• H&R Moderators: VerbalTruist | cdin | Lil'LinaptkSix

Are Anti-Depressants Over Prescribed

"Opiates were once used for depression because that's ALL THEY HAD! Certainly opiates and other escapist drugs are better than nothing when it comes to severe psychotic disorders/depression....but they pale in comparison to the efficacy of SSRIs and other antidepressants. Opiates also have FAR more potential for addiction (which SSRIs do NOT have...dependance is most certainly not the same as addiction, and SSRIs, unlike opiates, are very rarely abused).
Ultram is NOT an opiate, it is an opioid, and has significantly less abuse potential than true opiates. Furthermore, the reason it helps depression is because it has serotonin reuptake inhibiting properties...thus it ACTS LIKE AN SSRI...and may well have the same sort of 'neurotoxicicity issues' that you are so concerned about."
Ultram may indeed. It's adverse side effects are pretty long as well. You will note I compared it's actions to Venlafaxine (Effexor) a SNRI, because that is what it is. Effexor also has dopagenic action which contibutes to it's effects in the body. Thus I felt Ultram and Venlafaxine are comparable for what they do. "Is Ultram safer than SSRI's? Maybe, Ultram wouldn't be my first choice to use either." For the same reasons. As to the question of "abuse". Because a drug is or isn't abused recreationally by a portion of the population has no bearing on whether or not a drug is effective for a given purpose. Do you want effective treatment or something that can not be abused but causes a host of neurotoxic side effects and permanant damage ...Or one that works, and doesn't. SNRI's, SSRI's, and Opiates/Opioids cause physical dependence. They all have pronounced withdrawal syndromes. Many patients refuse to come off of SSRI/SNRI drugs because of the problems associated with withdrawal.
As to the second part of your statement about "efficacy", that brought a grin. Ever read how about the actual trials for getting FDA approval were conducted? Placebo beat out Serzone, and Effexor, and Prozac, and Zoloft in several of the trials. I don't have a link for the Prozac & Zoloft trials handy, but I do have one about the trials for Serzone and Effexor. Enjoy.
http://www.pssg.org/moore.htm
The FDA rules only state a drug has to be better than "nothing" to be approved for a specific purpose. If you had to run 8 trials, and your drug fails to be better than nothing in 6 out of the 8 does your drug get approved? Unfortunately it does. (...if you have enough money, and manipulate the data enough.)
I don't argue that SSRI's and SNRI's don't have some uses. I've never made any arguement that people should be "unhappy" and that's just a part of life. I seriously question the wisdom of doctors reaching for the prescription pad and writing out SNRIs and SSRIs though. There are other ways of achieving the same ends which involve less risk in many cases.
Someone mentioned not trusting adverse event reports posted on angelfire ..Okay..You can find the same data in other places, you can even order it from the government itself. It comes on a CD-ROM, you'll need to have a copy of GREP handy to use it as it's just an endless series of .DAT files. You *might* get lucky and have a medical school in your area that you can get into their library and review it, or your public library might have a copy of it in the reference section if you ask nicely.
You can order a copy of the adverse drug reaction report here (comes on CD-ROM) ...
http://www.ntis.gov/search/product.asp?ABBR=SUB5460&starDB=GRAHIST
They want quite a bit of money for it. $360 inside the US and nearly twice that much to ship it outside of the US. Quarterly reports are available for a lot less money.
------
One last bit of SSRI inspired (lack of) joy. SSRI's have also been documented to cause Amotivational Syndrome in rare cases. Which results from damage to the temporal lobes.
Garland EJ, Baerg EA: Amotivational syndrome associated with selective serotonin reuptake inhibitors in children and adolescents. Journal of Child and Adolescent Psychopharmacology 2001; 11:181-186. Correspondence to: Dr. Garland, Children's and Women's Health Centre of British Columbia, C429-4480 Oak St., Vancouver, British Columbia, Canada V6H 3V4; e-mail: [email protected].
Hoehn-Saric R, Harris GJ, Pearlson CD, et al.: A fluoxetine-induced frontal lobe syndrome in an obsessive-compulsive patient. J Clin Psychiatry 1991; 52:131-133.
Hoehn-Saric R, Lipsey JR, McLeod DR: Apathy and indifference in patients on fluvoxamine and fluoxetine. J Clin Psychopharmacol 1990; 10:343-345
 
