Talk:Causes of schizophrenia

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Hypoxia, as one option, in the neurodevelopmental model.[edit]


This work did not rely in any way on hypoxia. In 1993, Nature published Philip Seeman, Hong-Chang Guan & Hubert H. M. Van Tols work "Dopamine D4 receptors elevated in schizophrenia" (Vol 365, 30 September p441). In this work they found d4-like receptors to be elevated six times in schizophrenia. This result was replicated many times. Recently Dr Seeman said the most likely explanation for this is an alteration in the monomer:dimer ratio of the d2 receptor: "Dopamine Receptors: Clinical Correlates", Such alterations are caused by dopamine agonists or dopamine: Logan J; Fowler J. S.; Dewey S. L.; Volkow N. D.; GY S Gatley S J.; A consideration of the dopamine D2 receptor monomer-dimer equilibrium and the anomalous binding properties of the dopamine D2 receptor ligand, N-methyl spiperone: Short communication; 2001, vol. 108, no3, pp. 279-286, Journal of neural transmission, Dopamine itself can increase 1000% in striatal dialysates under hypoxia reversably provided (in part) the reuptake is not blocked.(Akiyama Y, Koshimura K, Ohue T, Lee K, Miwa S, Yamagata S, Kikachi H (1991) J Neurochem Sep; 57(3);997-1002 Notpayingthepsychiatrist (talk) 08:19, 25 March 2008 (UTC) Dr Seeman attributes the excess of monomers to "increased release of endogenous dopamine": Seeman P, Kapur S, Schizophrenia: more dopamine, more D2 receptors; Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):7673-5; a Google search reveals several possible causes of such release (as could be inferred from Philip Seeman, David Weinshenker, Remi Quirion, Lalit K. Srivastava, Sanjeev K. Bhardwaj, David K. Grandy, Richard T. Premont, Tatyana D. Sotnikova, Patricia Boksa, Mufida El-Ghundi, Brian F. O'Dowd, Susan R. George, Melissa L. Perreault, Pekka T. Männistö, Siobhan Robinson, Richard D. Palmiter, and Teresa Tallerico; Dopamine supersensitivity correlates with D2High states, implying many paths to psychosis; PNAS, March 1, 2005, vol. 102 no. 9, pp 3513-3518 (in which hypoxia is considered too)). One of the cited cause of release is amphetamine exposure. It turns out that amphetamines work by means of a hypoxic process: Alberto Del Arco, Jose´ L. Gonza´lez-Mora, Vicente R. Armas, Francisco Mora, Amphetamine increases the extracellular concentration of glutamate in striatum of the awake rat Neuropharmacology 38 (1999) 943–954. Involvement of high affinity transporter mechanisms and "endogenous release of dopamine" is attributed to hypoxia in: P. William Conrad, David E. Millhorn and Dana Beitner-Johnson, Novel regulation of p38γ by dopamine D2 receptors during hypoxia ; Cellular Signalling, Volume 12, Issue 7, July 2000, Pages 463-467 ; increase was also reported by Gary B. Freeman and Gary E. Gibson, Effect of Decreased Oxygen on In Vitro Release of Endogenous 3,4-Dihydroxyphenylethylamine from Mouse Striatum, Journal of Neurochemistry, Volume 47 Issue 6 Page 1924-1931, December 1986 and there is a natural period when the placenta is hypoxic: John D. Aplin, Hypoxia and human placental development, J Clin Invest. 2000 March 1; 105(5): 559–560: besides dysfunctional reasons for hypoxia.


As Dr Seeman pointed out, the original dopamine hypothesis suggested that not only may dopamine be more highly expressed in the brains of psychotic people, but they might be more sensitive to it Philip Seeman and Shitij Kapur "Schizophrenia: More Dopamine, More D2 Receptors" PNAS as at 2-01-08. He has written extensively and done many experiments with d2high, the highly sensitized receptor state for dopamine.

According to Dr Seeman et al, (SYNAPSE 60:319–346 (2006) p332 (full reference at the end of article)), The low affinity state of the receptor could be explained by the 'cooperativity model': when a dopamine-like chemical "binds to the vacant receptor, the occupied receptor interacts or 'cooperates' with the other receptors ... such that the affinity of the other receptors for the agonist is markedly reduced ..." - a 'negative cooperativity': the low state of the receptor. He says that, according to this model, increased d2high is a result of reduced 'negative cooperativity'.

