toxic psychiatry

part of the problem with those who critique the establishment is their tendency to over-exaggerate their case and use a substantial amount of rhetoric which undermines their credibility. while this book begins with some of that (and has some of this strategy dispersed within) it also contains a sophisticated analysis and critique of problems with the disease model of mental illness and biological treatments for them.

http://www.amazon.com/Toxic-Psychiat.../dp/0312113668

i haven't finished the book yet, but i have finished the section on schizophrenia. some of the claims that are made are:

- many years of searching for the neurological basis of schizophrenia were unsuccessful. (e.g., nazi scientists has brains on demand and they were unable to discover the neurological basis despite numerous autopsy's).

- since the development of neuroleptics (anti-psychotics) gross brain abnormalities have been found (enlarged ventricles, shrunken areas etc). seeing as these gross brain abnormalities were not described prior to the development of anti-psychotics (and they are gross, or extensive enough for them to have been visible to microscopic investigation upon autopsy) it seems reasonable to conclude that the gross neurological damage is caused by anti-psychotics.

- he describes what were taken to be the beneficial effects of lobotomy (by quoting those who advocated it). the beneficial effects were lack of interest / caring, lack of passion, muted emotional responses, not questioning and simply following orders and instructions (these look rather similar to the so called 'negative symptoms' of schizophrenia). the main beneficial effect of lobotomy is that the patients in the institutions were complacent and followed orders and didn't initiate much action off their own bat. lobotomy made them easier to manage, basically. it did not prevent their symptoms (e.g., delusions, hallucinations, thought disorder) rather it inhibited them from expressing their symptoms and by being so bothered by them.

- he describes how anti-psychotics were described as being a successful chemical alternative to lobotomy because it produced the same effects in subjects. he describes how lobotomy surgically cuts the frontal lobes and limbic system off from communication (inputs and outputs) with the rest of the brain and how neuroleptics chemically cuts the frontal lobes and limbic system (and the basil ganglia) off from inputs from the rest of the brain.

- he describes how the effects of chemical lobotomy are similar in mentally ill people, mentally 'normal' people, animals etc. the neuroleptic medications don't have the specific effect to rectify neurological damage (of which none has been found) rather they have the effect of disabling brain communication.

- he describes how chemical lobotomy (treatment with anti-psychotics) was thought to be preferable to physical lobotomy because chemical lobotomy was thought to be reversible (one could simply stop prescribing the medication).

- he provides studies to show that they don't help positive symptoms more than other seditives and that they weren't responsible for getting people out of institutions and living more productive lives (they were shuffled to other institutions such as nursing homes).

- he describes how tardive dyskinesia mimics a disease called 'lethargic encephalitus' and claims that the effect of neuroleptic medication is to cause this disease by creating neurological damage rather than to rectify neurological damage. (he cites studies where the non-neuroleptically treated control group didn't have a single case of movement disorder)

'Generally the profession tells the public and patients very little about tardive dyskinesia and greatly minimises the risk. A fortunate exception is psychiatrist Jack Gorman in his book 'The essential guide to psychiatric drugs (1990)'. He warns the potential patient, 'the risk of developing severe TD from antipsychotic drugs probably lies between 20% and 40%, but mild signs may appear in up to 70% of patents.'

- TD is caused by hyper-reactivity of the dopamine system in the basal ganglia area (where the hyper-reactivity is caused by the neuroleptic medication). One would expect that the dopamine system in the areas of the limbic system and the frontal lobes would also become hyper-reactive resulting in dementias (tardive dementia) and this is what is found.

- clozapine / clozaril doesn't supress dopamine transmission in the motor areas (basil ganglia) so isn't likely to cause movement disorder (TD). it does produce a profound lobotomy effect, however, and since it is more effective in blocking transmission to the frontal lobes one might expect more significant longer term to higher mental functions (tardive dementias).


hmm... something to think about...

(reasons to carefully examine the malfunction assumption methinks...)

wow.... heheh i had to go and look up every other word up in the dictionary i now have no idea about schizoprenia...hehehe i am so confused.... lalala i like grapes....
tc all
self

I have been treated for my MI off and on for over 35 yrs, I will be 50 in a few months.

When I was a teenager I was very mentally ill. Along with my lengthy hospitalizations were numerous anti-psychotics and ECT.....I was only 16. The Dr even discussed the possibility of a lobotomy with my parents and myself, and then moved to have a second series of ECT (8-12 "treatments") when we declined.

My parents had the good sense, after being prodded by the nurses, to change Drs. That Dr perscibed only the throazine and did much needed therapy with me.

Does that mean I think that all psychiatry is bad? That all medications are worthless? NO!

