.8.124.250 (talk) 18:31, 1 September 2011 (UTC)

The article contains a good deal of synthesis from primary sources, like binding assays, rat and mouse experiments. I have added the species in such cases and added fact tags. What we need is not conjectures by the editors from a variety of speculative primary sources and lab experiments, but peer reviewed clinical review articles. Otherwise such results belong into a separate section "animal and cell research", not with a discussion of clinical pharmacology, if at all into the article. Ihave also deleted a self-published ref due to WP:MEDRS, regardless who the researcher is. 70.137.154.143 (talk) 21:27, 22 September 2011 (UTC)

Wouldn't it be nice if we had review articles to support every single point? Because this is a narrow topic (not like, say, selective serotonin reuptake inhibitor), we can't, and won't. Reviews are preferred, but where unavailable, or not yet found by editors, we have the sources we have. Rest assured that academic peer review normally doesn't let any sort of nonsense be published in respected journals, Sokal affair notwithstanding. Alessandra Napolitano (talk) 04:48, 17 November 2011 (UTC)

I think 70.137.154.143 has a reasonable suggestion concerning segregating material about in vitro and in vivo animal research from anything that concerns humans (clinical trials or even speculations about what might happen in humans). IMHO, WP:SCIRS applies to the former while WP:MEDRS applies to the later. WP:SCIRS has a more permissive attitude towards high quality peer reviewed primary sources while WP:MEDRS for good reason insists on secondary sources. (I realize that WP:SCIRS has not been promoted to a guideline, but nevertheless I think it takes a balance and sensible approach to identifying reliable sources in the natural sciences.)

Furthermore, I believe that the Mirtazapine#Binding_profile and Mirtazapine#Chemistry sections falls under the scope of WP:SCIRS and not WP:MEDRS. In contrast, the section on Mirtazapine#Correspondence_to_clinical_effects I believe falls under the scope of WP:MEDRS. There are currently a lot of primary sources in this article, many of them in sections were they really should not be. Hence I would support a reorganization of this article to more cleanly separate the in vitro and animal experiments from the clinical observations. Boghog (talk) 20:22, 16 April 2012 (UTC)

Withdrawal "Equivalency"

I have removed the following from the article under Discontinuation:

"It should be noted that withdrawal effects from most psychoactive drugs are common, but generally lack certain characteristic features such as cravings and are less severe than those of drugs typically associated with withdrawal syndromes such as alcohol, benzodiazepines, and opioids."

I can't comment on the portions regarding withdrawal from benzodiazepines or alcohol, but I have experienced both very-high-dose Prozac withdrawal and withdrawal from several different opioids at very high doses, including morphine, oxycodone, and fentanyl. The idea that antidepressant withdrawal is less severe than opioid withdrawal or lacks drug cravings is simply WRONG. I am absolutely certain I am not the only person with this comparative experience. I do not believe the science in the references is sound as I am not aware of any studies concerning people like myself who have experienced both phenomena and therefore are in the best position, if anyone at all is, to make a call about something so subjective as which of them are "worst". In any event the whole sentence seems like a drug company spin control thing, just like their insistence on the use of the term "discontinuation syndrome" instead of the honest scientific term "withdrawal". If reasonable people in sound logic conclude I am wrong in this, put it back, but for the sake of accuracy, at least remove the reference to opioids, as I can tell you from experience that it is absolutely wrong. Opioid withdrawal is a special kind of hell, but it doesn't make you feel like your nervous system is tearing itself apart at the seams as antidepressant withdrawal can. There's no sense of water sloshing around in your head or electric zaps that go down your arms or legs or spine or all at once when in opioid withdrawal. Honestly, though, like I said before, I think the whole idea of comparing withdrawal symptoms and deciding that some are "worse" than others is deeply subjective and therefore specious to include in an article on a site like Wikipedia.

