The Pseudoscience of Anti-Psychiatry in PLOS Medicine
OR: How Does This Crap Get Into Reputable Journals?
Moncrieff J, Cohen D. (2006). Do antidepressants cure or create abnormal brain states? PLoS Med. 3:e240 [Epub ahead of print]Here we have a rare example of the anti-psychiatry movement in the realm of academic medicine. Another strain of this movement is represented by Tom Cruise.
Antidepressants are assumed to work on the specific neurobiology of depressive disorders according to a "disease-centred" model of drug action. However, little evidence supports this idea. An alternative, "drug-centred," model suggests that psychotropic drugs create abnormal states that may coincidentally relieve symptoms. Drug-induced effects of antidepressants vary widely according to their chemical class—from sedation and cognitive impairment to mild stimulation and occasionally frank agitation. Results of clinical trials may be explained by drug-induced effects and placebo amplification. No evidence shows that antidepressants or any other drugs produce long-term elevation of mood or other effects that are particularly useful in treating depression.
The essay's argument is incoherent and relies entirely on the following analogy:
Alcohol can relieve symptoms of social phobia, but this does not mean that alcohol corrects a chemical imbalance underlying social phobia.
The authors skip right over their (unstated) assumption that depression has nothing to do with the brain. Hmm, so moods and thoughts are not caused by the brain? Perhaps they are caused by "spooky stuff" -- Cartesian souls or spirits that exist in the ether somewhere.The last sentence of the essay:
We have proposed an alternative drug-centred model of drug action that is consistent with a demedicalised approach to depression.
Um, no they haven't. They gave absolutely no evidence that we should abandon a disease-centered model of psychotropic drug action. It's not clear how antidepressants work, true, but that doesn't mean they're useless. And the concept of "demedicalization" isn't mentioned until that final sentence.
...abandoning the disease-centred model of antidepressant action squarely challenges the notion of depression as a biologically based medical disease. The argument presented here supports claims that the medical concept of depression obscures the diversity of problems and experiences that come to be so labelled, and that social explanations and interventions have been undervalued.That statement about social explanations came out of the blue. But you can read all about it here:
Moncrieff J. (2006). Psychiatric drug promotion and the politics of neo-liberalism. Br J Psychiatry 188:301-2.Sure, overpromotion of psychiatric drugs is bad, the history of psychiatry is littered with many instances of abuse, and really, I'm left-wing and anti-consumption, but... this whole line of reasoning is like creationism, but in the guise of progressive political thought.
The pharmaceutical industry has popularized the idea that many problems are caused by imbalances in brain chemicals. This message helps to further the aims of neo-liberal economic and social policies by breeding feelings of inadequacy and anxiety. These feelings in turn drive increasing consumption, encourage people to accept more pressured working conditions and inhibit social and political responses.
posted by The Neurocritic @ 5:06 PM
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The authors skip right over their (unstated) assumption that depression has nothing to do with the brain. Hmm, so moods and thoughts are not caused by the brain?
I don't see how that's the underlying assumption. Their argument is centered around the assumptions relating to definitions of pathology and palliatives.
Here's their conclusion:
Many patients are led to believe, by their physicians and by advertising, that antidepressant drugs will act on the biological cause of their depressed state by rectifying a “chemical imbalance” [56]. On the contrary, our analysis indicates that there are no specific antidepressant drugs, that most of the short-term effects of antidepressants are shared by many other drugs, and that long-term drug treatment with antidepressants or any other drugs has not been shown to lead to long-term elevation of mood. We suggest that the term “antidepressant” should be abandoned. We have proposed an alternative drug-centred model of drug action that is consistent with a demedicalised approach to depression.
It is centered around (physicalist) mechanics, not metaphysics. Their main point seems to be that antidepressants are a fluke for some people, and shouldn't be labelled as such. In the grand scheme of things, it's a minor quibble. Until there are reliably and widely effective instruments to deal with psychopathology, so-called antidepressants are the best candidates to be named as such.