So the question is: does hypoxia promote positive or negative cooperativity. Unfortunately Dr Seeman doesn't refer to hypoxia and cooperativity in just mentioned article. Notpayingthepsychiatrist (talk) 10:19, 2 January 2008 (UTC)

Nitric Oxide is often stimulated by hypoxia (nitric oxide is elevated at high altitudes Nitric Oxide may be the brain's step towards vasomotor escape? however -

Nitric oxide's use results in a guanine nucleotide exchange: (as of 30-03-08). Dr Seeman says the role of guanine nucleotide is to alter the interreceptor cooperativity (332). The ability of some binding sites to bind with guanine nucleotides can "cooperatively increase their affinity" Paolo Migani, Rosamaria Fiorini, Ersilia Ferretti, Elena Manini, Stefano Chimichi, Gloriano Moneti (1997) Role of Guanine Nucleotides as Endogenous Ligands of a Kainic Acid Binding Site Population in the Mammalian Cerebellum Journal of Neurochemistry 68 (4) , 1648–1654 Notpayingthepsychiatrist (talk) 21:33, 2 January 2008 (UTC) And enhanced cooperativity results in more monomers rather than dimers has been found).Notpayingthepsychiatrist (talk) 09:14, 5 August 2009 (UTC)

Hi Notpayingthepsychiatrist, there is now a large amount of information on hypoxia in the article, nearly 3 screenfulls plus refs. Do you think it could be boiled down? Some of it reads as quite generalized or as constructing a technical argument, rather than a summation of the issue. The new section on future treatment is original research because it links two sources neither of which makes the link themselves, and I suspect some other parts are also doing this via generalized sources on hypoxia; I see from your talk page that you've been advised to avoid this before. It would be helpful to include a URL or ID link to the articles cited so it's easier for others to check/balance. For example, Schmidt-Kastner et al. is cited twice for a simple statement of the importance of hypoxia, but the article also says it's a hypothesis that relies almost exclusively on epidemiological studies, has some points of weakness or contradiction, and needs further research. I'm not intending to discourage these contributions of excellent sources and points, but they need to fit the context of the article and Wikipedia policies. EverSince (talk) 14:01, 12 August 2008 (UTC)

Will get right onto itNotpayingthepsychiatrist (talk) 16:34, 12 August 2008 (UTC)

After adding in the links to articles and checking them, I've edited it down a lot more - much of the content was argumentation drawn from sources that were not themselves linking hypoxia and schizophrenia. A lot of it interestingly linked early neurodevelopmental/motor abnormalities to schizophrenia, but not to hypoxia; I think that should be re-added here but within a section on early signs rather than on hypoxia. Some of the sources linked hypoxia to neurodevelopmental issues but not to schizophrenia; the summaries of those could be re-added to a hypoxia article rather than here. Having said that, most of the basic points seem to have survived, because they were briefly made by some source, but just without the extra points and connections made around them. If I've mistakenly taken anything out, of course feel free to reinstate it (preferably copying any citation from a version with the URL links added in). EverSince (talk) 22:59, 19 August 2008 (UTC)

Hey thanks for all your work in making this article more enclopaedic and having sources making the connection themselves. I read in a style guide for Wikipedia that - there is no need to say that Sadam Hussein was an evil man, just say he bombed his own people and the reader will draw the conclusion. So in keeping with this I found the quote which said 'motor coordination deficits are the hallmark of prenatal hypoxia'. I then pointed out the regularity of motor deficits in schizophrenia, letting the reader draw the conclusion that hypoxia was involved. This was a sizable part of the article. It was further followed up by the quote from Nature, (supplied to me by CopperKettle) which said hypoxic tel-tale signs are found near motor neurons, which I think bolstered the article.

I also assumed that readers would be familiar with schizophrenia which is why I included the effect of hypoxia on G-proteins, which readers would note had to do with schizophrenia with no more trouble than that an evil man bombs his own people. Other well-known (but possibly inconsistent) symptoms of schizophrenia are: increased d2 receptors and enlarged ventricles and faulty axon guidance.

Anyway, it is as it is and anyone who wants to see these points can look at the history of the article.

