Talk:Escitalopram/Archive 2

Archive 1

Archive 2

Addiction

This article sidesteps the issue of addiction. It should be made clear whether Lexapro is addictive or is not addictive, but instead the issue is mostly avoided and partly finessed.

Prescription drug addiction is no joke-- it is not like other kinds of 'mild' addictions--

Prescription drug addiction does tremendous damage to peoples lives and a lot of medical schools don't teach the full story about addiction (the implicit message is-- it's OK to turn a patient into an addict in order to 'treat anxiety or depression'). This is not so. Anxiety and depression can be successfully treated through therapy and / or non-addictive meds and there is NEVER a good reason to turn an anxiety or depression patient into a prescription drug addict in order to 'help' them.

The pharmaceutical industry is one of the most powerful and corrupt political lobbies in the country. Pharmaceutical company executives who try to cover over or minimize the harm caused by prescription drug addiction (and irresponsible Doctors who do the same) should be prosecuted. Any Doctor or Psychiatrist who thinks it's OK to turn a psych patient into a drug addict should have to spend years in jail. Ditto for drug company execs who do the same.

Sean7phil 19:45, 5 May 2007 (UTC)

128.138.230.144 19:39, 5 May 2007 (UTC)

To quote SSRI discontinuation syndrome, which is linked from this article and does address the issue:

SSRIs are not addictive in the conventional medical use of the word (i.e. animals given free access to the drug do not actively seek it out and do not seek to increase the dose), but suddenly discontinuing their use is known to produce both somatic and psychological symptoms, as described by researchers.

None of the symptoms listed in the article on discontinuation seem to be actively life-threatening either (unlike withdrawal of many genuinely addictive drugs), though some may be quite hard to bear.

Of course antidepressants and other such drugs should not be prescribed lightly by any means, and I do agree that the pharmaceutical industry is one of the most powerful and corrupt political lobbies, though I disagree that its malignant influence is limited to just your country (or indeed your continent). I disagree with your When-I-am-King penalties for doctors and psychiatrists, though. There are unfortunately many cases where turning the patient into an addict is better than any alternative course of action, and may even be the only feasible one. However, those who would make this decision lightly in cases where addictive medication is not the only feasible option should in my opinion have their licence to practise medicine revoked, at the very least.82.111.241.126 08:38, 15 October 2007 (UTC)

Withdrawal symptoms are not synonymous with addiction with regards to prescription drugs. Simple as that. Wisdom89 08:41, 15 October 2007 (UTC)

I'm pretty sure that withdrawal symptoms can be synonymous with addiction in regards to prescription drugs. I know people addicted to oxycontin who want to stop taking it but can't because they can't deal with the physical withdrawal it will cause them to go through. I know people who hate taking xanax every day but continue to do so because they've felt how bad the withdrawal is and they fear it. Also, how many cigarette smokers do you know that "want to quit" but don't, or can't, because they give in to withdrawal. That's obviously addiction, and to say that withdrawal symptoms can't be synonymous with addiction just because the drugs are prescribed, is ridiculous. The article severely side-steps the issues of addiction. —Preceding unsigned comment added by 24.251.185.162 (talk) 04:58, 31 May 2009 (UTC)

Addiction is not a medical term. Addiction is a term that is easily identifiable to the lay person and connotes all the negative things that one thinks of when using that term: seriously impaired functioning, neglect of responsibility, social decline, etc. Medically, one speaks of "dependence." Substance dependence is similar to the idea of "addiction" and requires meeting certain criteria which I won't list for the sake of brevity. However, impaired functioning is a central idea, as is the use of increased amounts of the substance. While depressed patients may require an increased dose of an SSRI for optimal efficacy, there is not a steady increase or a desire to seek out more and more of the substance. Furthermore, the goals of this drug is to increase one's daily functioning and generally does not limit it. By this definition, SSRIs are not "addictive." Then there is the matter of physiologic dependence, which requires tolerance or withdrawal. SSRIs do not exhibit tolerance. Now, concerning withdrawal, I will give an example that I think illustrates my point well. Older antihypertensive medications can cause rebound hypertension after sudden discontinuation, yet most people don't consider this a "withdrawal" symptom. It is the same with SSRIs. The symptoms that are felt in discontinuation syndrome are simply what occurs when your body re-adjusts itself to pre-medication metabolism, much like what happens in the rebound hypertension with clonidine, or even the rebound congestion with a short course of phenylephrine. To label these substances as "addicting" I think casts them in an undeserved shadow in that it only provides more resistance to a class of drugs that is already a tough sell to some people. This is even more a shame when you consider the fact that these drugs are effective in reducing symptom severity of a common and incapacitating disease, and do so with relatively benign side effects. Even all this argument seems to rest on the fact that discontinuation syndrome is unavoidable. It is easily treated by an easy taper of the medication in use. As both a doctor and a patient who has been treated for severe depression, I don't think SSRIs should be classified as addictive substances. —Preceding unsigned comment added by 98.109.159.82 (talk) 22:57, 7 March 2010 (UTC)