Hi daksya,
Thanks for stopping by. I do think the PLOS article (and others by those in the Critical Psychiatry Network) makes the assumption that mental illness does not have a biological cause, that it's entirely due to social conditions:
"Critical psychiatry is deeply sceptical about the reductionist claims of neuroscience to explain psychosis and other forms of emotional distress."
--Phil Thomas
I'm a neuroscientist, so I think it's preposterous to posit that schizophrenia is due to only social conditions and not to an intrinsic brain abnormality. How about this one?
Editorials
Patrick Bracken, Philip Thomas
Time to move beyond the mind-body split
BMJ 2002;325:1433-1434 (21 December)
The "mind" is not inside but "out there" in the social world.
Of course, stressful living conditions can have a profound effect on neurophysiology, but that doesn't invalidate the field of biological psychiatry.
mental illness does not have a biological cause, that it's entirely due to social conditions
To reiterate, their objection seems to be less a matter of metaphysics and more about the mechanics, specifically, the choice of schemata. To give an example, suppose I am feeling hungry and see a cookie, so I pick it up and then eat it. This hierarchy of events & conditions can theoretically be described using either folk psychology - "I ate the cookie since I was hungry" - or using neuroscience - "So and so activity in regions X,Y,Z led to a cascade in regions A,B,C which led to another cascade in regions D,E,F..etc". The choice of which frame to use, depends on utility, convenience, comfort..etc. The authors implicitly acknowledge that drugs i.e. physical agents, alter mental functioning (cf. the alcohol quote you cite). What they seem to have a problem with, is claiming that a description based on the grammar of neurotransmitter levels & other biochemical activity is the correct (or most useful) way to approach depression. Labelling certain physical agents as 'antidepressants', given their lukewarm efficiacy, is hence premature.
The authors also say,
"Taking a drug-centred approach to the treatment of depression, we would conclude that no presently known effects of any drugs, including antidepressants, are likely to do more good than harm in the long term."
So all the people who have benefited from antidepressants should stop taking them. Same goes for those taking drugs for bipolar disorder and schizophrenia.
Take a look at the conference agenda for THE LIMITS OF PSYCHIATRY
As it is phrased, the important clause is "no presently known effects of any drugs". They may be extremists but this latest PLoS paper isn't a good illustration of that. Members of this movement are most likely self-selected dualists and/or puritanicals, who probably subscribe because of the scientific veneer, but there's nothing majorly controversial in their latest paper.
...there's nothing majorly controversial in their latest paper.
Well, there is the claim that antidepressants don't work at all... One could put together a different meta-analysis to dispute the conclusions in the PLoS paper.
But I agree that the paper isn't nearly as radical as many elements of the movement... but it does provide the scientific veneer, as you mentioned.
there is the claim that antidepressants don't work at all
To be fair, the claim is that any relief provided is "coincidental".
But "coincidental" means there's no cause and effect. It's like if you started eating a strawberry Starburst fruit chew every day and then felt better in 4 weeks.
But "coincidental" means there's no cause and effect.
The alcohol quote belies that interpretation. I think what they mean is that these drugs aren't antidepressants, but that's what ends up happening in some proportion of the depressed who take them.
Of course Zoloft ads are misleading, which is why these parodies are so funny:
Proloxil
More ad parodies
Zoloft game
And of course, it would be nice if consumers were given more accurate information about antidepressants and their putative mechanisms of action (and it would be nice if Americans showed higher levels of science literacy).
Notice that I did say,
"Sure, overpromotion of psychiatric drugs is bad, the history of psychiatry is littered with many instances of abuse, and really, I'm left-wing and anti-consumption..."
so it's not as if I'm a drug company hack or something.
I also said,
"It's not clear how antidepressants work, true, but that doesn't mean they're useless."
In fact, I've written about antidepressants and neurogenesis (in a skeptical way):
Prozac and Progenitor Cells
Etiology or Epiphenomenon?
Finally, do you think the brains of depressed people are not at all different from those of non-depressed people?
some magical defect in the brain.
Magical has nothing to do with it, which is the point.
Medicine is interested in curing illness. Science is interested in describing how things work by providing mechanistic explanations.