References

-- 75.18.179.81 (talk) 11:11, 30 August 2012 (UTC)

Mirtazapine and paralysis

Neurological symptoms may happen while taking mirtazapine. This should be stated.(strange it is not mentioned and developed) On Jun, 25, 2011: 9,884 people reported to have side effects when taking Mirtazapine. Among them, 18 people (0.18%) have Paralysis.(http://www.ehealthme.com/ds/mirtazapine/paralysis) It is also reported in http://www.druglib.com/adverse-reactions_side-effects/mirtazapine/seriousness_disabling/ Often (but not always it seems) the condition is triggered by an association of mirtazapine with other drugs ( 1. Depromel 2. Rohypnol 3. Remeron 4. Vegetamin b 5. Lexotan) What I would like to know is if this paralysis is reversible or not. (Nothing being mentioned, I suspect irreversible) — Preceding unsigned comment added by 109.89.68.228 (talk) 18:04, 12 July 2011 (UTC)

Remeron IS mirtrazapine, so it does not qualify as an "other drug".--Bstard12 (talk) 02:20, 16 January 2013 (UTC)

2012-03-21

I've experienced something like paralysis when using Mirtazapine (7.5 mg, once daily) together with generic Dextroamphetamine (2.5 mg, 4-5 times daily). It only happens when I've slept too little for a long time, in other words when I'm exhausted. It usually only happens when I'm about to fall asleep, but has sometimes occurred just for a split second when I'm standing and feel sleepy. I lose muscle control before my mind starts sleeping, which best can be described as a feeling of falling.

An excellent idea would of course be to test if the symptoms disappear if I use only Mirtazapine without the amphetamine. However, that would make me unable to focus on work tasks, because of my ADHD. It happens very seldom and only when I've not slept enough. At least this specific form av paralysis (sleep paralysis?) is reversible, for me.

/JvA — Preceding unsigned comment added by 194.218.4.2 (talk) 10:42, 21 March 2012 (UTC)

Orphaned references in Mirtazapine

I check pages listed in Category:Pages with incorrect ref formatting to try to fix reference errors. One of the things I do is look for content for orphaned references in wikilinked articles. I have found content for some of Mirtazapine's orphans, the problem is that I found more than one version. I can't determine which (if any) is correct for this article, so I am asking for a sentient editor to look it over and copy the correct ref content into this article.

Reference named "Lancet":

• From Quetiapine: Leucht S, Cipriani A, Spineli L, Mavridis D, Örey D, Richter F, et al. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. The Lancet [Internet]. 2013 Jun 27 [cited 2013 Sep 19];382(9896):951–62. Available from: http://www.sciencedirect.com/science/article/pii/S0140673613607333
• From Ziprasidone: Leucht S, Cipriani A, Spineli L, Mavridis D, Örey D, Richter F, et al. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. The Lancet [Internet]. 2013 [cited 2013 Sep 29]; Available from: http://www.sciencedirect.com/science/article/pii/S0140673613607333
• From Aripiprazole: Leucht S, Cipriani A, Spineli L, Mavridis D, Örey D, Richter F, et al. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. The Lancet [Internet]. 2013 Jun 27 [cited 2013 Sep 17];382(9896):951–62. Available from: http://www.sciencedirect.com/science/article/pii/S0140673613607333
• From Paliperidone: Leucht S, Cipriani A, Spineli L, Mavridis D, Örey D, Richter F, et al. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. The Lancet [Internet]. [cited 2013 Sep 30]; Available from: http://www.sciencedirect.com/science/article/pii/S0140673613607333
• From Haloperidol: Leucht S, Cipriani A, Spineli L, Mavridis D, Örey D, Richter F, et al. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. The Lancet [Internet]. [cited 2013 Sep 29]; Available from: http://www.sciencedirect.com/science/article/pii/S0140673613607333
• From Ginkgo biloba: Schneider, L. S. (2012). "Ginkgo and AD: Key negatives and lessons from GuidAge". The Lancet Neurology. doi:10.1016/S1474-4422(12)70212-0.

I apologize if any of the above are effectively identical; I am just a simple computer program, so I can't determine whether minor differences are significant or not. AnomieBOT⚡ 13:37, 5 October 2013 (UTC)

Misleading placement of sleep apnoea under 'Medical uses'

Two references are cited for it's inclusion. The first (http://informahealthcare.com/doi/abs/10.1517/13543780902877674) doesn't mention it in the abstract, and the second (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2442407/) had negative results.