To be pedantic, the class of drug known as "neuroleptics" does not include SSRI's. The terms antipsychotic and neuroleptic are interchangeable, as are the terms antidepressant and thymoleptic (a term that is rarely used). I'm staying out of the actual discussion. :)
 
What's the principle action of anti-psychotic drugs? A reduction in dopamine levels.
(The simple version of) What happens when you put an SSRI in the body? Serotonin goes up dopamine goes down.
(You can call 'em what you like..They do the same thing. The secondary action has a lot to do with why we are seeing EPS now.)
http://www.wemove.org/emove/article.asp?ID=362
 
Well Sacred you make some good points and have some citations but I am afraid that you have been lead astray by some people with an ax to grind.
First of all in the one article we should read the author is quite obviously biased. Consider this sentence.
By contrast, medications only suppress symptoms. They are like crutches or Band-Aids. By themselves, they are never a cure.
The author here is a psycotherapist who clearly has a deep seated bias against medication. This isn't surprising as psychiatric medication challenges their entire career not to mention their theory of self and meaning in life.
This entire article consists of nothing more than ancedotal evidence. Hell TD has been associated with antihistamines, estrogen, birth control!! Ancedotal evidence is shit, movement disorders occur in people not taking drugs as well. Without a controlled study this only shows the bias of psychotherapists. I mean these case reports (his and the ones he cites) could just as well have been evidence that doctors offices cause TD.
Good summary of TD stuff.
http://www.emedicine.com/neuro/topic362.htm#target3
As the psychotherapist (doesn't it bother you that it appears to be psychotherapists and not researchers and neurologists talking about these symptoms). It is moreover written in classic scare tactic journalism (anyone who has any experience with drugs and the media should be wary of). Consider this
In light of these neurological side effects, we should especially question how freely these drugs are being prescribed to children. When major tranquilizers were in vogue, they were readily prescribed to children for mild anxiety, insomnia, or hyperactivity. The drugs are no longer used in this way on children because they cause tics. Current estimates are that serotonin boosters are being prescribed to over half a million children in this country, with pediatric use of the drugs one of the fastest-growing "markets." This in spite of repeated studies showing antidepressants are no more effective in children and adolescents than placebos. Should we not be protecting children, with their developing nervous systems, from drugs with potentially serious side effects?
Are the negative effects more likely to occur during development of the nervous system? He doesn't say but he plays the emotional appeal of protecting the "developing" children and by drawing attention to the word "market" is the a terrible attempt to unfairly bias the reader by trying to suggest these children are being exploited in an analogy with cigarettes. The dastardely dairy farmers of america attempts to tarket the children's "market" as well should I conclude they cause brain damage.
Hell lets take him at face value estimates (presumably the largest he could find) place the number of cases of TD from SSRIs in the thousands.
28 million adults are prescribed SSRIs. This means that at most about .02% are developing these side effects. This is crazy small...fuck you are probably more likely to kill yourself.
Moreover the principle of action of anti-psychotic drugs is as a dopamine antagonist. This is a far differnt effect than lowering of dopamine levels. in fact it RAISES dopamine levels to compensate which is one of the proposed theories for the cause of TD and EPS.
As to your arguments. I realize they are well intentioned but they are really about as scientific as "E puts holes in your brain". Hell they even boil down to the same basic premise "holes in your brain cause problems" "E causes problems" therefore E puts holes in your brain. The reasoning is just as bad from SSRIs and neuroleptics or MDMA share side effect X therefore they must both be neurotoxic.