Thanks EverSince. Notpayingthepsychiatrist (talk) 09:12, 20 August 2008 (UTC)

As I understand it, the point in the NPOV guideline about calling someone evil is about a neutral sticking to the facts, with subjective points of view attributed to those who hold them. A more relevant guideline here is Wikipedia:No original research. But as I say, I think many of the issues should be re-added here (which I will help work towards) but within sections on those issues (such as motor and neurological abnormalities as you mention) and reflecting the focus of the sources, rather than subsumed, via synthesis of a series of intermediate sources, under one possible cause. Will need to be careful with the use of primary sources though (e.g. one I noticed was cited by a failure to replicate). Readers can then indeed draw their own conclusions. EverSince (talk) 12:35, 20 August 2008 (UTC)

OK. But just so the left hand knows what the right hand is doing, it is now 3:45 in Australia and I am going to reinsert the information on motor dysfunction here, under its own title. Probably take half an hour. Then look forward to your editing. Notpayingthepsychiatrist (talk) 17:49, 20 August 2008 (UTC)

EverSince, have simply placed the information in a new section. Had to include the quote about hypoxia as the article is called 'Causes of Hypoxia' not 'Symptoms of hypoxia'. I leave it in your hands.

Steve Notpayingthepsychiatrist (talk) 18:14, 20 August 2008 (UTC)

EverSince, I have also reinserted the material on increased d2 receptors and ventricles under your banner of hypoxia, as these are perhaps the two most well-known symptoms. Steve Notpayingthepsychiatrist (talk) 18:27, 20 August 2008 (UTC)

I think splitting the section up (or rearranging them or whatever) was a very good idea on your part as it was getting too cumbersome. Notpayingthepsychiatrist (talk) 18:39, 20 August 2008 (UTC)

I think we have had a left-hand right-hand miscommunication, my fault for not commenting here to avoid it like you did. As you were writing the above, I was busy adding a new section on childhood development at the end of the article, based on your sources/comments previously in the hypoxia section, as well as some new for balance. I missed at least one of yours out, which need to re-add. It's not just about splitting it up btw; what you've readded still steers it all towards hypoxia in a way teh sources do not. EverSince (talk) 18:49, 20 August 2008 (UTC)

Excelent, I'm glad we're working at the same time. Please let me know what you decide to do. Steve Notpayingthepsychiatrist (talk) 19:00, 20 August 2008 (UTC)

Your having added the section at the end of the article is excelent. I will delete the section I just added on neurodevelopment. I wonder if there is a place for the comment that hypoxia shows as poor motor coordination?

Notpayingthepsychiatrist (talk) 19:13, 20 August 2008 (UTC)

Cool, I think some of the other content on neurological issues in those with schizophrenia can be added to the existing neural section. I think content on links between hypoxia and motor coordination can be added in the hypoxia section - if the sources support those links occuring in the development of schizophrenia. Got to go for a bit now. EverSince (talk) 19:19, 20 August 2008 (UTC)

Eversince, would it be OK to add the following sentence to the hypoxia section?:

After discussing variuous obstetric complications, which they say are related to hypoxia, Golan et al say evidence has been put forward that such complications may result in schizophrenia, for example, in later life (p338), They later say, motor deficits including coordination have been called the "hallmark of prenatal hypoxia". But the difference between subjects and controls is only visible in challenging tasks, not when "freely roving in a plain arena", and only when brain damage has been done [1]. —Preceding unsigned comment added by Notpayingthepsychiatrist (talkcontribs) 20:58, 20 August 2008 (UTC)