The previous commenter is 100% correct (maybe even more than that :) ). SSRIs are not addictive. People don't have urges to take more as they do if they become addicted to a drug like nicotine or heroin. Specific withdrawal symptoms (frequently known as SSRI discontinuation syndrome in this case; I'll shorten this to "DS") don't equate to addiction, which is not, in any case, a medical term (although it is unfortunately used carelessly by many doctors). SSRI DS can, as the previous commenter notes, be minimized or even eliminated by simply tapering off slowly and carefully. This is a common difficulty with these medications, but it's just like a side effect; it's not a sign of substance dependence, which is considered a mental disorder (and a notoriously hard-to-treat one at that). The same is true of many other drugs; some of them can be addictive (such as opioid pain medications), but experiencing a DS if you stop taking them abruptly after taking them frequently for a while doesn't automatically make you an addict, as it is a perfectly normal and expected reaction; tapering off slowly, sometimes after substituting a longer-acting drug of the same class, is usually the way to deal with this problem (provided there isn't an addiction *as well*). Addiction, or substance dependence (to use the "medically correct" term), has to do with the feeling of constantly wanting the drug, and difficulty controlling one's use of it; people often describe a sense of "craving." This is something I, at least, have never heard of with SSRIs or other thymoleptic/antidepressant drugs. Substance dependence really is not a matter of whether there is a specific DS or not, although the DS is sometimes part (but not all) of what makes it difficult for people to stop. In some cases, as for example with heroin, it is the out-of-control use of the drug that is more dangerous (because of the risk of overdose), while the DS, although certainly very painful and unpleasant physically and emotionally, is not actually life-threatening.

Regarding Xanax dependence: sometimes people find it easier to switch to a longer-acting benzodiazepine like Klonopin and then discontinue it. Discontinuation effects are a very unfortunate but normal side effect of this class of drugs. Unfortunately they can be life-threatening due to the possibility of seizures (particularly with the higher doses sometimes required in the treatment of panic disorder, although the benzodiazepines are still much safer than the older barbiturates, which are seldom used in outpatient settings anymore because of their many risks). I should note that this is pharmacologic dependence, *not* necessarily addiction or substance dependence (the mental disorder). You're confusing the nicotine cravings that smokers experience (which *are* a sign of pathological dependence or "addiction") with a DS, which could be seen as simply a kind of physiological rebound (for example, rebound insomnia and anxiety that a long-time user of Xanax would almost certainly experience if they tried to stop abruptly; or the examples the previous commenter offered: antihypertensives and decongestants). A question to ask is: is this a specific reaction to discontinuing this drug, or is it a general feeling of wanting or craving it? It isn't as obvious as you think that your friends are addicted to their sleeping pills or pain medications (although it is possible; there's not enough information to know for sure). Contrary to myth, plenty of people take these medications without becoming addicted; discontinuing them after your body has become used to them will lead to a rebound reaction or DS whether or not you are addicted. Unfortunately, some doctors may improperly assume patients are abusing medication if they have trouble stopping it because of a normal DS, and patients may be afraid to talk their doctors about difficulties they are having with the DS because they think it means they are addicted, or are afraid the doctor will think so. A good doctor will be able to help a patient taper off the medication with minimal discomfort and will not treat it as a failure on the patient's part.

To the previous poster: there is a phenomenon I've sometimes heard described as antidepressant tolerance, but I'm not sure if that's quite an accurate description: I've also heard the more colloquial description "poop-out" which seems a bit more descriptive. It isn't the same as the tolerance people sometimes experience with sleeping pills, say, where they gradually become less effective, resulting in a constant need to increase the dose. Instead, the antidepressant just stops working and as far as I know, increasing the dose doesn't help. I've heard sometimes adding adjunctive medications (like lithium or aripiprazole) may get the patient responding again. 174.111.234.195 (talk) 20:17, 1 September 2011 (UTC)

if you get withdrawl without it, it's addictive. Duh. 170.3.8.253 (talk) —Preceding undated comment added 15:12, 2 August 2012 (UTC)

The list

@Zxcv9:, what exactly was the problem with this edit? You need to give a reason for your revert, WP:BRD is not a reason (WP:BRD-NOT). I think their edit was justified well.

