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Posted by linkadge on February 11, 2006, at 8:44:31
In reply to Re: The dramatic rise of mental illness » detroitpistons, posted by yxibow on February 11, 2006, at 7:45:32
The problem as I see it is this devide that we create. Doctors and patients don't see any inbetween. We take black and white stances on the safety and efficacy of these meds. Drugs are either miracles, or they are the demonic. People don't take any inbetween ground.
We can easily push of stuff as fluff, but whenever I do that at least, there is always a voice that comes asking all the unanswered questions.For instance, the FDA ruled again just a little while ago, that drug companies do NOT have to provide long term information about the safety and efficacy of their medications.
The safety of these drugs is based on drug company's assumption that we are not going to use them for more than 6 months.
But when one injests these substances so chronically: months, years, decades even, there are absolutely no guarentees.
They didn't do the studies back whenever that showed that APs cause irreversable structural problems to the brain. Alterations that cannot be attributed to the disease since these changes can easily be produced in healthy mice taking the drugs.
Its easy to say, oh well this study sites Breggin, so I don't need to believe any of it. But no matter how I take my medication, there will always be those nagging telltale signs for me that perhaps these people are on to something.
Linakdge
Posted by Meri-Tuuli on February 11, 2006, at 8:57:49
In reply to Re: The dramatic rise of mental illness, posted by linkadge on February 10, 2006, at 19:21:27
I have to agree with you link.
I do think that we are overmedicated in general. People seem/demand/expect to take a pill for every slight nuance of disorder (or even for 'personality enhancement'), rather than trying to uncover the underlying problems. I think that pills just mask the underlying problems, and they won't go away once you've finished the pills. I likened it to taking an aspirin for a hangover headache - the aspirin masks the headache so it doesn't hurt, but you've still got a hangover, you just can't feel it anymore, but your bodies still recovering from all that alcohol you drank!
Anyway, perhaps the pill companies are very keen to have as many people as possible diagnosed with mental illness - thats one way to boost sales. You don't see counselling companies making the ftse 100 do you?
I also tend to think that there's this 'ideal' that we prescribe to - being super happy and successful all the time. Media stereotypes enhance this, making us feel more inadequant if we don't have supermodel looks, a brillant career etc etc, which, lets face it, who does?
And I also think that people are less likely to put up with negative life experiences without some form of chemical enhancement from the doc - life is very painful at times for everyone, thats just plain fact. And it wouldn't be human if we didn't experience these things. It is unrealisitic to expect to be full of energy/happy/productive/shiny at all times.
But then, there are severe instances out there that do need pills - what I'm saying is that we shouldn't be nearly so quick to pop pills in the first place and alot more emphasis should be placed on other approaches....okay so they might take alot more dedication/hard work (I'm thinking exercise/therapy/nutritional/time/etc other approaches) but they are harder work and people just want a 'quick fix' - I mean who doesn't? But thats not how it works, does it? Its like taking diet pills - you might lose alot of weight and fast, but when you start eating like you did and stop the pills, you put it straight back on. Permanent, lifestyle changes are needed - there's no quick fix.
Hmm....well just my two cents, or whatever the phase is.....
> You are right, everbody is on somthing.
>
> We use the excuse that this is a board of treatement resistant patients, and our experiences are by no means indicitive of the population at large. I would argue that our experiences are *very* indicitive of the effects in the population at large.
>
> We're just a group that is computer literate.
>
> Linkadge
>
Posted by linkadge on February 11, 2006, at 9:05:54
In reply to Re: The dramatic rise of mental illness » detroitpistons, posted by yxibow on February 11, 2006, at 7:45:32
I don't think we're all that advanced either. Sure we have more tools these days to poke around, but are people actually getting any better?
Sure there are cases of people commiting suicide before meds, and there are also cases of those who do so even on meds. My mother tried to commit suicide and she claimed it was the tegretol that made her so depressed.
We are so far from individually tailoring meds. If you are depressed, you three options, tweek your serotonin, tweek your norepinephrine, or both.
If the drugs were half as efficatious as doctors claim, we would see significant declines in mental illness, and suicide rates but we havn't.
Suicide rates have wobbled up and down since Thorazine. The lowest suicide rate in the century was pre-meds.I've been on more meds than people thrice my age, but they never really did anything. If we were really "hitting the target" then people wouldn't have to keep upping their dose every two weeks.