I currently take clozaril along with 2 anti-depressants. I am educated, I hold down a responsible job, and I have family and friends who love me and I them. Without medication I KNOW that I would not be able to say those things. Trust me I have tried it without meds, numerous times, and my best years (both for me and my family), were the ones where I was medication compliant!

The past seven years I have really worked hard at staying on my meds. I say "worked" because there is always that part of me that hates the meds.....not for the side effects (I have few), but the for the simple thought that I should even need them. Thinking that what I have is a simple character flaw and not an illness.

But when I try it without meds, I have a very brief window where my thinking becomes distorted and I still have time to act to begin taking the meds again. If I past that window, then a hospitalization is usually the only way to get me on the right course again. Although I can proudly say that I have had only 2 subsequent hospitalizations (since I was a teenager) in the past 35 years.

So what am I really trying to say after this long diatribe..........

Thank God for medication!!

Without it I have no doubt that I would be dead. And that I would have emotionally hurt many people along the way to that final outcome. But with my medication I have led a good and productive life and made a positive difference in many peoples lifes along the way.

Toxic psychiatry????? Only to those who have never truely experienced the before and after of a severe mental illness. I have.......

hey daniella.

i'm interested in what this guy has to say as another perspective on the matter.

you have never had the opportunity to have some brief respite and care in order to get you through an episode medication free?

if you suddenly stop taking your medication then your brain kind of rebounds so that things are twice as bad for a time before your brain adjusts to being off the meds.

> Without it I have no doubt that I would be dead. And that I would have emotionally hurt many people along the way to that final outcome. But with my medication I have led a good and productive life and made a positive difference in many peoples lifes along the way.

you could be a poster person for the med companies ;-)

there isn't any way to know whether you could have received the same (or better) results from drug free alternatives. because... you were given the medications and if you stop taking them (as you say) you have to get through the rebound (which would result in your hospitalisation and the commencement of medication).

if you are doing alright then that is great and more power to you (really).

> Toxic psychiatry????? Only to those who have never truely experienced the before and after of a severe mental illness.

the specific claim is that psychiatry is toxic in the sense that neuroleptics (and maybe other drugs - i haven't read those sections of the book yet) cause neurological damage.

that is an empirical matter (whether they cause neurological damage or not is an empirical matter). it seems as though... they do...

but... maybe not in every single case.

or... maybe you would be even smarter and so on if you had never taken the medication... perhaps.

do you have any TD (movement) type symptoms at all?

'medication compliant'... compliance is an interesting notion...

his alternative account of mental illness (seems to be) one of 'psycho-spiritual crisis'. he focuses on the role of EE (expressed negative emotion) in the family and the exquisite sensitivity of people who become mentally ill. he looks for meanings and themes in 'psychotic' communications... and states that while medications might make people care less about those concerns... they also supress creativity and expression and the process of meaning creation...

if you are happy on your meds then more power to you. i guess these thoughts are more likely to be gratefully received by those who are tossing up the virtues of 'compliance'.

I wish there was a long-term study done on these issues, but we have only a small handful.

Most studies, especially those that show a drug is "safe" and "effective" are done for 8 to 16 weeks. That's it. I don't know of anyone who takes a psychiatric medication for so short a period of time (excepting anti-anxiety drugs, which are short-acting).

I'd love to see the long-term studies that take fMRIs or something similar of people before treatment, 4-6 weeks after treatment begins, then a scan every month or every few months for the years they are on the medication.

As I understand it, to date, most of what we have to examine the real long-term effects of some medications are single case studies, which are often dismissed as "oh, that person was unique." I haven't read the book so I'm interested in what you're writing here... very interesting.

For the record, in the previous books I've read by Breggin, he seems to go a bit to the extreme to make his point. I think he'd be more effective if he didn't go to such extremes, because then his critics simply paint him as someone with an extreme view and his own agenda. But he does raise interesting questions.

John

> I'd love to see the long-term studies that take fMRIs or something similar of people before treatment, 4-6 weeks after treatment begins, then a scan every month or every few months for the years they are on the medication.

Yes, I'd love to see those studies too. What one would ideally also require, however, would be a medication free control group matched for severity of condition. I'm not sure that one could ethically randomly assign people to a 'no neuroleptic treatment' condition. Of course the ethics are begging the question here (assuming that those who aren't treated with medication are being harmed) but I do forsee ethical issues in obtaining a control group.

Without the control group... A finding of degenerative brain damage would probably be taken as evidence for the degenerative nature of schizophrenia rather than being taken as evidence for neuroleptics causing brain damage.

> As I understand it, to date, most of what we have to examine the real long-term effects of some medications are single case studies, which are often dismissed as "oh, that person was unique."

