Talk:Schizophrenia/Archive 6

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Meaningless, pseudoscientific term

"Schizophrenia" is a strictly meaningless diagnosis. There are a variety of different forms of madness which get thrown into this lazy, bucket term 'schizophrenia'. For example there are people who hear voices who are termed schizophrenic but who is to say that hearing voices is a bad thing? Joan of Arc heard voices and she became a saint to give just one example. There are people called schizophrenic who do not hear voices. We in the West take comfort in science and try and explain everyhing in it terms. 'Schizophrenia' sounds scientific but it really isn't. Even the derivation of the word is rubbish. The people we label schizophrenia have brains and ECG scans identical to those who are labelled as normal. There is no 'split brain'. It's just nonsense, nonsense spouted by the non-scientists known as psychiatrists. Africa witch-doctors say that the people labelled as schizophrenic are possessed by evil spirits and have just as much - or as little - success advising their patients to chew a piace of tree bark as the highly-paid western pyschiatrists with their expensive and untestable Amisulpride or Haloperidol. Many in the mad community resent this terminology and we are the ones supposedly suffering this psuedo-condition. If it was up to me I would put the whole subject in scare quotes. While I accept that this may be a minority view it one held by most of the people called by this term. SmokeyTheCat •TALK• 20:42, 14 January 2009 (UTC)

To illustrate my point about the worse than useless treatment dished out by the well-paid witch-doctors we call 'psychiatrists' here is a section from the Anti-psychotic drugs page:- "Some doubts have been raised about the long-term effectiveness of antipsychotics because two large international World Health Organization studies found individuals diagnosed with schizophrenia tend to have better long-term outcomes in developing countries (where there is lower availability and use of antipsychotics) than in developed countries.[21][22]" SmokeyTheCat •TALK• 20:53, 14 January 2009 (UTC)

I think if you leap immediately from "some doubts have been raised" to "worse than useless", it's going to be hard to contribute usefully to this article. We are all free to have our beliefs, but the article needs to be governed by what the best sources say. By the way it's not true that people diagnosed with schizophrenia have "brains and ECG scans identical to those who are labelled as normal" -- there are many statistically significant differences, but they are all subtle. Looie496 (talk) 01:06, 15 January 2009 (UTC)

Looie, the differences you mention are currently of little clinical use. You may want to read this piece of opinion. SmokeyTheCat however is wrong, see my reply below. Xasodfuih (talk) 22:33, 24 January 2009 (UTC)

Nowadays schizophrenia has good diagnostic concordance (aka diagnostic agreement). This isn't sufficiently mentioned/cited in the article (given that we don't even have a stub on the concept, why am I not surprised?) There's a bit too much emphasis on the criticism of the diagnosis. Any book by Andreasen should contain a good list of studies. Granted in the 1970s, the Americans used to diagnose (way) more patients with schizophrenia compared to the British, and this is a documented row (should be mentioned in the history section). By the way, mania is now in a somewhat similar situation; there was an article in Br J Psychiatry comparing US, British and Indian diagnoses (don't recall title/authors off the top of my head). Xasodfuih (talk) 22:08, 24 January 2009 (UTC)

N.B.: The 70's row is described in the last paragraph of the history section. Still more should be said about concordance studies. Xasodfuih (talk) 22:19, 24 January 2009 (UTC)

Question

Do schizophrenic deaf people hear voices? ★ QuackOfaThousandSuns | Talk ★ 20:25, 22 January 2009 (UTC)

Apparently yes, at least in some cases. Looie496 (talk) 23:45, 21 January 2009 (UTC)

Relative risk vs odds ratio

This change inserted the text "40% to 100%" in the sentence "Cannabis use is associated with a 40% to 100% dose-dependent increase in risk of development of psychotic disorders, including schizophrenia." (my italics). This change is incorrect. The cited source, Moore et al. 2007 (PMID 17662880), did not say that there was a 40% to 100% increase in risk (i.e., a relative risk); it gave odds ratios, which are quite different things. One cannot convert an odds ratio to a relative risk that easily. It's questionable whether it's worth giving the study's exact figures here, as this will require explaining odds ratios to the readers; we can't assume that readers know this stuff. However, regardless of whether the magnitude of the increase is an appropriate detail here, the current text is plainly incorrect, and for now I reverted the change. Eubulides (talk) 09:38, 24 January 2009 (UTC)

In the case of rare outcomes, the odds ratio is a good estimate of the relative risk. This is because, technically, an odds is defined as p/(1-p), so if p is low (traditionally set as less than 10 %), (1-p) will be near one, meaning that the ratio obtained by dividing two odds is close to the ratio obtained by dividing two risks. I agree with you that, technically, the two entities are very different, but the only reason why anyone is interested in the odds ratio in epidemiology is that a) it is usually a good estimate of the relative risk, b) exceedingly more easy to calculate than the relative risk in all but the most simple of cases. So I think the figures do belong in the article, and probably without explanations of odds ratios versus relative risks, as most readers will just be confused. However, I will not go into an edit war on this, so I'm hoping we can get a discussion going with other editors here as well, so we can decide what is best - have the numbers in the article or not. -Lilac Soul ^{(talk • contribs • count)} 10:45, 24 January 2009 (UTC)

Update: I have just checked the full-text version of the article (cannot link to it, though - you need a subscription), and the authors themselves interpret the odds ratio the way I presented it in the article here. Quoting directly from their discussion section:

“

The pooled analysis revealed an increase in risk of psychosis of about 40% in participants who had ever used cannabis. However, studies tended to report larger effects for more frequent use, with most studies showing a 50–200% increase in risk for participants who used most heavily.

”

The 50-200% figures refer to the confidence interval of the 100% increase, which is probably too complicated to be in the present article. Based on this, I am going to restore my edit. I hope this is okay with everybody. -Lilac Soul ^{(talk • contribs • count)} 11:33, 24 January 2009 (UTC)

Have you noticed this review, published by the same authors a year later, which comes to rather different conclusions? Looie496 (talk) 17:30, 24 January 2009 (UTC)

I wouldn't quite different "Cannabis use was consistently associated with increased relapse and non-adherence [to treatment]." "Confidence that most associations were specifically due to cannabis is low." Basically there's low confidence that association implies causation here, but association does not appear to be in doubt in the author's mind. Xasodfuih (talk) 13:34, 25 January 2009 (UTC)

Also, did anyone read all those letters to the editor(s) because replied appeared in different journals as well? Xasodfuih (talk) 13:05, 25 January 2009 (UTC)

After reading the letters, I think this should either be removed or seriously ammended, but the latter would take quite some space. The study results and interpretations have been contested (in the 3 letters) on:

statistical grounds (small stydy bias in metaanalysis when only a limited number of studies contribute to the assesment, citing BMJ 1997; 315:629-634 [did not read]).
confounding factors (comorbid addiction to other substances), in particular another study showing that smoking tobacco doubled the risk as well.
revese causation, in particular evidence that cannabis use lessens negative symptoms, suggesting that those smoking it already had developed some negative symptoms of schizophrenia.

In reply the authors basically agree that their numbers are only weakly supported. Xasodfuih (talk) 14:24, 25 January 2009 (UTC)

I agree with you (I think) that the current state of the literature doesn't support any claim that cannabis use causes schizophrenia, and that this article ought not to be hinting at any such claim. Looie496 (talk) 18:49, 25 January 2009 (UTC)

Hi there, I am not sure why a 'totally disputed' tag has been added to the paragraph as it does not suggest that there is a causal connection between cannabis use and schizophrenia, it reports, quite accurately, the debate and reports, again accurately, the results of the meta-analysis and the clear finding that there is an association while giving the caveats that other factors may also account for it. The fact that "the literature doesn't support any claim that cannabis use causes schizophrenia" is clearly false, as there is plenty of literature that does, although the conclusion is by no means certain as the meta-analysis makes clear. Uncertainty does not mean there is no effect. The fact that "this article ought not to be hinting at any such claim" is clearly NPOV as this is the single biggest debate in the cannabis and psychosis literature. I would also note that the letters referenced above suggest caveats but are not refutations in themselves - they largely give hypothesis for other ways the data need to be interpreted. Nothing in the current paragraph is currently disputed in the literature, I think the 'totally disputed' tag should be removed. - Vaughan (talk) 18:33, 26 January 2009 (UTC)

Lilac Soul added more qualifiers to the statement, so the tag can go for now, but I suggest using multiple sources and viewpoints to describe this issue since it is indeed controversial. If nobody else does it I'll get back to it later. Xasodfuih (talk) 18:53, 26 January 2009 (UTC)

It may be useful to expand the topic later, but the short version had problems that needed to be fixed regardless of later expansion. For a discussion of this please see #Recent cannabis edits still have problems below. Eubulides (talk) 23:54, 26 January 2009 (UTC)

Omega 3's

I've updated the info on that, but I've specifically omitted the review of Peet and Stokes PMID 15907142, which is more enthusiastic on omega 3's, because half of the RCTs they review were conducted by Peet et at. Emsley et al. (2003) also included one of their own positive RCTs in their review, but they were more balanced in their overall assessment. Xasodfuih (talk) 18:22, 24 January 2009 (UTC)

Impact of antipsychotics on negative symptoms

It think it's general knowledge that antipsychotics have less effect on negative symptoms, and this seems an important fact to mention. It shouldn't be hard to find citations from schizophrenia opinion leaders on this. Xasodfuih (talk) 18:34, 24 January 2009 (UTC)

Agree, important point. I have read over the article again and can see the need to include that somehow. (now for some review article or other...) Casliber (talk · contribs) 21:07, 24 January 2009 (UTC)

Added from recent reviews to boot. Xasodfuih (talk) 21:40, 24 January 2009 (UTC)

I've made this statement more general by eliminating any exceptions and adding two more refs; the 2006 one is a review dedicated to just negative effects, and the 2008 one, although very general, takes into account the CATIE results on negative symptoms (2007) [1] and another 2007 RCT from Arch Gen Psychiatry [2]. I can't find two reviewers to agree on what antipsychotic might work better for negative symptoms, so they're probably just writing their own bias in that area. Xasodfuih (talk) 11:14, 25 January 2009 (UTC)

Obesity

This barely mentioned in the wiki article, and it's a major comorbidity (twice the pop avg. in the US). It may not be entirely due to antipsychotics. If anyone cares to develop it PMID 16541087 (free) should be helpful. Xasodfuih (talk) 19:55, 24 January 2009 (UTC)

Thanks (so many chores, so little time...) Casliber (talk · contribs) 21:08, 24 January 2009 (UTC)

FGAs vs SGAs

The current version of the medication section has a ^{[citation needed]} for SGAs being better tolerated, followed by a paragraph sourced from the (rather dated now) 2003 Lancet metaanalysis that found SGA = FGA, which obviously contradicts the paragraph just above it. In the mean time CATIE and CUtLASS have found the same sad thing as the Lancet study. But then, OMG WTF BBQ, the World Psychiatric Association decided to do their own review PMID 18243663 that decided that SGAs are still better! You can also find other, somewhat older reivews, but still post-2003-Lancet, that declare the same result, e.g. PMID 15289815. The icing on the cake is that Lancet published another metaanalysis this month PMID 19058842, and you can guess what it says. So, I think it's fair to say there's a controversy here, and describe it. Xasodfuih (talk) 11:58, 25 January 2009 (UTC)

Hi there, the paragraph does not contradict itself. 'Better tolerated' refers to the number of drop outs in RCT studies, the paragraph that references the Lancet article notes they are "thought equally effective for the treatment of the positive symptoms" which is a completely different outcome measure. There is no contradiction here and I'll remove the tag shortly. What we have is an update because, as you rightly mention, CATIE and CUtLASS found that SGA are not better tolerated (e.g. see PMID 18310570). The WHO study is certainly an outlier, in comparison to all the other meta-analyses that find exactly the opposite (one more: PMID 18180760). I agree it's important to mention this in the paragraph. - Vaughan (talk) 18:53, 26 January 2009 (UTC)

This is indeed one of those murky areas in psychiatry and the stakes are very high. This is an important point and I agree the controversy needs describing. Casliber (talk · contribs) 22:38, 26 January 2009 (UTC)

Weight gain

Also, the 2009 Lancet review found that aripiprazole and ziprasidone did not cause weight gain, which is supported by older studies, e.g. PMID 15998156, and this should probably be mentioned as well, since it's rather important and doesn't take much space. Xasodfuih (talk) 11:52, 25 January 2009 (UTC)

Another valuable point and I agree this would be an important addition. - Vaughan (talk) 19:04, 26 January 2009 (UTC)

Agree. Xasodfuih I apologise as I have my finger in way too many pies at the moment. I am happy to leave tweaking the page to you - will try to look later. :) Casliber (talk · contribs) 22:34, 26 January 2009 (UTC)

Caption under Nash's picture misleading

From what I remember (from the book) he had finished grad school and the work for which he got the Nobel prize before he ever got medicated. Actually he even said at a psychiatry conference something along the lines: it would be amazing if someone got the Nobel prize for work done after recovering from mental illness. Xasodfuih (talk) 13:55, 25 January 2009 (UTC)

I wasn't overly fussed about the image, and I can see the good point made in terms of chronology there. Casliber (talk · contribs) 22:36, 26 January 2009 (UTC)

Smoking not discussed either

This is another well known comorbidity that is not discussed. And it needs to be, given that nicotine interacts with the dopamine system. There seems to be too much emphasis on historical events and etiological issues in comparison with clinical matters in this article. Xasodfuih (talk) 00:16, 26 January 2009 (UTC)

This is a valuable point and I think something on nicotine should be added. However, I strongly disagree that there is too much emphasis on historical events and etiological issues. It's an encyclopaedia article, not a clinical textbook. There is room for more in-depth clinical information in sub-articles, but for the general reader historical, etiological and conceptual issues are important. - Vaughan (talk) 19:03, 26 January 2009 (UTC)

To a certain extend I agree. We shouldn't transform this article into an issue of Psychiatric Times by brooding over the relative merits of various antipsychotics. On the other hand, I think that sections like "Alternative approaches" are overdeveloped relative to other parts of the article. No scientific book (let alone review) would give that more space than to the medication section. Two of the three books mentioned there don't even have a wiki article (The Origin of Consciousness in the Breakdown of the Bicameral Mind is a redirect to an article that only contains "schizophrenia" in the footnotes.) Just like this article shouldn't discussing every gene liked to schizophrenia, so it should discuss all the old alternative theories that were never proven. Xasodfuih (talk) 20:17, 26 January 2009 (UTC)

Recent cannabis edits still have problems

Recent edits to the sentence about cannabis still have problems.

The preliminary phrase "Though not necessarily implying causality" is redundant with the phrase "a clear causal connection between drug use and schizophrenia has been difficult to prove" that leads the paragraph. It's also redundant with the 2nd sentence of the paragraph, which clearly states that causation could be either way. We do not need to repeat the point again in the 3rd sentence, particularly since the sentence in question is about association, not causality. Better than repeating the point would be a wikilink to Association (statistics) and using the adjective "statistical" before "association", which will help make it abundantly clear that we're talking about statistical association, not causality.
The phrase "published in The Lancet" was added. There is no need for this sort of source puffery in the text. The citation contains the relevant info. Unless The Lancet itself is part of the story (as it is in, say, MMR vaccine controversy) it should not be mentioned in the main text.
It reinserted the text "40% to 100%" before "dose-dependent increase in risk of development of psychotic disorders, including schizophrenia". This insertion has several problems:

As mentioned above in #Relative risk vs odds ratio, this insertion is not directly supported by the cited source, Moore et al. 2007 (PMID 17662880); the "100%" figure is a result of our calculations based on the source, which is worrisomely close to WP:OR. The cited source says "40%" and then later "50–200%"; it does not say "40% to 100%".
The "40% to 100%" sounds like a confidence-interval range, but it's not: the 40% is the mean estimate for users in general, and the 100% is our approximation to the mean estimate for frequent users. This is not explained in our text and the percentages are therefore a mystery to the ordinary reader.
Most important, the authors of the study themselves say (Zammit et al. 2007, doi:10.1016/S0140-6736(07)61652-3):

"We followed the advice provided by Egger and colleagues—ie, that meta-analyses of observational studies are not inappropriate, but that the statistical combination of results should not be the main component of the review. In keeping with this, the primary focus of our review was not the strength of statistical evidence from the pooled results, but the thoroughness of any attempts made by each individual study to minimise the effects of bias, reverse causation, and confounding."

Given that "the statistical combination of results should not be the main component of the review", it is quite odd for us to be emphasizing the statistical combination in our very brief summary of that review. We should not be giving undue weight to a result that the authors of the result themselves say should not be emphasized.

I read 7 reviews and/or letters about the study:

Potvin & Amar 2008 (PMID 18223063) said it was "one of the most reliable estimates of the association". They noted that the odds ratios were low values, albeit significant.
Smye 2008 (PMID 18583502) found that the review "was comprehensive and used meta-analysis and narrative review methodologies effectively".
Nordentoft & Hjorthøj 2007 (PMID 17662860) said the review was "the most comprehensive meta-analysis to date of a possible causal relation between cannabis use and psychotic and affective illness later in life" and that "We therefore agree with the authors' conclusion that there is now sufficient evidence to warn young people that cannabis use will increase their risk of psychosis later in life."
Zullino et al. 2007 (PMID 17980730) raised the question whether there is a causal connection between addictive behavior in general (not merely addictive cannabis use) and schizophrenia.
Macleod et al. 2007 (PMID 17980727) said "The evidence that it [cannabis] additionally [that is, in addition to respiratory harm] causes mental health harm seems to us as equivocal and difficult to interpret as it always has been."
Schulte-Herbrüggen & Jockers-Scherübl 2007 (PMID 17980729) said that the paper "is a milestone in the recent psychiatric literature and clearly provides evidence for a dose-dependent effect of cannabis on the development and course of disease", and suggested that it might be due to early appearance of negative symptoms of schizophrenia that benefit from use of cannabis.
The authors' reply (Zammit et al. 2007, doi:10.1016/S0140-6736(07)61652-3) said that they agree that "it is not possible to be certain that the relation between cannabis use and psychotic illness is causal".

Given all the above, it is not controversial among reliable sources that there is an association between cannabis use and schizophrenia, or that the association is stronger with more-frequent users. However, it is controversial whether that "40% to 100%" is a reliable figure, or whether it represents a major cause or effect, so we should not be emphasizing it here.
To try to fix the above problems, I changed this text:

Though not necessarily implying causality, a meta-analysis published in The Lancet found that cannabis use is associated with a 40% to 100% dose-dependent increase in risk of development of psychotic disorders, including schizophrenia.

to this:

A 2007 meta-analysis estimated that cannabis use is statistically associated with a dose-dependent increase in risk of development of psychotic disorders, including schizophrenia.