Linkadge
Posted by ed_uk on February 11, 2006, at 9:08:54
In reply to Re: The dramatic rise of mental illness » yxibow, posted by linkadge on February 11, 2006, at 8:44:31
>The problem as I see it is this devide that we create. Doctors and patients don't see any inbetween. We take black and white stances on the safety and efficacy of these meds. Drugs are either miracles, or they are the demonic. People don't take any inbetween ground.
That's very true Link. I always try my best to see the middle ground.
Ed
Posted by linkadge on February 11, 2006, at 9:13:40
In reply to Re: The dramatic rise of mental illness, posted by Meri-Tuuli on February 11, 2006, at 8:57:49
I agree with everything you've said.
How to we create depression in animals? We subject them to mild chronic stressors.
Life can be a mild chronic stressor. I think the pain is a signal. A signal that something is wrong with the way we are doing things.
Its easy to push away all those signals and just say I am chemically imballanced.
I have a theory that poop out is simply: "your brain knows better, and it can't be fooled that easily"
Linkadge
Posted by pseudoname on February 11, 2006, at 12:00:21
In reply to The dramatic rise of mental illness, posted by detroitpistons on February 10, 2006, at 13:39:25
What a great thread. Thanks for starting it, DP.
I am also deeply ambivalent and skeptical about psych meds, even as I keep taking them. But without denying any of the comments in this thread, I still want to point to some problems in Whitaker's essay.
As others have said, our current infrastructure, motivations, and techniques for diagnosing mental illness are enormously different than they were even 50 years ago, let alone 100. The rates are just not comparable. From my own family's anecdotes, I know of a dozen cases in my extended family 1900-1950 that were not formally diagnosed or "in the system" but would surely be diagnosed and in the system now.
Whitaker cites Healy saying the response rate for in-patients was better 100 years ago, even though they were worse off at admission. But if one group is worse off, their higher improvement rate could be explained simply as regression to the mean. If there are different inclusion criteria, then the two groups are simply not comparable. And since the 1900-era inpatient non-horrific treatments are all still available and given at least to a lucky few (rest, seclusion, beautiful surroundings, etc), current persuasive data for that approach should be available. Whitaker doesn't cite any. I've tried the rest/seclusion thing: it's better than high-stress living, but it was no cure for me. Very sadly.
Whitaker focuses on SSRI-induced mania. But that real problem doesn't explain why there are more people diagnosed with depression (and thus taking the SSRIs) to begin with. Whitaker also doesn't back up his assertion that people who have bad responses to SSRIs are "well along on the road to permanent disability", but it's a sobering possibility.
Even if the actual incidence of mental illness is rising (not just the diagnoses), the fact that it roughly correlates with increased prescriptions proves nothing in itself. When sales of sunglasses increase, the rate of drownings also increases, but sunglasses don't cause drownings. Both are caused by a third factor, people going to beaches and pools in warm, sunny weather.
As others have posted, there are many possible "third factors" that may be making people today more likely to have mental illness. I always think of the study showing that exposure to lots of TV images before age 3 changes brain development and leads to attention problems at the very least.
Another factor Whitaker leaves out is current research showing that untreated depression leads to actual, long-term physiological changes in the brain and other increased illness and mortality. (Like Peter Kramer summarized in "Against Depression".) Maybe without psych meds, our overall statistics today would be even WORSE. That idea has as much of a basis as Whitaker's conclusion.
That said, I agree that psych meds are oversold by pdocs and the media, and the many problems with them are not considered enough by docs or authorities. Maybe articles like Whitaker's, for all the problems I see in them, help by getting more people talking about it. My fear is that they lead to defensive, dismissive reactions from the system's "experts".
Like I said, this is a great discussion. I hope I've contributed to it and not detracted from it. Sorry I went on so long.
Posted by ed_uk on February 11, 2006, at 12:20:28
In reply to but correlation is not causation, posted by pseudoname on February 11, 2006, at 12:00:21
An excellent post PN.
Ed
Posted by detroitpistons on February 11, 2006, at 12:20:55
In reply to but correlation is not causation, posted by pseudoname on February 11, 2006, at 12:00:21
> What a great thread. Thanks for starting it, DP.
Glad I could contribute!
