![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 103 to 127 of 143. Go back in thread:
Posted by linkadge on May 20, 2006, at 2:13:31
In reply to Re: Statistical question on SSRIs - ADDENDUM » linkadge, posted by Larry Hoover on May 15, 2006, at 9:54:44
>If antidepressant drugs caused a suicide, how >would you demonstrate that to another person? >How could you show that it was this one lone >variable that made the difference?
Thats exactly it. We can't prove anything yet. I'm not claming that the reason for my conclusion is at all scientific or provable in any sence yet.
>Anecdote. What is anecdote? It is an >uncontrolled experiment with one subject. What >have you got when you collect one thousand >anecdotes? One thousand different uncontrolled >experiments with one thousand different subject >populations. Anecdote is a point in space. How >do you extrapolate from one point?Hopefully anecdotal instances might persuade the initiation of a host of more systematic experimentation.
>Anecdote spurs people to create hypotheses, and >to consider experiments not yet done. How could >you design an experiment which would >demonstrate this suicidality, this inductive >effect? The fact is that you can't. Any >experiment that could do so is absolutely >unethical to perform.
We do have some experiements that show some interesting things. You take a regular clinical trial for an SSRI. Throughout the trial, you ask both groups a whole host of question relating to feelings of akathesia, acute feelings of suicidiality, feelings of hostility, increased feelings of self hatred or intent to self harm.
You compare the incidences of such events between both groups, and you discover what many such trials are indicating, that SSRI's statistically seem to increase the likelyhood of such feelings.Perhaps nobody actually kills themselves in such trials, but the information will lend merrit to many of the anecdotal reports.
>All we can really do, IMHO, is to manage the >drugs better than we did before. Serious drugs >for a serious disease require serious >management. I cannot fathom how the latter was >allowed to detach itself from the former, but >we let that happen. Thalidomide taught us a >lot. It turns out that thalidomide is a miracle >drug, when used in other contexts than for >morning sickness.I think that part of the mannagment, is in coming to terms with the extent of the problem.
There is still such a devide. Either they cause people to kill themselves, or they do no such thing.>It's the human component that we can influence. >No amount of posturing will affect the drugs >themselves. They are what they are. We have a >people problem, not a drug problem, IMHO.
Lets suppose that there is something really quite unique about the individuals who have such negitive reactions to SSRI's. Its like we've skipped back 40 some odd years, when MAOI's were not known to interact with tyramine. Sure, only some people were dying, and nobody knew exactly why. We still have yet to discover why people are reacting this way. It is still a drug problem, just like MAOI dietary interactions were a drug problem. It is my belief that we simply don't know the mechanism yet.
Linkadge
Posted by linkadge on May 20, 2006, at 2:21:35
In reply to Re: Statistical question on SSRIs - ADDENDUM » Squiggles, posted by Larry Hoover on May 15, 2006, at 14:57:10
>If you sample a population enough times, you >can always find a significant result, no matter >how absurd the hypothesis being tested.
>Much of the research that has been published is >not proof of anything at all
I do think that certain clinical trials can help to develop a clearer picture of what the drugs are doing, and the way in which an antidepressant may induce suicidiality. I have actually seen a few clinical trials in which *healthy vaulenteers* were given placebo, or active SSRI. It seemed that the SSRI's were actually producing things like acute apathy, acute akathesia, insomnia, agitation, and suicidal feelings, whereas placebo group experienced no such events.
This is an important type of trial, since in studies such as this we cannot lean back to the old "well this population was depressed anyway".
I have seen reports of psychiatrists self testing SSRI's and having similar findings.
Linkadge
Posted by linkadge on May 20, 2006, at 2:48:48
In reply to Re: Statistical question on SSRIs - ADDENDUM » Squiggles, posted by Larry Hoover on May 16, 2006, at 10:04:04
>But it is not relevant, IMHO, to even do such a >study. What would it tell us? We already know >what's missing from the care received by >depressed people. It is management of the >treatment. That's where we fall short. You >can't just hand a depressed person powerful >drugs, and leave him on his own.
