Childish anti-scientific nonsense
"The most common chemical indicated and treated for depression being serotonin[wp] ("happy hormone")". Really? No legitimate psychiatrist or neuroscientist in the last several decades has taken the "chemical imbalance" BS marketed by the drugs companies seriously. Nobody knows how they work (actually, they don't, google "Irving Kirsch") but it sure as hell isn't that simple. Rationalwiki seems to love "woo" and marketing hype when it gets the seal of approval of big pharma. What's the difference between the chemical imbalance lie and say, lies about homeopathy for example? --126.96.36.199 (talk) 21:44, 4 September 2016 (UTC)
gnostic 12:58, 12 January 2011 (UTC)
I'm writing a paper making a case for severely inadequate research into antidepressants, particularly when it comes to long-term studies on overall outcomes and wellbeing. Please share relevant research...IF you can find any!
Removed big pharma rant text
Also the leaflets still downplay the withdrawal symptoms which can be so severe and debilitating that people are not able to function for a very lomg time (many years!), or are forced to get back to the medication, even when the original indication for presciption is not actual anymore.
Though those patients are technically not addicted, they will be forced to take the medication forever and live with the possible side effects, only to keep away the withdrawal effects.
- I think the removed text is accurate. I'm not anti-pharma, but I think big pharma has earned some bad vibes for just this sort of thing and other things in this class of medications. I won't return such text, though, unless I find something to support it. MarmotHead (talk) 02:18, 30 May 2014 (UTC)
- Why I cut it:
- "Also the leaflets still downplay the withdrawal symptoms which can be so severe and debilitating that people are not able to function for a very lomg time (many years!)" < cut > Leaflets, which leaflets? "severe and debilitating" - it can be, but it's actually considered 2SD>mu, and therefore not the norm. Spelling and the parenthetical, with extreme time frames (and an exclamation!). Oh, and spelling.
- ",or are forced to get back to the medication, even when the original indication for presciption is not actual anymore." - which goes to an issue of professional practice, but the rest of the article intimated that the RX's get you 'hooked and addicted' which is kinda the hallmark of big-pharma conspiratorial scares. Extreme evidence=++claims!
- "Though those patients are technically not addicted, they will be forced to take the medication forever and live with the possible side effects, only to keep away the withdrawal effects." - This is the most objectionable, which displays a fundamental lack of knowledge of addiction neuroscience.And this is tricky since it makes such general assertions, which can also be used to draw the ridiculous assertion that dehydration is a withdrawal effect of addiction to water.
- Personally, I think the last paragraph flows fine without all of this, but the article seems much like a very personal diatribe with unknown motives, but with the suspicion that the adverse consequences happened to the original author. I am not stating that is the case, but it does come across that way to me, and I came with no preconceived notions Kassorlae (talk) 15:08, 30 May 2014 (UTC)
Help for someone who is depressed?
I was prescribed Prozac a few days ago, and today I stumbled upon this site:
Who runs it? I can't find who, and is the person who runs it a quack? It's really freaking me out. I just want to add that I feel like crap right now. (Chest pain, etc., but i hear that's completely normal for the first few weeks?--188.8.131.52 (talk) 01:23, 22 November 2014 (UTC)
- That site makes my FUD sense tingle. I'd take it with a big grain of salt, especially since googling around shows there may be a Scientology connection through James Harper. Unique pinion (talk) 02:04, 22 November 2014 (UTC)
- Ah, $cientology... Go figure. Thanks!--184.108.40.206 (talk) 02:08, 22 November 2014 (UTC)
- For anecdotal purposes, I've been on and off Prozac, Paxil, and generic fluoxetine starting about sixteen years ago. Now off, and on an even keel thanks to moderate exercise and the support of friends and loved ones. I think the SSRI helped more than it hindered me. I remember recognizing a certain feeling in my chest that came with being on that kind of medication, but it wasn't painful. You probably already know to keep paying attention to how you feel, both physically and emotionally, and to keep talking to someone about it. Unique pinion (talk) 02:19, 22 November 2014 (UTC)
- Ah, $cientology... Go figure. Thanks!--220.127.116.11 (talk) 02:08, 22 November 2014 (UTC)
Prozac and Flouride?