Posted by pseudoname on February 11, 2006, at 13:09:12
In reply to Re: but correlation is not causation » pseudoname, posted by ed_uk on February 11, 2006, at 12:20:28
Posted by pseudoname on February 11, 2006, at 13:36:48
In reply to Thanks! (nm) » ed_uk, posted by pseudoname on February 11, 2006, at 13:09:12
Sorry, I can't resist. :)
Another possible reason the DIAGNOSIS RATE of mental illness may be rising:
Almost all other diseases are getting diagnosed effectively. So a doctor in 1900 might say (half-guessing) that his patient had "poor blood" or whatever. Today's doc knows tons more about blood and has super-excellent blood tests. She rules out all blood problems and is left to say (half-guessing) that her patient is depressed.
Another possible reason the ACTUAL INCIDENCE of mental illness may be rising:
Most other diseases are getting treated effectively. So, people who would've died from infections, injuries, diabetes, heart attacks, etc, are surviving long enough to develop mental illness. If people had lived longer in 1900, they might've developed mental illness at the same rate.
Hmmm. Is that flawed reasoning?
(PS: Not saying ADs & APs are off the hook.)
Posted by zeugma on February 11, 2006, at 14:23:06
In reply to two other factors?, posted by pseudoname on February 11, 2006, at 13:36:48
cited in the article.
That study is now generally acknowledged to have used a dose of phenelzine that was inadequate (45 mg/day). Healy, in "The Antidepressant Era", cites this as the study which defined 'typical' depression as that which responds to TCA's, because MAOI's were 'shown' to be placebos. Hence the strange terminology imposed on the DSM in which 'atypical' depression is probably actually typical, if we take 'typical' to refer to commonest subtype. Now we have 'atypical' antipsychotics that appear to be typically applied to everything, including subtypes of bipolarity earlier generations of psychiatrists would doubtless have called anxiety disorders because they responded to benzodiazepines.
it's very easy to be impressed by studies, whether positive or negative. Too easy, I think.
-z
Posted by pseudoname on February 11, 2006, at 14:47:42
In reply to about that 1965 MRC study, posted by zeugma on February 11, 2006, at 14:23:06
> it's very easy to be impressed by studies, whether positive or negative. Too easy, I think.
A few months ago I read a scientist (not in mental health) saying that the best way to look at peer-reviewed, published studies is that they're just "suggestive", no matter how solid or persuasive they seem.
Posted by linkadge on February 12, 2006, at 15:07:08
In reply to but correlation is not causation, posted by pseudoname on February 11, 2006, at 12:00:21
The problem with the notion that antidepressnts improve the course of depressive illness is that there is not a lot of data to support the view.
There are arguements put forward that depression becomes a much more chronic illness, after it is treated with antidepressants.Practically everybody on Effexor these days has been told that their depression will require life-long treatment. I personally think that doctors are just trying to safe themselves the blame when a patient must go through a hellish withdrawl.
More specifically though, there have been recent articles on the notion that antidepressants are neuroprotective, and that they may reduce volumetric changes induced by depression.The truth is that in regards to neuroprotection, not all antidepressants were created equally. Many of the studies that claim "antidepressants are neuroprotective" used the drug Tianeptine, or lithium.
Direct comparisons between say fluoxetine and tianeptine show that tianeptine, but not fluoxetine prevents the stress induced morphological changes in cerebral metabolites.
Dr. Manjii was done extensive work into this. He has noted that antidepressants do not alter the progression of hippocampal morphology. He is biased towards lithium, because of his line of work, but his research is very extensive.
The below study compares Tianeptine to fluoxetine and desipramine. Neither prozac nor desipramine produced any neuroprotective effect.
http://www.tianeptine.org/tianeptine/tianeptine-2.htm
I am not the first one to bring up this point.
Also see:
http://ajp.psychiatryonline.org/cgi/content/full/161/7/1309-a
These are important things to clarify, because it is very necessary to get a clear image of what the drugs do, and don't do.
Linkadge
Posted by linkadge on February 12, 2006, at 15:09:06
In reply to two other factors?, posted by pseudoname on February 11, 2006, at 13:36:48
No, but it just makes one wonder. I remember doing a small poll in one of my classes. 1/4 of the class was on antidepressants.
I remember saying to myself, what the f*ck ?
Linkadge
Posted by linkadge on February 12, 2006, at 15:16:25
In reply to Re: about that 1965 MRC study » zeugma, posted by pseudoname on February 11, 2006, at 14:47:42
In addition, because of the addictive potential of the drugs, a lot more people are going to *stay* on the medications. People may have fully recovered, but they will never know it because they have to take their medications much longer than they need them.Withdrawl symptoms are often identical to original depressive symptoms so people just stay on their medications forver, because they just don't know what is well anymore.