Eubulides (talk) 23:54, 26 January 2009 (UTC)

Experience says that readers commonly take "there is an association between cannabis use and schizophrenia" to mean "cannabis use causes schizophrenia". Because the reviews are careful to say that the evidence does not justify the latter conclusion, I feel that we ought to guard against saying things in a way that will mislead readers. Looie496 (talk) 05:03, 27 January 2009 (UTC)

The text is already guarding against that misinterpretation. It precedes the discussion of the statistical association with two sentences talking about the lack of proof of causation. I don't see the need to add yet another "but that's not causality" phrase; it's already clear from context. Eubulides (talk) 08:52, 27 January 2009 (UTC)

One further thought I have is to remove the phrase "A 2007 meta-analysis estimated that" from the sentence about cannabis. That phrase adds little to the text, other than the (mistaken) impression that it may be controversial among reliable sources whether there is a statistical association. The date and type of study is easily available in the citation, for those few readers who want to know the details. Eubulides (talk) 18:46, 27 January 2009 (UTC)

Important Distinction Needs To Be Made

This article needs to state the difference between negative symptoms and major depression. Can anyone address this? 76.169.29.127 (talk) 22:58, 28 January 2009 (UTC)

The reason I ask this is because negative symptoms—e.g., affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), avolition (lack or decline in motivation), anhedonia (lack or decline in ability to experience pleasure), lack of concentration or social withdrawal (sometimes called social anhedonia) all appear to be symptoms of major depression. 76.169.29.127 (talk) 01:48, 30 January 2009 (UTC)

Minor quibble about a section heading

WP:MEDMOS recommends having separate top-level sections for causes/etiology and mechanism/pathophysiology. Shouldn't the "Neural" section be moved from "Causes" to "Mechanism"? Xasodfuih (talk) 09:42, 1 February 2009 (UTC)

I have read them again and tend to concur. Acutally the psychological one above would also be best under a mechanism category as both discuss changes before and during rather than some true antecedent. Casliber (talk · contribs) 12:33, 1 February 2009 (UTC)

I've added a "Mechanism" heading. Although it sounds rather bad, "pathophysiology" would sound even worse right before "psychological". Frankly the subheadings "psychological" and "neural" are a rather poor indicator of what's contained in those two subsections; also there's some mind-body dualism suggested by those headings, although there's thankfully none of that in the text there. I'd rather remove the subheadings them and simply have a top level heading "Neuropsychological mechanisms". Xasodfuih (talk) 14:47, 1 February 2009 (UTC)

Vitamin D lead.

My research and others has suggested a link to a vitamin D deficiency and symptoms that can be labelled as schizophrenia.

Hopefully someone can find other reliable sources and include them.

Vitamin D can treat schizophrenia ?

--Caesar J.B. Squitti: Son of Maryann Rosso and Arthur Natale Squitti (talk) 20:52, 14 February 2009 (UTC)

Foods is not a good enough source of Vitamin D.

CTV Report Vitamin D and sunlight

--Caesar J.B. Squitti: Son of Maryann Rosso and Arthur Natale Squitti (talk) 20:56, 14 February 2009 (UTC)

Unlikely, but if you can give a WP:PMID instead of the broken links above, I'll have a look. Xasodfuih (talk) 17:07, 15 February 2009 (UTC)

The Relationship between Trauma and Psychosis

Many experienced clinicians report that psychotic symptoms can be modified, or even stop with suitable psychotherapeutic intervention, without medication, and that medication may inhibit this process. These therapeutic interventions are based on based on the assumptions that the symptoms are the result of re-enactment of past trauma; see: Karon, B. P. (2008). Trauma and Schizophrenia. Journal of Psychological Trauma, 6 (2), 127-144. —Preceding unsigned comment added by Philbenjamin (talk • contribs) 02:55, 15 February 2009 (UTC)

I question the "many" here. Karon is a psychoanalyst whose publications have drawn little attention, and the Journal of Psychological Trauma is a small-press journal created in 2008 and not covered by PubMed, so we would need better sources. Since even Freud considered schizophrenia highly resistant to therapy, I am very skeptical of this. Looie496 (talk) 18:36, 15 February 2009 (UTC)

Changes to Issues and Controversies Section

Hi Xasodfuih,

Just a note to say thanks very much for some of the recent edits. They have really improved some of the more unfocused bits of the article. However, I just want to pick up on some of the changes to the 'Issues and Controversies' section. This has been changed so it reads like a list of people and their opinions, which is a quite misleading. For example, "Cognitive neuropsychiatrist Anthony David warned however that the definition of delusion is lacking consistency." This makes it seem as if it is just one individual with an opinion, when the reference is to a review article which covers a number of academic articles and research studies and is one of the most widely cited papers on the conceptual basis of delusions. The same problem pervades the rest of the section.

I think I fixed that. David's article isn't a review; it is a commentary on another article. It's in the last paragraph now. Xasodfuih (talk) 17:07, 31 January 2009 (UTC)

Also, I'm not sure where the 'psychologists vs psychiatrists' bit came from. The Campaign for the Abolition of the Schizophrenia Label have no psychologists as part of their team [3]. The reference quotes a psychologist and an nurse in favour of their position, and a psychiatrist and psychologist against.

From the BBC article that's given as reference. Xasodfuih (talk) 17:07, 31 January 2009 (UTC)

Richard Bentall, professor of experimental clinical psychology, from the University of Manchester, said: "We do not doubt there are people who have distressing experiences such as hearing voices or paranoid fears. "But the concept of schizophrenia is scientifically meaningless. It groups together a whole range of different problems under one label - the assumption is that all of these people with all of these different problems have the same brain disease."

I checked their web site and concluded taht the BBC article did not detail well enough who was involved. Updated. Xasodfuih (talk) 03:29, 1 February 2009 (UTC)

Furthermore, the paragraph on the political use of the diagnosis has just disappeared, despite these still being current concerns and genuinely important 'issues and controversies' in the diagnosis.

I moved to the history section since it was about Soviet practice, and expanded it a bit. I removed the stuff about Falun Gong practitioners since the references did not say that they were diagnosed with schizophrenia. As far as I know the Chinese Classification of Mental Disorders has some special disorder for that, so it should be discussed there instead. Xasodfuih (talk) 17:07, 31 January 2009 (UTC)

The addition of the section on schizoaffective disorder is a welcome addition, although it perhaps needs reference to recent molecular genetic studies from the Cardiff group on lack of genetic distinction between bipolar and schizophrenia and association with affective and non-affective psychosis (e.g. "The beginning of the end for the Kraepelinian dichotomy?" article etc).

Feel free to add it, I wasn't aware of it. Xasodfuih (talk) 17:07, 31 January 2009 (UTC)

N.B.: Craddock and Owen already get their fair share of wikispace in the genetics section. I've added their BJPsych editorial to the controversies section as you suggested. Xasodfuih (talk) 04:10, 1 February 2009 (UTC)

Anyway, I think the original version was much better and should be replaced so we can edit it from there to fix any inconsistencies and update it.

- Vaughan (talk) 15:20, 31 January 2009 (UTC)

Really? I found it rambling and repeating. Compare before after. The old version also mentions a non-contrversy (the Japanese renaming - I moved it to the [new] stigma subsection), a falsehood (the 65% bit - not to mention it was single small scale study), an irrelevant issue for the current criteria (Rosenham's study), improperly discusses David's commentary as being about thought disorder. As for repetition, it cited two of Bentall's books, in the 1st and 3rd paragraph, pretty much with same idea. It also completely ignored the new issues I've added: the reliability-validity trade-off and mood features. Finally, it allocated an entire paragraph to Green's book, which is a fairly minoritarian perspective even amongst the critics methinks. The flow of ideas was: validity/reliability - spectrum - def of delusion - nonspecificty of psychosis - reliabiltiy again (factually wrong and POV) - Japan - UK call for dropping the disorder (no mention of opposition) - neurocognitive definition(s) - political purposes Xasodfuih (talk) 17:07, 31 January 2009 (UTC)

I wondered about this Other UK psychiatrists opposed the move arguing that the term schizophrenia is a useful, even if provisional concept - I would think that "Most" was more accurate than "other". The BBC article quotes that as being stated by others and it would concur with my perception of my colleagues. Casliber (talk · contribs) 12:37, 1 February 2009 (UTC)

I agree that "most" is almost certainly a far better estimate. Trouble is, it's not something directly supported by the BBC story cited. I guess we could cite some NICE consensus statement; perhaps Vaughan can find it? Anyway, before I added that statement, just mentioning the call for sz to be scrapped in the UK looked rather unbalanced. Xasodfuih (talk) 14:19, 1 February 2009 (UTC)

Brand new NICE guidelines are due any month now. Draft edition on the web [4]. My favourite topic is there Earlypsychosis (talk) 12:21, 20 February 2009 (UTC)

Schizophrenia and over the counter drugs

The previous discussion on this item ignores the simple reality that the research found that inacurrate diagnosis resulted in the label "schizophrenia" being applied.

This research also does not mention faulty testing for "organic origins" of the disease. (lead for some link to this inforation)

- Phenylpropanolamine (PPA) is a sympathomimetic drug similar in structure to amphetamine which was formerly present in over 130 medications, primarily decongestants, cough/cold remedies, and anorectic agents.

- A report on PPA, from the Dept. of Psychiatry, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland. Pharmacopsychiatry 1988 stated:

We have reviewed 37 cases (published in North America and Europe since 1960) that received diagnoses of acute mania, paranoid schizophrenia, and organic psychosis and that were attributed to PPA product ingestion. Of the 27 North American case reports, more reactions followed the ingestion of combination products than preparations containing PPA alone; more occurred after ingestion of over-the-counter products than those obtained by prescription or on-the-street; and more of the cases followed ingestion of recommended doses rather than overdoses.

Failure to recognize PPA as an etiological agent in the onset of symptoms usually led to a diagnosis of schizophrenia or mania, lengthy hospitalization, and treatment with substantial doses of neuroleptics or lithium.

PPA is no longer available in any medication in the United States as of the year 2000.

--Caesar J.B. Squitti: Son of Maryann Rosso and Arthur Natale Squitti (talk) 17:07, 18 February 2009 (UTC)

A couple of images from Otis Archives

Otis Archives collection at Flickr has a couple of images (1 2), apparently a drawing on the wall made by a patient with schizophrenia. The license is CC-BY. It is written that the snapshots are made at the turn of XX century at St. Elizabeths Hospital. I wonder if they could be used; I'd upload them using Flickrtool -> to the Commons. Best regards. --CopperKettle 18:24, 25 February 2009 (UTC)

Uploaded to Commons:File:Reeve37257.jpg and Commons:File:Reeve37258.jpg --CopperKettle 18:29, 25 February 2009 (UTC)

Also upped the Commons:File:Reeve041788.jpg --CopperKettle 18:39, 25 February 2009 (UTC)

Archiving

This page is way long and gets substantial traffic. I propose to set up automatic archiving via Miszabot -- it seems to me that an archival cutoff of 30 days, and max archive size of 200K, would be reasonable. Are there any objections to that? Looie496 (talk) 18:48, 25 February 2009 (UTC)

Fine to me. --CopperKettle 19:04, 25 February 2009 (UTC)

Screening and Prevention

Screening and prevention

This needs some further consideration. The treatment of people who may never develop schizophrenia is not that controversial, in light of the work of leading prodrome clinics (PACE in Melbourne, OASIS in London). Most of these approaches involve a "active watching brief" and provide pharmacological and psychological treatments for non psychotic psychopathology (anxiety and depression). There is also a very good RCT on fish oils in an at risk group (Amminger et al 2008 or 2007).

I'm also of the view that early intervention initiatives prevents schizophrenia - but this is antecdotal, based on what I see, rather than a robust RCT (but I havent the time to wait for someone to do the research) —Preceding unsigned comment added by Earlypsychosis (talk • contribs) 07:46, 14 February 2009 (UTC)

Amminger Schäfer, Papageorgiou, Harrigan, Cotton, McGorry, Berger (2008). INDICATED PREVENTION OF PSYCHOTIC DISORDERS WITH LONG-CHAINOMEGA-3 FATTY ACIDS: A RANDOMIZED, PLACEBO-CONTROLLED TRIAL Schizophrenia Research, 102, 252- Earlypsychosis (talk) 07:21, 15 February 2009 (UTC) I am having trouble finding this article - I think it is maybe in Schizophrenia Bulletin? Earlypsychosis (talk) 21:35, 27 February 2009 (UTC)

I doubt that such treatment is not-controversial, because there are no precise tools to diagnose schizophrenia itself, let alone predict who will have it in the future, and pharmacological treatments have severe side-effects. How can we say that something prevents schizophrenia? To do this, there must at least be some way to recruit several at-risk groups using a unified method, prove that the groups have similar rates of schizophrenia in the later years. That will mean the method is working. Then take new groups and treat one of them, while leaving another without treatment. If the treated group will have lower rates of schizophrenia, then the treatment is good for prevention. And all this should take years and years, IHMO..--CopperKettle 10:33, 15 February 2009 (UTC)

could I suggest you read [5] and then the key articles written by A Yung in Melbourne, who has achieved what you suggest, that is, recruit at risk groups using a unified methods (CAARMS), placed them in a RCT, and then compare the rates of psychosis in each group. This has been achieved by treating with drugs, CBT ((Morrison et al, 2004) , and fish oil.(Amminger). Good summary in peer reviewed article. [6] Earlypsychosis (talk) 08:40, 18 February 2009 (UTC)

Tnank you, I'll take a look! --CopperKettle 10:37, 18 February 2009 (UTC)

As writes Jim Van Os in his latest article (via MindHacks), "..when a 'first episode' of psychotic illness is diagnosed, it may in fact be more correct to regard this as the poor outcome of the phenotype representing sublinical dimensions of psychosis that is transient in the great majority of cases.[3] Third, if psychotic experiences are frequent, their diagnostic value will be low in relation to the rare disorder of schizophrenia. Research has shown that even if the follow-up period is extended to more than 15 years, the probability of developing a psychotic disorder does not exceed 25%.[4]" O_o -CopperKettle 10:48, 15 February 2009 (UTC)

added a paper on ethics and early intervention - but would welcome direction to the WPpage to show me how to reference correctly (ie with PMID) Earlypsychosis (talk) 00:58, 20 February 2009 (UTC)

Add Clinical Scales

This article should include clinically useful scales for assessing and diagnosing schizophrenia. If added to the article, suggest including the BPRS.

The BPRS (Brief Psychiatric Rating Scale) assesses the level of 18 symptom constructs of psychosis such as hostility, suspiciousness, hallucination, and grandiosity. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 2-3 days. The patient's family can also provide the behavior report.--Cortamears (talk) 22:00, 6 March 2009 (UTC)

might be too far removed from the central topic of the article. maybe a brief mentioned within the text reference, but then BPRS is one of many ratings scales (what about PANSS), and is simply a measure of the symptoms of psychosis, rather than schizophrenia and I see you have already added to psychosis. Earlypsychosis (talk) 22:44, 6 March 2009 (UTC)

We have had a similar discussion on major depressive disorder about rating scales. The problem is the sheer volume of material to go in these articles. We ended up hiving it off to subpages. Actually developing them would be a great idea. Casliber (talk · contribs) 22:51, 6 March 2009 (UTC)

See Rating_scales_for_depression Casliber (talk · contribs) 22:52, 6 March 2009 (UTC)

A check of contribs shows that Cortamears (talk · contribs) has been adding paragraphs about scales to several psychiatric articles: Psychosis, Bipolar disorder, and Anxiety. The Hamilton scale mentioned in Anxiety seems well established, but the other are dubious. Without validation from strong sources this doesn't seem legit to me, and I'm inclined to remove them. I'm bringing this up here because there is already some discussion. Looie496 (talk) 01:05, 7 March 2009 (UTC)

dont remove them. the Brief Psychiatric Rating Scale is a well established scale. I thought about starting an article on it, but dont have the key references to hand. The Hamilton rating scales for anxiety and depression are also well known and well used. Its not hard to find references for them (I added the original reference to psychosis) and a quick check of current RCTs would show how common they are.... and this seems to be the key problem for wikipedia...a mismatch between the real world and wikipedia...finding evidence to show how common, well known and how widely used any topic is - requires a type of evidence that is difficult to demonstrate. Earlypsychosis (talk) 02:25, 7 March 2009 (UTC)

Yes, I have found that difficult - finding references for how psychiatry is practised has been very tricky at times. There are numerous scales for psychosis/schizophrenia/psychotic symptoms - the BPRS, the Positive and Negative Syndrome Scale (PANSS), the SAPS and SANS...part of the SCAN too...Casliber (talk · contribs) 04:13, 7 March 2009 (UTC)

(outdent) I also forgot about this one - Psychiatric assessment. Lots of pages to expand and crosslink. Casliber (talk · contribs) 04:17, 7 March 2009 (UTC)

loss of brain tissue

The statement Mihai cartoaje (talk · contribs) added "there is evidence that the neuroleptic drugs themselves cause loss of brain tissue" is not supported by the source. The interviewee was very careful to say they had only found a correlation, and proposed a possible reason. That is far from proving anything or finding "evidence". Her comments are based on unpublished studies that have not been subject to peer review. So even if interviews in newspapers were considered reliable sources for medical facts (which they are not, and WP:MEDRS is a guideline), the source fails WP:V because it doesn't support the text. Colin°^Talk 08:24, 1 March 2009 (UTC)

There was a study on macaque monkeys that in my view greatly corroborates Andreasen's conclusion (PMID 15756305 and PMID 17063154 and PMID 17945195); a combination of this and her words (and mention of critiqal remarks from Torrey) could be added in one phrase to let reader know the current state of thoughts in this area, and as soon as her study results are published the phrase could be swapped with one that only tells of human data. --CopperKettle 10:18, 1 March 2009 (UTC)

I can't remember any studies about schizophrenics and the purported long-term negative cognitive/brain size effects of antipsychotics, but off the top of my head I remember PMID 12590629, which associated cognitive impairment with the use of antipsychotics in bipolar I patients. (Also, I found PMID 16039620 which reiterated more or less the same results in bipolar I). If user User:Mihai cartoaje is interested in this, he should try to find some more reliable sources than a newspaper, since this is a contentious issue. Xasodfuih (talk) 11:04, 1 March 2009 (UTC)

Also PMID 12679233 may be of interest: "CONCLUSIONS: We failed to find evidence that hippocampal volume loss is associated with familial liability to schizophrenia but have confirmed the association between hippocampal volume reduction and exposure to obstetric complications." Xasodfuih (talk) 13:20, 1 March 2009 (UTC)