Xbao (talk) 10:02, 16 April 2015 (UTC)

Citation link incorrect

The citation link referenced 112 leads to the wrong page but I don't know how to change it. The correct URL is http://neuro.psychiatryonline.org/doi/full/10.1176/jnp.23.1.jnpe7 MarpoHarks (talk) 19:23, 21 September 2016 (UTC)

thanks, yes it was incorrect. i've removed it as it is a case study and weight gain was discussed in the very next ref cited. Jytdog (talk) 20:19, 21 September 2016 (UTC)

Thanks Jytdog! MarpoHarks (talk) 20:21, 21 September 2016 (UTC)

External links modified

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Remeron name

The IP has said several times that the brand name Remeron was chosen because of the effects on REM sleep. I have looked for a ref for that and have not found one. Would be interested to see it. (it makes sense and seems worth adding in the history section, but we need a ref) Jytdog (talk) 16:34, 22 July 2017 (UTC)

http://www.psychiatrictimes.com/sleep-disorders/effects-antidepressants-sleep

http://www.aafp.org/afp/2011/1101/od1.html

http://oxfordmedicine.com/mobile/view/10.1093/med/9780199674558.001.0001/med-9780199674558-chapter-9

https://www.sleepio.com/articles/sleep-aids/mirtazapine-and-sleep/

https://link.springer.com/article/10.2165/00023210-199911010-00005

https://pubchem.ncbi.nlm.nih.gov/compound/mirtazapine

https://selfhacked.com/blog/mirtazapine/

Also check out the above selfhacked link's external references for other uses of Mirtazapine (memory helping & nootropic - other studies also done for the same). — Preceding unsigned comment added by 112.79.153.91 (talk) 14:17, 22 August 2017 (UTC)

I looked at the reliable ones - not the ones like selfhacked -- and not a single one of them says that drug was named remeron because of its effects on REM sleep. I do not take kindly to having my time wasted, and I am not going to waste my time looking at other refs you cite in the future. Jytdog (talk) 00:06, 23 August 2017 (UTC)

Mirtazapine for veternary use

The article says Mirtazapine may be given cats or dogs to increase their appetite under certain conditions. Is this wellknown to an average vet or would he/she consider me to be lunatic if I asked for the appropriate dose? Or does anyone know how to calculate? --BlaueWunder (talk) —Preceding undated comment added 14:50, 25 June 2017 (UTC)

Does Mirtazapine really posses serotonergic action?

I think it's disputed:

A systematic review of the serotonergic effects of mirtazapine: implications for its dual action status. (2006). Gillman, P. K. Human Psychopharmacology. Clinical and Experimental 21: 117-125. https://www.ncbi.nlm.nih.gov/pubmed/16342227?dopt=Citation

• http://psychotropical.info/mirtazapine-dubious-evidence
• http://psychotropical.info/mirtazapine-a-paradigm-of-mediocre-science

--80.171.149.187 (talk) 05:28, 7 July 2017 (UTC)

The blogs are not useful. The Gillman ref is. I will post at WT:PHARM to see if someone wants to try to tackle this. It is complex to handle. Jytdog (talk) 14:11, 7 July 2017 (UTC)

Agree that the Gillman review is a valid source, but Gillman's views are not accepted by other valid sources. I think the best thing to do it to discuss Gillman's claims briefly but not allow them to dominate the article. Looie496 (talk) 15:32, 7 July 2017 (UTC)

@Looie496 Indeed, that sounds like a good idea... --78.50.179.210 (talk) 20:17, 8 July 2017 (UTC)

Responding from WT:PHARM, I'm not that familiar with the source material for mirtazapine, but I'm reasonably familiar with mianserin, and there certainly are a preponderance of sources that consider it to be at least in part serotonergic. All of these drugs have incredibly complex multi-receptor actions, so we should err on the side of not giving too much weight to single sources that assert less complex modes of action. --Tryptofish (talk) 20:13, 7 July 2017 (UTC)

I've definitely seen reviews indicate that it has 5-HT3 antagonism. TylerDurden8823 (talk) 01:18, 8 July 2017 (UTC)

5-HT2A and 2C antagonism at human GPCRs is listed by IUPHAR, with comparable affinity to its action at adrenergic receptors (see link). IUPHAR also states "Mirtazapine has affinity for several GPCRs, but has highest measurable affinity for the α2-adrenoceptors (IC50 order of potency: 2A>2C>2B [2]) and the serotonin 5-HT2A and 5-HT2C receptors (Ki order of potency 2C>2A>7>1A [1,3])." DrugBank lists 5-HT2A and 5-HT3A as receptors at which it is known to have pharmacological activity as an antagonist, citing human studies (see link). HMDB lists the 5-HT-2A, -2C, and -3A receptors as active targets (see link). I don't feel like sifting through and summarizing all of the bindingDB entries, but it clearly lists several serotonin receptors with pharmacological activity for mirtazapine in homo sapiens in this link.