So you've got drug companies pushing highly addictive drugs, to people who may not need them, of course the number of people dependant on SSRI's is going to go up.
I personally liked the study that compared Zoloft to exercise. The Zoloft group initially did better, but after a few months, the exercise group was significantly better that the zoloft group.
BUT, what was most interesting was that the exercise alone group was doing better than the Exercise + Zoloft group! This to me was evidence that the drug was actually hinerding recovery.
Linkadge
Posted by zeugma on February 12, 2006, at 15:29:29
In reply to Re: two other factors?, posted by linkadge on February 12, 2006, at 15:09:06
> No, but it just makes one wonder. I remember doing a small poll in one of my classes. 1/4 of the class was on antidepressants.
>
> I remember saying to myself, what the f*ck ?perhaps your classroom is an unrepresentative sample (just kidding).
but about neuroprotection and antidepressants:
this study claims that amitriptyline decreased age related impairments in water maze learning in rats. The same researchers then showed that fluoxetine failed to produce beneficial effects using the same parameters:
So are we to conclude that tianeptine, amitriptyline, lithium, but not fluoxetine are neuroprotective?
Anecdotal evidence: I am certain that my performance on spatial tasks has improved tremendously since starting my current regime of nortriptyline three and a half years ago. Extrapolating from my own experience, or that of tree shrews or aging rats, has its dangers. But we do have to decide what evidence we are to take seriously and what disregard, and our own experiences usually cast the final vote in these matters.
-z
>
> Linkadge
Posted by zeugma on February 12, 2006, at 15:44:05
In reply to Re: two other factors? » linkadge, posted by zeugma on February 12, 2006, at 15:29:29
this was the passage that I was thinking of when I said that AMI was neuroprotective in aged rats, in contrast to fluoxetine:
Interestingly, chronic amitriptyline treatment altered a specific aspect of water maze learning in the aged rats. The escape latency to find the hidden platform, thought to reflect the consolidation of spatial information via GRs (Oitzl and de Kloet, 1992), was unchanged. Furthermore, aged controls and amitriptyline-treated aged rats both had approximately equivalent declines in performance over the 6 month interval from initial testing in the water maze. This suggests that long-term memory does not appear to be preserved by amitriptyline treatment. In contrast, the search-escape strategies during the probe trial, thought to be more reflective of the actions of the MR (Oitzl and de Kloet, 1992), were enhanced in amitriptyline-treated aged rats. Together, this suggests that amitriptyline treatment may induce changes in hippocampal MR to alter the probe test times without affecting escape latencies. Previous studies have indeed shown that antidepressants, including amitriptyline, induce a more prominent effect on increasing hippocampal MR than GR expression and that the magnitude of this increase is dependent on treatment duration (Reul et al., 1993, 1994; Yau et al., 1995). Moreover, several studies suggest that it is the MR in the hippocampus (rather than the GR) that shows the more robust decline with aging (van Eekelen et al., 1991; Rothuizen et al., 1993; Hassan et al., 1999). >>
-z
Posted by pseudoname on February 12, 2006, at 18:00:39
In reply to Re: but correlation is not causation, posted by linkadge on February 12, 2006, at 15:07:08
> These are important things to clarify, because it is very necessary to get a clear image of what the drugs do, and don't do.
And a satisfactorily clear image is what we don't yet have, positive or negative. That's my feeling, anyway.
Posted by joslynn on February 12, 2006, at 21:53:52
In reply to Re: about that 1965 MRC study, posted by linkadge on February 12, 2006, at 15:16:25
(link wrote) "In addition, because of the addictive potential of the drugs, a lot more people are going to *stay* on the medications. People may have fully recovered, but they will never know it because they have to take their medications much longer than they need them.
Withdrawl symptoms are often identical to original depressive symptoms so people just stay on their medications forver, because they just don't know what is well anymore. " (end quote)
THAT is where I get all confused. I did feel depressed when I tried to taper off a while ago, but how do I know if it was withdrawal or the actual depression coming back? I was so afraid of a relapse that I went back to my usual dose. Before going on meds, I had two very severe depressions with several years of so-so living in between. The second episode required hospitalization. That was when I finally gave in and tried the meds.
Whenever I think of trying to go off again, I get scared by people saying that going off, then getting depressed again, and going back on the same thing to try to get better again doesn't work anymore.
So, it can be very confusing to decide what to do next. Since being on meds, my life and mood are much, much better. But I started therapy the same time that I started meds. So how do I know that wasn't what helped?