I think there is something to the idea that the Nazi scientists were unable to find a neurological basis to schizophrenia despite their numerous autopsy's. One would also need to know:
- whether the concept 'schizophrenia' (as used by the Nazi's) picked out roughly the same individuals as would be picked out by our present concept. I think it would be fair to assume that they would be picking out the most severe cases, however.
- whether their microscopic investigations were hampered by their lack of more advanced technology. I think it would be fair to assume that they would have been capable of finding enlarged ventricles and shrunken areas, however. how about more dopamine receptors? i'm not sure dopamine receptors had been discovered yet... that could be a potential problem.

I would like to check out the studies that he mentions in order to interpret them for myself. He does seem to offer a fairly sustained argument backed up by solid (and reputable) research, however. Sometimes I find psychology / psychiatry arguments to be lacking (claims are over-enthusiastic and obvious objections aren't considered). I found him to anticipate some of my objections, however, so was fairly impressed by that :-)

> For the record, in the previous books I've read by Breggin, he seems to go a bit to the extreme to make his point. I think he'd be more effective if he didn't go to such extremes, because then his critics simply paint him as someone with an extreme view and his own agenda.

Yes. I haven't read any of his other books, but the initial pages certainly had me thinking that.

To be fair, I think that advocates of all sides (including the biological psychiatrists) do that it is just that it is more apparent to us when we don't agree with (or question) some of their rhetoric.

Szasz is another who is often under-rated and IMHO unfairly dismissed by his critics. I've had psychiatrists say that he simply isn't taken seriously in psychiatric circles but I've certainly seen him getting a fairer hearing very recently with respect to the concept of mental disorder.

Often there are paradigms of research. The dysfunction assumption is thought to ground psychiatry as a science and hence anyone who challenges this assumption is probably going to be ignored. People tend to respond to that by trying to muster some interest (by their hyperbole and attempts to gain publicity) so that the others have to take them seriously enough to respond to their claims.

I think that there is a great deal more to the anti-psychiatry movement than is commonly acknowledged. It is precisely because of the anti-psychiatry movement (and the gay rights movement) that homosexuality was taken out of the DSM and that the DSM taskforce had a work group to look at which disorders should be included and which disorders should be excluded. The anti-psychiatry movement has forced psychiatry to be more accountable than it was previously and that has got to be a good thing.

A few snippets worthy of pondering...

<blockquote>RW: Here's just one real powerful study on this: Researchers with the University of Pittsburgh in the 1990s took people newly diagnosed with schizophrenia, and they started taking MRI pictures of the brains of these people. So we get a picture of their brains at the moment of diagnosis, and then we prepare pictures over the next 18 months to see how those brains change. Now during this 18 months, they are being prescribed antipsychotic medications, and what did the researchers report? They reported that, over this 18-month period, the drugs caused an enlargement of the basal ganglia, an area of the brain that uses dopamine. In other words, it creates a visible change in morphology, a change in the size of an area of the brain, and that's abnormal. That's number one. So we have an antipsychotic drug causing an abnormality in the brain.

Now here's the kicker. They found that as that enlargement occurred, it was associated with a worsening of the psychotic symptoms, a worsening of negative symptoms. So here you actually have, with modern technology, a very powerful study. By imaging the brain, we see how an outside agent comes in, disrupts normal chemistry, causes an abnormal enlargement of the basal ganglia, and that enlargement causes a worsening of the very symptoms it's supposed to treat. Now that's actually, in essence, a story of a disease process -- an outside agent causes abnormality, causes symptoms...

SS: But in this case, the outside agent that triggers the disease process is the supposed cure for the disease! The psychiatric drug is the disease-causing agent.

Source: Interview: Robert Whitaker

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As for the abnormalities that researchers have found with brain scans, Mosher thinks the antischizophrenic medication accounts for much of this. He says, "The Germans, who invented neuropathology, looked at the brains of thousands of schizophrenics before there were any neuroleptics. And they were never able to find anything. They never reported increased ventricular volume, which at postmortem you can measure quite easily. And they also never reported any specific cellular pathology, and they studied many, many, many brains." He adds that "there are a whole lot of people who don't have schizophrenia and also have enlarged ventricles. And there are people who have other psychiatric conditions who have enlarged ventricles, and there are a number of known causes of enlarged ventricles that are not schizophrenia. So, yes, there is a statistical difference, but it is not specific."

"On the other hand," Mosher continues, "there are studies that have shown that people treated with neuroleptics have changes in brain structure that are at least associated with drug treatment, dosage, and duration -- and have been shown to increase over time as drugs are given." He cites one "horrific study" of children between the ages of 10 and 15 in which the researchers measured the volumes of the kids' cortexes. "The cortex is what you think with, the part on the outside," Mosher explains. Over time, "They watched the cortical volume of these young people decline, while the cortical volume of the nonschizophrenic controls was expanding because they were adolescents and still growing." The researcher concluded that their schizophrenia had caused the decrease in the subjects. "And yet every single one was taking neuroleptic drugs," Mosher says.