Ill mention a few glaring points.
>Do SSRIs cause brain damage? Well, first we have to define “brain damage”. Changes in the structures of the brain would seem to qualify.
You have change in the structure of the brain simply from learning and big changes from things like adolescence puberty etc.. etc.. How do you propose you every remember anything if there isn't change in the structure of the brain. Fuck if we want to make unhappy people happy we have to change the structure of their brain. Guess what stopping SSRIs is going to cause changes in structure as well. So you better keep everyone who has SSRIs prescribed on them as it will cause brain damage to change.
> It’s my opinion that the effects you see from serotonin agents like SSRIs are precisely that. They inflict a chemical trauma to the brain & the body reacts to that trauma.
Really, well if thats your opinion im fucking convinced! Under that theory meth or mdma which can cause significant trauma in one sitting are going to be alot better anti-depressants right? It is true that SSRIs do not work simply by causing a rise in serotonin levels (actually neither does E given r-MDMA seems to lack the fun) the fact that it takes so long to notice changes is no doubt a result of some longer term process like tolerance occuring in the brain. So what?
The point is there is no simple version of what happens when you put SSRIs in the body. Serotonin levels rise sure, but where, what systems develop tolerance and how much? Dopamine levels fall? (which cite was this in?) where do they fall? Is it both addictive and drops dopamine levels in the Nucleaus Accumbens? That would be highly surprising.
What do you mean when you say it is addictive. Some people report adverse effects leaving the drug? Some people don't want to leave the drug. Well fuck if that wasn't true it wouldn't be an anti-depressant.
100,000 adverse reaction reports big deal. 28million people are taking the drug currently. Either I am really addiction resistant by managing to get off the SSRI gravy train so easily or these people are choosing to keep taking it b/c the side effects aren't that severe for them since they keep taking their drugs. The fact that the responses are so varied is GOOD NEWS as it suggests that what we are seeing is normal crap that happens to people not effects of SSRIs. CNS affecting drugs, just by causing mental effects are probably more likely to generate adverse symptom reports.
Go read some FDA data on cipiro, acne drugs, anything prescribed by a physician, vaccinations, you will find alot of case reports of adverse reactions. Since docs have a good idea of how say antibiotics work when you come in with a headache they are far less likely to file an averse report than with SSRIs.
Brain scans don't mean anything. No one has any real clue how to use them to view subtle things like you are describing. There isn't much difference bbetween scans of E users and SSRI users because their isn't much difference between either of these scans and control. Alot of scientists seem to think of this sort of brain imaging as "false color psuedo-science." It may look great on oprah's nodding audience (dear god I want to jump through my TV and kill them for being that dumb) but has little to no hard evidence to back it up.
As for efficacy this has always been a bothersome issue with SSRIs. However, while the link you gave describing serazone and effexor studies was of a much higher quality (as it points out uncontrolled studies are crap) it still was misleading and didn't give enough information to let us make informed deciscions. Yes alot of the SSRI trials didn't show significant effect at the normally prescribed levels but they did show it at higher levels. Doctors are dumb and for some reason want to prescribe most of the SSRIs at 20 mg a day even though there is considerable variation in their strength/half lives.
Also the increase in suicides isn't really meaningfull. I mean this is common across all psychiatric drugs and the normal explanation (which seems to be fairly convincing) is that it gives patients the willpower and energy actually to go out and do the deed. Also these were severely depressed people if it made even a small percent worse while helping others it would also have these effects.
 