The exact quote from Andreasen, as given in NYT, is "Another thing we’ve discovered is that the more drugs you’ve been given, the more brain tissue you lose." Since this is unpublished research, but she is an authority in the field, it could be mentioned as long as the source, the venue, and the fact that this research has yet to be published, are clearly mentioned. Xasodfuih (talk) 13:28, 1 March 2009 (UTC)

I have reworded the sentence accordingly. Xasodfuih (talk) 13:37, 1 March 2009 (UTC)

Also, two questions later she says: "Q. ARE YOU WORRIED YOUR FINDINGS MIGHT BE MISUSED? A. The reason I sat on these findings for a couple of years was that I just wanted to be absolutely sure it was true. My biggest fear is that people who need the drugs will stop taking them." and "Q. WHAT ARE THE POLICY IMPLICATIONS OF THIS FINDING? A. Implication 1: that these drugs have to be used at the lowest possible dose, which often doesn’t happen now. There’s huge economic pressure to medicate patients very rapidly and to get them out of the hospital right away. Implication 2: we need to find other drugs that work on other systems and parts of the brain. Implication 3: whatever medications we use need to be combined with more nonmedication-oriented treatments, like cognitive or social therapies." Xasodfuih (talk) 13:41, 1 March 2009 (UTC)

"Implication 1" could possibly mentioned as well, although I'm weary of transforming this article in an Andreasen quote farm. Xasodfuih (talk) 13:45, 1 March 2009 (UTC)

Thank you! --CopperKettle 13:50, 1 March 2009 (UTC)

Published research in this area exists for humans as well, although it only supports Andreasen's hypothesis for typical antipsychotics. I've added it. Xasodfuih (talk) 14:14, 1 March 2009 (UTC)

In case you wonder whether this my WP:SYNT, rest assured that the contrast with the earlier studies in humans was made in this context in the discussion section of PMID 17063154. Xasodfuih (talk) 14:17, 1 March 2009 (UTC)

Andreasen's interview in the newspaper has no place in this article. Schizophrenia (and drug treatment) is very well researched and documented. There is simply no need to cite such an inferior source for an encyclopaedia article. And we never cite unpublished research. So that sentence should go. As for the "Published research in this area only supports Adreasen's hypothesis" follow-on sentence, I have rarely seen such flagrant WP:OR. We can only say such things if the sources say "Adreasen's hypothesis is supported by ...". Directly citing research on non-human primates means you as a WP editor has decided such studies are clinically relevant. Not on. We can only link animal research to effects in humans if our cited sources do so. And PMID 15809403 does not "support Adreasen's hypothesis". It fails to prove any reason for the brain differences on the two drug-treated groups. They offer many possible reasons, but the one they find most compelling is that olanzapine is protective against the "underlying pathophysiology and progressive nature of schizophrenia". I have no particular POV to push. If there is strong evidence that these drugs are damaging (or protective) then we should mention this. But we need to cite the secondary literature here, not play scientists and perform our own primary literature search ourselves. The final two sentences in that paragraph fail two of our fundamental policies, which allows for their deletion. It is the responsibility of editors wishing to add material to find suitable sources for it. Colin°^Talk 20:09, 1 March 2009 (UTC)

I agree that the newspaper interview should not be used, however I don't think it is OR to cite PMID 15756305 -- it's a top quality source, Darrel Lewis is a highly reputed expert on the neuropathology of schizophrenia, and it does discuss the human relevance of the findings. And on principle, an effect of this type found in macaques at clinical doses has a high likelihood of carrying over to humans. Looie496 (talk) 21:45, 1 March 2009 (UTC)

Agree that we should not be citing the newspaper interview, and concerned about OR as pointed out by Colin above. SandyGeorgia (Talk) 22:22, 1 March 2009 (UTC)

Sorry for inadvertently presenting the first episode haldol vs. olanzapine studies as supporting Andreasen's hypothesis; that was due a superficial 1st reading of those studies on my part. Since those studies have been published, I don't see much point in keeping Andreasen's unpublished work. Because primate studies explicitly cite them for contrast (as I mentioned above, but Colin did not seem to read), I think this version is reasonably free of issues; feel free to adjust as necessary. There's some chance that the 2005 studies have been cited in reviews, but I won't be looking for those today. I'm signing off for now. Xasodfuih (talk) 01:23, 2 March 2009 (UTC)

I've replace all the primary studies in that paragraph with reviews in this version. Happy WP:MEDRSing. Xasodfuih (talk) 03:17, 2 March 2009 (UTC)

IIRC, haloperidol vs. olanzapine was Eli Lilly marketing. It's one of those marketing scams like when Janssen took people who were recently taking high doses of neuroleptics as their placebo group and people who were not taking neuroleptics recently as their Risperdal group and since their "high doses of neuroleptics/placebo" group still experienced EPS as an after-effect, used it to claim that Risperdal has the same indicidence of EPS as placebo. Since it is marketing, it is partisan, and therefore not a good source per WP:RS. --Mihai cartoaje (talk) 08:05, 9 March 2009 (UTC)

MEDRS is not a guideline. Many of its supporters admitted a conflict of interest, were pov pushers, and there was too much opposition. Even MEDRS allows the New York Times because it is a social issue. The wording of the sentence "there is evidence" was written by Vaughan and I did not change that part. The New York Times is a reliable source so it is against policy to remove it. This is just a cover-up. The APA has admitted to political lobbying, as I pointed out on the MEDRS talk page, and they also have a conflict of interest in making their jobs easier, so writing that only a partisan, conflict of interest, advocacy group is allowed as a source would be biased. Both sides deserve fair representation per WP:NPOV. --Mihai cartoaje (talk) 08:05, 9 March 2009 (UTC)

Even if newspapers were a reliable source for medicine, not everything published in a newspaper is governed by their editorial policy. In an interview, the interviewee can say what they like. Andreasen might think the moon was made of cheese and the NYT would be accurate in reporting that. The effect of a drug on brain tissue is not a "social issue". As for the rest of your comments, please note that article talk pages are not a forum for editors to voice opinions on the state of the world. Colin°^Talk 13:49, 9 March 2009 (UTC)

It is a social issue because forced-drugging advocates have been arguing that the brain shrinkage is because of schizophrenia being a disease and therefore, according to them, innocent people should be victimized. --Mihai cartoaje (talk) 00:31, 10 March 2009 (UTC)

You can only buy Wikipedia space in proportion to how much coverage you buy in the peer-reviewed real world venues. Once Andreasen gets over her reluctance to publish the stuff, we can include. Xasodfuih (talk) 15:57, 9 March 2009 (UTC)

There's no such rule. --Mihai cartoaje (talk) 01:10, 10 March 2009 (UTC)

WP:MEDRS. Xasodfuih (talk) 02:37, 10 March 2009 (UTC)

What actually happens to the brain of men or monkeys is not a social issue, but a purely scientific one, and non-scientific material on this is not reliable, and not even relevant. If one is writing about the public perceptions of the issue, then non-scientific publications are primary data, and academic asocial science is the relevant reliable sources. it is relevant. If one is writing about the public policy implications of what happens, then it is a social issue and although one might with Socrates make a case for only those qualified in the study of social ethics having relevant opinions, the usual modern Western view on matters like this is that all ethical views are equally valid for political purposes--so all wp need do is achieve balance. My own view is that such matters as perceptions of a scientific field, or its political or ethical or religious implications, scientific or medical field belong in separate articles, because the nature of the sources is so radically different. What the effect is of psychotropics is a scientific question on which politicians or the public have nothing to say; whether they should be permitted or even required, is quite the opposite. It would be possible to argue that while effective and safe, they are still destructive of personal freedom--a view I emphatically do not share, but one where my opinion is no better than yours. Only those who understand the science can give a valid opinion about safety or effectiveness. One might even argue that even if dubious safe or effective, they might still be used to maintain hope. That again is back to ethics. DGG (talk) 02:26, 11 March 2009 (UTC)

Taraxein

Taraxein is claimed to be a hallucinogenic protein that has been claimed to be extracted from humans with schizophrenia. PubMed indexes 14 papers with “taraxein” in the title, mainly from the 60's and 70's. Some of these papers are available online.

The Merriam-Webster definition of the word states that the initial studies were disproven. Does anyone know which research put the nail in the coffin of this theory? What were the flaws in the multiple studies that confirmed the psychoactivity of taraxein? If someone is informed on this subject, please create the article. — StrawberryCube (talk) 03:52, 16 March 2009 (UTC)

I have never ever heard of this...weird....Casliber (talk · contribs) 09:19, 16 March 2009 (UTC)

I hadn't either, but a look at Google Scholar tells the whole story: the idea of a psychotogenic blood protein was pushed by some Russian writers and by the rather infamous Robert G. Heath in the late 50's, and definitely ruled out somewhere around 1960. It really doesn't even make sense, since the supposed proteins were found in serum, and as proteins wouldn't have been able to cross the blood-brain barrier. Looie496 (talk) 17:15, 16 March 2009 (UTC)

Thanks! That's useful. I'll dig on Google Scholar and try a write-up at Taraxein. I first read about it in a book published in ’77, which said it was the only hallucinogenic extracted from humans. I guess they were behind on their research, even for their time :). — StrawberryCube (talk) 02:36, 17 March 2009 (UTC)

There was another one-hit-wonder, the so-called "Pink spot" that came up in urine analysis of the patients. A number of confounding factors were found eventually, as far as I remember. --CopperKettle 03:21, 17 March 2009 (UTC)

concerning Psychosis

The psychosis article could use a few more eyes -- it's been getting some edits recently whose validity is not clear to me. I'm not enough of an expert to be assertive there, though. I'm bringing it up here because of the close relationship of the topics and because I don't want to canvass individuals. Looie496 (talk) 23:05, 14 March 2009 (UTC)

Good point. It also was a Featured Article once - and is a good place to discuss the relationship with substance use as it can higlhight both schizohrenia and drug-induced psychosis. Casliber (talk · contribs) 11:39, 26 March 2009 (UTC)

Type 1 and Type 2

Makes no mention of Type 1 and Type 2 (reactive/acute and process) that I can see. Need to break it down with the normal things under each one as bullet points and further explanation. desk003 (talk) 06:43, 25 March 2009 (UTC)

Old terminology not used anymore. Casliber (talk · contribs) 08:14, 25 March 2009 (UTC)

Well that's interesting. I'm currently studying Psychology and that's how I'm being taught. desk003 (talk) 00:26, 26 March 2009 (UTC)

What textbook? Looie496 (talk) 00:54, 26 March 2009 (UTC)

We use Comer's Abnormal Psychology Sixth Edition. However, now that I'm specifically looking for it (and not all annoyed and studying for a test) I can't find anything stating Type I or Type II in it.. I thought I was just annoyed and impatient last night when I was looking. I guess it's just the professor here at Vincennes University that's teaching us Type I and Type II.. So that's annoying.. desk003 (talk) 01:18, 26 March 2009 (UTC)

new publication treatment guidance

The UK based National institute for health and clincal excellence (NICE) has recently published treatment guidance. It is a good read and a reliable source of information that needs to be added to here [7] Earlypsychosis (talk) 09:48, 12 April 2009 (UTC)

Genetic burdon of common diseases likely carried by large numbers of rare varients.

In the Genetics section of this article we have "it has been suggested that schizophrenia is a condition of complex inheritance, with several genes possibly interacting to generate risk for schizophrenia or the separate components that can co-occur leading to a diagnosis."

Change requested: I would like to see some of the following incorporated into the article's section on genetics. I cannot edit semiprotected pages yet.

David B. Goldstein, a Duke University Professor wrote in this weeks issue of the The New England Journal of Medicine "that the genetic burden of common diseases must be mostly carried by large numbers of rare variants. In this theory, schizophrenia, say, would be caused by combinations of 1,000 rare genetic variants, not of 10 common genetic variants."

"This would be bleak news for those who argue that the common variants detected so far, even if they explain only a small percentage of the risk, will nonetheless identify the biological pathways through which a disease emerges, and hence point to drugs that may correct the errant pathways. If hundreds of rare variants are involved in a disease, they may implicate too much of the body’s biochemistry to be useful."

^[1]

-jdh —Preceding unsigned comment added by Xeropoint (talk • contribs) 18:37, 16 April 2009 (UTC)

Drug induced psychosis

This section Schizophrenia#Drugs says that only cannabis can cause psychosis but I strongly disagree. Whilst cannabis appears to be a fairly common factor in psychosis, a wide range of drugs of abuse are associated with psychosis, including amphetamines (especially methamphetamine), LSD, PCP (angel dust), Ketamine, alcohol (alcoholic hallucinosis, korsakoff's syndrome). Although it is a secondary source (a review paper), I could find hundreds I am sure of other reviews on psychotic disorders triggered or caused by other drugs of abuse. Also the review paper is actually misquoted. It says at least in its abstract that only cannabis causes psychopathology, so they are basically saying that all other drugs of abuse cause no mental health problems whatsoever, even depression or anxiety etc. I am uneasy with the statement that only cannabis. What are other editors views?--Literaturegeek | T@1k? 20:23, 26 March 2009 (UTC)

Ah, the problem is that in DSM IV TR, one of the diagnostic criteria for schizophrenia is the absence of a general medical condition or a substance, such as abuse of a drug or medication, as a cause. Thus, detailed discussion on the links between substances and schizophrenia on this page will continue to be argued about ad nauseam until DSM evolves into a more sophisticated classification system. However, the debate is firmly in the sphere of psychosis which is a term for the psychotic disorders, much like mood disorder is for depression, bipolar, dysthymia etc. Casliber (talk · contribs) 23:18, 26 March 2009 (UTC)

PS: Dual diagnosis is a good article for worsening of prognosis with comorbid substance use, and I have just discovered that Drug-induced psychosis ~~(official name)~~ (sorry, my bad - old term) is actually a redirect to Amphetamine psychosis....hmmmmmmm. Casliber (talk · contribs) 23:20, 26 March 2009 (UTC)

I see what you are saying that schizophrenia has specific diagnostic criteria in the DSM. That would be fine if the article said "other drugs of abuse are not associated with increased risk of schizophrenia but several other drugs of abuse can cause a substance induced psychosis".

I could build up a drug induced psychosis section in the psychosis article and then it could be used as a see also link.--Literaturegeek | T@1k? 09:47, 27 March 2009 (UTC)

Yes. and linked to from hither. Casliber (talk · contribs) 09:51, 27 March 2009 (UTC)

Looky what I found :). This ref seems to be saying just what we seem to be agreeing on (I think). The ref says in summary,,,, Alcohol, cannabis, amphetamines and cocaine may cause a substance induced psychosis in individuals with or without a history of psychosis. Only cannabis has been shown to increase the risk of schizophrenia. The evidence for other substances of abuse increasing the risk of schizophrenia is less clear due to limited data.

I wonder would it be worth replacing the current review used at the end of the drugs section with the review I just found? Then we could wiki redirect link substance induced psychosis to a subsection in the psychosis article.--Literaturegeek | T@1k? 10:31, 27 March 2009 (UTC)

Amphetamines also increase schizophrenia or only cannabis?

I recall a discussion with a professor of psychiatry and is a psychopharmacologist who is the clinical director of a large psychiatric hospital who stated to me that a large number of his patients that he sees who meet the diagnostic criteria for schizophrenia or schizo-effective disorders often have a past history of stimulant use for ADHD. I found a review article which confirms his observation. In his opinion the amphetamines during childhood causes brain damage and he believes his colleagues in child psychiatry and pediatrics are unwittingly brain damaging a number of their clients with amphetamine based drugs. Anyway, I came across an interesting review article which finds a high association of childhood use of amphetamine based stimulants for ADHD with schizophrenia, schizoeffective disorders and bipolar disorders, independent of ADHD. Although the citations I found do not conclude that the stimulants themselves cause brain damage to children, it might be of value citing this association? Also what are people's thoughts? I am just not convinced that cannabis is the only drug which increases rates of schizophrenia. Chronic amphetamines aren't healthy for the brain either, at least in susceptible people. See the italiced text below for info on schizophrenia and amphetamine use during childhood.

Methylphenidate an amphetamine derivative and potent central nervous system stimulant,^[2] can also in some people lead to a psychosis from chronic use. Although the safety profile of short-term methylphenidate therapy in clinical trials has been well established, repeated use of psychostimulants such as methylphenidate is less clear. The long term effects of methylphenidate such as drug addiction, withdrawal reactions and psychosis has recieved very little research and thus the long term effects of using stimulants for ADHD are largely unknown.^[3] Some publications suggest a rate of psychosis of 6% in children on long term methylphenidate.^[4] The long term effects on mental health disorders in later life of chronic use of methylphenidate is unknown.^[5] Concerns have been raised that long-term therapy might cause drug dependence, paranoia, schizophrenia and behavioral sensitisation, similar to other stimulants.^[6] Psychotic symptoms from methylphenidate can include, hearing voices, visual hallucinations, urges to harm oneself, severe anxiety, euphoria, grandiosity, paranoid delusions, confusion, increased aggression and irritability. Methylphenidate psychosis is unpredictable in who it will occur. Family history of mental illness does not predict the incidence of stimulant toxicosis in ADHD children. High rates of childhood stimulant use is found in patients with a diagnosis of schizophrenia and bipolar disorder independent of ADHD. Individuals with a diagnosis of bipolar or schizophrenia who were prescribed stimulants during childhood typically have a significantly earlier onset of the psychotic disorder and suffer a more severe clinical course of psychotic disorder.^[7]

Reviews cited above, clickable. See full text of review article. An abstract of another review and another abstract of a review and another review.--Literaturegeek | T@1k? 19:34, 21 April 2009 (UTC)

Note, that when talking about amphetamines and increased schizophrenia, they are talking about past use, not current transient amphetamine induced psychosis.--Literaturegeek | T@1k? 21:01, 21 April 2009 (UTC)

Amphetamine induced psychosis is widely recognised. It gets murky when a person is chonically using amphetamines and chronically psychotic. Again we have the conundrum about DSM IV and origin. Casliber (talk · contribs) 21:11, 21 April 2009 (UTC)

I understand the conundrum Casliber but the refs on schizophrenia, as far as I am interpreting them are not talking about people still taking amphetamine based stimulants but are talking about people who have a past history (not current use) of using stimulants for ADHD in childhood. So I don't believe that the conundrum of DSM IV exists in this case.--Literaturegeek | T@1k? 21:17, 21 April 2009 (UTC)

It is the last reference and this text "There is little evidence to suggest that other drugs such as alcohol cause psychosis" in this section Schizophrenia#Drugs that I have a problem with. It is seriously misleading to the general public and health professionals to say that other drugs do not cause psychosis (drug induced or not). Even you yourself say that amphetamine psychosis is widely recognised so why is there a ref basically saying little evidence to support amphetamine psychosis or any other drug induced psychosis other than cannabis. It also says alcoholic psychosis does not exist, whilst it may not be as common as amphetamine or cannabis psychosis it clearly is established as a disorder. Is korsacoffs a myth? You see my point I hope.--Literaturegeek | T@1k? 21:31, 21 April 2009 (UTC)

If I am a lone wolf in this I will not go on about it and let it rest. I don't intend or want to be a pest.--Literaturegeek | T@1k? 21:34, 21 April 2009 (UTC)

These are good points and the same have been debated long and loud on many psychiatry forums. Incidentally, Korsakoff's psychosis was a bad choice of names for Korsakoff's syndrome which has nothing to do with psychoses as commonly understood. Casliber (talk · contribs) 21:50, 21 April 2009 (UTC)

I think in the meantime the word "psychosis" should be renamed to "schizophrenia" or better still "chronic schizophrenia" to clear up confusion as in its current form it implies that alcohol cannot cause drug induced or withdrawal related psychosis and it currently reads to say that drug induced psychosis such as amphetamine psychosis is effectively a myth with in their words "little evidence".