He concedes that the German neuropathologists working earlier in the last century didn't have access to PET scans, a tool that Mosher categorizes as being a significant advance. "They show you activity, not just structure. They show which parts of the brain are working at a given task. And okay -- there they do find differences between people who've been labeled schizophrenic and normal people." But how, Mosher asks, can anyone tell if those differences cause the psychotic behavior or result from it? He says he's not at all surprised that the frontal lobe metabolism of drug-naïve schizophrenics looks different on PET scans than that of normal people. "Because if you meet such people, you know that they are in an unusual state of consciousness. They may be going 100 miles a minute. They may be totally distractible. You could measure a lot of other things, and they'd all be different at that point in time. But you don't know if that's a cause or an effect of the way they are."

Source: <a href=http://laingsociety.org/colloquia/thercommuns/stillcrazy5.htm>Still Crazy After All These Years</a>

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The issue of medication is a complex and controversial one. On the one hand, there are numerous people who identify medication as being helpful to them; on the other, there are numerous others who don't. My position on the matter is that what helps is what helps. Regardless of whether an individual personally finds medication to be beneficial, I firmly believe they are deserving of information such as the above. If the drug you are taking carries a high risk of stroke, diabetes, tardive dyskinesia, etc., that is information you are entitled to know. Without that information you cannot truly give your informed consent.

Just as vital, individuals are entitled to know that many people recover from schizophrenia without the use of medications. That's not to say that all people can but, rather, to counteract the perpetuated myth that medication is essential to recovery. This is simply not true.

thanks for the links.

> The issue of medication is a complex and controversial one. On the one hand, there are numerous people who identify medication as being helpful to them; on the other, there are numerous others who don't. My position on the matter is that what helps is what helps. Regardless of whether an individual personally finds medication to be beneficial, I firmly believe they are deserving of information such as the above. If the drug you are taking carries a high risk of stroke, diabetes, tardive dyskinesia, etc., that is information you are entitled to know. Without that information you cannot truly give your informed consent.

> Just as vital, individuals are entitled to know that many people recover from schizophrenia without the use of medications. That's not to say that all people can but, rather, to counteract the perpetuated myth that medication is essential to recovery. This is simply not true.

I agree 100%.

I agree 100% that Nazi Scientists would have measured ventricular enlargement on autopsy if it was there to be measured. The fact that they did not find it does seem to strongly support the 'medication may cause ventricular enlargement' hypothesis.

With respect to the studies that have been done on neurological degeneration the conclusion that 'medication may cause degeneration' hypothesis isn't terribly supported because there is a possibility that they didn't rule out by including a control group. To play devils advocate here... The findings are also consistent with the hypothesis 'schizophrenia is a degenerative brain disorder'. In order to rule out the latter hypothesis (and hence more strongly support the former hypothesis) they would need to have a control group of people with schizophrenia (who are as severe as those who were taking the medication) in order to show that their brains did not degenerate over time. That way the neurological degeneration would be shown to be due to the medication rather than the degenerative nature of schizophrenia.

fMRI and other neuroimaging scans really don't tell us a hell of a lot... There is so much divergence between different 'normal controls' that particular individuals with schizophrenia often resemble particular normal controls more than they resemble the hypothetical construct (average) 'schizophrenic brain'. typically... it is one or two individuals with schizophrenia who throw the whole average out.

This is very interesting. Has there ever been testing done to see if someone who has quit these medications still has the brain abnormalities? Would it heal itself? I would guess not. Its very concerning.

the first Pdoc, here, put me back on prozac and handed me "two brain graphics"....he said, "here's how you brain looks without prozac and here's how it looks with it"...now i'm seeing another Pdoc and when the first Pdoc saw me, in the hall, last week, he was upset that i'm tapering off the prozac. i immediately thought of those graphics and just grinned at him........

i agree, MRIs and re-checks.....when i had Rocky Mountain Spotted Tick Fever, i had several MRIs. the very capable neurologist (who saved me) said it takes several scans to see how the brain is handling the meds. so, we know then that ADs and such call for MRIs.......at $3200 a pop, here, that's unlikely.

alexandra_k: In order to rule out the latter hypothesis (and hence more strongly support the former hypothesis) they would need to have a control group of people with schizophrenia (who are as severe as those who were taking the medication) in order to show that their brains did not degenerate over time.

At risk of repeating myself...