(I'm here because I edited this article when I was using this medication, and it has since been on my watchlist.) — Jeraphine Gryphon ^(talk) 09:31, 26 April 2015 (UTC)

My Edits (Josh)

Hello all. I would like to help clean up this article as it is of concern to me. I have started by correcting the statement that "Escitalopram has the strongest affinity for SERT of SSRIs on the market," which is not true. Escitalopram has SERT affinity of 1.1nM. Sertraline (Zoloft) for example has 0.3nM SERT affinity, Paroxetine 0.1nM. 1.1nM is strong but not even close to the strongest. However, I believe what was meant is that Escitalopram has highest selectivity. I see some debate about this above. It is a known fact and I will add textbook citation momentarily. S-Citalopram has SERT / NET selectivity of >7000x, the highest of any SSRI on the market. It is very reasonable to say that low NET and DAT affinities along with high SERT affinity makes it a generally-well-tolerated drug. In the future I will be looking to clear up some of this 'controversy,' as I believe it is blown out of proportion in this article. No one can dispute the known, numeric affinities of S-Citalopram, and they are arguably quite better than those of the racemic mixture. More to come on that :) Thank you 68.11.161.74 (talk) 22:42, 11 June 2015 (UTC)

Questionable claims

The following unconfirmed statements are doubtful and not acceptable within the article.
Re: "They are not by definition untrue if there is no reference, they are waiting for that."
ReRe: They've already got their waiting time. Now, let them wait on the talkpage (until the end of time(?)) ;-)

• "R-citalopram has been shown to counteract the antidepressive effect. Escitalopram is the most selective SSRI."
• "However, preclinical and clinical data have shown differentiated effects of citalopram and escitalopram. In particular escitalopram has shown to be more effective in depressive patients and particularly shows higher efficacy vs. citalopram and other SSRI in severely depressed patients."

As soon as scientific references are provided, you can of course add information into the article. Note, that otherwise anyone could write contributions such as: "this stuff is extremly toxic and the ingestion of nanograms of it leads to death within seconds.". Such a style is inappropriate and based on the intention to spread misinformation; it weakens article quality.--84.136.220.223 19:11, 7 September 2006 (UTC)

Three days is not what I call 'they've already got their waiting time.' I must confess, I am not a specialist in this area, but the main reason why I reinserted the claims was, that they were deleted by an anon-IP without a good reason. Wikipedia would soon go down in volume if all unreferenced data would be removed. When the deletion is performed by an anon IP (nothing personal, sometimes IP-numbers are shared between nonrelated people) that could be because someone with a lot of knowledge on the subject knows they are untrue, it could be plain vandalism, or it could be a company trying to hide information! (the same is not necessarily true for a named account, one can then check what other edits this person has done, and guess the persons expertise .. new named accounts may still have to build some faith). Things that do not have a reference, are not by definition untrue, and I have the good faith that the sentences were put there because someone with some knowledge thought them true (I will have a look who added the info, anyway). I would have had no objection if you would have questioned the facts on the talk page, given it a couple of weeks, and then deleted the sentences. And I can also be OK with the solution that you have chosen now. The best solution would of course be, provide facts which counter the data, though I know that 'un-proof' is sometimes hard to find. I hope I did not bite too hard (see WP:BITE), I come across a lot of vandalism, sometimes it is difficult to separate vandalism/spam from genuine edits. --Dirk Beetstra ^{T C} 20:05, 7 September 2006 (UTC)

To say it forthright: It's advertisement. There is not the slightest hint that esc. actually is so unequally better than c., as the claims suggest. It is an info page and not a stage for advertisement. If the studies were provided (if they exist at all!), the reader could judge himself and he could also have a close look at their (potential) weak points.
I have no problem with unreferenced texts, but my credo is: provide reliable refs or remove the passages (to the talkpage or nirvana resp.) if there is a single one who mistrust them! Quality comes first!
P.S.: I am (quite) well aquainted with WP.--84.136.247.196 02:23, 8 September 2006 (UTC)

I know, I have not checked who put these lines there, so they may be. I see your point, this is not about whether or not your edit was genuine, they way you edit may as well be vandalism as genuine. If you create an account, people would be able to check. Now I see two edits from this very IP (84.136.247.196), so if you would have deleted a line without providing a reason, and send them to walhalla, it would have been vandalism to me! You might be well aquainted with WP, I have no way to check. I am sorry. --Dirk Beetstra ^{T C} 07:25, 8 September 2006 (UTC)