I still feel that it should be cited that childhood use of stimulants is highly associated with later development of schizophrenia because that is what a review of the evidence found. Perhaps korsacoffs was a bad example and I never realised there was controversy surrounding its name, I learnt something new. :) I do have a ref here which associates alcoholism with schizophrenia and this ref on alcoholic psychosis being misdiagnosed as schizophrenia. Perhaps alcohol is not relevant to this article, but I feel the high association of stimulant use in childhood is as notable if not moreso than cannabis. I guess my point is why is the association with cannabis in the article but with amphetamines it is not in the article? Is the evidence base not strong enough for a featured article in your opinion for stimulants compared to cannabis being associated with increased rates of schizophrenia?--Literaturegeek | T@1k? 22:10, 21 April 2009 (UTC)

I can't see anything in your sources that says that stimulants cause schizophrenia, or increase the incidence of it. It is a mistake to go from psychotic symptoms to schizophrenia without further support. Looie496 (talk) 00:00, 22 April 2009 (UTC)

It was the first review link that I gave that states the high levels. See full text of review article

Here is a copy and paste from the full text.

Retrospective data from patients with schizophrenia or bipolar disorders document high rates of childhood stimulant use—generally higher even than other groups with attentional dysfunction (26) and histories of stimulant-associated adverse behavioral effects (27). In these patients, a history of stimulant use is also associated with an earlier age at onset (28) and a more severe course of illness during hospitalization (29). Stimulant exposure in vulnerable individuals may hasten the onset or worsen the course of bipolar or schizophrenic illnesses (26, 30). Thus, while stimulants are clearly beneficial for the vast majority of children with ADHD, there may be a small subgroup for whom the medications worsen the long-term course of other illnesses. Research aimed at determining whether such a subgroup exists and how to identify it is warranted.

I said that it is highly associated. Cause and effect similar to cannabis is speculative and difficult to prove. The high association exists just like with cannabis, perhaps higher than cannabis.--Literaturegeek | T@1k? 00:18, 22 April 2009 (UTC)

You misread me, when I said above about causing psychosis, I was talking about drug induced psychosis (usually transient, lasting weeks or months). The article reads as if to say drug induced psychosis only occurs with cannabis. That is a seperate issue. The other issue regarding schizophrenia being highly associated with past stimulant use in childhood I did not say was caused (as that is speculative as with cannabis).--Literaturegeek | T@1k? 00:22, 22 April 2009 (UTC)

I guess I have two comments. First, at this point it's not clear to me exactly what you're trying to say. Second, what is clear is that you have a preconceived opinion and are hunting for sources to support it. That's always a recipe for portraying the literature in a distorted way. One must read the literature with an open mind in order to represent it in a properly balanced way. Regards, Looie496 (talk) 00:33, 22 April 2009 (UTC)

I am trying to say the same as what the secondary reliable source that I gave you says. Errm, I am not trying to hunt for sources to fit my POV. I used a review article, not a primary source first of all. Second of all I have yet to read a study which finds no association of stimulant use and high rates of schizophrenia, so your accusation is false, unfounded and unwarranted. My motives are this, lots of schizophrenics and mental health workers are going to read this article, the drug section and think that drug induced psychosis only occurs with cannabis and no other drugs illict or licit. Can you give me an example of where I have distorted the literature?--Literaturegeek | T@1k? 00:51, 22 April 2009 (UTC)

I did a bold mini edit to resolve the main issue I had with this article. I think that it is a fair edit. Article is on schizophrenia anyway not transient drug induced psychosis so I think edit is accurate and doesn't mislead the reader like the previous version. If it gets reverted oh well. Since this has degenerated into accusations and is getting personal I think that I will back away from the article. I prefer if people want to criticise my edits that they do so by producing reliable sources to back up their accusation or position rather than randomly claiming that the literature really says something different and I am distorting it. I await a review paper showing no association between stimulant use and schizophrenia otherwise we will leave it as an unfounded false accusation against me that I am distorting the literature.--Literaturegeek | T@1k? 01:00, 22 April 2009 (UTC)

I just did a scan of pubmed on schizophrenia and methylphenidate and couldn't even find a primary source finding no association of use of methylphenidate and schizophrenia so if you can even find a primary study, let me know. I am NOT distorting the literature and reject that accusation. Infact I am 100% inline with the literature.--Literaturegeek | T@1k? 01:33, 22 April 2009 (UTC)

I personally have no problem at all with that mini-edit. Regarding the other stuff, the difficulty with "associations" is that it is very hard to tell whether they arise because people with incipient schizophrenia seek drugs, or because drug use promotes schizophrenia. To talk about causality in this article, we need more than sources that find associations, we need sources meeting MEDRS that explicitly talk about causation. Looie496 (talk) 01:52, 22 April 2009 (UTC)

Good, looks like my main problem is resolved. Glad you have no problems with the edit. I understand that, but cause and effect of cannabis is controversial as well and hotly debated and not resolved but is cited in this article. This review does state that chronic use of stimulants such as methylphenidate can cause schizophrenia so that is a ref for causation. Then there is also the review finding a high correlation of childhood history of stimulant use and schizophrenia so I personally don't see why cannabis is cited in the article and not childhood exposure to stimulants. I understand that this is a featured article as well and that the standard bar is higher on such articles so if we can't get consensus I am not going to push things. At least it appears that my mini edit is not a problem and I am happy with that outcome. Hopefully we can also set aside are minor fall out on this page and get 2 good outcomes. :)--Literaturegeek | T@1k? 02:31, 22 April 2009 (UTC)

Explanation

It's a metamorphosis of the mind, kind of like a caterpillar becoming a butterfly. Except, it never ends and it never gets beautiful. And, ultimately, all the energy expended is entirely exhausting. SharkD (talk) 05:30, 21 April 2009 (UTC)

No Nobel

Nash never won a Nobel Prize. He won a Memorial prize in Economics. Please correct the picture caption. 89.180.182.21 (talk) —Preceding undated comment added 01:07, 22 April 2009 (UTC).

Have you read Nobel Memorial Prize in Economic Sciences? It seems to justify simply referring to it as a Nobel prize. Looie496 (talk) 03:05, 22 April 2009 (UTC)

Potassium ion channels and isoform 3.1 of KCNH2

A new paper may be of interest: Huffaker SJ, Chen J, Nicodemus KK, Sambataro F, Yang F, Mattay V, Lipska BK, Hyde TM, Song J, Rujescu D, Giegling I, Mayilyan K, Proust MJ, Soghoyan A, Caforio G, Callicott JH, Bertolino A, Meyer-Lindenberg A, Chang J, Ji Y, Egan MF, Goldberg TE, Kleinman JE, Lu B, Weinberger DR (3 May 2009). "A primate-specific, brain isoform of KCNH2 affects cortical physiology, cognition, neuronal repolarization and risk of schizophrenia". Nature Medicine. doi:10.1038/nm.1962. {{cite journal}}: Unknown parameter |laysummary= ignored (help)CS1 maint: multiple names: authors list (link)

Could be handy in the Causes of schizophrenia article --CopperKettle 15:51, 6 May 2009 (UTC)

nature of hallucinations

I'd like to discuss the most recent change to the lead made by Editor182 (talk · contribs). To my understanding, somatosensory disturbances are more common than visual, and perhaps olfactory too; but I'm not enough of an expert to be sure of this. Any input? Looie496 (talk) 15:13, 7 May 2009 (UTC)

Somatosensory disturbances do occur but are not often prominent and overlap with delusions. They are much more a feature of stimulant intoxication ("formication" etc.). I wouldn't have it in the lead. Casliber (talk · contribs) 20:36, 9 May 2009 (UTC)

recognizing psychosis

Popular Hollywood films such as The Soloist and A Beautiful Mind provide true stories from the lives of patients and their families. Often relatives are not aware of key signs, nor, that early intervention can be helpful. Local mental health groups support families to seek medical advice and steps to a clear diagnosis.

Scientists collaborate in Schizophrenia Research Forum, to bring together experts from neurology, brain imaging, pharmacology to address this puzzling disease. www.schizophreniaforum.org 99.234.95.84 (talk) 15:08, 9 May 2009 (UTC)

I agree with the mentioning of The Soloist and Schizophrenia Research Forum (a helluva website). --CopperKettle 15:35, 9 May 2009 (UTC)

Schizophrenia etymology

Schizophrenia does not literally mean "I split" it means "Split Mind". —Preceding unsigned comment added by Mattyb54 (talk • contribs) 07:08, 25 May 2009 (UTC)

I am not sure to which you are referring - the word pieces are discussed separately. Casliber (talk · contribs) 19:55, 29 May 2009 (UTC)

Heritability

The article states that "Estimates of the heritability of schizophrenia tend to vary owing to the difficulty of separating the effects of genetics and the environment although twin studies have suggested a high level of heritability."

This language makes it sound as if heritability measures of schizophrenia are inconclusive, which does not appear to be the case. I just did a quick Google Scholar search and the estimates were all in the 80-90% range. This is an extremely high level of heritability and would warrant a much stronger conclusion than is given in the article.

I can address this myself after the semester is over, but I thought I'd throw this out there in case somebody wanted to tackle it in the next few weeks.

Josh (talk) 07:24, 25 April 2009 (UTC)

Studies of incidence of monozygotic twins have 40-50% as the rate of the second twin getting it if the first has. Casliber (talk · contribs) 07:45, 25 April 2009 (UTC)

One large latest study estimates genetics share at only 64% for SZ and 59% for bipolar; see PMID 19150704 and "Large Family Study Links Genetics of Schizophrenia, Bipolar Disorder" at Schizophrenia Research Forum. --CopperKettle 08:38, 25 April 2009 (UTC)

Apparently my quick Google Scholar search was insufficient. Well, we should at least include some of these numbers in the article. It's vague as it is and can be more informative. Josh (talk) 15:15, 26 April 2009 (UTC)

It is a fascinating subject - finding the 'best' sources (haha) can be a little tricky sometimes...our problem is the article is huge already. Might be good to exand on causes of schizophrenia. Casliber (talk · contribs) 20:05, 26 April 2009 (UTC)

I know someone with this disease, for more than 20 years.His mother, now more than 80 ears old, never had any mental problem.His father died many years ago and never had any emntal problem;he died of prostate cancer and old.Any of his six sisters or brothers has any mental problem.He is the only case of schizophrenia is his big family.Anyone reallly knows what causes schizophrenia.The cause of this disease remains a mistery.Agre22 (talk) 23:20, 31 May 2009 (UTC)agre22

If anything the article does not canvass all the etiological theories and weight them properly. The pathogen theory is barely mentioned despite its long history and strong advocates, and yet the 'bad parenting' theory, which has long since been discredited, is given weight along with pure speculation like Jaines's hypothesis that schizophrenia is the default state of the bicameral mind absent acculturation. The heritability hypothesis lacks an adequate examination of the patterns that characterize genetic diseases, as shown by longitudinal studies. What's more, statistical studies that do not give the maxima and minima for the studied populations are suspect. Left-handedness is known to make up about ten per cent of all human populations, but the genetic argument has never been credibly made. The maxima and minima of studied populations do not support it.Uniquerman (talk) 01:53, 5 July 2009 (UTC)

Arguments such as this could only be used in the article if there are recent review papers in strong books or journals that advocate them. Are there? Looie496 (talk) 15:58, 5 July 2009 (UTC)

I'll see what I can do. No promises.Uniquerman (talk) 21:54, 13 July 2009 (UTC)

Unsourced additions

This edit adds text to existing text, based on a source where only the PMID is easily available. Is the new text really covered in that article? Does anyone have the full text to verify? In fact, is all of the text sourced to that article really in that article, since it's about speech and doesn't seem very broad, based on the PMID alone? Can someone check, and either remove or source this new text? This kind of text creep, that appears to be sourced but may not be, has to be watched. Regards, SandyGeorgia (Talk) 13:38, 29 May 2009 (UTC)

I'll take a look. Actually anhedonia is a bit of a borderline one too. Casliber (talk · contribs) 19:56, 29 May 2009

(UTC)

Yoga and link with Schizophernia

Thinking at a lower level of perception that can be explained physically and logically is considered social and acceptable, but the higher level of perception of an individual is considered unusual. This altered state of mind which it is unable to have commuinication with mass minds is Schizophernia. Newton, Nash are only one of few known and popular examples who have had the ability to climb down from unique mind to mass minds. Other die or cause death by inability to return or die (leave the body) as they find a free state of choosing reality they are in comfort.

See page 20 Times of India New Delhi edition for title Kids bring mom home after 20 years jungle stay.

This proves that Schizophernia can be not a threat if such persons stay in forest and even animals have a respect for such an individual in deep meditation.

Life is not as simple as is known. —Preceding unsigned comment added by 123.239.106.205 (talk) 13:15, 24 May 2009 (UTC)

How many schizophrenics have you known? I've know hundreds in a professional sense - sorry, they are not some existing on some "higher plane of conciousness" with "higher levels of percetion"... 132.38.190.10 (talk) 15:31, 20 July 2009 (UTC)

Ditto. One wonders which is worse, the blithe ignorance or the fantastic conception of mind at work. In any case, the comment is out of place.Uniquerman (talk) 17:18, 23 July 2009 (UTC)

Famous persons with schizophrenia

Many persons, including kings and presidents, had this disease.The article hasn't a list of persons with this disease.Agre22 (talk) 23:15, 31 May 2009 (UTC)agre22

It would be helpful for you to list a few famous people who have been diagnosed with or show clear signs of schizophrenia. Remember, it is a debilitating disease with a preponderantly juvenile onset.Uniquerman (talk) 17:15, 23 July 2009 (UTC)

Cognitive and emotional features of schizophrenia

The following section was in the Causes of schizophrenia article, but as it's about the cognitive features of schizophrenia and not its etiology, I deleted it from that article. I'm not sure where or if this should go in the Schizophrenia article, but I thought I'd put the text here incase any of it is useful.Dgf32 (talk) 20:59, 26 July 2009 (UTC)

A number of cognitive biases and specific cognitive deficits have been found in people diagnosed with schizophrenia. These include attribution biases in social situations, difficulty distinguishing inner speech from speech from an external source (source monitoring), difficulty in adjusting speech to the needs of the hearer, difficulties in the very earliest stages of processing visual information (including reduced latent inhibition), and an attentional bias towards threats.

Some of these tendencies have been shown to worsen or appear when under emotional stress or in confusing situations. As with the related neurological findings, they are not shown by all individuals with a diagnosis of schizophrenia, and it is not clear how specific they are to schizophrenia.^[8] However, the findings regarding cognitive difficulties in schizophrenia are reliable and consistent enough for some researchers to argue that they are diagnostic.^[9] Impaired capacity to appreciate one's own and others' mental states has been reported to be the single-best predictor of poor social competence in schizophrenia,^[10] and similar cognitive features have been identified in close relatives of people diagnosed with schizophrenia.^[11]

A number of emotional factors have been implicated in schizophrenia, with some models putting them at the core of the disorder. It was thought that the appearance of blunted affect meant that sufferers did not experience strong emotions, but more recent studies indicate there is often a normal or even heightened level of emotionality, particularly in response to negative events or stressful social situations.^[12] Some theories suggest positive symptoms of schizophrenia can result from or be worsened by negative emotions, including depressed feelings and low self-esteem^[13] and feelings of vulnerability, inferiority or loneliness.^[14] Chronic negative feelings and maladaptive coping skills may explain some of the association between psychosocial stressors and symptomology.^[15] Critical and controlling behaviour by significant others (high expressed emotion) causes increased emotional arousal^[16] and lowered self-esteem^[17] and a subsequent increase in positive symptoms such as unusual thoughts. Countries or cultures where schizotypal personalities or schizophrenia symptoms are more accepted or valued appear to be associated with reduced onset of, or increased recovery from, schizophrenia.

Related studies suggest that the content of delusional and psychotic beliefs in schizophrenia can be meaningful and play a causal or mediating role in reflecting the life history, or social circumstances of the individual.^[18] Holding minority socio-cultural beliefs, for example due to ethnic background, has been linked to increased diagnosis of schizophrenia. The way an individual interprets his or her delusions and hallucinations (e.g. as threatening or as potentially positive) has also been found to influence functioning and recovery.^[19]

Whose definition of reality?

199.117.69.8 (talk) 21:24, 2 August 2009 (UTC)

Is this supposed to be an objection to something in the article? Looie496 (talk) 21:37, 2 August 2009 (UTC)

Association of Schizophrenia with Seasons

An article in the journal Schizophrenia Research contradicts the seasonal relationship of schizophrenia.

Volume 66, Issue 1, Pages 1-6 (1 January 2004)
 
No association between season of birth of patients with schizophrenia and risk of schizophrenia among their siblings
 
Jaana M. Suvisaari, Jari K. Haukka, Jouko K. Lönnqvist
 
Received 11 June 2002; accepted 14 November 2002.
Abstract 
 
Previous studies on the relationship between the season of birth of patients with schizophrenia and the risk of schizophrenia among their siblings have  
yielded contradictory results. We investigated whether proband's month of birth affects siblings' risk of developing schizophrenia. We used the Finnish  
Hospital Discharge Register to identify all patients born in Finland from 1950 to 1976 who had been hospitalized because of schizophrenia at least once 
between 1969 and 1995. Their siblings were identified from the National Population Register, and data on siblings were linked to the Hospital Discharge 
Register to obtain information on any hospitalizations. We used logistic regression to investigate a sibling's probability of developing schizophrenia, 
defining the proband initially as the first sibling in calendar time to develop schizophrenia, then as the affected sibling with lowest onset age. Within-
family dependence was taken into account by using robust standard error estimates. Neither models found any association between proband's month of birth 
and siblings' odds of developing schizophrenia. Our results support those previous studies that found no association between proband's month of birth and 
family history of schizophrenia, and suggest that the winter–spring excess of births among patients with schizophrenia is not caused by any genetic or
environmental risk factor that operates independently of other risk factors.  —Preceding unsigned comment added by 66.27.102.110 (talk) 05:14, 12 August 2009 (UTC)

--66.27.102.110 (talk) 05:18, 12 August 2009 (UTC)

Prevalence

Reference #3 - 'Goldner EM, Hsu L, Waraich P, Somers JM (2002). "Prevalence and incidence studies of schizophrenic disorders: a systematic review of the literature". Canadian Journal of Psychiatry 47 (9): 833–43' States that the prevalence of schizophrenia is 0.34, and the incidence is 0.55. The article states that its prevalence is 0.55.