<blockquote><font color=red>Most Americans are unaware that the World Health Organization (WHO) has repeatedly found that long-term schizophrenia outcomes are much worse in the USA and other developed countries than in poor ones such as India and Nigeria, where relatively few patients are on anti-psychotic medications. In undeveloped countries, nearly two-thirds of schizophrenia patients are doing fairly well five years after initial diagnosis; about 40% have basically recovered. But in the USA and other developed countries, most patients become chronically ill. The outcome differences are so marked that WHO concluded that living in a developed country is a strong predictor that a patient will never fully recover.</font>

Source: Drugs May Hinder Recovery

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<font color=blue>...85% of our clients (all diagnosed as severely schizophrenic) at the Diabasis center not only improved, with no medications, but most went on growing after leaving us.

-- Dr. John Weir Perry</font>

Source: Trials of the Visionary Mind

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<font color=green>There have now been three World Health Organisation studies showing that the outcome for schizophrenia in Developing countries is better than in the Industrialised world. This is extraordinary. How can places without psychiatrists, psychiatric nurses, psychiatric facilities, rehabilitation programs, medication and therapies come up with results considerably better than our sophisticated, scientific industrialised world? A country such as the USA spends 1% of its GNP on one illness, schizophrenia, and has results far worse than countries that don’t spend anything!

-- Dr. Simon Bridge</font>

Source: The Developing World Experience

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<font color=purple>The WHO Study of Schizophrenia is a long-term follow-up study of 14 culturally diverse, treated incidence cohorts and 4 prevalence cohorts comprising 1,633 persons diagnosed with schizophrenia and other psychotic illnesses. Global outcomes at 15 and 25 years were assessed to be favorable for greater than 50% of all participants. The researchers observed that 56% of the incidence cohort and 60% of the prevalence cohort were judged to be recovered. Those participants with a specific diagnosis of schizophrenia had a recovery rate which was close to 50%. [...] The course and outcome for persons diagnosed with schizophrenia were far better in the “developing countries” than for such persons in the “developed” world of Western Europe and America.

-- Dr. Brian Koehler</font>

Source: Long Term Follow Up Studies

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<font color=maroon>Among those who went through the OPT program, incidence of schizophrenia declined substantially, with 85% of the patients returning to active employment and 80% without any psychotic symptoms after five years. All this took place in a research project wherein only about one third of clients received neuroleptic medication.</font>

Source: Dialogue is the Change

See also: Schizophrenia & Hope

Gemstone: Has there ever been testing done to see if someone who has quit these medications still has the brain abnormalities? Would it heal itself? I would guess not. Its very concerning.

It's been understood for a very long time that many people recover from schizophrenia -- fully and completely. Why that fact should remain such a secret is the mystery.

<blockquote>... long term studies however ... done in 12 different countries now indicate that irrespective of treatment, 30% of schizophrenics completely recover within 25 years. There have been studies from Switzerland, Italy, Scandinavia, the United States, Germany... they all find the same thing. Unfortunately, the best of the American studies -- that of Courtney Harding, which studied patients from Vermont -- found that the patients got better in 20 years but the patients who stayed on their medication as long as their doctors told them to, none of them ever recovered. 50% of the patients eventually stopped taking their medication against medical advise and all of the patients who had a full recovery were in that group.

PTR: So what you're saying Dr. Karon is first of all that schizophrenia is really an experience, an experience of terror ...

BK: Right.

PTR: And secondly, if someone continues to take the medication as prescribed by psychiatrists and doctors, that the odds are that they won't improve and get better. They're better off stopping the medication.

BK: Taking the medication may make them easier to manage but it gets in the way of full recovery.

Source: Dr. Bertram Karon: Schizophrenia & Psychotherapy

I just wrote a paper that explores genetic and experiential causes of differences in the brain, and effects or symptoms associated with those differences. The genetic factors that I looked at were "Schizotaxia" - a set of schizophrenic-like symptoms, including negative symptoms but no positive symptoms, observed in first-degree relatives of people with schizophrenia; and DAMP syndrom - basically ADHD + developmental coordination disorder. I also discussed the effects of child abuse on the brain, and related outcomes seen in adult survivors of abuse and neglect.

Not only are there apparently genetic conditions that are associated with differences in the brain and outcomes in life, and which respond to medication, but similar differences are also seen in children who have been abused or neglected. Adult survivors even have the enlarged left ventricles and decreased left hippocampal volume similar to what is seen in schizophrenia. Adult survivors are also more likely to suffer disorders like PTSD when traumatized as adults than adults without a history of child abuse.

Other reading I've been into discusses how both epilepsy and bi-polar disorder, and probably depression too, can be kindled (created by inducing the symptoms at first), and each subsequent seizure or episode happens more easily, with less or no stimulus, and tends to be more severe.