That study is primary but another Golan et al. study cites it and is a review: The effect of prenatal hypoxia on brain development: short- and long-term consequences demonstrated in rodent models (2006) It does state in the intro that "obstetric complications may be associated with psychopathology in later life, e.g. schizophrenia..." citing two other sources, while also mentioning other conditions like learning disability or cerebral palsy. It does then frame its review of rodent fetal hypoxia studies as potentially providing "some insight into the nature and extent of neurodevelopmental abnormality that may be expected in affected children and are integral to the development of therapeutic interventions." So it does seem to just about make the link, indirectly, and only as one example - and it doesn't say that any of the findings are specific to it. Personally I guess it could support a brief statement about rodent models and findings of a range of sensorimotor & learning/memory deficits in some cases following fetal hypoxia. Btw the other animal model study cited here, "Neonatal intermittent hypoxia impairs dopamine signaling and executive functioning", I can't access but it appears to be making a similarly distant and non-specific link? The citation currently next to it, Jucaite et al, is on ADHD and doesn't mention schizophrenia so isn't suitable.
It seems like we really need a section on obstetric factors in general, with hypoxia as one subsection within that. The Mallard guinea pig article currently cited under hypoxia is about complications involving numerous factors, only one of which was hypoxia and the effects of which it wasn't able to differentiate. One of the two studies cited in Golan above, PMID 15063096, more specifically and explicitly links animal models to schizophrenia but covers various obstetric issues. Other studies are also more general than just hypoxia, including the one Copperkettle has added below. This 2005 review article, The role of obstetric events in schizophrenia seems very good and perhaps could be used as the overall summary (it also very interestingly puts the findings in context). EverSince (talk) 23:30, 20 August 2008 (UTC)

Thanks, I'll include it. Other editors can always delete it. Notpayingthepsychiatrist (talk) 00:14, 21 August 2008 (UTC)

message for eversince[edit]

Hi Eversince,

thank you very much for properly formatting the crude material I had there.

Could the material fro CopperKettle - included at the end of this discussion page, and also at my UserTalk page be incorporated.

If you look at one of my previous revisions it says poor axonal guidance is related to schizophrenia. CopperKettle's article says this can be because of hypoxia. His Nature article also points to the proximity between hypoxic trademarks and motor neurons. I checked with him (see my talk page) and he says the edit is good.

But you've done enough already.

Thanks again. Steve Notpayingthepsychiatrist (talk) 05:21, 22 August 2008 (UTC)

Hi Steve,
I don't think there's any doubt that the article posted by Copperkettle above is relevant and should be added...somewhere within the obstetric section?
The article on parkinsons mentioned in passing that axonal guidance has been linked to schizophrenia, but didn't cite it. The others didn't mention schizophrenia. Thought I'd read something interesting on it in more detail re schizophrenia, maybe in one of the sources in the article, but couldn't find it. Must be a good source somewhere and seems like it should be mentioned, maybe in the neural section. Just one opinion as one editor anyway.
Thanks for fixing the point on the different school data sets by the way. EverSince (talk) 12:36, 22 August 2008 (UTC)

Hypoxia and axonal guidance - an answer to the Notpayingthepsychiatrist[edit]

Prevention of schizophrenia[edit]

If excessive hypoxia beyond a certain tolerance results in activating the hypoxic schizophrenic genes, why not test all fetus' with and treat by giving the mother HBOT?

Notpayingthepsychiatrist (talk) 18:08, 18 August 2008 (UTC)

Please refer to this site for a cure rate of 66% for IUGR fetus'? with HBOT

Notpayingthepsychiatrist (talk) 18:30, 18 August 2008 (UTC)

motor abnormalities[edit]

Hi Notpayingthepsychiatrist, The new additions still seems to be selecting bits from different sources & putting them together to make the link more than the sources do. e.g. "A predictive cohort of over 12,000 children says: "Altered motor development in schizophrenia is, therefore, fairly robust across many different study designs" - but is it linking that to hypoxia or a range of possible causes? The two quotes from teh book that are run together - are they related to each together in the book? "a 0.004% chance of their being no relation between hypoxia and schizophrenia" - is this referring to the 0.0004% probability from the statistical significance testing? It seems misleading/exaggerated to use that for a general statement like that, and the article also reports some prior null findings. Just some thoughts as per your query. EverSince (talk) 14:19, 27 August 2008 (UTC)

Hi Eversince,

I included the study which said there were modest relationship with hypoxia because it is on the same cohort. But I realise there are two articles making the link. The book indeed links the two itself. Just below the quote it gives animal examples of how hypoxia links schizophrenia. The quote I made is the first human example of the quote. I think the quote about the significant p value is linked because the article itself is trying to remedy why there is not significant reporting of hypoxia in this sample which is why it adopted this technique and the customised NSS. The null findings are the reason for its methodology not supporting its conclusion on purpose.