Correct me if i'm wrong, but here is copied text from the abstract: 'Heterogeneity analysis revealed significant differences across 1-year and lifetime prevalence and 1-year incidence of schizophrenia. The corresponding pooled rates were: 0.34 per 100, 0.55 per 100'

See it here: http://www.ncbi.nlm.nih.gov/pubmed/12500753 —Preceding unsigned comment added by 222.152.15.118 (talk) 10:00, 12 August 2009 (UTC)

No, the cited figure in our article is right, and matches the reference. It's just that the abstract is written in a grammatically complex manner. Here's the full text of those two sentences "Heterogeneity analysis revealed significant differences across 1-year and lifetime prevalence and 1-year incidence of schizophrenia. The corresponding pooled rates were: 0.34 per 100, 0.55 per 100, and 11.1 per 100,000, respectively; the variation in rates between studies was generally between 2- and 5-fold."

So, that is:

1-year prevalence rate: 0.34 per 100
lifetime prevalence rate: 0.55 per 100
1-year incidence: 11.1 per 100,000

Cutting off the end of the second sentence leads the reader to miss that there were three measures (1-year prevalence, lifetime prevalence, and 1-year incidence) and three statistics (0.34 per 100, 0.55 per 100, and 11.1 per 100,000). The article correctly states the lifetime prevalence as 0.55 per 100. The incidence of schizophrenia is 11.1 per 100,000. Edhubbard (talk) 13:52, 12 August 2009 (UTC)

The Five Senses

The beginning of the article says "may affect all five senses, including sight, hearing, taste, smell and touch". "Including" implies that what follows is just a few select examples, yet it goes on to list ALL FIVE of the five senses. You wouldn't say "I have three friends, including John, Lucy and Bob", would you? Perhaps "may affect the five senses: sight, hearing, taste, smell and touch"?

(I would change it myself but I can't because it's semi-protected.) —Preceding unsigned comment added by 94.195.25.249 (talk) 17:08, 8 August 2009 (UTC)

Well, there are some very daft people in this world whom couldn't name one of the senses. —Preceding unsigned comment added by 91.75.70.102 (talk) 17:48, 31 August 2009 (UTC)

I would've specified the five "classical" senses, because there are many, many more... think Kinesthesis. Cerebrospinal pH. etc. —Preceding unsigned comment added by 210.8.69.49 (talk) 02:28, 14 September 2009 (UTC)

Causes and models

The intro to the "Causes" section says this:

The idea of an inherent vulnerability (or diathesis) in some people, which can be unmasked by biological, psychological or environmental stressors, is known as the stress-diathesis model.[46] The idea that biological, psychological and social factors are all important is known as the "biopsychosocial" model.

I must say, I don't see the differences between these two models. If some people have an inherent vulnerability, and it gets triggered by outside stressors (stress-diathesis model), that implies that biological, psychological and social factors are all important (biopsychosocial model). It would be helpful if somebody clarified the differences between these two models. —MiguelMunoz (talk) 21:53, 11 August 2009 (UTC)

Even the Biopsychosocial model and Diathesis–stress model pages give very similar definitions, but the diathesis-stress model has only one reference, which seems blank unless I'm doing something wrong. "The diathesis–stress model is a psychological theory that explains behavior as both a result of biological and genetic factors ("nature"), and life experiences ("nurture")." The biopsychosocial model attempts to explain more than just mental health. "There are also theories that the state of mind directly affects the immune system, and there are many carefully-planned studies that show this to be the case; see psychoneuroimmunology. Psychosocial factors can cause a biological effect by predisposing the patient to risk factors. An example is that depression by itself may not cause liver problems, but a depressed person may be more likely to have alcohol problems, and therefore liver damage."

That sentence also tells me that the inherent vulnerability is more important in the diathesis-stress model.

From [8]: "In contrast to the biopsychosocial model, which describes the interdependence of depression causes, the diathesis-stress model talks about the relationship between potential causes of depression, and the degree to which people may be vulnerable to react to those causes."

From [9]: The risk factors have been placed into a simple biopsychosocial model known as the diathesis-stress model.

So, the diathesis-stress model focuses on the stress factors and reactivity to these factors while the biopsychosocial model covers a lot more. The former is basically a sub-model of the latter, and the diathesis-stress model explains that vulnerability (through all of the factors) isn't enough. For example, I read (here) that having one parent who has gone through a major depressive episode leads to a 10% chance of depression in the children, 30% if each parent had had an episode, and that after the first episode, another is 50% likely, and a third after that, 80% likely. Even if you're faced with that 80%, the depression isn't going to happen randomly, there must be a trigger (stress).

This is my understanding. MichaelExe (talk) 03:56, 15 August 2009 (UTC)

Thanks. The part that most clarified it was when you wrote "The former is basically a sub-model of the latter." Maybe it should be explained in the article this way. —MiguelMunoz (talk) 02:29, 18 September 2009 (UTC)

Genetic

"There is little doubt about the existence of a fecundity deficit in schizophrenia. Affected individuals have fewer children than the population as a whole. This reduction is of the order of 70% in males and 30% in females. The central genetic paradox of schizophrenia is why, if the disease is associated with a biological disadvantage, is this variation not selected out? To balance such a significant disadvantage, a substantial and universal advantage must exist. Thus far, all theories of a putative advantage have been disproved or remain unsubstantiated."

The entire paragraph is too subjective; some discussion of the content would be great. The fact that schizophrenics have fewer children is not necessarily biological, because they might believe that they lead a dangerous life, and such a life would not provide the best means to raise a family. So, some more details as to why schizophrenics tend to have a "fecundity deficit" would help a lot, because the statistics do not suffice. The question doesn't make much sense, either: if biological disadvantages were selected out all of the time, innate disorders such as autism (whose etiology is attributed almost entirely to heritability) would not be so common. Also, from Causes of autism#Genetics (or the original source, http://www.ncbi.nlm.nih.gov/pubmed/18578904): "One hypothesis is that autism is in some sense diametrically opposite to schizophrenia, and that autism involves increased effects via genomic imprinting of paternally expressed genes that regulate overgrowth in the brain, whereas schizophrenia involves maternally expressed genes and undergrowth." MichaelExe (talk) 03:05, 15 August 2009 (UTC)

I'm still looking for others' thoughts on this. MichaelExe (talk) 21:16, 13 October 2009 (UTC)

Semi-protection

This page needs some minor copy-editing, but is this not possible as it is a semi-protected article?Alpinehermit (talk) 13:42, 23 August 2009 (UTC)

"Semi-protected" means that accounts have to be at least four days old and have at least ten total edits in order to be able to edit the article. So if you make another four edits (feel free to make trivial edits to this talk page or your talk or user pages), you'll be able to do it. Regards, Looie496 (talk) 17:29, 23 August 2009 (UTC)

BDNF

There seems to be an edit war starting: Beland (talk · contribs), who clearly is very interested in BDNF, added a sentence saying, "There is a correlation with low levels of brain-derived neurotrophic factor (BDNF), but it is unclear whether this is a cause or a symptom.". The sentence was then removed by Earlypsychosis (talk · contribs), and the removal was then reverted by Nutriveg (talk · contribs). There has been some discussion on Earlypsychosis's talk page, resulting in a reference being added by Nutriveg. However, I am going to remove the sentence again for now, for two reasons: first, because the sentence is too vague to be meaningful; second, because the source does not meet MEDRS. Schizophrenia is correlated with hundreds of things, and there needs to be strong community opinion that an important causal role is likely in order for such statements to belong. The main thing, though, is that I urgently ask that this issue be settled by discussion here rather than by revert-warring. Looie496 (talk) 18:42, 3 September 2009 (UTC)

I guess the other issue is whether it has been an important enough development to get discussed in a review article, which I am not aware of to date. Casliber (talk · contribs) 18:49, 3 September 2009 (UTC)

That's what I meant by "source does not meet MEDRS"; sorry, should have been clearer. Looie496 (talk) 18:50, 3 September 2009 (UTC)

also happened to other many conditions including anorexia, dementia, bulimia as per discussion on WikiProject Medicine discussion Earlypsychosis (talk) 22:48, 3 September 2009 (UTC)

The cited sentence doesn't reflect the one I added and I don't see why the source used doesn't meet WP:MEDRS. Casliber, the source I used fits as secondary source and there are reviews as well: Angelucci, F.; Brenè, S.; Mathé, A. (Apr 2005). "BDNF in schizophrenia, depression and corresponding animal models". Molecular Psychiatry. 10 (4): 345–352. doi:10.1038/sj.mp.4001637. ISSN 1359-4184. PMID 15655562.--Nutriveg (talk) 14:53, 4 September 2009 (UTC)

I still think "there is a correlation" is not informative enough to be useful, and the sentence as placed in the article seemed totally out of context. If that review, which I agree fully meets MEDRS, has anything strong and specific to say about schizophrenia and BDNF, then I don't see any problem with mentioning it, as long as the mention is properly integrated into the text. (The source used in the original edit, PMID 18408624, is not a secondary source, it's a primary research study.) I just want to add that if this were a start-class article, it would be okay to be more aggressive in adding material, but this is an FA and we need to be sure to integrate things in a way that keeps the writing up to FA level. Regards, Looie496 (talk) 15:56, 4 September 2009 (UTC)

Rewrite it then.

The article in the original edit, although a primary source for the conclusions of that particular study is a secondary source when it analyzes previous studies in the same article: "Functional experiments have suggested that BDNF may be involved in the etiology of schizophrenia."--Nutriveg (talk) 17:38, 4 September 2009 (UTC)

I'm going to resist that interpretation -- merely having a discussion section (which every paper does) doesn't make a paper into a secondary source. For one thing, I can tell you having reviewed numerous papers myself that authors are typically given a lot of latitude for interpretation in the discussion sections of data papers. Review papers are usually written by recognized experts in the field and aim to describe the mainstream consensus of opinion; they are much better sources. Looie496 (talk) 18:12, 4 September 2009 (UTC)

Well, I've also cited review papers, so that kind if discussion is unnecessary. Read another one while you talk.Shoval, G.; Weizman, A. (May 2005). "The possible role of neurotrophins in the pathogenesis and therapy of schizophrenia". European Neuropsychopharmacology. 15 (3): 319–329. doi:10.1016/j.euroneuro.2004.12.005. ISSN 0924-977X. PMID 15820422.--Nutriveg (talk) 18:41, 4 September 2009 (UTC)

kalirin

http://www.sciencedaily.com/releases/2009/08/090810174305.htm Thoughts? Are you ready for IPv6? (talk) 03:22, 12 October 2009 (UTC)

From Kalirin: "One of the isoforms, Kalirin-7, was found to be necessary for the remodeling of synapses in mature cortical neurons and is thought to be important in the development of schizophrenia, as demonstrated by adolescent development of schizophrenia-like symptoms in kalirin knockout mice." The sources in that article look good, so I don't see why we shouldn't include it (in the Neural subsection under Mechanism). Just note how "is thought" is used, in order to not state it as fact. MichaelExe (talk) 03:32, 12 October 2009 (UTC)

Please see WP:MEDRS regarding sourcing of medical articles and also WP:RECENTISM; if kalirin is mentioned in recent peer-reviewed journal-published articles, perhaps something can be added. Unless a recent journal review mentions Kalirin, the info shouldn't be added here. What is in other Wiki articles (which are not a reliable source) isn't relevant to the standards expected of a featured article, or a medical article. SandyGeorgia (Talk) 05:48, 12 October 2009 (UTC)

Agree, better add the mention in the "causes of schz" article and only if mentioned in a review. Seems that candidate genes play tiny roles individually, alas.. so adding each would bloat the article.. --CopperKettle 05:57, 12 October 2009 (UTC)

I'm a bit lost on this. Are you saying that it needs more reviews and studies before it can be determined if the kalirin thing is true? Are you ready for IPv6? (talk) 06:13, 12 October 2009 (UTC)

It may be true, but for what? Schizophrenia is a hodgepodge of conditions that boil down to psychosis or deterioration. In some patiens, kalirin may turn out to be one of the culprits, in some it may turn out to be unaffected. The work so far is done on mice. Mice have tiny brains and are unable to have schizophrenia, so research is done using endophenotypes like prepulse inhibition and working memory performance. When the full scheme of molecular interactions leading to schizophrenia is finally unraveled, it will be similar to a blueprint of the supercollider, having many interacting parts.. if we start adding molecules to the main article on schizophrenia as the research goes on, it will bloat and still give no clear picture. Hundreds of molecules affect synapses. If we add kalirin, why not throw in reelin? And then why not add COMT, MTHFR, Akt, PKC, NPAS3, DISC1, NRG1.. and so on. So, as I understand, we add the molecule if it is mentioned in a review, it may be important, and its gene has at least a semi-proven association with schizophrenia. --CopperKettle 06:59, 12 October 2009 (UTC)

Reply to IPv6: no, I am saying that Wiki medical articles must conform with WP:MEDRS. It isn't our "job" to determine the truth, rather to report what reliable sources say-- in this case, recent, peer-reviewed journal-published sources. SandyGeorgia (Talk) 14:20, 12 October 2009 (UTC)

Here are the 4 references used in the Kalirin article tying it to Schizophrenia: http://www.ncbi.nlm.nih.gov/pubmed/18031682 http://www.ncbi.nlm.nih.gov/pubmed/19020030 http://www.schizophreniaforum.org/new/detail.asp?id=1408 http://www.ncbi.nlm.nih.gov/pubmed/19403804. The third is the secondary source, and the other three, primary sources. The primary sources are from 2007, 2008 and 2009, respectively. MichaelExe (talk) 16:18, 12 October 2009 (UTC)

This is the sort of situation where a broad familiarity with the literature is really helpful. People who have done a lot of reading will know that there are about a hundred things that are at least as promising as kalirin, maybe several hundred. There's no way a top-level article like this can cover all of them -- the only way to get appropriate perspective is to rely as far as possible on review articles in top journals to guide our coverage, as WP:MEDRS recommends. Looie496 (talk) 17:10, 12 October 2009 (UTC)

Also, the schizophreniaforum link doesn't conform with WP:MEDRS; journal reviews, pls. SandyGeorgia (Talk) 17:14, 12 October 2009 (UTC)

So we won't use it as a source, but it can still help us choose our wording. The other three meet the standards, but this article should see only brief coverage of the link between Kalirin and Schizophrenia (as per WP:WEIGHT). The same length as the coverage in Kalirin would be appropriate.

Is it against Wikipedia policy to copy and paste from other Wikipedia articles? You can't plagiarize your own work. XP MichaelExe (talk) 17:41, 12 October 2009 (UTC)

How do primary sources here meet WP:MEDRS standards? SandyGeorgia (Talk) 17:45, 12 October 2009 (UTC)

"In general, Wikipedia's medical articles should be based upon published, reliable secondary sources whenever possible. Reliable primary sources can add greatly to a medical article, but must be used with care because of the potential for misuse. For that reason, edits that rely on primary sources should only describe the conclusions of the source, and should describe these findings clearly so the edit can be checked by editors with no specialist knowledge. In particular, this description should follow closely to the interpretation of the data given by the authors, or by other reliable secondary sources. Primary sources should not be cited in support of a conclusion that is not clearly made by the authors or by reliable secondary sources, as defined above (see Wikipedia:No original research)."

"Individual primary sources should not be cited or juxtaposed so as to "debunk" or contradict the conclusions of reliable secondary sources, unless the primary source itself directly makes such a claim (see Wikipedia:No original synthesis). Controversies or areas of uncertainty in medicine should be illustrated with reliable secondary sources describing the varying viewpoints. The use and presentation of primary sources should also respect Wikipedia's policies on undue weight; that is, primary sources favoring a minority opinion should not be aggregated or presented devoid of context in such a way as to undermine proportionate representation of expert opinion in a field."

I understood that primary sources can be used to fairly represent minority views, as long as they do not contradict conclusions by reliable authors, and as long as it isn't original research. Imo, the three sources do not consist of original research, but of minority views. There are 19 doctors from 3 different universities in support (or involved in the research) of the link between Kalirin and Schizophrenia. MichaelExe (talk) 18:03, 12 October 2009 (UTC)

It's not necessary to quote the page; a link suffices (and most editors of FAs know policy :) Have you reviewed WP:MEDRS andWP:UNDUE? SandyGeorgia (Talk) 18:10, 12 October 2009 (UTC)

Yes, and primary sources can meet Wikpedia's standards, but only in certain situations (the ones I've underlined above). Do you think the primary sources consist of original research or of a minority viewpoint? A consensus on this should decide whether the sources are used or not. MichaelExe (talk) 18:27, 12 October 2009 (UTC)

For the reasons outlined by others above, unloess it is well covered in recent journal-published reviews, inclusion here is not warranted. SandyGeorgia (Talk) 18:29, 12 October 2009 (UTC)

It is not against policy either. Overall, I think its inclusion would be an improvement. MichaelExe (talk) 18:35, 12 October 2009 (UTC)

There is not room in this article to cover every factor for which there is some evidence of association with schizophrenia. We need reliable reviews to support the choices of the factors that we mention in our (necessarily) brief summary. This area is extremely well reviewed; there should be no need to cite primary sources in such a well-travelled locale. Eubulides (talk) 07:52, 13 October 2009 (UTC)

Let me just note that PMID 18597863 is a MEDRS-quality review that has a section on the relationship of Kalirin-7 to schizophrenia. I can't download it from my current location so I can't check what it says, though. Looie496 (talk) 19:10, 12 October 2009 (UTC)

It has a paragraph that advocates kalirin-7's role in schizophrenia. Here's a quote (QQ):

"The molecular mechanism by which dendritic spine morphogenesis contributes to schizophrenia is still in early stages of investigation, but several lines of evidence suggest that a role for modulators of dendritic spine morphology such as kalirin-7 might be important.... Taken together, these lines of evidence suggest that abnormal kalirin-7 signaling could contribute to the synaptic pathology associated with schizophrenia, potentially by interfering with spine formation, maintenance or activity-dependent plasticity, leading to the observed endophenotype of reduced dendritic spine density that might underlie schizophrenia-related cognitive dysfunction. Much work is still required to better establish kalirin-7's role in schizophrenia. Additionally, other signaling molecules that play a similar integrative role in dendritic spine dynamic regulation might contribute to schizophrenia pathogenesis."