As to opiates. First of all it whether or not ultram is a opiate or opiod is really a red herring. Not only is this distinction not well defined (I *can* make opiods using synthesises wchih start with natural morphine...hell I can make anything) it doesn't mean much unless you are going to start telling me fentanyl is a better anti-depressant than morphine for similar reasons.
Being an opiod really doesn't give one less addiction issues. Fentanyl is way more addictive than codeine. Yes, there is a subtle issue that morphine and presumably sufficently close analogs cause almost no receptor endocytosis which methadone and other more distant relatives cause it significantly.
Ultrams low addictivness comes from both its receptor profile and the fact that its more active component (just as with codeine) is produced through the saturatable CYP2D6 pathway.
Yes it is also an SSRI but have they really done side-by-side studies of ultram vs. comparable doses of other opiates (god damn't if that terminolory is good enough for my pharm prof it is good enough for me.
Sure they didn't have many anti-depressants back then but greater efficacy isn't the reason they don't use opiates now. Both our puritanical fear of things which make us feel good and addiction do.
Addiction wouldn't be a problem if the drug was prescribed legally. Okay im addicted to fentanyl, guess I will just have to keep that patch on all the time...big deal. Hell I am really bothered by the lack of addictiveness of current anti-depressants. Maybe its just me but drugs which make me feel better make me want to keep doing them. The more they make me feel better the more they make me want to keep doing them/
Finally I don't see what is more escapist about them. Sure shooting heroin might be but in this situation you are getting fucked up so much you can't do normal things and the association of the reward with the usually anti-social ritual of injection. Personally on opiates (especially long term dosing with codeine) I was less escapist, took more pleasure being social, going to concerts even going to classes. It did exactly what an anti-depressant should be doing, made things simply feel better. Unlike ketamine, or ecstasy bad things are not made to disappear, consequences still exist and you are aware of them.
In short fairnymph for all that you attack Sacred's posts for lack of good data I want some data that contrary to personal several month long experimentation with regular codeine vs. regualr prozac, opiates are not an effective AD.
 
There isn't data directly comparing the efficacy of opiates vs antidepressants, so we'll probably be arguing about this issue for a while.
As for your other points (in response to Sacred), I am in complete agreement, quale. You said it as well as I could have.
 