Then there's the possibility that children with certain genetically-based predispositions that increase the likelihood of being victimized, and it all compounds each other. It's impossible at this point to say what causes what.

Rapunzel: I just wrote a paper that explores genetic and experiential causes of differences in the brain, and effects or symptoms associated with those differences. The genetic factors that I looked at were "Schizotaxia" - a set of schizophrenic-like symptoms, including negative symptoms but no positive symptoms, observed in first-degree relatives of people with schizophrenia

Do you have a source? I ask because I was reading the work of Dr. Jonathon Leo of late and this has raised some questions in my mind about the validity of research in which the back story is unknown, i.e.,

<blockquote>The three methods most frequently cited in support of genetic factors in schizophrenia are family studies, twin studies, and adoption studies. Kandel says that all three of these methodologies support the role of genetics in schizophrenia. In this article, we examine the data that Kandel presents for each of these approaches and we will also point out the problems with each approach.

...

Kandel presents a table claiming that 14% of the biological relatives were diagnosed with schizophrenia, while only 3.4% of the control relatives were so diagnosed (Kandel, 2000, table 60-1, p. 1194). If this evidence is valid, and if the study is otherwise methodologically sound, it makes a strong case for the role of genes in schizophrenia. In Kandel’s words, “In addition to documenting the importance of genetic factors in schizophrenia, these studies of adoptees in whom schizophrenia developed showed that rearing does not play a major role in the disease” (p. 1194). But is the evidence valid?

Problem #1: The widening of the schizophrenia spectrum. The only way that Kety et al. could diagnose 14% of the biological relatives with schizophrenia was to greatly broaden the definition of schizophrenia to include diagnoses such as “latent schizophrenia,” “uncertain latent schizophrenia,” and “inadequate personality.” Kandel claims that these categories are “thought to be a mild form of the disease, a nonpsychotic condition related to schizophrenia” (p. 1194). But why should these cases be included in the overall totals when there is little evidence that chronic schizophrenia and the spectrum disorders are genetically related (Joseph, 2001a)? Kandel also claims, on the basis of family studies, that “odd” people are found among the relatives of people diagnosed with schizophrenia: “they are socially isolated, have poor rapport with people, ramble in their speech, tend to be suspicious, have eccentric beliefs, and engage in magical thinking” (p. 1194). The claim that “odd” people are found among the relatives of people diagnosed with schizophrenia means little, and was often made on basis of non-blind diagnoses by investigators devoted to the genetic position. In addition, it could just as easily be the result of the negative psychological and social environments experienced by family members. The fallacy here is that correlation is seen as being directly related to genetic causation, when there is little evidence to support this view.

If one limits the comparison to cases of chronic schizophrenia among the Kety et al. 1975 biological relatives, one is left with 5 cases of chronic schizophrenia among the 173 biological relatives of index adoptees (2.9%) and zero cases of chronic schizophrenia among the 174 biological relatives of control adoptees. Yet, 5 cases of chronic schizophrenia out of a group of 173 individuals (2.9%) is not much higher then the general population rate of 1% (Joseph, 2001b).

Source: Medical students are taught it’s all in the genes, but are they hearing the whole story?</blockquote>

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Rapunzel: It's impossible at this point to say what causes what.

Fortunately, it's not impossible to say that full recovery is a very good possibility, regardless of the (unknown) cause.

the WHO study and the fact that many people with schizophrenia recover from schizophrenia (or schizophrenic symptoms) without neuroleptics doesn't have any bearing on whether they also have ventricular enlargement.

it could be the case that they do have degenerative ventricular enlargement.

the only way to rule that out would be to neuroimage them and find out...

we do know that people without schizophrenia have ventricular enlargement and that people with schiozphrenia don't have ventricular enlargement.

randomised double blind control trials are considered to be the best scientific methodology because they are much more effective in ruling out alternative hypotheses than other kinds of trials. in particular, if we had a group on neuroleptics and a control group (matched for severity) not on neuroleptics and we neuroimaged them progressively over time then the study would presumably show whether the degeneration that was found was due to the neuroleptics or neural degeneration that occurs in the absence of neuroleptics. we need the control group to fix the base rate...

alexandra_k: the WHO study and the fact that many people with schizophrenia recover from schizophrenia (or schizophrenic symptoms) without neuroleptics doesn't have any bearing on whether they also have ventricular enlargement.

What I was primarily addressing was this...

alexandra_k: The findings are also consistent with the hypothesis 'schizophrenia is a degenerative brain disorder'. In order to rule out the latter hypothesis (and hence more strongly support the former hypothesis) they would need to have a control group of people with schizophrenia ...