Anyway, on another question, if we want to include failed Wikipedia contibutions on our own web site (as was the case of my measuring hypoxia etc), do we still have to attribute them to Wikipedia if they were rejected. Please check I think I could get into trouble if I attribute them, because it turned out to be not Wikipedia's stance, but then if I don't they were mentioned in Wikipedia.

If after this you still feel the sources arn't linked themselves, please delete them.

I should tell you that one of my motives for focusing on motor abnormalities is there are not a lot of measures for fetal hypoxia. Motor abnormalities have been stated as one symptom. Genetic studies have had some success but fail to be replicated. I have been a patient in some myself.

The symptoms described in the previous version of the article make fetal hypoxia an alternative, which could be widely responsible as neuromotor defects are widely symptomatic.

Waiting for your reply. Steve Notpayingthepsychiatrist (talk) 21:57, 27 August 2008 (UTC)

Hi Steve, I realised there was a link to the book pages, and that it addresses the whole issue. Thanks for explaining the issues with the other points also. I will try some rewords in due course (which of course you might want to re-re-word, etc), but it seems like there should be enough to support the links as you mention.

Regarding the attribution to Wikipedia, I think you'd be fine because all you're saying is that it was here at some point, and it's in the very nature of the content to be co-edited and changed over time (and not necessarily meaning prior was rejected; e.g. much of the original in this case is still in this article but in diffferent ways/sections, and still some other pieces to re-cover). By the way I did read ages ago that if you personally created and added some particular content to Wikipedia, then you retain copyright and do'nt need to attribute it; but can't remember where in the help/guideline pages that I saw that so best check... EverSince (talk) 23:19, 27 August 2008 (UTC)

(Have added another source to childhood antecedents which says those with poor motor abiliities are not likely to progress to High school. Looks like the same study except two new authors ) Notpayingthepsychiatrist (talk) 19:40, 22 December 2008 (UTC)

change to personality section[edit]

Included factors which contribute to delusions, section on HVA refers to schizophrenia specifically. Notpayingthepsychiatrist (talk) 10:42, 10 September 2008 (UTC)

lack of holistic approach and structual approach[edit]

Neurotransmitters are only modulators of 'trigger level' of specific autosopher or perceptron network. i would like to point out @ A.Jakubik's findings about how information processing disorders are related to psychoses.

factors like infecteous damage of limbic system (i.e. due to viral, bacterial or parastic infection) which is usually rich supported by blood (so also circulatory system issues can contribute) and 'draws' lot of blood for quick enough information processing might be the 'key' to understand schizophrenia, which was afterall described as 'information metabolism' disorder by A.Kepinski.

also perserveration of perception and perserveration of emotional state can be put into this model nicely, as emotional system exists in limbic system structures, which are very prone to perserveration, due to their structural design.

so , reorganising the problem : schizophrenia is disorder of information metabolism in individual, with core axis symptom - autism - which is disorder of relation of individual with environment.

causes of either of disorders can be easily spot then (i.e. information/social memory overload, organic damage of information processing structures or tracts connecting them with other parts of the brain, or repetative (or very intense) environmental influences. separate section could include modelling of limbic system in early childchood, altrough this could be aswell accounted into organic damage. (talk) 06:22, 4 April 2008 (UTC)


Just noting that this article seems to need some tidying... repeated bits, disproportionate coverage e.g. hypoxia, informally worded bits. EverSince (talk) 08:38, 30 July 2008 (UTC) & separately sourced stuff on causes before the causes section even starts. EverSince (talk) 08:44, 30 July 2008 (UTC) Ack tried some things but it's impossible really... EverSince (talk) 09:27, 30 July 2008 (UTC)

Just to note here in advance, I'm intending to move the points mixed together under "environment" out into individual sections, grouped by type in some way or other. And then genes would be in its own section too. EverSince (talk) 15:10, 22 August 2008 (UTC)

Bot report : Found duplicate references ![edit]

In the last revision I edited, I found duplicate named references, i.e. references sharing the same name, but not having the same content. Please check them, as I am not able to fix them automatically :)

  • "fn_23" :
    • Dalby, JT, Morgan D & Lee, M (1986). Schizophrenia and mania in identical twin brothers. ''Journal of Nervous and Mental Disease'' 174, 304–308. PMID 3701318
    • Huttunen MO, Niskanen P. (1978). Prenatal loss of father and psychiatric disorders. ''Archives of General Psychiatry'', 35(4), 429–31. PMID 727894