These two pursuits have different goals. Most doctors aren't particularly invested in knowing exactly how medications alleviate the suffering of their patients, rather they're invested in knowing whether the drugs improve symptoms. How long was aspirin used as a pain reliever before prostagladins were discovered?
Do drugs used to treat other illnesses show the same magnitude of placebo effect?
Yes, some drugs and treatments do.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=PureSearch&db=pubmed&details_term=%22placebo%20effect%22%5BMeSH%20Terms%5D%20OR%20placebo%20effect%5BText%20Word%5D
Drugs and treatments for the relief of arthritis pain, for instance, as one example:
Neustadt D, Caldwell J, Bell M, Wade J, Gimbel J. Clinical effects of intraarticular injection of high molecular weight hyaluronan (Orthovisc) in osteoarthritis of the knee: a randomized, controlled, multicenter trial. J Rheumatol. 2005 Oct;32(10):1928-36.
The effectiveness of the 3-injection regimen (O3A1) was masked by a possible placebo effect from the needle injection procedure in the A4 (control) group.
...creates what the authors of this paper call an "abnormal brain state" that makes patients more capable of thinking through their problems, not because 5-HT2 agonist activity directly results in some underlying change in chemical activity.
Assuming your example of psychedelic therapy is accurate, as a reductionist, I maintain that 5-HT2 agonist activity (and its cascade of consequences) causes patients to be more capable of thinking through their problems. Changes in brain states cause changes in mental states. How does an "abnormal brain state" make patients more capable of thinking through their problems? Wouldn't it be due to neuropharmacological and physiological changes caused by the psychedelic?
Consciousness is a state of the brain.
Not only the conclusions and premises of the authors of this study are wrong, none of their arguments stand ground under careful scrutiny. I have published a post on my blog, http://the-mouse-trap.blogspot.com/2006/08/down-in-dumps-time-to-pop-sleeping.html, that methodically refutes all the steps of their argumnets and may be instructive for those who are debating this artcile. Although, my post is not as strongly titled as Neurocritic's, the feelings are same viz. how does this sort of crap gets punblished?
You seem to have misunderstood what this article is arguing.
It argues that 'antidepressants' should be explained from the action of the drug in the brain (common in many other areas of medicine), rather than on a specific neurochemical marker for a disease.
The latter is problematic in depression because there is no reliable evidence of monoamine deficiency linked to depression. Try and find some on PubMed, all you'll find is inconsistent radiotracer studies and 5HTP washout studies that induce a mild dysphoria at best. See this recent article in Nature Reviews Neuroscience for a review.
The rest of the evidence is taken from the action of certain antidepressants. Hence the circular argument.
Furthermore, nowhere do the authors argue against a biological explanation for depression, only against biological reductionism which is an argument for an exclusively biological explanation.
Calling this article pseudoscience and antipsychiatry is just nonsense, the authors just argue for something which you (and in some place, I) don't agree.
In fact, the article specifically argues for certain drug treatments for depression, based on their interpretation of the literature.
This hardly puts the authors in the same category as Scientology. Your ad hominem attack on the authors really adds nothing to your argument.
gonesavage - thanks for your comments, they illustrate how harmful it can be to deny the existence of an underlying brain abnormality in depression and other psychiatric illnesses. As if you're supposed to get better from talking yourself out of it or CBT alone. I'm glad you found a drug that works for you. Unfortunately, some in the anti-psychiatry movement are ex-patients themselves.
Sandy G - thanks for posting the link to your excellent commentary.
Simon - here's another example of the placebo effect (with a 60% response to placebo).
Clegg DO et al. (2006). Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med. 354:795-808.
RESULTS: ... Overall, glucosamine and chondroitin sulfate were not significantly better than placebo in reducing knee pain by 20 percent. As compared with the rate of response to placebo (60.1 percent), the rate of response to glucosamine was 3.9 percentage points higher (P=0.30), the rate of response to chondroitin sulfate was 5.3 percentage points higher (P=0.17), and the rate of response to combined treatment was 6.5 percentage points higher (P=0.09). The rate of response in the celecoxib control group was 10.0 percentage points higher than that in the placebo control group (P=0.008). For patients with moderate-to-severe pain at baseline, the rate of response was significantly higher with combined therapy than with placebo (79.2 percent vs. 54.3 percent, P=0.002).