So, in conclusion, yes, mirtazapine really does posses serotonergic action in homo sapiens based upon these four databases which aggregate binding data from research articles. Seppi333 (Insert 2¢) 23:32, 8 July 2017 (UTC)

antagonistic activity, not agonistic activity. There is a huge difference... --78.50.179.210 (talk) 09:53, 9 July 2017 (UTC)

I didn't realize until I saw your comment that you are talking specifically about serotonergic agonism, not serotonergic activity in general. This is a more specific question, and obviously it cannot be directly answered by binding studies alone. So could it be an antagonist at some 5-HT receptor subtypes, but be, or not be, an agonist or partial agonist at another subtype? I don't know. --Tryptofish (talk) 17:06, 9 July 2017 (UTC)

If this issue pertains solely to receptor agonism, then the question wasn't really worded that well because the term "serotonergic" implies any pharmacological effect that directly impacts serotonin neurotransmission. Seppi333 (Insert 2¢) 00:52, 10 July 2017 (UTC)

You are right, in a way. My problem is that most people assume that "serotonergic activiy" implies the possibility of Serotonine Syndrome when combined with other "Serotonergics", but it's not that simple, because it depends on if it's agonism, antagonism, inverse-agonism and so on. Sorry for my imprecise question ;=) --78.54.135.223 (talk) 03:32, 10 July 2017 (UTC)

According the the sources cited in the Interactions section, it's apparently very unlikely to elicit serotonin syndrome. (That actually does not prove anything about agonism, because agonism or partial agonism can be masked by effects at other receptors, such as noradrenergic.) --Tryptofish (talk) 20:07, 10 July 2017 (UTC)

Refs about hypnotic

User:112.79.141.7 thanks for providing updated refs in this this dif. You also added content there, in the Pharmacology section, that wasn't about pharmacology. I used the refs to replace old/outdated ones in the medical use section, in these diffs. You have now added back the content and the already-used refs twice, here and here, without giving policy-based reasons. Please discuss. Thanks. Jytdog (talk) 16:24, 11 July 2017 (UTC)

Mirtazapine's specific inaction on REM sleep is a rare psychopharmacological effect often talked in discussions about hypnotics. So its wiki page having no mention of sleep architecture would be a waste. REMeron wasn't named remeron just like that. So my wordings from the citations themselves are very relevant, and I would say important to Mirtazapine page. — Preceding unsigned comment added by 112.79.141.20 (talk) 16:29, 11 July 2017 (UTC)

Thanks for your reply. There are other people who watch this page; lets see what they have to say about the content and where it might belong. Jytdog (talk) 16:34, 11 July 2017 (UTC)

the ref added here was a primary source; we don't use them per MEDRS. Jytdog (talk) 17:01, 11 July 2017 (UTC)

Lift off?

While looking at the interactions section of the page, I saw the link to the page on California rocket fuel, and that page strikes me as not worth a standalone page. We don't need a dictionary-ish definition of what appears to be a rather obscure slang term.

I propose that we make California rocket fuel a redirect to Mirtazapine#Interactions, where the term gets about as much coverage as it does on the standalone page. --Tryptofish (talk) 20:14, 10 July 2017 (UTC)

Well, now that the IP has so emphatically removed their comment, I want to ask everyone else: are there any objections to going ahead with this? --Tryptofish (talk) 16:24, 12 July 2017 (UTC)

not from me. may want to do something on the other ingredient pages? Jytdog (talk) 18:26, 12 July 2017 (UTC)

Yeah, that occurred to me too. Obviously, I can't have a redirect go simultaneously to two pages. Venlafaxine is the other ingredient, and I'm not seeing a mention of California rocket fuel there, but the lead includes "A combination of venlafaxine and mirtazapine...", so it will link here. --Tryptofish (talk) 18:46, 12 July 2017 (UTC)