I am putting into queston the studies section of this section, as it doesnt match our ratonal bais, and seems a bit like woo. Any comments? Bubba41102Anonymous user is almost, but not quite, entirely unlike an editor 19:28, 22 August 2015 (UTC)
Just to make a small point, (edit: lol "small", oh well) in case *someone* is crazy enough to use the article page as a primary source, that only modified-release Venlafaxine/Effexor has a long half life - and it's actually listed as 15 hours (maybe +/- 2 hours?), not 17. And if you graph it out, a small change in halflife can have a very big effect on how rapidly the drug clears out of your system to a level where it's essentially undetectable, as well as how stable a level of it can be maintained in the blood. The regular stuff has a HL of a mere 5 hours, though one of its also-effective derivative substances (IE what the body turns the precursor in the tablet into) is something like 11 hours, with the overall aggregate being somewhere in between over the period you're meant to split the doses (I can't remember exactly what I worked it out to, but the idea is that if you split it 3 per day, by the time you take the next there's ~roughly~ half of the previous tablet left, and it all builds up over several doses to a more uniform level) as they aren't present in a 50/50 ratio. Thing is the extended release is meant as a one-a-day drug, and takes longer to kick in after swallowing, so, it's sort of swings and roundabouts as to the min/max levels and how it affects you at different times of the day.
Background on this: patient currently taking it, and having had serious problems with side effects on various ADs without much positive impact (I'm a heck of a cynic, so basically only the drugs which have a real and quite strong effect have even half a chance of cutting through ;), with VF being pretty much the last fallback available before moving to stuff that has a haymaker wallop in terms of desired effects but only in conjunction with a list of sideeffects that would probably leave me bedridden for a while. Thankfully, it seemed to have some benefits once the right dose was achieved (fun times - the side effects kick in first at lower doses, but not the intended ones, and it's only at higher levels that the tables turn ... my doctor, not being super experienced in it all, prescribed an initial dose equivalent to what I had been trying before, and when it reduced me to a bit of a wreck, experimentally ~reduced~ it before jacking it up after that made things worse...), but it was hella peaky. After finding out about the half-life and stuff, I chucked the numbers into Excel and it looked like a sawtooth wave on an oscilloscope, no matter how I tried to divide it up (other than breaking the tablets up with a dremel and taking the fractions religiously once an hour), a problem made worse in real life by difficulty faced with taking them at regular intervals.
However in the course of that I also found out there's "modified release" / "extended release" (etc) versions available that are basically a bunch of tiny pills in cellulose coatings inside a hard-to-digest capsule, with the much longer halflife - that is actually not a clearance halflife (the VF is processed by the liver and other internal organs at exactly the same speed) but in fact a combination of that and the *digestion* halflife. The graph for that therefore, which was a somewhat complicated one to work out as it involved simulating a particular, varying dose every half hour (the resolution of my table :p) instead of just one every 4, 6, 8 hours or whatever, looked a lot smoother, especially over several days.
I've only been on the slow release type a few days now but it seems to be working better, though I need to figure out the best time to take it in order that the remaining peaks and troughs occur at suitable times; a rising limb (ie going from low to high blood concentration) seems to have a sedative effect, whereas a falling one is more stimulant, so defying the doctor's orders and having it just before bedtime might actually be best... theoretically. However experience hasn't much borne it out as I've found myself waking up at 4am and then being a wreck at 7am, not the best for trying to get to work. So perhaps having it at breakfast may indeed be the best, who knows.
FWIW the regular ones are just "Venlafaxine" (generic) or "Effexor" (original branded version), but the modified ones have all kinds of names, usually with an "XR" or "XL" on the end, including those two better known ones and, for some reason, "Vensir" (XL), which is what's printed on the package I got from the pharmacy... some kind of sub-brand, bit weird... the ingredients are listed as exactly the same as the generic or original though.
Still remaining skeptical about how much use all this might be, but seeing as it's kind of a condition of not losing my job that I seek some kind of treatment for mental health issues that caused a lot of friction here, and to comply with doctor's orders, I'm remaining in a scientific and "suck it & see" mood. Maybe it'll work, maybe it won't, but we'll never know until we try, and at least I'm not a teenager being duped into taking something that might lead to an otherwise avoidable suicide (in my 30s instead, ysee).
I noticed no one had updated the recent study, which analysed data from 522 trials involving 116,477 people, and found that 21 common anti-depressants were all more effective at reducing symptoms of acute depression than placebos (Source: http://www.bbc.co.uk/news/health-43143889). I've also noticed a trend among the loony right to demonise antidepressants - which they call "SSRIs". These people are basically encouraging people to go off their meds! Do you they realise that? Do you think they realise that they are encouraging people who may be on antipsychotics to not take their meds? Holy shit! Levi Ackerman (talk) 20:14, 23 February 2018 (UTC)
- Ja, I added it at the beginning as a citation.