As if you're supposed to get better from talking yourself out of it or CBT alone.
On its own, CBT is typically as effective as antidepressants, and is more effective in preventing relapse. The most effective treatment for depression is a combination of CBT and antidepressants.
CBT causes significant brain changes during treatment which partially overlap with the changes caused by antidepressant drugs.
The dichotomy you seem to be making between depression as a 'brain' problem, or as a 'social' or 'psychological' problem is a false one. All psychology happens in the brain and hence depression is related to brain function.
This does not mean that the 'low serotonin' theory of depression is a good theory of what happens in the brain when someone becomes depressed.
Vaughan - It's disappointing that you're defending a view espoused by the Critical Psychiatry Network.
Of course CBT is effective for many people, typically with milder forms of depression. But it doesn't work for everyone, and it didn't for gonesavage (for instance). How do you label those who don't improve with CBT alone?
Depression cannot be cured by willpower, praying, wishing, supplication, toughness, piety, denial or guilt.
I'm aware of neuroimaging studies on CBT. The one you cite says the following:
In studies of major depressive disorder, cognitive behavioral therapy and interpersonal therapy were associated with markedly similar changes in cortical-subcortical circuitry, but in unexpected directions. For any given psychiatric disorder, there was only partial overlap between the brain-imaging changes associated with pharmacotherapy and those associated with psychotherapy.
-Roffman et al. (2005)
The Nature Reviews Neuroscience article says,
It should be noted that the chemical and network hypotheses are not mutually exclusive, but are complementary.
-Castrén (2005)
I'm quite familiar with the neurogenesis hypothesis, and will reiterate that I've written about it in this blog.
Of course CBT is effective for many people, typically with milder forms of depression. But it doesn't work for everyone, and it didn't for gonesavage (for instance). How do you label those who don't improve with CBT alone?
Approximately 30% of people show no effect to antidepressants. How would you label those people? Actually, I wouldn't label them at all. Different treatments work for different people. This is one of the most common findings in medicine. It doesn't mean they don't have similar pathology.
It's disappointing that you're defending a view espoused by the Critical Psychiatry Network.
Again, this is an ad hominem attack. I would rather you addressed the issue rather than the attacking the people who make it.
The fact that one of the authors of the original paper is a member of the Critical Psychiatry Network is really beside the point. It has been made by plenty of other people who are not members of this organisation in the scientific literature.
I fully agree with both the quotes you mentioned. I am not arguing against a neurochemical explanation (neither was the PLoS paper), only an exclusively neurochemical one, or one that is over-simplified to the point of nonsense (i.e. the 'low serotonin hypothesis').
Your article largely attacked the paper based on "their (unstated) assumption that depression has nothing to do with the brain."
I see no such assumption in the paper. You further seem to be suggesting that arguing against the monoamine hypothesis or against the efficacy of antidepressants is "antipsychiatry" and "pseudoscience".
Considering both the monoamine hypothesis and the efficacy of antidepressants have been a matter of much debate in the mainstream psychiatric literature this seems to be a very odd accusation.
BTW, I am not a member of the CPN and do not want to join, but I would not disagree with something purely because someone from the CPN also believes it. As it turns out, I agree with some of what they say, and not other things.
In terms of the PLoS paper, my own opinion is that I agree that the 'low serotonin theory' is largely nonsense based on the current evidence. I don't agree that antidepressants are useless in treating depression, although their efficacy has been overstated in some of the literature.
Importantly, nowhere in the paper does it make the assumption "depression has nothing to do with the brain". In fact, the paper argues exactly the opposite. Otherwise, how could they come to the conclusion that some drugs create brain states that are useful in treating the condition?
I feel you've both misrepresented their argument and used slurs instead of your usual insightful analysis. Perhaps a more considered commentary next time?
Vaughan - Surely, this is a very emotional topic. My reaction to the PLoS article was informed by the authors' other writings on these issues, for instance the implication that neoliberal economic policies cause mental illness...