DumZiBoT (talk) 22:58, 12 August 2008 (UTC)

Obstetric-genetic interaction: risk for schizophrenia[edit]

At Molecular Psychiatry: Serious obstetric complications interact with hypoxia-regulated/vascular-expression genes to influence schizophrenia risk

The etiology of schizophrenia is thought to include both epistasis and gene-environment interactions. We sought to test whether a set of schizophrenia candidate genes regulated by hypoxia or involved in vascular function in the brain (AKT1, BDNF, CAPON, CHRNA7, COMT, DTNBP1, GAD1, GRM3, NOTCH4, NRG1, PRODH, RGS4, TNF-) interacted with serious obstetric complications to influence risk for schizophrenia. A family-based study of transmission disequilibrium was conducted in 116 trios. Twenty-nine probands had at least one serious obstetric complication (OC) using the McNeil-Sjostrom Scale, and many of the OCs reported were associated with the potential for fetal hypoxia. Analyses were conducted using conditional logistic regression and a likelihood ratio test (LRT) between nested models was performed to assess significance. Of the 13 genes examined, four (AKT1 (three SNPs), BDNF (two SNPs), DTNBP1 (one SNP) and GRM3 (one SNP)) showed significant evidence for gene-by-environment interaction (LRT P-values ranged from 0.011 to 0.037). Although our sample size was modest and the power to detect interactions was limited, we report significant evidence for genes involved in neurovascular function or regulated by hypoxia interacting with the presence of serious obstetric complications to increase risk for schizophrenia.

--CopperKettle (talk) 05:21, 20 August 2008 (UTC)

Reelin and schizophrenia[edit]

I've accumulated some evidence and hypotheses linking reelin to schizophrenia (see the subsection there). You might find it neccessary to integrate this information into this article somehow. --CopperKettle (talk) 03:39, 27 August 2008 (UTC)

Seems that a summary of the issue should be added, maybe under "other" in neural processes? I'm not sure incidentally if the neural section need reorganizing or anything...don't know what you think. EverSince (talk) 11:41, 1 September 2008 (UTC)

Original research/Synthesis in Development of specific delusions section[edit]

That section is chokefull of statements not attributable to the original sources. Examples: writing that "Jealousy, a common delusion, ranked requiring less dopamine in both experiments." based on PMID 10533332 (a study on mice fertility!) and PMID 11185930, a case report on one guy that got jealous while taking amphetamine; or non-sensical statements like "This state-created 'personality' is well-known in the culture of a society."

Also, I question the specificity of the section to this article. It should be moved to the Delusion article if not outright deleted. Xasodfuih (talk) 14:10, 16 February 2009 (UTC)

Hi Xasodfuih, I am the author of this section and agree with what you say. The style is amateur, and the section on personality is a bit non-sequeteur. My motivation for writing it was many schizophrenics have delusions which they assimilate into their personality and assume, for example, that their gender is changing; when it is not, and this is a neurotransmitter problem. There is valuable information here for families and patients, so I would like it recorded somewhere - could it be retained in the talk pages? It is a central question schizophrenics ask - am I psychologically causing this delusion or is it medical. I had this symptom myself, and the answer is in another section of the DSM to schizophrenia (GID), and the study on amphetamines is not available on the net, so the answer is hard to find for those panicking their gender is changing. Notpayingthepsychiatrist (talk) 08:20, 18 February 2009 (UTC)

Notpayingthepsychiatrist (talk) 01:12, 9 March 2009 (UTC)

Notpayingthepsychiatrist (talk) 18:06, 9 March 2009 (UTC)

I agree that specifics of schizophrenics delusions are very poorly described, i suggest learning more from bibliography related to findings of Andrzej Jakubik ( [171][172][173][174][175][176][177][178][179][180][181][182][183][184][185] ). Some delusions like jealousy are NOT related to schizophrenia per se , but occur also in other psychoses (i.e. drug related psychoses, alcohol related psychoses, etc), and are consequence of oxytocin and dopamine system damage BUT they are SEPARATE SYMPTOMS , which are of psychotic class, but not 'schizophrenia' itself, and can occur (and do) also in common neuroses and wide range of other medical conditions.