There is a control group of people with schizophrenia who do not take medication. They are found in other nations, cultures and settings, and captured within international studies such as that conducted by WHO. It has been repeatedly demonstrated that those individuals have a higher recovery rate. This is an indication that schizophrenia is not a degenerative brain disease -- a matter which has already been demonstrated as false through the work of individuals such as Courtenay Harding. Whether they also have larger or smaller ventricles is -- to me -- an irrelevant matter, since ventricle size itself is not an indication of schizophrenia.

Even if we were able to conduct neuroimaging studies on those groups of people, what would it tell us? If they did not have enlarged ventricles would it tell us that they did not have schizophrenia, or would it indicate that the use of neuroleptics produces a change in ventricle size? If we wish to prove a correlation between the use of anti-psychotic medication and ventricle size the study might be useful, but if we wish to demonstrate that schizophrenia is not a progressive disorder of degeneration... that's already been demonstrated via the WHO study and numerous others.

> There is a control group of people with schizophrenia who do not take medication. They are found in other nations, cultures and settings, and captured within international studies such as that conducted by WHO.

Yeah, I guess that is true. They aren't neuroimaged such that we can compare their neuroimaging with the neuroimaging of a bunch of people who are on neuroleptics though, are they? It would help our case if they had been...

> It has been repeatedly demonstrated that those individuals have a higher recovery rate.

Yes. We have no idea why, however. Some people say that it is due to the lack of medication. Some people say that it is due to the relative lack of social stigma. Some people say that it is due to a closer family structure.

We don't know whether ventricular enlargement occurs before schizophrenic symptoms (in the cases where people with schizophrenia do have ventricular enlargement) or whether the gradual progression of ventricular enlargement results in more severe symptoms over time (in the cases where people with schizophrenia are developing ventricular enlargement). We don't know whether the causes of the ventricular enlargement are due to a gene switching on or whether they are due to a neuro-degeneration in the brain or whether they are due to a loss of social supports or whether they are due to medication. We don't know whether the ventricular enlargement shrinks as people recover from schizophrenia or whether people recover despite ventricular enlargement.

Sure there have been some studies done... Most often the methodology is criticised (because most often the methodology isn't as rigerous as it should be and so the criticisms are fair). What is interesting is... Trying to find something of a consensus of what you would need to find that would persuade the sceptics of your hypothesis that your hypothesis is most likely to be correct. Design that study and hopefully it will be done one day... At present... Well... Studies often do come up with hopelessly contradictory findings for quite some time... That is the nature of science (and that is how come they change their opinions on such things as whether eggs are good for you).

> This is an indication that schizophrenia is not a degenerative brain disease -- a matter which has already been demonstrated as false through the work of individuals such as Courtenay Harding. Whether they also have larger or smaller ventricles is -- to me -- an irrelevant matter, since ventricle size itself is not an indication of schizophrenia.

It is an indication that schizophrenia is not a degenerative neurological disorder but it doesn't actually rule out the possibility that people recover from the behavioural symptoms of schizophrenia DESPITE ventricular enlargement. We simply don't know whether they have ventricular enlargement or not without neuro-imaging / autopsy.

I don't think that it has been falsified that schizophrenia is a degenerative neurological disease. In the sense that... I don't think that it has been falsified that mental illness is a neurological malfunction. I'm sceptical that it is but I haven't seen a knock down argument against it... Also... Failure to find a neurological abnormality doesn't at all entail that there isn't one there to be found...

The malfunction assumption is one of the framework assumptions of psychiatry. I suppose they are concerned about what would be left of their discipline if the malfunction assumption was shown to be false. That might well make them ignore some of the evidence that seems to support the notion that the malfunction assumption is false. Still... It might well be that there are facts that can ground psychiatry as a science that don't rely on the neurological malfunction assumption. Maybe mental disorders can be characterised as *cognitive* (or *mental*) disorders rather than *neurological* disorders. They have to be careful of encroachment from neurology too...

> Even if we were able to conduct neuroimaging studies on those groups of people, what would it tell us? If they did not have enlarged ventricles would it tell us that they did not have schizophrenia, or would it indicate that the use of neuroleptics produces a change in ventricle size?

If the neuroleptic group showed evidence of progressive neurological degeneration...
And the control group showed lack of neurological degeneration...
(I anticipate problems with how you figure 'degeneration' from 'maturation' or 'functioning okay' from 'abnormal')

Then on the assumption that the neuroleptic and control group were matched for severity and similar in all other relevant respects (which unfortunately is an assumption that has to be made...) then it would follow that if there was a statistically significant difference... Neuroleptics cause neurological degeneration.