The pharmaceutical industry has popularised the idea that many problems are caused by imbalances in brain chemicals. This message helps to further the aims of neoliberal economic and social policies by breeding feelings of inadequacy and anxiety.
Moncrieff J. Psychiatric drug promotion and the politics of neoliberalism. The British Journal of Psychiatry (2006) 188: 301-302.
...and also by the fact that I know people who have suffered greatly under the point of view that mental illness can be cured by sheer willpower. Throw away your drugs! The diagnosis of schizophrenia is just a means of social control!
Some in the network espouse these sorts of views:
The Right to be at Risk
Wait till you get to the part about how the author got an erection while listening to a young female patient describe her history of self-mutilation. This was a lecture given at the Critical Psychiatry Network Conference on, "The Limits of Psychiatry," London, 13 June 2003.
Or this:
Understanding psychiatry's resistance to change
...a psychosocial hypothesis regarding the causation of schizophrenia is at least as valid as the hypothesised biochemical theory.
Granted, it's unfair to tar every member with the same brush, and for that I apologize. However, I have not seen any attempt to distance themselves from those viewpoints.
Certainly, there has been much heated debate and disagreement with the meta-analyses cited in the PLoS article:
Throwing out the baby with the bathwater
Efficacy of antidepressants in adults: a partial account of a complex problem
Finally, I'd like to draw your attention to an excellent profile of Helen Mayberg in Scientific American Mind, August/September 2006 (by David Dobbs):
Then, in early 2004, she published a study that drew wide notice and — and threw her for a loop. She scanned two groups of depressed patients undergoing treatment — one with Prozac, one with cognitive behavioral therapy, or CBT. The Prozac patients showed the same pattern as other studies had found – depressed frontal activity that increased in those that got better, and a hyperactive Area 25 that calmed. The CBT patients, however, displayed a new and confounding dynamic: when CBT treatment worked, Area 25 slowed down, as expected, but the frontal areas showed less activity — not more, as had been the case in every other patient group.
P.S. - and I'm really not a cheerleader for the 'low serotonin theory' of depression...
Hi from Shrink Rap. Thanks for inviting us to comment. You've already got a whole discussion flying here, complicated stuff.
Sometimes, it doesn't matter what I read, I'm left with the fact that patients who've really struggled tell me they feel much better on a specific medicine and they want to continue on it. Anecdotal, yes, but somedays we just take what works. Other things are going on as well-- you never give meds in a vacuum-- people's lives change, the psychotherapy helps, the seasons change, other uncontrolled variables occur, sometimes we stop the meds and see and often depression recurs. Since I'm not a neuroscientist, in clinical practice I'm most interested in having people feel better, not in the fine details of their neurotransmitters.
Thank you for commenting, Dinah. And welcome! We've been talking about depression from a neurobiological perspective, but your experience in clinical practice illustrates my previous observation:
Medicine is interested in curing illness. Science is interested in describing how things work by providing mechanistic explanations.
These two pursuits have different goals. Most doctors aren't particularly invested in knowing exactly how medications alleviate the suffering of their patients, rather they're invested in knowing whether the drugs improve symptoms.
The supposedly-proposed drug-centred model is never actually outlined or described as a functioning model in this article (actually an essay). It consists of four criteria, in Table 1:
- drugs create an abnormal brain state [this is also useful in supporting Moncrieff's other recent papers on how antidepressants cause depression and the return of symptoms after drug discontinuation is due to the drugs and not an underlying disorder. How fab it all fits together so well!]
- therapeutic effects are coincidental and depend on social context [contradicts the entire theory put forth that drugs act on symptoms]
- effects do not differ between patients and volunteers [a bizarre and medically naive line of reasoning]
- paradigm: alcohol for social anxiety [rather irresponsible for a psychiatrist to promote the "benefits" of alcohol for anxiety complete with idyllic photo of beer drinking]
Essentially they claim that medications thould be employed based on their subjective psychological effects, rather than pharmacokinetics. A drug that makes you feel happy might be an antidepressant rather than a pharmaceutical that acts on a cluster of targets to relieve a set of symptoms. If antidepressants work, it's because they have mildly sedative effects, so the claim goes. But even this grudging concession is contradicted: "No evidence shows that antidepressants or any other drugs produce long-term elevation of mood or other effects that are particularly useful in treating depression."