Granted, the SSRI market has taken a drop in sales since the introduction of such reports.
It is still absolutely necessary to guage the extent of the problem so long as SSRI's are being prescribed.Consider a lesser problem induced by the SSRI's. Sexual side effects are not argued against, (except by some doctors). Initially, such side effects were thought to occur in only a very small number of patients treated. As time progressed, we can piece together a better picture based on may different types of evidences, that a significantly greater proportion than originally estimated are thought to experiences such effects.
We need to get inventive. Where there is a will (plus a little cash) there is a way to find out what we are dealing with. No it won't be exact. But, I am willing to make decisions based on stastical significance.
The problem is important, and could be underestimated for many reasons. The "excuse" is that the patient group is depressed to begin with. Looking from another angle, this is an additional reason why the problem can be *underestimated*, these people are depressed to begin with. It is highly likely that such a group could confuse drug induced suicidiality with the feelings of their own illness. Same thing went with sexual side effects, its just going to be pawned off as a "consequence of depression".These are peoples lives, and if we cared, we'd get inventive.
>IMHO, the problem has never been the drugs. It >has always been the people who were let down by >other people. We haven't taken the illness >seriously enough. Don't forget, fifty years >ago, nobody talked about mental illness at all. >We built great buildings, and populated them >with people who otherwise virtually ceased to >exist. We haven't come too far from that period >of great stigma. Don't kid yourself.Management can only go so far, you first have to admit there is a problem, and understand the problem. Its like saying to an MAOI user, "call me if you start to have chest pain", thats useless; too little too late. Again, the patient may be suicidal to begin with. Suicidal means, I don't want to live anymore. You make sombody suicdial and they can go at any moment. You cannot underestimate suicidality, and you cannot make a paitent responsible for their own suicidiality. That is why it is absolutely necessary to try and identify who may be at increased risk of such occurances.
It has always been the drugs. Somebody would never say that SSRI induced anorgasmia and genital anesthesia was not an effect of the drugs. SSRI's are very effective chemical castration. That is a *real* drug induced side effect. I don't see how all of a sudden drug induced suicidialty falls a whole new category of "meh".
Oh, its too difficult to ascertain, so lets just sweep the notion under the carpet.
Its not too difficult to ascertain, but we need to be inventive.
Linkadge
Posted by linkadge on May 20, 2006, at 3:03:59
In reply to Re: Statistical question on SSRIs - ADDENDUM » Squiggles, posted by Larry Hoover on May 16, 2006, at 11:44:42
"It is a class effect of pharmacological treatment of mood disorders. If you're going to treat depression with drugs, you get this effect."
Thats not true at all. Its called SSRI induced akathesia. Some drugs induce more akathesia. Some drugs have a higher likelihood of inducing such events. To try and package it all as one deal is foolish, and reeks of carelessness.
The shear body of evidence, for instance, indicates that lithium prevents suicides better than depakote does. That is statistically significant. It is not a "bipolars are going to blow off their heads anyway so it doesn't really matter much what we give them".
There are better treatments, and there are worse treatments.
Some antidepressants made me suicidal, others did not. No, I don't know the exact mechanism, but I sure don't think that it was just coincidence. Just like citalopram gave me anorgasmia and remeron did not. Drug induced suicidality is not a general consequence of drug treatment of depression, and if it is currently, then it needent be. A drug should make you better, not worse.
Opium never made a depressed suicidal insomniac want to jump off a bridge. If somebody is about to jump of a bridge, shoot them in the leg with a dart of MDMA. I'm shure they'd first step off the ledge, then they'd come give you a warm hug for saving their life.
It's called SSRI's are lousy. We simply need better antidepressants.
Good antidepressants work.
Linkadge
Posted by linkadge on May 20, 2006, at 3:16:57
In reply to Re: Statistical question on SSRIs - ADDENDUM » SLS, posted by Squiggles on May 16, 2006, at 20:30:31
>For some mysterious reason Larry got
>upset with my remark, that medication
>takes priority over bed-side manner in
>curing diseases. What is care? In
>serious mental illness, it's got to be
>drugs. I don't know why he go upset
>at that.I agree with you. If soothing talk and kindness could relyably cure depression, then I'm sure a patient could get well from the comfort of their own home. They go to the doctor to get treatment for a debilitaing disease. Unfortunately depression is not as clear cut as treating other diseases.