The context is a review that focuses on kalirin-7 and its possible role in schizophrenia, autism, Down syndrome, bipolar disorder, epilepsy, etc. It's a bit of a "I've got a hammer and there sure to seem to be a lot of nails around here" review. It'd be better to rely on reviews that focus on schizophrenia etiology, to give us a better feel for the relative weights to give to the potential causes. Possible reviews include Tandon et al. 2008 (PMID 18514488) and van Os & Kapur 2009 (PMID 19700006). Eubulides (talk) 07:52, 13 October 2009 (UTC)

"Much work is still required to better establish ... " is an indicator that adding this info to the article would be premature, unless other, general reviews mention it. SandyGeorgia (Talk) 13:55, 13 October 2009 (UTC)

And the Causes in this article are presented with "suggested", "thought to", and "found to"; none of which are entirely objective. What it comes down to is whether or not it consists of an improvement to the article. Do you think those interested in the etiology would rather not know about a possible link with kalirin, confirmed or not (and most of the wording in this article imply the latter)? Also, the journals are dated to 2007, 2008 and 2009. 2009 is definitely new, but the others support the same conclusion. MichaelExe (talk) 19:50, 13 October 2009 (UTC)

Unless something new surfaces, I think we're done here. We don't add every bit of non-peer-reviewed data to articles, much less a featured article, where due weight is a careful consideration. SandyGeorgia (Talk) 19:54, 13 October 2009 (UTC)

I think I may have found a reliable secondary source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118058/ MichaelExe (talk) 20:45, 13 October 2009 (UTC)

Please see WP:MEDRS on reviews. PMID 18031682 does not appear to be a review, but Eubulides would know better. SandyGeorgia (Talk) 20:58, 13 October 2009 (UTC)

Scroll down; that page has 50 references. It would also help if you'd quote which lines exactly of these policies and guidelines are relevant, because I don't feel like re-reading them every time you throw one around. There's an essay on this; whether you choose to follow it or not is evidently wouldn't result in any formal consequence, but it would definitely make things easier for the rest of us. MichaelExe (talk) 21:14, 13 October 2009 (UTC)

Since you are editing across numerous featured articles, it would be helpful if you would read the policies. It will save you, and everyone else, a lot of time, and all of the editors working to maintain featured articles are busy. The relevant information about reviews is shown prominently in the Nutshell at the top of the page, but reading the rest of the page might help. SandyGeorgia (Talk) 21:23, 13 October 2009 (UTC)

I said "re-read". I have read them. You are not telling me what specifically makes the source unreliable. It's a published (by NIH and PubMed) and peer-reviewed secondary source from the "Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago". While it may not represent all of psychiatry, it is not original research, and minority views should be included in articles (otherwise, we would be breaking WP:NPOV). MichaelExe (talk) 21:45, 13 October 2009 (UTC)

I'll try again. "PMID 18031682 does not appear to be a review, but Eubulides would know better." Do you see the Review Tab at the PubMed entry, which indicates it is not a review? It isn't always accurate; as I said Eubulides would know better. Do you see the posts above from Eubulides, discussing reviews? We are spending inordinate amounts of time on issues of semantics and undue weight now on several articles; fortunately, Eubulides has the patience of a saint. SandyGeorgia (Talk) 21:49, 13 October 2009 (UTC)

That's not the link I've been talking about; this is. MichaelExe (talk) 21:54, 13 October 2009 (UTC)

Unless you're seeing something that I'm not, it's the same article. You're linking to the PMC full text, while we typically link to the PMID abstract on talk. The PMID abstract links to the same PMC you link to, and doesn't seem to indicate it's a review (although Eubulides sometimes disagrees). This page may help you understand sourcing in medical articles: Wikipedia:Wikipedia Signpost/2008-06-30/Dispatches. When working on well-vetted featured articles, it does help to have a solid understanding of policy and guidelines. You are also misunderstanding the use of the term minority views as it compares to primary studies and WP:RECENTISM, although several editors above have explained to you that we don't include every new piece of speculation in an overview featured article. It's about WP:UNDUE and WP:RECENTISM and reliable review sources, not minority viewpoints. In other words, it's still unproven, and hasn't been mentioned in reliable top-level reviews, so we don't include it yet. SandyGeorgia (Talk) 22:03, 13 October 2009 (UTC)

Then what makes a review a review? This obviously isn't original research; it has 50 references. I have yet to see anything in the source (the link I suggested) that does not conform to the definition of Systematic review. MichaelExe (talk) 22:11, 13 October 2009 (UTC)

There are lots of clues. The abstract says "Here we report that..." and "our study identifies a...". The introduction says "in this study we investigated...", "We report that ...", "We show that ...", "We demonstrate that ...", "our study identifies a ...". A literature review doesn't have a "Results" section, nor does it have a "Discussion" section that analyses the results of the presented study, nor does it describe the "Experimental procedures" of the study. A systematic review would document the selection process used to choose the [other] studies for review. It might perform a statistical analysis of the results from these multiple studies. The Introduction has similarities with a Literature review but is not considered as good a source as a proper literature review article. Colin°^Talk 22:36, 13 October 2009 (UTC)

All references to schizophrenia are sourced: [10] (this one does not mention schizophrenia in particular, but "brain function and disease" instead), [11], [12], [13], [14], [15] and [16]. MichaelExe (talk) 23:02, 13 October 2009 (UTC)

Ok, I see that that source is not a review. These might be (some of them require purchase): http://www.jneurosci.org/cgi/content/full/29/17/5367, http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0V-4SWFGV1-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=8756df972f9d7129270888731cabe59a, and http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586970/?tool=pubmed (or [17]). This last one does not require purchase. MichaelExe (talk) 23:22, 13 October 2009 (UTC)

Can you please provide PMID links instead, so we're all on the same page? That is the most common convention on medical talk pages. You only have to type PMID followed by the PMID number, and they are automatically linked (see samples in my edits or Eubulides' edits above). SandyGeorgia (Talk) 23:26, 13 October 2009 (UTC)

[18] and [19]. MichaelExe (talk) 23:50, 13 October 2009 (UTC)

They are both reviews, but neither PMID 19403804 nor PMID 18597863 have free full-text available, so you'll need to get the full text of the articles to see what they say before they can be quoted or added. Also, neither of them are general schizophrenia reviews-- needed for due weight issues. See comments above about reviews on Kalirin compared to general reviews on Schizophrenia. SandyGeorgia (Talk) 00:02, 14 October 2009 (UTC)

Of course we wouldn't include a paragraph worth of information. I'm inclined to say a sentence or two. I wasn't asking for any more than this in the first place. MichaelExe (talk) 00:31, 14 October 2009 (UTC)

Using only the abstract of PMID 18597863, we can get something like: "An implication of Kalirin-7 in the synaptic pathology in schizophrenia, among other disorders, has been suggested." It shouldn't elaborate much more (or any more) than this, anyway. If one wanted to delve further into the subject without purchasing the review, reading the subtitles in the article outline would suffice. MichaelExe (talk) 02:04, 14 October 2009 (UTC)

Please see #We need better sources than those two below. Eubulides (talk) 08:49, 14 October 2009 (UTC)

We need better sources than those two

Re the two sources suggested above:

Sommer & Budreck 2009 (PMID 19403804) doesn't mention schizophrenia and is unsuitable as a source here.
I quoted from Penzes & Jones 2008 (PMID 18597863); see (QQ) above. That review is about kalirin-7, and as I mentioned, it suggests kalirin-7 as possibly being involved in a wide variety of disorders. As the quoted text makes clear, the involvment of kalirin-7 in schizophrenia is speculative, and I agree with SandyGeorgia that that source alone isn't enough to justify mentioning kalirin-7 here.

Better would be an review on the etiology of schizophrenia, which we could then use to see whether it's worth mentioning kalirin-7 (along with the zillions of other factors that have hypothesized to be involved in etiology). I suggested two such reviews above, namely Tandon et al. 2008 (PMID 18514488) and van Os & Kapur 2009 (PMID 19700006). Reviews like these should be used instead of reviews on factors that are possibly associated with many conditions. Eubulides (talk) 08:49, 14 October 2009 (UTC)

Isn't the involvement of anything in schizophrenia more-or-less speculative? Either way, it doesn't necessarily have to be included into etiology (of course, if there are so many small theories, we could start a new article devoted to them, like with autism and causes of autism); there's also the Neural (Mechanism) section, where I think it would be more relevant, anyway. Also, most articles (this one included) rarely use more than 2 sources. We've got the two reviews, and 3 primary sources to support the link. Orr, [[20]]. MichaelExe (talk) 11:09, 14 October 2009 (UTC)

You could work on causes of schizophrenia, which is in dismal shape, in need of cleanup, and nowhere near the featured quality of this article, but text included on Wikipedia has to meet our sourcing policies whether in that article or this one. Eubulides has already explained the problems with these two reviews well, so I won't repeat. SandyGeorgia (Talk) 11:41, 14 October 2009 (UTC)

I agree. The causes of schizophrenia is welcome place for any hard evidence, even small, and needs some attention anyway. --CopperKettle 04:27, 15 October 2009 (UTC)

You may be right about PMID 19403804, but the "behaviour" in the title implies that there probably would be mention of mental disorders. I'll ignore this review, then.
However, PMID 18597863 (if you check here) actually has a subsection devoted to schizophrenia, and another to Alzheimer's disease (which is another article that could be updated with this information). We've also got 3 primary sources directly supporting the implication of kalirin-7 in schizophrenia. The review meets WP:MEDRS standards (unless someone can give me a good reason why it doesn't), and not including it would be a violation of WP:NPOV. This article is already bordering on cluttered, so I will probably add to the causes of schizophrenia article instead. MichaelExe (talk) 20:07, 14 October 2009 (UTC)

I agree that Penzes & Jones 2008 (PMID 18597863) has a subsection on schizophrenia: I read that subsection before making my first comment in this thread, and quoted its main points; see (QQ) above. As I said there, that review is not good evidence that kalirin-7 is important enough to be mentioned in Schizophrenia's rather cramped quarters, though I agree the topic is suitable for Causes of schizophrenia. Eubulides (talk) 22:06, 16 October 2009 (UTC)

FA level

I dont believe that this article is even close to FA let alone GA or A level anymore..I will be outting it up for FA review in a week or so....pls comment if you like Buzzzsherman (talk) 17:44, 21 October 2009 (UTC)

Would you like to list the specific problems here first and see what can be done? Casliber (talk · contribs) 19:16, 21 October 2009 (UTC)

no problem...citations are missing - as well the new size is a problem see also toolbox -since 2004 when this article was promoted standers have changed and i see in 2008 all this was brought up.

not trying to downgrade article just think its time for editors to look at it again. It has been edited thousands of time since last look and not all is flowing well...........I have asked tw0 others to take a look before i put it up for review..if they belive it would pass FA review at todays standers i will leave it alone.Buzzzsherman (talk) 19:52, 21 October 2009 (UTC)

Yea, these highly edited articles are a bit like building sandcastles at the beach - you can see the erosion right before your eyes (and that is even with semiprotection!). We did develop a Causes_of_schizophrenia and a Treatment of schizophrenia daughter articles to help with the size issues, so that some more esoteric or research-level material can go there. I will look at the fact tags too. Casliber (talk · contribs) 20:01, 21 October 2009 (UTC)

i have talk the two reviewers about this and was told that the article has a very hight view counts here on wikipidia ...They do not believe it needs downgrading .but They do believe an update is badly needed (copy edit) ..external links are not to bad and only 2 redirects....... BUT alt text is now a mandatory feature for all GA to FA Level articles >>> however since there is only a few pics i was told to mention it needs to be added ....I will do this my self soon if no one gets to it in dew time. Sorry did not mean to make waves.Buzzzsherman (talk) 20:17, 21 October 2009 (UTC)

The article is too damn long (takes forever to load), and should be pruned and carefully checked for primary sources. SandyGeorgia (Talk) 15:40, 17 November 2009 (UTC)

The issue of the scientificity of schizophrenia should be more integrated into the article

Subsection Diagnosis\Controversies and research directions and the last two subsections under Causes, seem to be Criticism sections that marginalize/demote positions critical the concept of schizophrenia iself. The lead section should also devolve a line or two on the fact that there is a debate on the validity of the concept of schizophrenia.--Sum (talk) 15:33, 17 November 2009 (UTC)

How much context?

Hi all, doing some housekeeping and was ruminating on some things which I will post here. Casliber (talk · contribs) 04:23, 25 November 2009 (UTC)

In the beginning of the Confusion_with_other_conditions section we have:

Part of a larger controversy over biopsychiatry, the validity of schizophrenia as a diagnostic entity has been criticised by number of psychologists as lacking in scientific validity and diagnostic reliability.

My question for all is, is the bolded bit necessary for context?

I would say no Casliber, as it does not sound accurate. I don't think that there is a "large" controversy over the validity of the diagnosis of schizophrenia. "Number of psychologists" should be put into context as well. Perhaps it should say "a vocal but small number of psychologists and psychiatrists have criticised/questioned,,,,, or something like that.--Literaturegeek | T@1k? 11:05, 25 November 2009 (UTC)

I agree that the bolded bit doesn't add anything useful to the sentence, but I don't see a need to tone down the rest of the sentence -- I think there are quite a number of people who have doubts about the validity of "schizophrenia" is a unitary entity. Looie496 (talk) 16:45, 25 November 2009 (UTC)

The rest of the sentence was fine by me too, it was just the first bit (i.e. good bit of extra context vs. veering into OT soapboxing). okay, I think it can go. Casliber (talk · contribs) 19:14, 25 November 2009 (UTC)

I suggest a number of psychologists could be deleted to WP:AWW and maybe some references added e.g. Part of a larger controversy over biopsychiatry, the validity of schizophrenia as a diagnostic entity has been criticised as lacking in scientific validity and diagnostic reliability (e.g. Schizophrenia: a scientific delusion? Mary Boyle). Earlypsychosis (talk) 07:09, 26 November 2009 (UTC)

Size and scope of causes and treatment sections

The size of this article is such that the only way to keep it manageable is to restrict the main article to really core theories of causes, and widely used core/standard treatments. It is frustrating I know, but the more experimental and research material can be discussed properly at Treatment of schizophrenia and Causes of schizophrenia. Any suggestions on promoting a triadic nature of the three articles would be much appreciated. cheers, Casliber (talk · contribs) 23:15, 30 November 2009 (UTC)

You could probably move this entire section Schizophrenia#Other proposed causes to Causes of schizophrenia. That should get the size of the article down quite a bit.--Literaturegeek | T@1k? 23:21, 30 November 2009 (UTC)

Good point and done - it is all in the causes page already and can be expanded upon there. Casliber (talk · contribs) 00:02, 1 December 2009 (UTC)

Looks good to me. I am not sure if you want to shorten the article any further? If you do, then this section might be a candidate for being moved or shortened.Schizophrenia#Controversies and research directions I am not usually a fan of deleting content outright from wikipedia. If you do want to delete it perhaps it could be moved to some other article, like biopsychiatry controversy or a new article started perhaps?--Literaturegeek | T@1k? 19:46, 1 December 2009 (UTC)

That section is a little more notable and central to discussion of the concept than material removed thus far. I am musing on it and find most of it probably worthy of staying, although the bit on continuum in the middle with the cite tag might be worth removing. Casliber (talk · contribs) 23:21, 1 December 2009 (UTC)

Ok, I will go with and trust your instincts as you know much more about this subject matter than I. I can't think of what else could or should be deleted unless other sub articles are created. Everything seems relevant to the subject matter of the article.--Literaturegeek | T@1k? 23:45, 1 December 2009 (UTC)

I had not been paying as much attention to it lately, and Sandy alerted me to it. I'll ask her again. Casliber (talk · contribs) 02:52, 2 December 2009 (UTC)

infobox image

I am not convinced that the image of Bleuler is a good one for the infobox, because Kraepelin was the first person to use an accepted classification. I also feel that the introduction is imbalanced, because it only mentions Bleuler and not other significant people. Snowman (talk) 18:26, 1 December 2009 (UTC)

Okay, you feel that an image of Kraepelin is better for the infobox then? I am receptive to that idea. I can add a line about Kraepelin to the intro I guess (it is quite large as is) or do you think we should remove Bleuler? Casliber (talk · contribs) 19:39, 1 December 2009 (UTC)

I am not quite sure, I think I slightly favour no images of people in the infobox as it would put too much emphasis to that person. I think I would know when it looks right. What about a diagram of some of the salient symptoms and signs? Snowman (talk) 20:09, 1 December 2009 (UTC)

A diagram? Can you elaborate over what you have in mind? Interesting idea possibly. Casliber (talk · contribs) 23:18, 1 December 2009 (UTC)

I was originally thinking of a diagram to show the clustering of symptoms. I while ago I went to a lecture where a professor explained the diagnosis of schizoaffective disorder using a drawing of symptoms as axis in 3D (on 2D drawing board) to show symptom clusters and therefore showing that this is a difficult diagnosis to make. It might not catch on here. Perhaps symptoms and signs arranged with those more likely to be diagnostic written towards the centre of a target and the more common symptoms and signs written bigger. Or perhaps just histograms. Or is there a relevant work of art? Snowman (talk) 00:42, 2 December 2009 (UTC)

Okay, I can see where you're coming from now (schizoaffective...there's an even bigger headache..), but I worry that the interrelationship between symptoms is highly subjectives. I have often had patients where it has been actually quite difficult to distinguish between a referential delusion/misinterpretation, auditory hallucination, or systematized delusion...or all three. There was a longterm issue on psychoactive drug about a chart which I and some others felt actually misinformed more than it enlightened. I did feel bad as the author of the diagram had clearly put alot of work into it. These articles are very hard to find specific free images for. See the archives for a long discussion on one recent example of some signs in a person's window. No obvious artwork springs to mind but google images and some well-chosen keywords might be a good starting point. Casliber (talk · contribs) 02:50, 2 December 2009 (UTC)

I have had a look at the "psycotrophic drug" diagram of circles, and it is fascinating. I am puzzled to see that the "psycodelics" circle overlaps with the "antipsychotics" circle. I did not see lithium there. Snowman (talk) 10:58, 2 December 2009 (UTC)

Lithium isn't psychoactive at all, just psycho-prophylactic as it were. Same with sodium valproate. Actually, for many people most antidepressants might not be either, but there were alot of problems with both incarnations of the chart which were discussed in the archives. Casliber (talk · contribs) 13:07, 2 December 2009 (UTC)

re: Soteria

I don't think Soteria gets enough attention in this article. .--Myth (talk) 15:33, 5 December 2009 (UTC)

The article is enormous - in order not keep the article to a manageable size, treatments can be discussed in more detail, and more research etc. can be placed at Treatment of schizophrenia. You are welcome to expand there. Casliber (talk · contribs) 05:41, 6 December 2009 (UTC)

Review of primary sources needed

The size of this article is better now, there are still some citation tags, but more importantly, a review of the use of primary sources (per WP:MEDRS) is urgently needed. The size of the reference list indicates that the article is not sourced primarily to reviews, and this article has tended to take on whatever anyone wants to add, based on primary sources. The article should be sourced mainly to secondary reviews. See Wikipedia:Wikipedia Signpost/2008-06-30/Dispatches and WP:MEDRS. This work should be done in the next month, or the article should go to WP:FAR. SandyGeorgia (Talk) 15:27, 6 December 2009 (UTC)

links between autism and schizophrenia which mean a genetic test could be developed for schizophrenia and/or autism

Microchip08 21:15, 6 December 2009 (UTC)

see the below article for full details of the new research and implications

http://www.vancouversun.com/health/researchers+find+link+between+autism+schizophrenia/2295674/story.html —Preceding unsigned comment added by Darwinerasmus (talk • contribs) 18:49, 6 December 2009 (UTC)

This material which isn't in general use is best placed at causes of schizophrenia article. There are announcements like this quite often which never make it to clinical use. The article is too big to include them all. Casliber (talk · contribs) 19:42, 6 December 2009 (UTC)

Additionally mention should be made of the user movement to change the name of schizophrenia as so few doctors agree on what it is , see http://www.caslcampaign.com/ suggested alternate names include :

This discussion has been closed. Please do not modify it.