Also they dispute that sleep disturbance is a symptom of depression and criticize the HAM-D and other scales for including questions on sleep, claiming that an improved score would be the result of improved sleep and not an improvement in depression. Separating depression from somatic symptoms is another attempt to reposition depression as a purely psychological illness.
The article displays a profound (or stubborn) lack of understanding of neuropsychopharmacology or indeed, pharmacology and biology in general.
But that's unsurprising given their conclusion:
...abandoning the disease-centred model of antidepressant action squarely challenges the notion of depression as a biologically based medical disease [my emphasis]. By contrast, a drug-centred model allows drug treatment to be considered without necessarily accepting a disease model.
How convenient! Hope they enjoy eating that cake.
I'm inclined to agree with this letter to the BJP in response to one of Moncrieff's tireless and varied attacks on psychiatric drugs:
Perhaps the most worrying aspect of Moncrieff's editorial was the implication that we should take either a psychosocial or a physical approach to the treatment of depression. Surely we should have put this rather tired dualist view of psychiatry behind us by now? A holistic view combining drug and psychological treatments is to be preferred [emphasis mine] and evidence is accumulating that this leads to better outcomes. - Anderson and Haddad, 2003, The antidepressant debate should move on.
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Vaughan - the low serotonin hypothesis itself is an ad hominem, since it's not one popular in science. It's an advertising concept and the issue is really one of mass media and not Nature Rev Neuro. Treatment models using a systematic approach combining treatments need to be similarly popularized before that changes in the minds of consumers.
Arguing against something doesn't argue in support of something else. Antipsychiatry suffers from a lack of proposed alternatives, one reason it causes this kind of debate, because it echoes the undercurrent denying existence of illness even when not explicitly stated.
I agree antidepressant is an inaccurate term considering how many other uses they have. What's a better name?
(Probably chemical castration agents wouldn't catch on...)
I agree antidepressant is an inaccurate term considering how many other uses they have. What's a better name?
To just describe the drug's main action or structure. e.g. SSRI, SNRI, NRI, tricyclic, tetracyclic or whatever.
To just describe the drug's main action or structure.
I'm all for that. Specificity is much preferred, whenever possible.
As seen here, from someone who is acknowledged to be at the heart of the alternative treatment crowd.
The point is, are these valid cuases, and do physicians routinely test for these when they dignose schizophrenia?
29 Medical Causes of Schizophrenia – well-known, less-known, and almost unknown
Well-known
1. Dementia paralytica
2. Pellagra
3. Porphyria
4. Hypothyroidism
5. Drug intoxications
6. Homocysteinuria
7. Folic acid/B12 deficiency
8. Sleep deprivation
9. Heavy metal toxicity
Less Well-known
1. Hypoglycemia
2. Psychomotor epilepsy
3. Cerebral allergy
4. Wheat-gluten sensitivity
5. Histapenia – copper excess
6. Histadelia
7. Pyroluria
8. Wilson's disease
9. Chronic Candida infection
10. Huntington's chorea
Almost Unknown
1. Prostaglandins
2. Dopamine excess
3. Endorphins
4. Serine excess
5. Prolactin excess
6. Dialysis therapy
7. Serotonin imbalance
8. Leucine, histidine imbalance
9. Interferon, amantadine, anti-viral drugs
10. Platelets deficient in MAO (monoamine oxidase)
UPDATE: the finding of altered 5HT2A binding in unmedicated, remitted former depressives provides strong evidence against the "drug-centred" view of depression, unless Moncrieff and Cohen now want to postulate that drug effects linger on forever!
Zubin Bhagwagar, Rainer Hinz, Matthew Taylor, Sabrina Fancy, Philip Cowen, and Paul Grasby (2006). Increased 5-HT2A Receptor Binding in Euthymic, Medication-Free Patients Recovered From Depression: A Positron Emission Study With [11C]MDL 100,907. American Journal of Psychiatry 163: 1580-1587.