It is wrong (IMHO) to conclude that drug induced suicidiality is somehow due to a flaw in the doctor-patient relationship.
Linakdge
Posted by SLS on May 20, 2006, at 8:28:01
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by linkadge on May 20, 2006, at 3:16:57
> It is wrong (IMHO) to conclude that drug induced suicidiality is somehow due to a flaw in the doctor-patient relationship.
I agree. However, I think that inadequate patient education and monitoring by the doctor will allow for a higher suicide completion rate.
I keep seeing the word "akathisia" thrown around as if it were a common occurrence with SSRIs. I question this. My guess is that it is agitation and anxiety that is producing suicidality, and not akathisia per se. Prozac probably produces more agitation and anxiety than the other SSRIs.
- Scott
Posted by Squiggles on May 20, 2006, at 14:34:25
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by SLS on May 20, 2006, at 8:28:01
> > It is wrong (IMHO) to conclude that drug induced suicidiality is somehow due to a flaw in the doctor-patient relationship.
>
> I agree. However, I think that inadequate patient education and monitoring by the doctor will allow for a higher suicide completion rate.Hi,
I'd like to say something about this. Are not
the two (i.e. doctor-patient relationship) and
monitoring/patient education of the patient
somehow similar? In either case, this would be
an interesting variable in explaining the results in the small "Prozac Survivor" group in a medically causal way.
>
> I keep seeing the word "akathisia" thrown around as if it were a common occurrence with SSRIs. I question this. My guess is that it is agitation and anxiety that is producing suicidality, and not akathisia per se. Prozac probably produces more agitation and anxiety than the other SSRIs.
>
>
Regarding "akathisia" - the word is from the Greek, a-kathisia, meaning non-restfullness. Restlessness in the midst of depression can be a very dangerous thing. This is so especially because restlessness can vary from nervousness, to anxiety, to mania. The word "akathisia" does not have a one-to-one reference in behaviour. It is a pointer to the many facets of a spectrum of behaviour under SSRI or other drug conditions. In some, "akathisia" can lead to suicide.Squiggles
Posted by linkadge on May 20, 2006, at 17:01:16
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by SLS on May 20, 2006, at 8:28:01
True. Although it is hard for a patient to identify a reaction that they have never been educated about.
I remember feeling absolutely horrid the first few weeks on my first SSRI. It wasn't till I later became educated that I could assign some names to it.
Linkadge
Posted by linkadge on May 20, 2006, at 17:04:51
In reply to Re: Statistical question on SSRIs - ADDENDUM » SLS, posted by Squiggles on May 20, 2006, at 14:34:25
The thing about akathesia is that (for me at least) time was the big thing.
Akathesia made me feel physically restless, but also very mentally restless. A strange feeling of urgancy. A feeling of having to get out, that something needed to be done right away.
Its a very ansy feeling. Like I can't wait till the next bus stop to pee, I have to go "NOW".
For me, I was luck that large doses of caffiene were able to restore some ballance.
Even when I got horrid akathesia on risperdal, caffiene was able to help.
Linkadge
Posted by Squiggles on May 20, 2006, at 18:12:57
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by linkadge on May 20, 2006, at 17:04:51
> The thing about akathesia is that (for me at least) time was the big thing.
>
> Akathesia made me feel physically restless, but also very mentally restless. A strange feeling of urgancy. A feeling of having to get out, that something needed to be done right away.
>
> Its a very ansy feeling. Like I can't wait till the next bus stop to pee, I have to go "NOW".
>
> For me, I was luck that large doses of caffiene were able to restore some ballance.
>
> Even when I got horrid akathesia on risperdal, caffiene was able to help.
>
>
> Linkadge
>That feeling you describe sounds very much
like the "fight or flight reaction". I am not
sure what sounds the alarm for that physically.It seems paradoxical that coffee should help, though.