The entire assertion that escitalopram is in any way superior to citalopram, especially in the abscence of any references to studies that support such claims, seems highly questionable. Frankly it reeks of either guerillia promotion by the manufacturers or escitalopram or promotion by someone that has been influenced elsewhere by drug company materials... the latter being more likely as even drug companies usually at least cite their own biased in-house studies. Will attempt to search the literature for a more definitive source on this myself now. --Condolini 14:56, 10 March 2007 (UTC)

• The Australian Medicines Handbook 2007, and independently published source of prescribing information for medical doctors (as opposed to the more common drug company sponsored MIMS Handbook) states that escitalopram is the active isomer of citalopram; no significant advantage over the other SSRIs has been demonstrated. While this is not a direct source it does come from an independant publication produced jointly by three of Australia's major professional societies, most notably the Royal Australian College of General Practitioners. Will keep looking for a primary source. --Condolini 15:18, 10 March 2007 (UTC)
• Right found it, not to sure myself how to put references into a wiki yet however I did find this review article by Manfield et al. that states that The manufacturer has claimed that the entantiomer has a larger effect with a faster onset of benefit. However, intention-to-treat analysis of pooled data has found no clinically important efficacy or safety advantages. Elsewhere they go on to say that while some studies have shown a slight advantage of escitalopram over citalopram, those studies have been only of very small samples and that the improved efficacy of escitalopram stated in them did not prove to be statistically significant. Full reference: Mansfield P, Henry D & Tonkin A. Single-enantiomer drugs: elegant science, disappointing effects. [Review] [23 refs] Clinical Pharmacokinetics. 43(5):287-90, 2004. --Condolini 16:05, 10 March 2007 (UTC)
• Ok I replaced previous erroneous claims with information supported by direct quotes from the source I have referenced in my last post (and indeed in the article itself). Unfortunately only the abstract of the article is available to those without a subscription to the journal, but fortunately I was able to access the full version of the article through my university. --Condolini 16:25, 10 March 2007 (UTC)

There are a couple of potentially-irrelevant asides in the Controversy section that are designed to question or diminish the nature of the controversy:

• In the following sentences, there are a couple of implications that this person generated controversy by filing his suits. This seems like an ad hominem attack rather than a dispute with whatever evidence he may have had: "One, a non-practicing physician Joseph Piacentile makes his living filing False Claims Act suits against pharmaceutical companies. (Whistleblowers are accorded a portion of damages, if the suit wins)."
• Further, I don't think that the last clause of the following is relevant: "Christopher Gobble was disturbed at what he witnessed at Forest, his first job out of school." It doesn't matter how many jobs you've had, in my view - whether this is your first job or your 100th, unethical behavior is unethical behavior.

I'm fairly new to the community so reluctant to make these significant edits myself, but let me know what you all think. --Artichokedance (talk) 20:28, 10 December 2009 (UTC)

That section needs improvement. If you can make it flow smoother, go for it. The Sceptical Chymist (talk) 11:36, 11 December 2009 (UTC)

Escitalopram is the most selective SSRI

Regarding citation needed for "Escitalopram is the most selective SSRI": There are plenty hits associated with escitalopram if one searches the web with a web search engine using the phrase "most selective SSRI". Most seem to reference J. Hytell (January 1994), "Pharmacological characterization of selective serotonin reuptake inhibitors (SSRIs)", Int Clin Psychopharmacol 9(suppl.):19-26, which I do not have access to. — fnielsen 10:11, 15 March 2007 (UTC)

I found the author is actually J. Hyttel and it is listed in PubMed [1] — fnielsen 10:14, 15 March 2007 (UTC)

Well, the above reference was actually for citalopram not escitalopram. A reference for escitalopram is [2].— fnielsen 20:53, 15 March 2007 (UTC)

Citalopram is the same substance as escitalopram. Escitalopram merely refers to the one optical isomer in citalopram that is medically active, whereas the other does nothing. —Preceding unsigned comment added by 82.111.241.126 (talk) 08:43, 15 October 2007 (UTC)

The last statement above is not correct: the R-enantiomer of racemic citalopram actually has an inhibitory effect on receptor binding by the S-enantiomer, escitalopram. Therefore, gram for gram, escitalopram is more than twice as potent as citalopram.[3] Sgouveia (talk) 23:07, 14 October 2008 (UTC)

This is No Longer Controversial in the Medical World!

Hi guys, I understand some of this may have been questionable at the time. However it is now 2015 and we have medical reference books that show very clear differences between S-Citalopram and the racemic mixture. There is no longer grounds to call it controversial or some kind of underhanded scheme to promote Lexapro.