How many doctors know what FDA form 3500 is? Not too many. There are doctors who go their entire careers never filling one out. In an age where a doctor spends less than 6 minutes (and 3 being closer to average) with any given patient, how many doctors are willing to spend 30-45 minutes filling out a form for an agency that probably wont even act on it?
How many in the general public even know what FDA form 3500 is? Even fewer. How many have filled them out? Not many.
The most "generous" estimates I have seen claim form 3500 gets filled out for less than 1% of adverse events.
100,000 adverse event reports thus equals 10,000,000 adverse events. That's not very good for a class of drugs that is precibred to a little over 3X that amount of people. (31,000,000 was the last US number I read, you cited 28,000,000)
This shouldn't be at all suprising. The average patient treated by a psychiatrist tries 4-5 drugs duing a course of treatment for depression. The vast majority quit one drug because of excessive side effects or the drug just doesn't work. Either of those two statements should give you pause.
The second, being simply, that these drugs aren't effective. We know that. The clinical trials pretty much established it. Placebo beats them almost every time. The wealth of first hand experience in patients should also tell you that.
But it creates another problem -- a legal problem -- causality. If a patient gets seriously injured and he took 4 drugs, which one caused the damage? So that is a problem, and it's a problem with medical reprucussions as well. How do you know an adverse event for Prozac wasn't caused by Effexor when the patient took both in a course of treatment? You are looking at a patient who took both, one maybe longer than the other, one at a higher dose than the other. You can say "Well, the side effect didn't occur till I tried XXX drug.." But did the damage occur before that or after? Add in synergistic effects that many of the drugs have with each other in relation to neurotoxicity & that complicates the issue as well. There are limits and always will be limits in what the data can tell you about that. Controlled trials are needed, as are CT's and MRI's before and after for a large number of people in treatment.
The first issue: quitting because of side effects. Should give you pause for another reason. Many people go through the course of treatment gaining no relief from their symptoms - but only experiencing side effects bounced from one drug to another. Again, this is *not* an unusual occurence. Nor is it an usual occurence for patients to state that the drugs made their conditions worse. (and quite a bit of medical evidence for these drugs making certain conditions worse as well.)
This might be "harmless" if the medications were not neurotoxic and didn't cause damage to other systems in the body. Unfortunately we know this isn't the case.
As to your comments about "doctors not filling out reports for antibiotics". Vanko - Vancmyacin is near the top of the list. Yet if you check the Rx 200 most prescibed drugs for the past couple years it doesn't even register. Now I'll give you that this may be "special" in that this drug has some unnerving side effects like hearing loss and patients seeing flashes of light that aren't there in addition to the other side effects of being one of the few antibiotics currently in use that is very toxic. Cipros reports went up after the anthrax attacks, but they did so in porportion to it's use and it's still no where near Prozac.
I'll return the adverse events for a moment. TD is a small number of reports out of the total of all reports, but EPS is not.
Quale, I followed you "TD" & "EPS" link. I found one thing very sriking. With the exception of 5 agents on that list, one of which is an antimalarial drug that most doctors will never use in the US -- every one of those drugs is commonly used in what field? Psychiatry. A few at the top of the list being used to manage side effects from drugs at the bottom of the list. No suprise there. Even "compazine" in the middle is an antipsychotic medication that just happens to be a pretty good antinausea drug.
As to "Why does this come from a psychiatrist and not a neurologist". Who uses the drugs? A neurologist may write a very low dose of Elavil for a patient with migrains or some other pain syndrome - just as pain management specialist may use them in equally small doses on a very limited bases -- but outside of psychiatry who uses them at doses 5-20 times that amount? Who else but a psychiatrist would have enough experience to observe the effects of those drugs at those dosages and familiarity with the syndromes they can cause? A neurologist, or even a GP isn't going to see those often enough to make a connection.
You mentioned "suicide", I did not. But lets be honest about the studies for a minute. "Seriously depressed people". Pretty much all of the patients who had serious enough depression to have to be hospitalized were kicked out of the study. Just as well, they didn't respond to the medication. I've seen this in the Prozac trials, Zoloft trials, Effexor trials, and in trials of Serzone. It's pretty much standard operating proceedure to kick those who don't respond to drug treatment out of your trials, and psychiatric patients that have to be hospitalized tend not to respond to the medications. Could it be, just maybe, that those who exhibit the strongest symptoms and most fit the definition of "depression" don't respond because the drugs don't work? Could it be that's why they get kicked out of the studies over and over again?
If a particular diabetes drug was causing the level of adverse events the SSRIs are -- you would see it pulled off the market.
-- "Everything causes brain changes" ... There is a world of difference between the changes in the brain that occur from reading a book, learning a new riff on the guitar -- and those that come from administering neurotoxic chemicals in high doses to the brain every day for a period of months or years on end. SSRI's & SNRI's are starting to cause exactly the kinds of changes in CT's and MRI's that we have seen from neuroleptic agents. It took about 35 years for medicine to come to terms with reality on that and actually start taking CT's of people *before* they had any drugs pumped through them and after. This proved the old argument of "brain differences were a result of the disease and not the treatment" dead wrong. This excuse/explanation was commonly used for people with schizophrenia and I'm sure you've heard it before. It's been used for conditions like "Borderline Personality Disorder" as well.
The sad truth is, no one is doing the work that needs to be done. No drug company is willing (for obvious financial reasons) to fund that kind of study. The FDA wont do it. It's strictly a matter of buyer beware and you have to dig to find the truth. I'm the first to come out and say we need more studies. We need images of people in drug naive states and after, and it'll be expensive work to do. But based on what I've seen so far, I don't like where it leads. Do you know what the effects of these agents will be 2...3...10...years down the line? We don't know, but we have some pretty disturbing indicators in those reports.
I've seen this cycle before: with neuroleptics, redux, thalidomide (which is a good drug if you control which may the molecules bind, causes birth defects if you don't!), toradol, and several others. It just seems to take 30+ years longer in psychiatric drugs to come full circle. There is tremendous bias on the part of the medical community towards those patients.
 