Squiggles
>
Posted by linkadge on May 20, 2006, at 19:35:54
In reply to Re: Statistical question on SSRIs - ADDENDUM » linkadge, posted by Squiggles on May 20, 2006, at 18:12:57
I attributed the extreme inner restlessness as akathesa due to the SSRI causing acute decrease in dopamine activity. The caffiene probably couteracted some of the negitive effects of the SSRI on dopamine release.
Linkadge
Posted by Squiggles on May 20, 2006, at 19:43:27
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by linkadge on May 20, 2006, at 19:35:54
> I attributed the extreme inner restlessness as akathesa due to the SSRI causing acute decrease in dopamine activity. The caffiene probably couteracted some of the negitive effects of the SSRI on dopamine release.
>
> LinkadgeWhy would any chemist make an antidepressant
that interferes with the release of dopamine?
Isn't dopamine supposed to alleviate depression and other negative emotions?Squiggles
Posted by SLS on May 20, 2006, at 20:46:49
In reply to Re: Statistical question on SSRIs - ADDENDUM » SLS, posted by Squiggles on May 20, 2006, at 14:34:25
> > I keep seeing the word "akathisia" thrown around as if it were a common occurrence with SSRIs. I question this. My guess is that it is agitation and anxiety that is producing suicidality, and not akathisia per se. Prozac probably produces more agitation and anxiety than the other SSRIs.
> Regarding "akathisia" - the word is from the Greek, a-kathisia, meaning non-restfullness.
Akathisia is a term used in medicine to describe a specific syndrome. It is part of medical nomenclature and has a medical definition. It really doesn't matter what the etymology of the word is. Unfortunately, the description of akathisia is not unambiguous.
Akathisia (from the Greek "not to sit") was first described by Haskovec in 1901
Akathisia is generally acknowledged to have two components:
1. Subjective: feelings of inner restlessness and urge to move.
2. Objective: repetitive movements including rocking while standing or sitting, lifting feet as if marching in place and crossing and uncrossing the legs while sitting
There are several akathisia rating scales, but the Barnes's Akathisia Scale is the one most often employed.
- Scott
Posted by Squiggles on May 20, 2006, at 20:49:47
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by SLS on May 20, 2006, at 20:46:49
> >........
> There are several akathisia rating scales, but the Barnes's Akathisia Scale is the one most often employed.
>
>
I did not know that :-)I'm glad there is a scale.
Squiggles
>
Posted by Dr. Bob on May 20, 2006, at 22:07:51
In reply to I rescind the DNP, posted by Larry Hoover on May 16, 2006, at 23:06:01
Posted by linkadge on May 20, 2006, at 23:27:39
In reply to Re: Statistical question on SSRIs - ADDENDUM » linkadge, posted by Squiggles on May 20, 2006, at 19:43:27
>Why would any chemist make an antidepressant
>that interferes with the release of dopamine?
>Isn't dopamine supposed to alleviate depression >and other negative emotions?This is it. Fast acting antidepressants generally work via affecting dopamine release.
When you take an SSRI, you are stimulating a number of serotonin receptors that will indirecectly supress dopamine release (for a while at least untill some sort of compensatory adapation takes place)
5-ht1a, 5-ht2a/c, 5-ht1b, (and others) act as indibitory pathways on dopamine function.
Sure SSRI's are selective to serotonin, but not to specific serotonin receptors, as a result the final product is often a wild free for all.
In contrast however, consider some endogenious neuromodulators such as anandamide. Anandamide agonizes 5-ht1a but antagonizes 5-ht2, 5-ht3, and other. Very rarely in nature, will you find compounds that affect the system as bluntly as the SSRI's do. The result, like I said, is a free for all. Doctors often try to augment with atypicals, since they block some of the undesirable serotonin receptors.
Linkadge
Posted by Squiggles on May 21, 2006, at 6:45:11
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by linkadge on May 20, 2006, at 23:27:39
> >Why would any chemist make an antidepressant
> >that interferes with the release of dopamine?
> >Isn't dopamine supposed to alleviate depression >and other negative emotions?