If the individuals in the control group showed similar deterioration then that would be evidence that neuroleptics either don't cause deterioration (because the deterioration would likely have happened if the subject hadn't taken the medication). If the individuals in the control group showed less deterioration (but still a significant amound of it)... perhaps compared to neurological changes in a non mentally ill control group over time... then that would show that neuroleptics make the degeneration worse.

If the neurology between the control group and the neuroleptic group is relatively similar (that might be problematic) then it would be interesting to see whether neurological abnormalities found in the initial samples rectified (due to neural plasticity) as the people got better over time...

I dunno. The studies haven't been done... I'd be interested to know, however.

> If we wish to prove a correlation between the use of anti-psychotic medication and ventricle size the study might be useful...

It would show *causation*. Either support or disconfirmation of the hypothesis that 'neuroleptics cause ventricular enlargement' (where the relevant sense of 'cause' is comperable to the notion in 'smoking causes cancer' which is not at all to say that EVERY individual who smokes or who takes neuroleptics has the nasty consequences but just that enough of them do to support the causal claim. How strong the causation is... Would be shown by the study)...

> ...but if we wish to demonstrate that schizophrenia is not a progressive disorder of degeneration... that's already been demonstrated via the WHO study and numerous others.

They aren't studying the presence or absence of neurological degeneration. As such they seem to be silent on the issue. Perhaps one thing we might say is that... When people do deteriorate that is due to neurological deterioration. When people don't deteriorate that is because they have been misclassified as schizophrenic (ha!). That isn't a very satisfactory response in one sense, but it is fairly satisfactory in another. That is why it would be interesting to know what is going on (both behaviourally, neurologically, and cognitively) in individuals who have been diagnosed with schizophrenia over time...

Here, I'll attach my paper if you would like to read it (with identifying information removed). Although I don't say so in the paper, this has lots of personal implications for me since my brother was schizophrenic, and I might meet the criteria for schizotaxia (and would have more certainly a few years ago before I started getting effective treatment - which has not included medication other than St. John's Wort, btw). The Schizotaxia article indicates that patients with Schizotaxia improve with Risperdal - they have negative symptoms only, no positive symptoms - so that means lessening of the negative symptoms.

I also feel that DAMP applies to me and to my brother, and I do have some abuse history also. Everything that I wrote about probably applies to me in some way. I would be interested in what my own MRI would show.

Here is my reference list:
References
De Bellis, M. D. (2005). The psychobiology of neglect. Child Maltreatment, 10, 150-172.
Gillberg, C. (2003). Deficits in attention, motor control, and perception: a brief review. Archives of Diseases in Childhood, 88, 904-910. Retrieved June 13, 2007, from http://bmjjournals.com
Grotberg, E. H. (1995). A guide to promoting resilience in children: strengthening the human spirit. Retrieved June 13, 2007, from The International Resilience Project: http://resilnet.uiuc.edu/library/grotb95b.html
Messman-Moore, T. L., Long, P. J., &amp; Siegfried, N. J. (2000). The revictimization of childhood sexual abuse survivors: an examination of the adjustment of college women with child sexual abuse, child sexual assault, and adult physical abuse. Child Maltreatment, 5, 18-27.
Rasmussen, P. &amp; Gillberg, C. (2000). Natural outcome of ADHD with developmental coordination disorder at age 22 years: a controlled, longitudinal, community-based study. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 1424-1431.
Tsuang, M.T., Stone, W.S., Tarbox, S.I., &amp; Faraone, S.V. (2001). An integration of schizophrenia with schizotypy: identification of schizotaxia and implications for research on treatment and prevention. Schizophrenia Research, 54, 169-175.

If you can't find any of those articles and want them, I can email them to you individually, but I can't post the articles publicly.

First post here. I am 71 years old (That's 'way over 60, but guess what? We geezers are still human.) and have had quite a bit of experience with psychiatry, lots of which I consider to have been toxic. But even at an advanced age learning to see some light seems possible -- in spite of so much "teaching" to the contrary.

Diagnoses? Having had so many, I have little interest in them any more. Consequences of childhood experiences, all.

I also have two cats (brother and sister). One of them is, I think, my best friend besides the T. [I have read enough on the forums to know that is the correct terminology.] Whitie the human cat.

thanks for the posts guys.
i have conference so i'm going away for a week.
today and tomorrow... i really need to write my paper eep!
i'll be sure to respond properly when i return.

thanks.

http://www.msnbc.msn.com/id/15196598

You might be interested in this too. I don't know what I think of it. I guess I don't really buy what this doc is saying, but I do think that the categories are no where near as separate and black and white as the labels make it appear. Everyone is different, and probably had symptoms of more than just what they are diagnosed with. Treatment really needs to be individual, not cut and paste according to the category or diagnosis. It's not like medical diagnoses where if you have tonsilitis, that's definitely what you have, and there is a specific treatment for it.