 Done. --Tryptofish (talk) 23:15, 17 July 2017 (UTC)

hay fever, comparative information

User:112.79.162.224, about this - the cochrane review is great, thanks for bringing it, but you didn't summarize it well. You also included a lot of primary sources behind that. The content about allergy/hay fever was not supported by MEDRS sources; I looked at pubmed and found nothing about using this drug for that purpose. Jytdog (talk) 04:22, 21 July 2017 (UTC)

request

Requesting full edit protection for vandalism, edit wars and deletion of MEDRS sourced citations and content. — Preceding unsigned comment added by 112.79.155.168 (talk • contribs)

Not done: requests for increases to the page protection level should be made at Wikipedia:Requests for page protection. DRAGON BOOSTER ★ 15:25, 22 July 2017 (UTC)

2010 UK Study

2010 follow up study comparing 14 antidepressants meets all MEDRS criteria and is fairly comprehensive if one takes time to read it. Yes Jytdog you have completely removed all mention of it along with 2009 study. 2009 study can be replaced as it is outdated. But 2010 study with statistically significant results needs to be mentioned if those are also mentioned for escitalopram, venlafaxine and sertraline. If I revert your edit you will claim edit war. Double standard here. For some reason it seems you are portraying that you really have no interest in the improvement of this particular article. You only seem interested in downgrading the page so that you don't have to monitor it at all. I am not being personal here and not even attacking you, but last few edits are really COI and POV based reeking of bias, at least from an outside perspective. Do you have COI here? — Preceding unsigned comment added by 112.79.142.13 (talk) 09:04, 22 July 2017 (UTC)

Please read the entire NICE study and its recommendations. I quote "There is evidence suggesting that there is a statistically significant difference favouring mirtazapine over SSRIs on reducing symptoms of depression by the end of treatment, but the size of this difference is unlikely to be of clinical importance". Also "There is evidence suggesting that there is a statistically significant difference favouring mirtazapine over other antidepressants on increasing the likelihood of achieving remission by the end of treatment as measured by the HRSD".

"There is strong evidence suggesting that there is a clinically important difference favouring mirtazapine over other antidepressants on reducing the likelihood of patients leaving treatment early due to side effects (K � 15; N � 2637; RR � 0.69; 95% CI, 0.55 to 0.87)." Results from NICE Study "Mirtazapine appears to be the most cost-effective option among those assessed for both moderate and severe depression, producing the highest number of QALYs and the lowest costs among all drugs assessed (dominant option)." — Preceding unsigned comment added by 112.79.142.13 (talk) 09:15, 22 July 2017 (UTC)

Just comparing it with SSRIs doesn't make sense now since SSRIs are a generation behind the more commonly prescribed SNRIs and a generation behind Mirtazapine (except escitalopram). So the statistical evidence of comparison of 14 most commonly prescribed treatments should be mentioned as I had mentioned. — Preceding unsigned comment added by 112.79.142.13 (talk) 09:23, 22 July 2017 (UTC)

I think I will go ahead and request page protection of Mirtazapine from harmful edits. 112.79.142.13 (talk) 11:14, 22 July 2017 (UTC)

User:112.79.142.13, about this:

A 2010 NICE study comparing 14 most common antidepressants found Mirtazapine as the most efficacious and cost-effective treatment for moderate to severe depression.

References

The table you are citing, is directly from the Cipriani et al. (2009) ref.

What NICE itself recommends, is described now in this article via this diff, which I will quote below:

NICE published a guideline for treating depression that included a review of antidepressants. It recommended generic SSRIs as first line choices, as they are "are equally effective as other antidepressants and have a favourable risk–benefit ratio." With respect to mirtazapine, it found: "There is no difference between mirtazapine and other antidepressants on any efficacy measure, although in terms of achieving remission mirtazapine appears to have a statistical though not clinical advantage. In addition, mirtazapine has a statistical advantage over SSRIs in terms of reducing symptoms of depression, but the difference is not clinically important. However, there is strong evidence that patients taking mirtazapine are less likely to leave treatment early because of side effects, although this is not the case for patients reporting side effects or leaving treatment early for any reason."