>
> This is it. Fast acting antidepressants generally work via affecting dopamine release.
>
> When you take an SSRI, you are stimulating a number of serotonin receptors that will indirecectly supress dopamine release (for a while at least untill some sort of compensatory adapation takes place)
>
> 5-ht1a, 5-ht2a/c, 5-ht1b, (and others) act as indibitory pathways on dopamine function.
>
> Sure SSRI's are selective to serotonin, but not to specific serotonin receptors, as a result the final product is often a wild free for all.
>
> In contrast however, consider some endogenious neuromodulators such as anandamide. Anandamide agonizes 5-ht1a but antagonizes 5-ht2, 5-ht3, and other. Very rarely in nature, will you find compounds that affect the system as bluntly as the SSRI's do. The result, like I said, is a free for all. Doctors often try to augment with atypicals, since they block some of the undesirable serotonin receptors.
>
>
>
> Linkadge
>
>There seems to be a vogue for "agonizing" (i guess that is stimulating) serotonin receptors, which a friend of mine tells me are all over the the brain and body and the most numerous. I guess they are a bit like endocrine glands on a neurological level. BTW, I see here that anandamine is what cannabis stimulates:
http://www.steve.gb.com/science/nervous_system.html
But as you probably know, that really gets you stoned.
Are there any drugs that stimulate the dopamine receptors; Or even drugs that stimulate or are a clone of dopamine for depression? L-dopa is used in Parkinson's disease, and one of its side effects is the same as the effect of an anti-depressant.
p.s. It's amazing how simple and different the action of lithium is in comparison to man-made ADs.
Squiggles
Posted by Squiggles on May 21, 2006, at 7:27:25
In reply to Re: Statistical question on SSRIs - ADDENDUM » linkadge, posted by Squiggles on May 21, 2006, at 6:45:11
p.s. It's amazing how simple and different the action of lithium is in comparison to man-made ADs.
>
>
> Squigglesoops, not so fast, and not so simple;
but lithium does feel simple and natural
in comparison to man-made drugs for some reason;
i suppose the same can be said for many others, e.g. cannabis, heroin, quinine, caffeine.http://bipolar.about.com/od/lithium/
Squiggles
Posted by linkadge on May 21, 2006, at 15:46:42
In reply to Re: Statistical question on SSRIs - ADDENDUM » linkadge, posted by Squiggles on May 21, 2006, at 6:45:11
Yeah, there are serotonin receptors in the stomach, and hence the initial nausia and GI problems that SSRI's can cause.
Anandamide is like the brains version of THC. Ie both bind to the cannabanoid CB1 receptors.
Linkadge
Posted by Larry Hoover on May 22, 2006, at 17:32:04
In reply to Re: I rescind the DNP, posted by Squiggles on May 19, 2006, at 15:54:49
> I just dropped by ASDM and saw your post
> to me. It was very clever of you to
> post it there and not here, as it would
> not have met the civility bounds here.Dr. Bob does not allow certain forms of communication. I clearly said that, in the opening sentence. Not clever. Attentive. I saved you from being blocked, Squig. You're welcome.
Lar
Posted by Larry Hoover on May 22, 2006, at 17:58:03
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by linkadge on May 20, 2006, at 2:13:31
> >Anecdote. What is anecdote? It is an >uncontrolled experiment with one subject. What >have you got when you collect one thousand >anecdotes? One thousand different uncontrolled >experiments with one thousand different subject >populations. Anecdote is a point in space. How >do you extrapolate from one point?
>
> Hopefully anecdotal instances might persuade the initiation of a host of more systematic experimentation.Unfortunately, I'm not arguing against that.
> You compare the incidences of such events between both groups, and you discover what many such trials are indicating, that SSRI's statistically seem to increase the likelyhood of such feelings.
When a recent study was published, and posted here, you dismissed the evidence made available by it. Pre-treatment suicidality was substantially higher than post-treatment measures, in the study population.
http://ajp.psychiatryonline.org/cgi/content/full/163/1/41
If you only look at the immediate post-treatment period, then your a priori assumptions force the effect of treatment itself to be your new baseline for the observation period. However, if you compare pre-treatment to post-treatment, the suicidality is substantially reduced. You are blinded by your experimental protocol, link.