If anyone is really wondering about it, a good place to start is Goodman and Gilman's The Pharmacological Basis of Therapeutics (12th edition), page 406. And there you have right before you the numbers showing exactly how the two are different, and you can clearly see the higher affinity of S-Citalopram for SERT and, perhaps more importantly, the lower affinity for NET (hence higher selectivity). This stuff is now factual, quantitative information. You will also see (on the same page), as I have mentioned below, that S-Citalopram does indeed have the highest SERT / NET selectivity of any SSRI on the market. I would strongly suggest that anyone wanting to discuss affinities or selectivity in medical articles in the future please use a reference textbook. 68.11.161.74 (talk) 22:56, 11 June 2015 (UTC)

Gold standards and POV

This article says something to the effect that escitalopram (Lexapro) has advantages over an equal amount of the same drug, supplied as a 50:50 enantiomeric mixture (generic Celexa), and says something the effect that such studies are the "gold standard" in clinical trials. Well, not quite. The gold standard is where at least two such studies (one to confirm) show something, where at least one is funded by people with nothing to gain, like a government, not a pharm company. Single controlled study findings funded by the drug company with most to gain from the finding should always be suspect, and the one quoted, the only one I can find that shows this effect clearly, was funded by none other than H. Lundbeck A/S, licencers of escitalopram and holders of the patent. This is Int Clin Psychopharmacol. 2005 May;20(3):131-7. Prospective, multicentre, randomized, double-blind study of the efficacy of escitalopram versus citalopram in outpatient treatment of major depressive disorder. Moore N, Verdoux H, Fantino B. Département de Pharmacologie, INSERM U657, Université Victor Segalen, Bordeaux, France. nicholas.moore@pharmaco.u-bordeaux2.fr, referenced in this Wiki. This group has also argued recently that escitalopram is expected to be cost effective because it results in fewer hospitalizations! (by calculation from the earlier study). Also a calculation funded by H. Lundbeck A/S. This is not to claim that the Moore group is corrupt, but it's a known fact that studies funded by drug companies are more likely to find positive results for the drug than studies of the same drug funded independently. People find a way to see what they want to. How "double blind" the data analysis is, sometimes takes a magician like Randi to figure out. In the meantime, I'm skeptical. That's MY POV. But not being a drug company, I haven't published this. And thus does money influence Wikipedia, WP:N standards or not. Studies and publication cost $. SBHarris 02:16, 5 January 2008 (UTC)

This is, IMO, why it is important to come back to quantitative data. You can cite studies and question them all day long, but once we have quantitative affinity profiles, facts can be asserted without chance of bias. Such quantitative information is available for both S-Citalopram and R,S-Citalopram. Also, please understand that of course it will be the developer of the drug who studies it the most. 68.11.161.74 (talk) 23:01, 11 June 2015 (UTC)

FDA approval date ?

FDA approval date ? Citalopram received U.S. Food and Drug Administration approval in 1998. ~~ Xb2u7Zjzc32 (talk) 19:30, 12 July 2015 (UTC)

Edit on statement regarding morphine and codeine

Hi all, first time editing a Wikipedia article here.

There was a statement regarding the conversion of codeine to morphine being reduced due to inhibition of CYP2D6 by escitalopram. While not factually incorrect, the statement is given undue weight by inclusion, given morphine is a minor metabolite of codeine and not primarily responsible for codeine's analgesic properties. I didn't add that explanation into the article because it would be incredibly off topic.

http://www.ncbi.nlm.nih.gov/pubmed/11092114 — Preceding unsigned comment added by 129.96.83.86 (talk) 02:06, 30 October 2015 (UTC)

So I went over a good chunk of the literature on this, and it's very headache-inducing. I think I might have found yet another relatively major project to work on though, as it seems that the information on Wikipedia related to codeine/morphine and their metabolites has a number of important issues to resolve. Not sure that I want to tackle that any time soon though.

Anyways... While it's true that only a small portion of the codeine is converted to morphine, it is important to recognize that morphine has an extremely high affinity for the µ-opioid receptors relative to codeine and a number of its metabolites (a factor of 200-600 in favor of morphine). Basically, morphine is clearly the primary analgesic, so the claim that "much of the effect of codeine is attributable to its conversion to morphine" is very well supported by the literature (and it's a pretty good broad simplified summary to use here too).

Please review WP:MEDRS, as this is a major factor here, and it will help you understand how to correctly approach the literature in the future. Garzfoth (talk) 21:36, 1 November 2015 (UTC)

Systematic IUPAC naming conflict

Hi, I'd like to share a concern I have regarding the systematic IUPAC name for this molecule:

(1S)-1-[3-(Dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile

(S)-1-[3-(Dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile

2600:8807:C203:7200:2DC6:DF69:694C:75DF (talk) 15:41, 21 October 2016 (UTC)