OBJECTIVE: A previous positron emission tomography (PET) study reported increased serotonin 5-HT2A receptor binding in unmedicated depressed patients with high scores on the Dysfunctional Attitudes Scale. The purpose of the present study was to use the highly selective 5-HT2A receptor ligand [11C]MDL 100,907 in a PET imaging paradigm to assess 1) 5-HT2A receptor binding potential in euthymic subjects with a history of recurrent depression and 2) the relationship between receptor binding and scores on the Dysfunctional Attitudes Scale. METHOD: Cortical 5-HT2A receptor binding was measured in 20 unmedicated, fully recovered unipolar depressed patients and 20 age- and gender-matched comparison subjects. Regional estimates of binding potential were obtained using a reversible plasma input function compartmental model and the cerebellum as a reference region to estimate the free and non-specifically bound [11C]MDL 100,907 in brain tissue. RESULTS: Relative to the comparison subjects, the recovered depressed patients demonstrated significantly higher 5-HT2A receptor binding potential in the frontal cortex (mean increase: 19%), parietal cortex (mean increase: 25%), and occipital cortex (mean increase: 19%). 5-HT2A receptor binding potential correlated negatively with age in both patients and comparison subjects and positively with the Dysfunctional Attitudes Scale in the recovered patients. CONCLUSIONS: These findings should be considered preliminary but suggest that recovered subjects with a history of recurrent major depression have elevated binding potential of cortical 5-HT2A receptors. The correlation of increased 5-HT2A receptor binding potential with increased scores on Dysfunctional Attitudes Scale supports earlier work suggesting that increased 5-HT2A receptor availability characterizes a group of depressed patients with high levels of dysfunctional attitudes.
My issue is Zyprexa which is only FDA approved for schizophrenia (.5-1% of pop) and some bipolar (2% pop) and then an even smaller percentage of theses two groups.
So how does Zyprexa get to be the 7th largest drug sale in the world?
Eli Lilly is in deep trouble for using their drug reps to 'encourage' doctors to write zyprexa for non-FDA approved 'off label' uses.
The drug causes increased diabetes risk,and medicare picks up all the expensive fallout.There are now 7 states (and counting) going after Lilly for fraud and restitution.
--
Daniel Haszard
I disagree with you on this one Neurocritic. Antipsychiatry is not a science like psychiatry. It's instead social commentary, something that misses from today's science. And yes, there are social factors concerning mental disease. Not everything is biological. I have linked to this page as an opposing view, concerning my own article on the subject at http://encefalus.com/sociopolitical/psychiatry-antipsychiatry-history-mental-disease/ . If you wish check it out
Are you saying that moods and thoughts are diseases? Can you prove that?
In my experience, I have been imprisoned in a psych ward, threatened with ECT, and I now have serious health problems caused by lithium.
"Therapy" has been no more structured or helpful than a long chat with a bartender.
This was posted long, long ago, so who knows if anyone is still reading or paying attention to it, but I still feel compelled to comment...
Somebody else's quote:
There's no reason to believe that HT2 agonist activity directly results in some underlying change in chemical activity.
Referring to the use of psychomimetic drugs to treat depression on an experimental basis. Well, LSD, DMT, and so forth, are indeed 5HT2A serotonin agonists, but they're also dissociatives, so we don't know for sure which effect contributes to the supposed AD effect. Very few legal drugs are 5HT2A agonists. One is, however; it's Topamax, an antiepileptic drug, and I take it. It's a last-ditch AE drug because the side effects can be terrible (and it's also used, not very effectively, for bipolar disorder). I take it as experimental treatment for post-traumatic stress disorder. For this disorder, it is powerful, stunning, and life-shattering. I'm one of the very few who has been able to stay on it. Most people just aren't willing to do it. It has offered me the opportunity to rebuild everything, but it is like walking voluntarily through fire to get to my true self on the other side. There is NOTHING else like it. But it's not an antidepressant!!