In other words, under the paradigm you envision, you are doing a within-groups comparison, but you don't realize it. They're all treated subjects, but you're thinking as if the placebo is not treated. That is not the case. Placebo is a treatment.
> Perhaps nobody actually kills themselves in such trials, but the information will lend merrit to many of the anecdotal reports.
If anybody did kill themselves, and it was part of your experimental hypothesis, then you would be forced to terminate the study. That's what I'm saying, link. You can't do the research you envision, on ethical grounds. You'd never get it past an ethics committee. And even if you did, the moment you collected any evidence, you'd have to shut it down.....before you had any statistically meaningful evidence.
> I think that part of the mannagment, is in coming to terms with the extent of the problem.We know the extent of the problem. It seems, though, as if you wish to extrapolate your experience to all people. The study I linked to, above, is clearly inconsistent with your thesis.
> There is still such a devide. Either they cause people to kill themselves, or they do no such thing.
I only wish *any* science was that clear cut. With people as subjects...??? Forget about it.
> Lets suppose that there is something really quite unique about the individuals who have such negitive reactions to SSRI's. Its like we've skipped back 40 some odd years, when MAOI's were not known to interact with tyramine. Sure, only some people were dying, and nobody knew exactly why. We still have yet to discover why people are reacting this way. It is still a drug problem, just like MAOI dietary interactions were a drug problem. It is my belief that we simply don't know the mechanism yet.
>
> LinkadgeDid we stop using MAOIs? No. Did we modify the drugs? No. Did we manage patients better, based on what we learned? Yes.
The MAOIs haven't changed one lick. We did. We manage them better. We have a medical management issue here, not a drug issue. The drugs are what they are. We either manage them in such a way that nobody gets hurt, or we don't. So far, we weren't doing very well. So far, we believed the marketing hype. Even wise doctors got hoodwinked. By our own human nature. We wish it was as easy as taking a happy pill. Oh, we wish.
Lar
Posted by Larry Hoover on May 22, 2006, at 18:03:15
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by linkadge on May 20, 2006, at 2:21:35
> I have actually seen a few clinical trials in which *healthy vaulenteers* were given placebo, or active SSRI. It seemed that the SSRI's were actually producing things like acute apathy, acute akathesia, insomnia, agitation, and suicidal feelings, whereas placebo group experienced no such events.
I can give insulin to healthy volunteers and kill them with it, whereas the target population finds the "drug" to be a wondrous benefit. Perhaps what you are describing is the inappropriate use of the drugs, all the while. Perhaps, if these things happen, you're proving the person didn't need the drug.
Unfortunately, there is no way to know. Not that I can think of, and I've spent a lot of time trying to figure a way. I'd love to prove your hypothesis, one way or the other. I really would. SSRIs nearly killed me. Serzone was perhaps one day from taking out my liver. I really am on your side, link. I only wish we could answer the question. If the evidence was available, I would be thrilled to post it here.
> This is an important type of trial, since in studies such as this we cannot lean back to the old "well this population was depressed anyway".
>
> I have seen reports of psychiatrists self testing SSRI's and having similar findings.
>
> LinkadgeSo long as there is an alternative plausible explanation, then you have not proven your case. I believe I gave a very plausible alternative theory.
Lar
Posted by Larry Hoover on May 22, 2006, at 18:12:05
In reply to Re: Statistical question on SSRIs - ADDENDUM, posted by linkadge on May 20, 2006, at 3:03:59
> "It is a class effect of pharmacological treatment of mood disorders. If you're going to treat depression with drugs, you get this effect."
I now realize I was actually thinking of antidepressant treatment. My apologies. Please allow for the rephrasing, to read "treatment of depression" rather than of mood disorders. My first sentence and second one were not well matched.
> Thats not true at all. Its called SSRI induced akathesia. Some drugs induce more akathesia. Some drugs have a higher likelihood of inducing such events. To try and package it all as one deal is foolish, and reeks of carelessness.