- >" These people are basically encouraging people to go off their meds! Do you they realise that? Do you think they realise that they are encouraging people who may be on antipsychotics to not take their meds? Holy shit!" THESE PEOPLE ACTUALLY PISS ME OFF SO MUCH. This line of thought that meds are the easy way out angers me beyond any reasonable measure. Ibrahim Moizoos (talk) 20:30, 23 February 2018 (UTC)
- The average effect of these drugs as shown in the Cipriani study in your BBC link , is 0·3 SMD, which is less than a clinically significant response. No one contests that drugs have a statistically significant response (except for those that claim bias), but what matters if the drugs are clinically significant. The UK National Institute for Health and Care Excellence has previously suggested that three points on the Hamilton scale or a 0·5 SMD should be used as criteria for clinical significance Neiltyson1fan (talk) 22:11, 28 December 2018 (UTC)
I got slammed one day on a social media post I made after Chester Bennington died and it took me a long time to figure out why the stuff this person was saying to me was wrong, but there is a really good episode of the Science VS Podcast that helped me learn more about this.
Irving Kirsch is a major voice behind pushing the anti-antidepressant thing. He's not an unbiased voice though, he has spent a large part of his career studying the placebo effect and some of that research obviously is useful, but he does this switch when talking anti-depressants that isn't honest. Clinical Significance is what FDA tests go by, but when he says anti-depressants aren't shown to be effective, he's actually using statistical significance, which isn't the standard in that context. So he switches these terms under the radar, and also bases the efficacy results on a test called the Hamilton Rating Scale, which includes many things that are related to depression but not necessarily identical, so if you have a mood improvement but an antidepressant is upsetting your stomach, your score may not change that much or it might go down and he'll say the drug isn't effective when it really has alleviated the important thing it's supposed to help.
- https://www.gimletmedia.com/science-vs/11-antidepressants#episode-player That episode is a good overview, and then this is the study that people cite without acknowledging the difference between clinical and statistical significance: http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0050045 After that study, Kirsch is quoted in things like Time, not calling out the difference and being a little misleading about the results: http://healthland.time.com/2012/01/18/new-research-on-the-antidepressant-versus-placebo-debate/
And then a later study showing SSRIs are more effective than placebos from Nature: https://www.nature.com/articles/mp201553.pdf
And over time this has turned into sites like this generalizing unsupported claims: https://www.naturalnews.com/055056_antidepressants_junk_science_depression_drugs.html 18.104.22.168 (talk) 14:56, 27 March 2018 (UTC)
- Right now Wikipedia has a nice section listing known meta-analyses on anti-depressants. I cannot find one study where there is a clinically significant response (more than a 3 point decrease in HDRS according to the National Institute for Health and Care Excellence), including Ciprianis latest meta-analysis . A look at Kirsches dataset reveals only clinical significance at the tail end of the very severely depressed (about 10% of patients). Which only yields a 4.28 HRDS decrease. Fournier et. al 2010 also only found about 10% of patients pass the NICE criteria for a clinically significant response to antidepressants . Just 30 half an hour of treadmill walking for 10 consecutive days is sufficient to produce a clinically relevant and statistically significant reduction in depression (reduction of 6.5 points from baseline on HRDS).. The exercise part aside, my point is the meta-analyses do not show a clinically significant response to antidepressants with the exception of maybe the top 10% most severely depressed patients. Neiltyson1fan (talk) 22:07, 28 December 2018 (UTC)
I see this perspective better now, the issue looks one way when we limit it to changes in the hdrs results, but the Hamilton Scale defines depression in a very broad and abstract way. When that definition requires us to say that because a patient experienced a decrease in suicidal ideation but an increase in insomnia, therefore the pills aren't working, the system seems inadequate. Or at least that's the content of the debate I've had with people, it's not literally increasing their Hamilton score, and that's not relevant to them because they're willing to tolerate some side effects to experience relief from their depression.
The big Cipriani meta analysis includes the interpretation "All antidepressants were more efficacious than placebo in adults with major depressive disorder." 22.214.171.124 (talk) 00:01, 20 September 2019 (UTC)