With regard to the economic analysis section, the NICE paper says the following:

These findings highlighted the need for de novo economic modelling for this guideline. The objective of economic modelling was to explore the relative cost effectiveness of antidepressants for people with depression in the current UK clinical setting, incorporating the results of a recently published network meta-analysis (Cipriani et al., 2009), as described in Section 10.11.....The choice of interventions assessed in the model was determined by the antidepressants included in the network meta-analysis by Cipriani and colleagues (2009).

... 10.12.6. Conclusions

The findings of this preliminary economic analysis suggest that mirtazapine might be more cost effective than other antidepressants in the treatment of people with moderate and severe depression and support the findings of Cipriani and colleagues (2009) regarding the clinical superiority of mirtazapine. However, these economic findings are subject to considerable uncertainty arising from the limitations of the current model and lack of incorporation of data on the relative adverse effects of the drugs in the model. Addressing these issues may alter the outcome of the model.

The two key things from this are:

1. The authors were developing a model and used the Cipriani analysis as a basis for that
2. The authors themselves do not consider the results definitive, and indeed the final recommendations for drug selection do not take this analysis into account. NICE recommends SSRIs as first choice drugs.

We cannot give more WEIGHT to this part of the NICE analysis, than NICE itself did. Please stop doing that.

The Cipirani study was published in 2009 and that is now too old per MEDDATE. Even the 2010 NICE study and the 2011 Cochrane review are too old but those are the most recent things we have. And they do not agree at all with the content you keep trying to add in that mirtazapine is The Best. The content you are adding, that I cited at the top of my response, misrepresents what NICE actually recommends.

Also please stop capitalizing the name of the generic drug. =

References

Jytdog (talk) 14:15, 22 July 2017 (UTC)

Have you read the 'Results' section, at all? What you are citing is the discussion and by saying they were developing the model you have completely ignored the 2009 study which was the basis of the 2010 study.

Results from NICE Study "Mirtazapine appears to be the most cost-effective option among those assessed for both moderate and severe depression, producing the highest number of QALYs and the lowest costs among all drugs assessed (dominant option)."

Is that wrong? Or am I just an idiot and you have all the better info right? — Preceding unsigned comment added by 112.79.155.168 (talk) 14:26, 22 July 2017 (UTC)

As I noted above, you are accurately quoting a section of the NICE recommendations, but a) that section itself notes that it was modelling things and that its results were provisional and b) the actual recommendations for drug selection do not reference that work at all. The actual recommendation for 1st line treatment are SSRIs. You cannot make it seem as though NICE recommended something that it did not or that NICE itself found the economic analysis very important (again, NICE itself did not use it, in the recommendations it made in the same document). We call the problem you are creating WP:UNDUE. Jytdog (talk) 15:34, 22 July 2017 (UTC)

Official Request for full page protection has been raised at the Page protection requests. Please don't edit the page further as this would constitute an edit war for which I will be notifying respective admins and also for possible case of COI. — Preceding unsigned comment added by 112.79.155.168 (talk) 14:39, 22 July 2017 (UTC)

@Fuse809 The NICE study of which the tables are a part of include 14 most common antidepressants including St. John's Wort.

Why wouldn't a drug name be a proper noun? The word has no other connotation or usage. Its like the name of a person. It's not a common thing so its not a common noun. Original and non-repetitve names are proper noun by convention. — Preceding unsigned comment added by 112.79.155.168 (talk) 15:10, 22 July 2017 (UTC)

We do not capitalize generic drugs names anywhere in Wikipedia. They are not proper nouns any more than "book" is a proper noun. Jytdog (talk) 15:31, 22 July 2017 (UTC)

Weight gain

Is listed as one of the common side effects. Not sure why it was removed?

Mechanism of action is listed as unknown, not sure why that was removed?

Which ref says it is often used with venlafaxine?

Why is this notable " it is closely related to mianserin" enough for the lead?

Doc James (talk · contribs · email) 21:49, 9 December 2018 (UTC)

Common side effects

Not sure why "dizziness" was removed? Ref says "Common Adverse Effects: Somnolence, increased appetite, weight gain, dizziness." Doc James (talk · contribs · email) 15:17, 12 April 2019 (UTC)

Sleep

Does it help with sleep 2A02:C7C:523F:1400:ED3E:7BFE:50E2:BDCC (talk) 09:59, 11 July 2023 (UTC)