Suicidality is higher with tricyclics and MAOIs than with SSRIs, according to the BMJ data published earlier this year. Current, real-time data gives SSRIs a lesser, but similar effect. I did not mean to suggest identical.
> The shear body of evidence, for instance, indicates that lithium prevents suicides better than depakote does. That is statistically significant. It is not a "bipolars are going to blow off their heads anyway so it doesn't really matter much what we give them".
Fair enough.
> There are better treatments, and there are worse treatments.
>
> Some antidepressants made me suicidal, others did not. No, I don't know the exact mechanism, but I sure don't think that it was just coincidence. Just like citalopram gave me anorgasmia and remeron did not. Drug induced suicidality is not a general consequence of drug treatment of depression, and if it is currently, then it needent be. A drug should make you better, not worse.In fact it *is* a general consequence of antidepressant treatment, and it always has been the case. The data are consistent, through our historical experiences with the drugs.
I wish you were correct, but I believe that you are not.
> Opium never made a depressed suicidal insomniac want to jump off a bridge. If somebody is about to jump of a bridge, shoot them in the leg with a dart of MDMA. I'm shure they'd first step off the ledge, then they'd come give you a warm hug for saving their life.
Getting someone high is hardly a long-term solution to anything.
> It's called SSRI's are lousy. We simply need better antidepressants.
>
> Good antidepressants work.
>
> LinkadgeI feel your pain. I really think I know it well. I just can't find any evidence for true antidepressant efficacy or safety, anywhere. But they're better than the alternative, when averaged over the population. Some individuals will suffer excessively. I'm sorry that's the case for you.
I'm stopping now.
Lar
Posted by linkadge on May 23, 2006, at 17:14:17
In reply to Re: Statistical question on SSRIs - ADDENDUM » linkadge, posted by Larry Hoover on May 22, 2006, at 17:58:03
>When a recent study was published, and posted >here, you dismissed the evidence made available >by it. Pre-treatment suicidality was >substantially higher than post-treatment >measures, in the study population.
I dismissed nothing. Different studies say different things. You believe what you want to.
>If you only look at the immediate post->treatment period, then your a priori >assumptions force the effect of treatment >itself to be your new baseline for the >observation period. However, if you compare pre->treatment to post-treatment, the suicidality is >substantially reduced. You are blinded by your >experimental protocol, link.
Often in such studies, if a researcher has reason to believe that a treatment is indeed increasing suicidiality, then the treatment is withdrawn.
Many studies are simply ended if researchers believe that the active treatment is causing suicidialtiy. So, is that information taken into consideration? Probably not. In addition, I don't trust studies in general.
>In other words, under the paradigm you >envision, you are doing a within-groups >comparison, but you don't realize it. They're >all treated subjects, but you're thinking as if >the placebo is not treated. That is not the >case. Placebo is a treatment.Of course placebo is treatment. It is treatment without the burdon of side effects. This is why the placebo often produces a more robust clinical effect.
>If anybody did kill themselves, and it was part >of your experimental hypothesis, then you would >be forced to terminate the study. That's what >I'm saying, link.
No, thats what I am saying. Think of all the clinical trials that we don't know about. The trials which might support my hypothesis, but were ended because of the conclusions which were reached.
>You can't do the research you >envision, on >ethical grounds. You'd never get >it past an >ethics committee. And even if you >did, the >moment you collected any evidence, you'd have >to shut it down.....before you had any >statistically meaningful evidence.You seem to think that my opinion is going to be swayed in any way by my lack of conclusive "scientific" evidence. I never set out to try and convince anybody but myself.
There are plenty of bits and pieces of information which I piece together to come to my conclusions. Studies are just studies. They need to be taken with a grain of salt.
For instance. I saw a study intitled: "Wellbutrin has strong Antianxiety Properties", published in the journal of clinical psychiatry. Do I believe such a study? No, I think it is GSK trying to attack the one reason that their medication is not prescribed more, which is that it is precieved to increase anxiety. Straight from the boardroom: "Design us a study that shows Wellbutrin does not increase anxiety"
>We know the extent of the problem. It seems, >though, as if you wish to extrapolate your >experience to all people. The study I linked >to, above, is clearly inconsistent with your >thesis.