The bottom line is this: for someone so seriously depressed/anxious/etc that they are going to DIE (either through suicide or a less direct means) unless they don't start getting better, antidepressants can be a godsend.
I was severely clinically depressed this summer. I doubt that I would be here today had I not gone on antidepressants a couple months ago.
As 'evil' as you may consider antidepressants, they can and do save lives. And being alive sure as hell beats anything else. I'd rather be alive and have some side effects -- wouldn't you?
 
Even that "benefit" may be non-existent.
In the work that has been done...:
You are 5.5 times more likely to kill yourself while taking Effexor XR vs Elavil.
You are 3.4 more times as likely to kill yourself while taking Effexor XR than Placebo.
You are 5.2 times more likely to kill yourself on Serzone than placebo.
Effexor Placebo
Patients treated
3,082 739
Suicides
7 1
Suicide attempts
36 2
Chance of event
1 in 72 1 in 246
Here are the results for Serzone:
Serzone Placebo
Patients treated
3,496 875
Suicides
9 0
Suicide attempts
12 1
Chance of event
1 in 166 1 in 875
Similar results were listed for Prozac.
...and this was in trials where they kicked "suicidal people" out.
Hospital admissions for people experiencing severe agitation, and mania from antidepressants account for 8% of all psychiatric admissions.
Less than 10% of people taking Effexor XR will achieve any clinical benefit from taking it in real world practice. "The results of this study suggest that, if 100 patients came to a general practice for treatment for depression, perhaps 40 would either not need the active drug (strong placebo responders) or find it intolerable (drop outs), or be at greater risk of having unwanted effects. Of the 60 patients remaining, 27 on the active drug would not have a relapse or recurrence of depression for one year - though 18 patients would have done as well on placebo. In other words, the advantage claimed might be in practice be available to about one in patient in every ten."
On the balance of things, that isn't very good.
Very high risk to benefit ratio. Findings aren't much different for other drugs in the SSRI/SNRI class.
The reality is: You can dye aspirin green and give it to patients and they'll improve *more* than they would on Zoloft, Prozac, Paxil, and Effexor without the risk of side effects and a much reduced risk of permanent injury and they will be far less likely to take a gun to their head as well.
Similar results are out there for "self-harm".
In just about every category SSRI's increase that too.
I don't believe SSRI's are "evil". I believe they are the equivalent of snake oil in the hands of those who currently profit from them. If one out of ten gets a real benefit -- find a way to identify that one out of ten quickly so the rest of us can be spared. I feel the same way about people who advocate genetic "drug addiction". Find those genes quick guys, so the rest of us can shoot smack with impunity!
I'm willing to use science. ...This is what the science tells me.
 
"I'm willing to use science. ...This is what the science tells me. "
Your "science" is pure BS. You quote "articles" from websites called "Prozac Survivors". You have NO clue how many people have been helped by these drugs.
You, my friend, are the victim of modern-day witchhunt and hear-say.
 
SacredNaCl, science says you are a moron. Overemphasis leads to distortion of the truth, just remember that.
 
FLAMING IS NOT TOLERATED IN THIS FORUM!
SacredNaCl has the right to express an opinion - you don't have to agree with it. A coherent rebuttal would go a lot further towards expressing your opinion than abuse does.
 
SacredNaCl, you have no idea what you're talking about. An Angelfire homepage is NOT a credible source. take your preaching elsewhere...
 
One thing that really bugs me is that my folks are both on anti depressents and when they take stuff like that, they don't think twice about it, but when i take an opiate or opiod recreationally to feel better its like i killed somebody. Not to mention when i went to go get prescribed Anti Depressents, the doctor gave me a choice practically and let me make the descision. Any other drug type, it would of never of happended. I couldn't be like i like percocet over vicodins so i want that. They hand that shit out like candy, much like ritalin, adderoll, dexedrine, etc. I do believe opiates make you feel better, but areant any way to solve depression. Before you know it you'll be depressed and have a dope problem, making you royally fuct.
 
Top