thank you
I will be honest enough to admit I don't even understand a lot of the technical aspects of what you are talking about. As a person with Bipolar Disorder, however, I am one of the people living in the trenches who gets "caught in the crossfire" of the pychiatry-anti-psychiatry debate. Everyone has a right to their own opinion, but what is inexcusable and deeply hurtful and offensive, not to mention ultimately ridiculous, is the view of some people that mental illness doesn't even exist. They use the "chemical imbalance is a myth" mantra as "evidence" that mental illness is not real. Bipolar disorder is one of the most dangerous, and deeply unpleasant illnesses a person can possibly have. I really don't care what the causes are...I want help. If a medication helps keep me out of jail, out of the hospital, or out of a state of mental/emotional hell then it is worth taking. Jail or side effects? That is a real choice that some patients have to make. Put yourself in that position for a moment. Until you have lived it, you can't understand the critical nature of it. A bit off topic maybe, but as Depression is a huge component of Bipolar Disorer, I felt obliged to make a comment.
Depressed patients feel sad all day long, they have loss of interest in things, everything seems in shades of grey. They commit suicide if left untreated.
There is no single biological defect that can be concretely identified in them, but it does not mean their suffering is false or non-existent.
Medications have their own limitations. Medications have their own side-effects, This is true for medications used for hypertension as well as for diabetes and hyperlipidemia.
Anti-tubercular treatment also has a definite failure rate, does not mean it is useless to treat TB. No one knows the reason why certain autoimmune diseases occur - 'idiopathic' is the term used in most cases. Steroids are used blindly by physicians with drastic results in infections mistaken to be autoimmune diseases. It is an equally blind therapy.
The significant point made by this paper, is that there isn't conclusive evidence of the 'monoamine hypothesis' peddled to this day by the psychiatry/big pharma machine. Not after several decades and billions spent trying. There can also be no doubt that there is a strong genetic component to the world's depression burden - just consider for a second that each parent passes on an average of thirty germline mutations to their children and that it holds the instruction set for developing and maintaining a healthy brain. It is time to move on, have a look at recent studies on ketamine which instantly alleviates drug resistant depression for several days after a single administration, as opposed to the sluggish indirect and weak effects of SSRIs. It acts on ion channels which are much more sensitive to mutation compared to other cellular components (ie they cause dominant disease phenotypes as opposed to recessive seen for most other genes).
People know lots of stuff don't they.
How many books have been written on psychiatry, neuroscience,neurobiology,social psychology, or stuff with the social-genetic lean that ALL claim to have these issues wrapped up nice and tight, having all the answers?? Sure such people do have all the Answers. Yet these people never seem to have a Solution. Odd isn't it?
So talk all you like about how Anti-psychiatry is Pseudoscience OR how Psychiatry is Pseudoscience. Argue all you want. Show the world how clever you are with words. Cause you're just foolin' your selves.
If people cared half as much about each other as they do for going online and picking out on one another-treating each other like they aren't even Human- If all you arguing smarty pants would put compassion first and deny your urges to self-satisfy your ego- All us Crazys can be done with your "answers" and finally have a practical SOLUTION. [One that wouldn't involve a nice brain scrambling with an ice pick. Or ECT to produce the proper amount of brain damage to 'help' the diseased. Or the pharmaceuticals that frickin' Barbeque a person's nervous system.] Yet all such 'treatments' seem perfectly logical to the highly educated or the want-to-beeees. Odd too!
Bottom line: we're being lied to. And if you're going to then base all your points of view, opinions, or overall interpretations of reality upon such lies, you can't very well hope to be saying much of any useful...for any one; Regardless of your IQ, the amount of money you make, the title you hold, or any other thing one can use to strengthen their delusion.
Belief, even scientific belief, is just BELIEF. Research Psychiatry and understand what you're talking about. See how many lives have been destroyed and are still being destroyed because of Psychology's/Psychiatry's hold over the general public's mindset. There is no grey area here. Your Delusion that your Perception fueled Believezzz are enough to talk about Human life like it's just a kid's science project just won't do.
the BENEFITS of Mental illness - http://www.black-op.org/benefitsofmentalillness.html
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