We do not know what the extent of the problem is. That is why we are asking ourselves (and currently creating the studies to test the hypothesis) whether or not the increased indicidence of SSRI induced suicidiality actually extends to adults.
>I only wish *any* science was that clear cut. >With people as subjects...??? Forget about it.I am not saying that the science is that clear cut. All I am saying is that it is a binary situation. Either the person was going to kill themselves anyway and the med had no effect. Or, the person was not going to kill themselves and the med pushed them over the edge. No, I realize nobody can know for sure, unless we had a time machiene. But it can still be considered a binary situation nonetheless.
>Did we stop using MAOIs? No. Did we modify the >drugs? No. Did we manage patients better, based >on what we learned? Yes.
Well, the rate of prescription of MAOI's is significantly less than what it would have been had the meds not had this problem. So in a sence, yes, we did stop using the drugs (though not entirely) based on our findings. Many doctors believe they are superior antidepressants, but they are shunned because of this side effect. Perhaps when newer antidepressants come out, doctors will say, "oh we don't like to use the SSRI's anymore cause they can make some people suicidal".
>The MAOIs haven't changed one lick. We did. We >manage them better. We have a medical >management issue here, not a drug issue. The >drugs are what they are. We either manage them >in such a way that nobody gets hurt, or we >don't.I wish it was that easy. If doctors believed that the potentially lethal side effects of the MAOI's could be completely mannaged, then the drugs would likely hold a larger portion of the market. But the fact remains, that even the best management cannot completely eliminate their risks. Its the same with SSRI's. There is absolutely no way that doctors can contain SSRI induced suicidialty. Perhaps it can be limited, or reduced. All the management in the world is not going to change the nature of the drug, or the nature of how people respond to it. We can't lock people up till they get over that "hump".
Linkadge
Posted by linkadge on May 23, 2006, at 17:30:33
In reply to Re: Statistical question on SSRIs - ADDENDUM » linkadge, posted by Larry Hoover on May 22, 2006, at 18:03:15
>I can give insulin to healthy volunteers and >kill them with it, whereas the target >population finds the "drug" to be a wondrous >benefit. Perhaps what you are describing is the >inappropriate use of the drugs, all the while. >Perhaps, if these things happen, you're proving >the person didn't need the drug.
Anyone, for whom the drugs are not fixing a genuine chemical imbalence, does not need the drugs. Thats a lot of people who are probably responding similarly to the "healthy vaulenteers".
In a fantasy world, it all fits together. You start with the assumption that the drugs are actually fixing something that is wrong with the depressed brain. Under those pretenses a whole host of false conclusions can be reached. Ie. the conclusion that the depressed brain is going to mystically respond completely differently to the drugs than healthy vaulenteers, which may or may not be true. You can predict almost every other side effect of SSRI's with healthy vaulenteers, from insomnia, to sexual side effects. Why does the line stop at suicidial ideation ?
We are wrong in thinking that one size fits all depressed people. Depression is a manifestation of perhaps dozens of different biochemical peterbations.>Unfortunately, there is no way to know. Not >that I can think of, and I've spent a lot of >time trying to figure a way. I'd love to prove >your hypothesis, one way or the other. I really >would. SSRIs nearly killed me. Serzone was >perhaps one day from taking out my liver. I >really am on your side, link. I only wish we >could answer the question. If the evidence was >available, I would be thrilled to post it here.
I agree its very up in the air. Heck, you might even find some doctor who would convince you that luvox is safe for you to try again, and that your reaction was a freak outburst of your clinical condition. But you know what you know. I'm certainly not asking you to explain to me why you decide not to take luvox again. You know whats best for you, and you don't really need the science to support you.
>So long as there is an alternative plausible >explanation, then you have not proven your >case. I believe I gave a very plausible >alternative theory.
But thats what I don't understand. I am not trying to proove anything. An evolutionist, for instance, can argue his points, but he cannot proove anything. If you are looking to be convinced, your talking to the wrong person.
Linkadge
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