The following discussion has been closed. Please do not modify it.

Abnormal Brain Pattern (ABP)

Abundance of Energy Mutation (AEM)

Active Spellbound Disorder

Affective Behavioral Cognitive Dysphoria

(ABCD; or “the letter disorder”)

Altered Brain Chemistry (ABC)

Altered Reality Syndrome (ARS)

Altered States Disorder (ASD)

Alternate Reality Perception Disorder

Alternative Dementia (AD)

Alternative Mindsplit Perception (AMP)

Alternative Perception (AP)

Amazaphren

Amazaphrenia

Bad Behavior, Emotional Disturbances,

Irrational Thinking (B BEDIT)

Biogenetichemosis

Biogenetichemphrenosis

Biologenetichemosis

Biological Brain Dysfunction (BBD)

Bleuler

Brain Anomaly Dysfunction

Brain Chemical Disorder (BCD)

Brain Circuit Dysfunction (BCD)

Brain Disorder

Brain Interpreting Reality Disease (BIRD)

Chemical Imbalance in Brain Syndrome

(CIBS)

Cognitive Transmitting Impairment

Common Neurotic Syndrome

De Interruptus

Deficit Spectrum Disorder

Delusional Brain Disorder (DBD)

Delusional Psychosis

Delusional-Hallucinatory or “-tery”

Illness (DHI)

Dementia Praecox

Dementia Praecox Syndrome (DPS)

Dereistic Syndrome

Differentiation Disorder

Disorder of Emotions, Behavior, and

Irrational Thinking (DEBIT)

Disorganized Thinking Disorder

Dissociative Thought Disorder

Distorted Reality Disorder (DRD)

Disturbed Emotions, Bizarre Behavior,

Irrational Thinking (DEBBIT)

Double Life

Emotional Aphasia

Emotional Dysphasia

Encefalo-Neuro-Pathic Syndrome Disease

Excess Dopamine Syndrome (EDS)

Extra Grace Required Syndrome (EGRS)

False Belief Syndrome (FBS)

Freneticism

Frontal Cortex Disorder (FCD)

Frontlobe Disease

Genetibiochemosis

Genetic Brain Disorder (GBD)

Harmony Syndrome

Heightened Awareness Disorder (HAD)

Hyper-Imaginative

Hyper-Responsive Dopamine Disorder

Illusionary Perception (IP)

Imagination Extremes

Innocentia

Insidious Mood Disorder (IMD)

Integration Disorder

Intensive Hypo Cognitive Sensory

Disturbance Disorder (IHCSDD)

Irrational Thinking, Disturbed Emotions,

Bizarre Behavior (IT DEBB)

Kraepelin’s Disorder

Limbic Hyperdopaminergia

Lobefront Disease

Martyrdom

Mind Brain Disorders (MBD)

Mind Computer Complex Disorder

Mind Distorted Disorder (or Syndrome)

Misperception Disease (MD)

Moodus

Multi-Cognitive Perceptual Disorder

(MCPD; “Mc Pea Dee”)

MultiFocal Psychosis

My-Mind-Lies-To-Me, or Mymindliestome

Neural Pathway Disorder (NPD)

Neuro Biochemical Disorder (NBD)

Neuro Biological Disorder–Vincent Van

Gogh (NBD-VG)

Neuro-Cognitive Dysphoria

Neurological Disorder

Neuroschizoterrafirmia

Non-Normal Perceptive

Objective Experience Disorder

Occipatalphrenia

Orthomolecular

Paci

Paranoid/Irrational Thought Syndrome

(PITS)

Perception Deficit Disorder

Perception Distortion Syndrome (PDS)

Perception Dysfunction Disorder (PDD)

Perceptionitis

Persistent Early Dementia Syndrome (PEDS)

Persistent Early Onset Dementia Syndrome

(PEODS)

Persistent Thought Disorder

Person with a Dangerous Gift (PDG)

Personal Reality Disorder

Personality Disorder

Pervasive Thought, Delusional Hallucination

Disorder (PTDHD)

Phrenia-Affective

Phrenmalady

Positive-Negative Disorder

Pseudo Perceptual Syndrome

Psychotic Spectrum Disorder (PSD)

Raptasess

Reality Deficit

Reality Impairment Syndrome with

Distortion of Perception, Thinking, and

Behavior

Reality Perception Disorder (RPD)

Romans 7:15

Schizostein

Secondary Perception (SP)

Sensory Dysfunction (SD)

Sensory Overload Syndrome

Serenfendil

Skidzo

Smartpolar

Spin Disease

Spiral Disease

Spiridis - Spirit Disorder

Stravinsky Syndrome

Supplementary-Eradicate

Disorder

Thera-Affective

Theraphren

Theraphrenia

Thought Disorder

Thought Disorder Syndrome

(TDS)

Voices

Whispering Mind

i am diagnosed schizophrenic and my favourite is 'alternative perception'

Again, thanks for the interest, name changes really only come up very rarely. Most doctors use the term and there is a broad agreement on universal criteria. How they are interpreted on the edges of diagnosis does differ between clinicians however. Once name changes are discussed in the DSM IV or broadly within the medical or psychological community with review articles etc. we can make some space (which is surely lacking here). Casliber (talk · contribs) 19:55, 6 December 2009 (UTC)

Cannabis research reference

I would just like to add another refrence backing up the claim that Cannabis use and Schizophrenia occurence is just a mere coping factor.

There is a sentence in drug abuse section that states "There is little evidence to suggest that other drugs including alcohol cause schizophrenia, or that psychotic individuals choose specific drugs to self-medicate; there is some support for the hypothesis that they use drugs to cope with unpleasant states such as depression, anxiety, boredom and loneliness.[70]"

I would also like to back this up with another additional reference. Here it is: http://www.ncbi.nlm.nih.gov/pubmed/15298320?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1

I also believe that the words "other drugs including alcohol" in this sentence should be replaced with "other drugs including cannabis" seeing as how the previous sentence had it's subject revolving around cannabis as well. Alcohol would fit into the "other drugs" category, but the main point of the sentence should clearly explain that it is the cannabis that this study is controversial about - not the alcohol.

Thanks guys.

MidnightToker666 (talk) 05:05, 18 November 2009 (UTC) MidnightToker666

I've since deleted this bit on my sandbox page on social construction of schizophrenia , but feel it is relevant to this part of the debate :

[Professor Nutt views links between cannabis and schizophrenia difficult to unentangle, in a UK populous study, :

"The other paradox is that schizophrenia seems to be disappearing (from the general population), even though cannabis use has increased markedly in the last 30 years. So, even though skunk has been around now for 10 years, there has been no upswing in schizophrenia. In fact, where people have looked, they haven't found any evidence linking cannabis use in a population and schizophrenia." ^[20]

Dutch research says there is no connection between cannabis useage and schizophrenia . The drug based hypothesis for onset of schizophrenia is therefore partially nullified : "The scientists say the drug only seems to affect people who are genetically predisposed to getting schizophrenia (meaning they will get it anyway). As schizophrenia manifests itself during adolescence, and many people start taking cannabis during adolescence - it is just coincidence that some people develop the mental illness soon after they start taking the drug."^[21]]

My thoughts on professor nutts comments which are indeed contradictory if you read the full guardian article as he suggests smoking weed increases the chance of getting schizophrenia 2.8 times are something akin to that , are A/ that schizophrenia isn't dissapearing from the general population , rather it is being used less as a diagnostic label by uk psychiatrists. I know of several people who are diagnosed bi-polar but have had schizophrenic symptoms. B/ That schizophrenia exists as a hereditary genetic condition and taking perception altering drugs may trigger the switches in the genes responsible for schizophrenia perhaps on a temporary basis. Darwinerasmus (talk) 13:23, 11 December 2009 (UTC)

Alternative perception spectrum

Not sure if this is the best place to do it, but I'd like to give a pointer to this new article for any who might be interested (I have nothing to do with it). Looie496 (talk) 00:19, 10 December 2009 (UTC)

I think that it should probably be deleted and I might nominate it for deletion. Much of it is poorly sourced. Does an article not already exist where this topic is already discussed, eg stigmatising effects of mental health labels or of schizophrenia?--Literaturegeek | T@1k? 09:51, 10 December 2009 (UTC)

I nominated it for deletion because there are no sources even unreliable sources which actually mention this alternative label for schizophrenia. It is original research IMHO.--Literaturegeek | T@1k? 09:57, 10 December 2009 (UTC)

I have been discussing this with literature geek on the alternative perception spectrum discussion page and have since began to rewrite the article as the social construction of schizophrenia in my sandbox which i have also copied to alternative perception spectrum - i think that stands barely as alternative perception already redirects to schizophrenia and thus is another name for schizophrenia spectrum but agree that it would be better to archive/delete alternative perception spectrum and concentrate on developing a social construction of schizophrenia page as there is a fair amount of research in that area . i am looking to get a hold of an athens password from a colleague at Northumbria University so i can access the full source materials of some of the current research around narrative and myths in schizophrenia to develop it further . I invite comments in my sandbox discussion page here http://en.wikipedia.org/wiki/User:Darwinerasmus/social_construction_of_schizophrenia Darwinerasmus (talk) 11:59, 11 December 2009 (UTC)

I still am not entirely sure social construct is the best name, because some of the people who want a different name for schizophrenia would reject the social construct theory, which is a minority opinion. From my limited knowledge on this subject there seems to be people who want a different name for similar reasons that manic depressive was changed to bipolar. I would have thought that criticisms of schizophrenia would have been better article name to cover a diverse range of aspects of schizophrenia. Then some of the content of the main schizophrenia article can be merged into it if it ever needs another pruning session (this article is currently quite big). Any article will need to be well sourced and I encourage you to read WP:MEDRS. If it promotes minority opinions using weak sources and nothing much else you run the risk of the article being deleted. If you created an article with the name I suggested you could do pubmed searches and find a variety of good quality sources discussing various criticisms and controversies. I do worry that this will become a WP:POVFORK and I hope that you will cover other aspects of criticisms and viewpoints and not just about the name schizophrenia and social construct.--Literaturegeek | T@1k? 03:07, 13 December 2009 (UTC)

Moore THM, Zammit S, Lingford-Hughes A, Barnes TRE, Jones PB, Burke M, Lewis G. “Cannabis use and risk of psychotic or affective mental health outcomes: A systematic review.” The Lancet. 2007 July 28; 370:319-328.

The Lancet reviewers consulted with experts to identify population-based longitudinal studies, as well as case-control studies.   
The reviewers zeroed in on the studies of developing a psychotic disorder based on research in Sweden,  New Zealand, and a Dutch study combined data from the three studies showed an increased likelihood of psychotic disorders in individuals who had ever used cannabis (adjusted odds ratio 1.08-6.13).  They determined people who used marijuana had roughly a 40% higher chance of developing a psychotic disorder later in life.

Whether cannabis causes persistent psychotic symptoms was reviewed with 35 studies (longitudinal & population based). There is an increased risk of any psychotic outcome in individuals who had ever used cannabis. Findings were consistent with a dose-response effect, with greater risk in people, who used cannabis most frequently.

The overall risk remains very low. Zammit said the risk of developing schizophrenia for most people is less than 1%. The prevalence of schizophrenia is believed to be about five in 1,000 people. Because of the drug's wide popularity, the researchers estimate that about 800 new cases of psychosis could be prevented by reducing marijuana use. Moore pooled results, finding an increased risk of psychotic outcomes in people who had ever used cannabis, controlling for confounding factors the schizophrenia risk has an adjusted odds ratio 1.20-1.65: 1.0.

The scientists found a more disturbing outlook for "heavy users" of pot, those who used it daily or weekly as their risk for psychosis jumped to 200%.

An analysis of six studies that assessed frequent use, found that individuals who often used cannabis were about twice as likely (adjusted odds ratio lies between 1.54 - 2.84: 1.0). There is now sufficient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life.

Nordentoft M, Hjorthøj C. “Cannabis use and risk of psychosis in later life. Meta-analysis Supports Case for Cannabis in Etiology of Psychosis” The Lancet. 2007 July 28; 370: p 293-294. M. Nordentoft and C. Hjorthøj of Copenhagen Hospital write, “The assessment of adjustment for confounding factors and transitory effects of cannabis intoxication is done more thoroughly than in previous reviews.”

A prior meta-analysis, led by Cécile Henquet of Maastricht Univ, Netherlands (Henquet et al., 2005), estimated that previous cannabis use doubles the risk of developing psychosis, independently of possible confounding factors. Zammit and colleagues ruled out alternative explanations. In addition, they looked at affective as well as psychotic outcomes.

The new meta-analysis by S. Zammit and T.H. Moore, Cardiff University, addresses methodological issues and causal links between psychosis and cannabis which affects dopaminergic, GABAergic, and glutamatergic neurons.

Dr. Wilson Compton, at the National Institute on Drug Abuse in Washington, called the study persuasive. There are consistencies across all of the studies with psychoses — but not in 7 studies of anxiety, and 15 studies of depression. Scientists cannot rule out that pre-existing conditions could have led to both marijuana use and later psychoses, he added. People with mental illness in their families could be at higher risk. For them, marijuana use "could unmask the underlying schizophrenia," said Dr. D.C. D'Souza, at Yale University.

Scientists think it is possible that marijuana causes psychoses by interrupting important neurotransmitters such as dopamine and other brain communication systems. Researchers have raised the possibility that cannabis use by young people, whose brains are still developing, may be particularly likely to increase psychosis risk. According to Moore “Arguments for why earlier use of cannabis might have more harmful effects are intuitively compelling, but no robust evidence supports this view.”

Age at first-use from the Dunedin evidence suggests it could be through effects of the catechol-O-methyltransferase (COMT) gene, in those who started 99.234.95.84 (talk) 00:31, 7 January 2010 (UTC)

FAR overdue

This article has been listed at Wikipedia:Featured articles/Cleanup listing for much too long, without issues being addressed; I'll wait one more week before taking it to FAR. There are still citation cleanup needs, and the Treatment section could benefit from better use of summary style. A serious review of use of primary sources, per WP:MEDRS (leading to undue weight) is needed. And this edit rightfully cut text to a daughter article, but left this article without a Summary. SandyGeorgia (Talk) 20:29, 13 December 2009 (UTC)

I would have put in summary text in for the History of Schizophrenia but there wasnt any obvious text to use.--Penbat (talk) 20:52, 13 December 2009 (UTC)

Incidentally it would be nice if somebody beefed up Paranoid schizophrenia--Penbat (talk) 21:32, 13 December 2009 (UTC)

I have cherry picked salient/core points for potted summary of History section - a new subarticle means that subarticle can now grow alot (very feasible)) Casliber (talk · contribs) 23:11, 13 December 2009 (UTC)

Yes, I can see a few links/sources which need updating now. Casliber (talk · contribs) 04:25, 24 December 2009 (UTC)

PS: this and/or this being two places to start to get the latest epidemiology. I need a bit of time to get and digest the fulltextsCasliber (talk · contribs) 04:46, 24 December 2009 (UTC)

I think it's time to take it to FAR. I hope it will be de-featured, so it can be edited more freely withtout users moaning about changes to a FA.--Sum (talk) 17:16, 6 January 2010 (UTC)

In what way do you feel it fails to meet criteria then? Casliber (talk · contribs) 19:35, 6 January 2010 (UTC)

Alternative interpretations

I suggest adding the following to the alternative methods section just to indicate that there exist essentially different interpretations of the subject that are not based on a medical model:

Jungian psychiatrist John Weir Perry argued that psychosis, more specifically schozphrenia was not an "illness" but a reconstitutive process of the psyche in deep crisis, and there is no nead for medication or specific treatment. In his view, if this process can develop and unfold in a supportive, understanding environment, the patient returns "weller than well" - that is, the person does not simply returns to his old self but emerges as more integrated, "healthier". He put his ideas to test in the center Diabasis where he accepted young "full blown" schizophrenics. He claimed that his patients revovered spontaneously after about three months.^[22]). In his theoretical work Perry introduced the idea that there is meaning in the seemingly chaotic, senseless content of the psyche in psychosis. He found parallels between mythical stories and psychotic content, and argued that while mythology serves to keep and renew mental balance in a social level, psychosis has the same purpose for the individual.^[23] Even though he claimed to find an effective, brief, inexpensive way of treatment that helps patients leave schizophrenia behind (as opposed to lifetime medication), his work remains largely unnoticed or ignored.