And when I think, well, I will know by going off meds, I get scared that then that same med will not work as well if I need it again.
The fact that I am not depressed today is something I am eternally grateful for, but in addition to God, should I thank the meds, or therapy, or just time, or what? And will I get a brain tumor one day and wonder, hmm, was it the meds that did it?
It is very hard to understand your own brain with your own brain! To me, it feels like trying to step on your own shadow while you are walking.
Posted by linkadge on February 13, 2006, at 10:01:05
In reply to Re: two other factors? » linkadge, posted by zeugma on February 12, 2006, at 15:29:29
Well I know that amitryptaline certainly worsened my water maze learning :)
But I guess what I am trying to say is that there have been some studies that show certain effects on cognition and neuroprotection, but we need to not extend those findings to an entire class of medications.
For instance, one study showed zyprexa use led to increase in temporal lobe grey matter, but that all other AP's tested lead to waning of grey matter in the region.
Linkadge
Posted by linkadge on February 13, 2006, at 10:10:38
In reply to clarification, posted by zeugma on February 12, 2006, at 15:44:05
There have also been a number of studies done on the detrimental effects of TCA's on memory and leaning. Amitryptaline is a potent anticholinergic. Its effects on water maze learning may be due to an enhancement of noradrenergic function, but this is only one test of memory.
http://biopsychiatry.com/dumbdrug.htm
Linkadge
Posted by linkadge on February 13, 2006, at 10:17:59
In reply to Re: but correlation is not causation » linkadge, posted by pseudoname on February 12, 2006, at 18:00:39
I realize, but one's brain is a very complex thing. You need to ask yourself how you are going to approach such a situation when safety data is nonexistant or withheald.
If this was the 70's one could keep taking their Thorazine and hope for the best. Perhaps people taking that medicine back then had a hunch too, that it may be doing strange things. I wouldn't ingore a hunch just because it is not scientific.
But I guess if you were being treated for psychosis and you became paranoid that the medicine was damaging your brain, you would have to increase the dose to overcome *that* piece of paranoia.
Its just like antidepressants and pregnancy. Just because the data was not there 10 years ago doesn't mean that the drugs didn't still increase the risk of complications to offspring.
Linkadge
Posted by linkadge on February 13, 2006, at 10:27:14
In reply to Re: about that 1965 MRC study, posted by joslynn on February 12, 2006, at 21:53:52
I went of meds a year ago. The first 6 months I felt more suicidal than I did before I ever started the meds. Right now, I am just back to dysthemic old me :), but I am certainly more functional off meds.
I cannot tell anyone to come off meds because that may not be a good idea. All I know is that depression, even when left unmedicated, almost always resolves within a certain timeframe.
My greatgrandmother went through 4 depressions in a lifetime, each lasting a little over a year. We may say she could have got faster nowadays, and perhaps. But when she got better, she was completely normal, and didn't have to feel drugged for the rest of her life. So AD's may speed recovery, but at what cost.
I am sure that having blunted sex drive for 6 good years of my adolecent development has impacted me now. (I think I may have missed my shot - I don't know if thats possable :)?)
Linkadge
Posted by zeugma on February 13, 2006, at 16:12:46
In reply to Re: but correlation is not causation, posted by linkadge on February 13, 2006, at 10:17:59
Perhaps people taking that medicine back then had a hunch too, that it may be doing strange things. I wouldn't ingore a hunch just because it is not scientific.>>
nor would i. healy tells the story of how patients on Parnate in the early '60's would complain of splitting headaches after eating cheese. the doctors they complained to would laugh and tell them that their imaginations were running away with them. but of course the patients were right and the doctors had to learn about tyramine the hard way (not as hard as their patients of course :-( )
it's like that with many things, the cytochrome P450 sytem was discovered in the 50's I believe, but its clinical implications did not become clear until patients on Prozac and amitriptyline would occasionally die despite 'therapeutic' dosages of amitriptyline. No one wants to find out about these things the hard way so caution is advised, even in the face of a doctors' smirk (and i can imagine a doctor smirking about patients' blaming cheese for their headaches, before the nature of the reaction was described in the Lancet)
-z
Posted by linkadge on February 13, 2006, at 17:18:29
In reply to Re: but correlation is not causation » linkadge, posted by zeugma on February 13, 2006, at 16:12:46
Yeah, I can imagine the doctors reaction.
"whoopsy"
Linkadge
This is the end of the thread.
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