1. The far side of madness. Englewood Cliffs, N.J., Prentice-Hall, 1974.

2. Roots of renewal in myth and madness. San Francisco, Jossey-Bass Publishers, 1976.

I also suggest adding http://en.wikipedia.org/wiki/Elyn_Saks within the list of people with schizophrenia who make cultural contributions. she is due to give a keynote speech at the second biannual schizophrenia international research conference. http://www.schizophreniaconference.org/page4.html 92.233.236.143 (talk) 01:11, 13 December 2009 (UTC)

I am not sure I use refs correctly. --LonesomeCowboyBurt (talk) 13:01, 31 October 2009 (UTC)

If anything, this article is much too long, and should be aggressively trimmed, routing out primary sources and using review sources only in the process. I don't support the proposed addition. SandyGeorgia (Talk) 13:09, 31 October 2009 (UTC)

Agree, but since there are good sources, there is no reason why LonesomeCowboyBurt couldn't create a John Weir Perry article to cover this material. Looie496 (talk) 18:18, 31 October 2009 (UTC)

Basic info

(1) what is this disease? as a mother, i've found that we need basic information on: what is psychosis versus what is a mental disorder DSM/ICD. Because of the long period of DUP duration of undiagnosed psychosis of 4-7 years, we turn to wiki in the middle of the night to clarify terminology. Yes, some can be viewed as a spectrum but WiKi is best at outlining the major categories. (2) is it genetic? i strongly suggest adding the july Nature results from huge studies; the bottom line seems to be a small contribution from a large number of genes. (3) please add a solid explanation of negative symptoms because these appear before positive symptoms. Negative symptom means an observable pattern of withdrawal, alienation, ahedonia, fear. (4)cannabis - when used at an early age and/or when used weekly does triple the risk of full SZ. yes it can be used as self-medicating later on; but this risk is well proven. as one factor, this article should distinguish: predisposition of susceptible people vs behaviours of choice in adults. (5)one source very helpful is :SCHIZOPHRENIA RESEARCH FORUM - The mission of the SRF is to help in the search for causes, treatments, and understanding of the devastating disease of schizophrenia. Our goal is to foster collaboration among researchers by providing an international online forum where ideas, research news, and data can be presented and discussed. The website is intended to bring together scientists working specifically on schizophrenia, scientists researching related diseases, and basic scientists whose work can shed light on these diseases. In this way, we hope that the Schizophrenia Research Forum will be a catalyst for creative thinking in the quest to understand a deeply complex disease. It is our goal to create and maintain up-to-date content of the highest quality. The website is free of charge to users, independent of industry sponsorship, and open to the public. Though geared toward researchers, we welcome other visitors—people with mental illnesses, families, the media, and others who need accurate information on research into schizophrenia. We do, however, require that users who wish to post comments and other materials be registered members. All such materials are subject to approval by the editorial team. As a "forum," we encourage participation and welcome feedback from the community. thank you Iris 99.234.95.84 (talk) 00:54, 7 January 2010 (UTC)

Probably a Typo

In Signs and Symptoms,under Positive and Negative symptoms, it says: "Negative symptoms are symptoms that are not present in schizophrenic persons but are normally found in healthy persons.| If negative symptoms are NOT present in schizophrenic persons, why do we consider them as symptoms of schizophrenia? Don't you think we should remove the "not"?

It's not a typo, just very awkwardly written. If you remove the "not", it will be a description of positive symptoms, not negative symptoms. I'll try to make it easier to understand; thanks for pointing it out. Looie496 (talk) 17:47, 27 December 2009 (UTC)

Source: Elliot Valenstein and Robert Whitaker

"Increased dopamine activity in the mesolimbic pathway of the brain is consistently found in schizophrenic individuals. The mainstay of treatment is antipsychotic medication; this type of drug primarily works by suppressing dopamine activity. "

According to one accredited neuroscientist and a award winning medical journalist this was established by studying the drugs and not the brain with the belief that the drugs worked based on the observed behavior of the individual. They cite studies that show that drugs like PCP that increase dopamine do not resemble the psychosis seen in Schizophrenics and that autopsy studies of Schizophrenic people show inconsistencies in this matter. They both also cite numerous studies from the National Institute Of Mental Health and The American Psychiatric Association itself that decreasing dopamine in the brain creates a "therapeutic parkinsons" and a "chemical straight jacket". I know I'm probably not the ten thousandth person to bring this up and have something reverted and I know many bots are set on this page but these peoples credibility amongst scientists who have no ties to drug companies is impeccable so I think that some bits of their work should be cited here on this wikipedia page. 24.236.234.23 (talk) 13:05, 15 January 2010 (UTC)

What you are saying is quite correct, I think, but it doesn't actually contradict the sentences you quoted. The sentences might be misleading to some readers, but they are factually correct. Increased dopamine activity is indeed found in schizophrenia, although it may not be the cause of the disease; dopamine antagonists are the mainstay of treatment, although they are clearly far from perfect. Regards, Looie496 (talk) 16:49, 15 January 2010 (UTC)

Metacognitive training

I just added a description of the metacognitive training in the psychological and social intervention section and so I would suggest to update the schizophrenia article in this manner, too. See Treatment of schizophrenia to look at what I wrote there! Thanks! --Neuschrank (talk) 17:13, 21 January 2010 (UTC)

omega-3 treatment/cure for schizophrenia and weblinks

I've been following the omega-3 research for about 9 years (as well as taking 5grams of omega-3 fish oil for much of this time), and recently an interesting report came out about omega-3's link to schizophrenia. I am pasting some of the web-links here.

Fish oil pills show promise in preventing schizophrenia http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20100202/omega_100202/20100202?hub=Health

Fish oil may prevent onset of mental illness: Study http://www.themoneytimes.com/featured/20100202/fish-oil-may-prevent-onset-mental-illness-study-id-1099134.html

Omega-3 Fish Oils Tested as Preventative Approach to Schizophrenia, with Positive Results http://www.schizophrenia.com/sznews/archives/005788.html

Fish oil hope for schizophrenia patients http://www.abc.net.au/news/stories/2010/02/02/2808143.htm?section=justin

Low omega-3 linked to schizophrenia risk http://www.upi.com/Health_News/2009/12/18/Low-omega-3-linked-to-schizophrenia-risk/UPI-14731261118188

Essential Fats Found Deficient in Brains of Men with Schizophrenia http://www.schizophrenia.com/sznews/archives/004864.html

Several years ago I also read research about how taking 5grams of omega-3 fish oil a day helped prevent relapse in manic-depressive disorder.

I think the time for skepticism of the massive benefits of omega-3 is long past, compared to the alternative of taking pharmaceutical drugs to mask illnesses it is really a no-brainer to take a natural oil that can CURE many diseases. This encyclopedia should step past the pro-pharmaceutical media bias and unflinchingly publish the honest truth about omega-3. Many people are needlessly suffering at the mercy of the pharmaceutical/psychiatric establishment who have largely ignored omega-3 as there is no money in finding a natural treatment or cure for diseases. There are many skeptics of game-changing science, but omega-3 truly is a game changer. It is likely that for many psychiatric patients omega-3 could replace psychiatric medication for treatment, with better outcomes and no side-effects. Please if you are interested in natural cures for disease do your research and you will see that they are out there.

cheers, Jamie 24.108.77.192 (talk) 12:48, 8 February 2010 (UTC)

the links arent working ? I edited them.

this is the reference I know Amminger Schäfer, Papageorgiou, Harrigan, Cotton, McGorry, Berger (2008). "Indicated Prevention of Psychotic Disorders with Long-Chainomega-3 Fatty Acids: A Randomized, Placebo-Controlled Trial", Schizophrenia Research, 102, 252 Earlypsychosis (talk) 18:12, 8 February 2010 (UTC)

Jamie it is best to use review papers especially for featured articles, per WP:MEDRS. Here is a recent review paper which could be used. The medical literature does not seem to be quite as enthusiastic as to declare it as a cure but nonetheless it does show benefitial effects in schizophrenia and those at risk of developing schizophrenia. Worth citing I think.--Literaturegeek | T@1k? 18:39, 8 February 2010 (UTC)

Addition of information about Yi gan san

It has been proven it a few studies for schizophrenia to reduce psychotic symptoms in conjunction with antipsychotics. Also, there is going to be a study out on Glycine as a standalone antipsychotic in high doses 30g/day to more. Please someone look at the sources and see if it worth adding. I am not good with wikipedia. So i do not want to edit this page. This page looks pretty good. I would love to see alternative therapies included into it. Such as fish oil, glycine and yi gan san(yokukan san). I would have really appreciated for someone to suggest these to me. If someone knows any other scientifically backed herbs or herbal medicine. Please put it in the discussion page for me to peruse. Why is there no mention of the groundbreaking study on fish oils for preventing schizophrenia? Are the pharmaceutical companies icing any mention of that stuff for their own benefit?—Preceding unsigned comment added by 76.122.99.157 (talk) 23:46, 8 February 2010 (UTC)

Laing

Psychiatrist, R.D. Laing was at the forefront of a whole new approach to treating schizophrenia around the time of the 1960s, but has since passed more or less into obscurity. There is only sparse mention of him at points in this article, and I feel that more should be made. His theory encompassed an interesting mixture of existential philosophy and phenomenology. Not only that, but the man was regarded as a sort of a 'guru' who could very easily connect with and get to know people--even those in states of acute psychosis. He regarded schizophrenia as a withdrawal from the world which an individual finds too threatening to his or her insecurely-built identity. His methods of treatment did not include psychotropic drugs; rather, he focused on how he actually 'treated' his patients as individuals and as persons, not viewing them as objectified and diseased patients. He was successful in a great number of cases, and had somewhat of a cult following for a time within the psychiatric community. His theories have since been mainly ignored by the establishment, which adheres strictly to the biomedical model of psychiatry. I feel that this article, in the interest of fairness and an unbiased view (even if the medical establishment itself is biased against Laing or Laing-esque approaches) desperately requires further mention of the theoretical work put forth by R.D. Laing. Perhaps dedicated sections under the following headings would be most appropriate: causes; mechanisms; management; prognosis.

p.s., I would have written the damned sections myself without any of this nonsense, but this article is strangely under lockdown.. I didn't fancy Wiki as such a bureaucratic and strict website.

Source(s):

Laing, R.D. The Divided Self. New York, Pantheon, 1960. —Preceding unsigned comment added by Andrew.slusher (talk • contribs) 06:42, 10 February 2010 (UTC)

If you make a few more edits and wait a few days, your account will be "autoconfirmed" and you will be able to edit the article yourself. The article is currently semi-protected because it is frequently vandalized by unregistered editors. Note that I am not expressing any opinion here on the changes you would like to make. Regards, Looie496 (talk) 18:52, 10 February 2010 (UTC)

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^ Tarrier N, Turpin G (1992). "Psychosocial factors, arousal and schizophrenic relapse. The psychophysiological data". Br J Psychiatry. 161: 3–11. doi:10.1192/bjp.161.1.3. PMID 1638327. {{cite journal}}: Unknown parameter |month= ignored (help)
^ Barrowclough C, Tarrier N, Humphreys L, Ward J, Gregg L, Andrews B (2003). "Self-esteem in schizophrenia: relationships between self-evaluation, family attitudes, and symptomatology". J Abnorm Psychol. 112 (1): 92–9. doi:10.1037/0021-843X.112.1.92. PMID 12653417. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ Birchwood M, Meaden A, Trower P, Gilbert P, Plaistow J (2000). "The power and omnipotence of voices: subordination and entrapment by voices and significant others". Psychol Med. 30 (2): 337–44. doi:10.1017/S0033291799001828. PMID 10824654. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ Honig A, Romme MA, Ensink BJ, Escher SD, Pennings MH, deVries MW (1998). "Auditory hallucinations: a comparison between patients and nonpatients". J Nerv Ment Dis. 186 (10): 646–51. doi:10.1097/00005053-199810000-00009. PMID 9788642. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^ The cannabis conundrum
^ Cannabis does not induce schizophrenia, Dutch scientists say
^ (1
^ (2)

[1] Wade, Nicholas "Genes Show Limited Value in Predicting Diseases" New York Times Research April 15, 2009 http://www.nytimes.com/2009/04/16/health/research/16gene.html?em

[2] Auriel E, Hausdorff JM, Giladi N (2008). "Methylphenidate for the Treatment of Parkinson Disease and Other Neurological Disorders". Clin Neuropharmacol. doi:10.1097/WNF.0B013E318170576C. PMID 18978488. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[3] Ashton H, Gallagher P, Moore B (2006). "The adult psychiatrist's dilemma: psychostimulant use in attention deficit/hyperactivity disorder". J. Psychopharmacol. (Oxford). 20 (5): 602–10. doi:10.1177/0269881106061710. PMID 16478756. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[4] Cherland E, Fitzpatrick R (1999). "Psychotic side effects of psychostimulants: a 5-year review". Can J Psychiatry. 44 (8): 811–3. PMID 10566114. {{cite journal}}: Unknown parameter |month= ignored (help)

[5] Kimko HC, Cross JT, Abernethy DR (1999). "Pharmacokinetics and clinical effectiveness of methylphenidate". Clin Pharmacokinet. 37 (6): 457–70. PMID 10628897. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[6] Dafny N (15). "The role of age, genotype, sex, and route of acute and chronic administration of methylphenidate: A review of its locomotor effects". Brain research bulletin. 68 (6): 393–405. PMID 16459193. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Cite has empty unknown parameter: |1= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

[7] Ross RG (2006). "Psychotic and manic-like symptoms during stimulant treatment of attention deficit hyperactivity disorder". Am J Psychiatry. 163 (7): 1149–52. doi:10.1176/appi.ajp.163.7.1149. PMID 16816217. {{cite journal}}: Unknown parameter |month= ignored (help)

[8] Broome MR, Woolley JB, Tabraham P; et al. (2005). "What causes the onset of psychosis?". Schizophr. Res. 79 (1): 23–34. doi:10.1016/j.schres.2005.02.007. PMID 16198238. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[9] Lewis R (2004). "Should cognitive deficit be a diagnostic criterion for schizophrenia?" (PDF). J Psychiatry Neurosci. 29 (2): 102–13. PMC 383342. PMID 15069464. {{cite journal}}: Unknown parameter |month= ignored (help)

[10] Brüne M, Abdel-Hamid M, Lehmkämper C, Sonntag C (2007). "Mental state attribution, neurocognitive functioning, and psychopathology: what predicts poor social competence in schizophrenia best?". Schizophr Res. 92 (1–3): 151–9. doi:10.1016/j.schres.2007.01.006. PMID 17346931. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[11] Sitskoorn MM, Aleman A, Ebisch SJ, Appels MC, Kahn RS (2004). "Cognitive deficits in relatives of patients with schizophrenia: a meta-analysis". Schizophr Res. 71 (2–3): 285–95. doi:10.1016/j.schres.2004.03.007. PMID 15474899. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[12] Cohen AS, Docherty NM (2004). "Affective reactivity of speech and emotional experience in patients with schizophrenia". Schizophr Res. 69 (1): 7–14. doi:10.1016/S0920-9964(03)00069-0. PMID 15145465. {{cite journal}}: Unknown parameter |month= ignored (help)

[13] Smith B, Fowler DG, Freeman D; et al. (2006). "Emotion and psychosis: links between depression, self-esteem, negative schematic beliefs and delusions and hallucinations". Schizophr Res. 86 (1–3): 181–8. doi:10.1016/j.schres.2006.06.018. PMID 16857346. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[14] Beck AT (2004). "A cognitive model of schizophrenia". Journal of Cognitive Psychotherapy. 18 (3): 281–8. doi:10.1891/jcop.18.3.281.65649.

[15] Horan WP, Blanchard JJ (2003). "Emotional responses to psychosocial stress in schizophrenia: the role of individual differences in affective traits and coping". Schizophr Res. 60 (2–3): 271–83. doi:10.1016/S0920-9964(02)00227-X. PMID 12591589. {{cite journal}}: Unknown parameter |month= ignored (help)

[16] Tarrier N, Turpin G (1992). "Psychosocial factors, arousal and schizophrenic relapse. The psychophysiological data". Br J Psychiatry. 161: 3–11. doi:10.1192/bjp.161.1.3. PMID 1638327. {{cite journal}}: Unknown parameter |month= ignored (help)

[17] Barrowclough C, Tarrier N, Humphreys L, Ward J, Gregg L, Andrews B (2003). "Self-esteem in schizophrenia: relationships between self-evaluation, family attitudes, and symptomatology". J Abnorm Psychol. 112 (1): 92–9. doi:10.1037/0021-843X.112.1.92. PMID 12653417. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[18] Birchwood M, Meaden A, Trower P, Gilbert P, Plaistow J (2000). "The power and omnipotence of voices: subordination and entrapment by voices and significant others". Psychol Med. 30 (2): 337–44. doi:10.1017/S0033291799001828. PMID 10824654. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[19] Honig A, Romme MA, Ensink BJ, Escher SD, Pennings MH, deVries MW (1998). "Auditory hallucinations: a comparison between patients and nonpatients". J Nerv Ment Dis. 186 (10): 646–51. doi:10.1097/00005053-199810000-00009. PMID 9788642. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

[20] The cannabis conundrum

[21] Cannabis does not induce schizophrenia, Dutch scientists say

[22] (1

[23] (2)

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

[9]

[10]

[11]

[12]

[13]

[14]

[15]

[16]

[17]

[18]

[19]

[20]

[21]

[22]

[23]

Meaningless, pseudoscientific term

Question

Relative risk vs odds ratio

Omega 3's

Impact of antipsychotics on negative symptoms

Obesity

FGAs vs SGAs

Weight gain

Caption under Nash's picture misleading

Smoking not discussed either

Recent cannabis edits still have problems

Important Distinction Needs To Be Made

Suggested External Link

Minor quibble about a section heading

Vitamin D lead.

The Relationship between Trauma and Psychosis

Changes to Issues and Controversies Section

Schizophrenia and over the counter drugs

Schizophrenia and over the counter drugs

A couple of images from Otis Archives

Archiving

Screening and Prevention

Add Clinical Scales

loss of brain tissue

Taraxein

concerning Psychosis

Type 1 and Type 2

new publication treatment guidance

Genetic burdon of common diseases likely carried by large numbers of rare varients.

Drug induced psychosis

Amphetamines also increase schizophrenia or only cannabis?

Explanation

No Nobel

Potassium ion channels and isoform 3.1 of KCNH2

nature of hallucinations

recognizing psychosis

Further Reading

Schizophrenia etymology

Heritability

Unsourced additions

Yoga and link with Schizophernia

Famous persons with schizophrenia

Cognitive and emotional features of schizophrenia

Whose definition of reality?

Association of Schizophrenia with Seasons

Prevalence

The Five Senses

Causes and models

Genetic

Semi-protection

BDNF

kalirin

We need better sources than those two

FA level

The issue of the scientificity of schizophrenia should be more integrated into the article

How much context?

Size and scope of causes and treatment sections

infobox image

re: Soteria

Review of primary sources needed

links between autism and schizophrenia which mean a genetic test could be developed for schizophrenia and/or autism

Cannabis research reference

Alternative perception spectrum

FAR overdue

Alternative interpretations

Basic info

Probably a Typo

Source: Elliot Valenstein and Robert Whitaker

Metacognitive training

omega-3 treatment/cure for schizophrenia and weblinks

Addition of information about Yi gan san

Laing