It could be noted though that schizophrenia CAN lead to development of such symptoms due to information metabolism disruption , changes in attitude, and neuroendocrine response due to prolonged stress (and emotional attitude of both affected individual and society interactingh with subject). (talk) 22:09, 28 March 2009 (UTC)

I may have misinterpreted the article on 'subtype and course of schizophrenia' in that subtype may have been meant to refer to deficit, non-deficit types or undifferentiated, paranoid type, which is further reason for it to be deleted perhaps? Notpayingthepsychiatrist (talk) 21:51, 30 March 2009 (UTC) Fixed - still relevant. So far everyone agrees the section should be moved to delusions?Notpayingthepsychiatrist (talk) 13:32, 31 March 2009 (UTC)

Hi, I would like to question whether the section introduces any new ideas. It is true that it uses supporting facts; but each section starts with a quote from a source which introduces these facts. I think this is within the guidelines of Wikipedia. Notpayingthepsychiatrist (talk) 08:11, 5 July 2009 (UTC)


Care must be taken to ensure that the reasoning elaborated for heritability explains why it is specifically genetic. Otherwise you are in the same position as explaining why someone who has an incarcerated relative is at greater risk of being incarcerated than the general population. Few believe that criminal tendency is part of the genetic code, even though having an aunt, uncle, parent, grandparent, sibling, or cousin behind bars puts one at an approximately 45% risk of becoming incarcerated at some point.

The pat answer, that schizophrenia must be written into the genetic code because family statistics entail the inference, is insufficient to settle the issue. —Preceding unsigned comment added by Uniquerman (talkcontribs) 20:45, 6 July 2009 (UTC) Uniquerman (talk) 20:49, 6 July 2009 (UTC)

It could be that it is genetic but not heritable, as is true of the vast majority of cases of Down's syndrome, where a meiotic disjunction event takes place in the gamete.Uniquerman (talk) 18:28, 3 September 2009 (UTC)


Like the section on cannabis use, the general notion that schizophrenia is a typology of symptoms rather than a primary disease is not properly weighted as to its probability. If professionals actively involved in the treatment, diagnosis, and management of schizophrenia were canvassed, most of them would be as nonplussed by the finding that any number of diseases, events, and susceptibilities can cause the same variable cluster of symptoms as they would be by the finding that smoking pot is one of them. Indeed, it would be very strange if it were not a primary disease. It's hard to think of any other cluster of specific symptoms, however variable, that is caused by multiple types of events, diseases, toxicologies, weaknesses, etc.

To see it otherwise, and to weight all manner of evidence equally, is somewhat akin to giving Jack London's observation of Samoan culture the same authority as Margaret Mead's. —Preceding unsigned comment added by Uniquerman (talkcontribs) 21:01, 6 July 2009 (UTC) Uniquerman (talk) 21:06, 6 July 2009 (UTC)


I tagged this article as "confusing." I did so even though I appreciate the amount of content it has. My concern is that there are so many hypotheses and anecdotes that it becomes difficult for the general public reader to navigate. Perhaps it would be better to decrease the large number of primary references and their often-anecdotal accompanying text, and limit the page to ideas that have been reviewed by secondary sources. --Tryptofish (talk) 22:04, 21 July 2009 (UTC)

I agree in part. There is no use in an article that is unreadable. But I think the state of the article reflects the state of science in this area and perhaps this should be made more clear in the introduction - that there are various hypotheses. It would be good to retain the comprehensiveness of the article though - our audience who look to the article are those connected with the affliction and they have a wide variety of experiences. So I would be for: a more explicit stating that the cause is unagreed upon and may not be singular and a more comprehensive encaptulation of the different experiences and their cause - which would reflect our readership. One thing we want to avoid is pretending that we are speaking authoritatively on an agreed upon and proven cause - which would be misleading.Notpayingthepsychiatrist (talk) 08:13, 22 July 2009 (UTC)

I think we clearly agree more than we disagree. Just to clarify my point, though, I feel that, for the very reason that we, indeed, do not want to speak authoritatively on a single proven cause, this is more than just saying explicitly up front that there are multiple theories. Whether our audience includes those touched by the affliction, or also those from the general public who want to learn more, we owe it to them not to give undue weight to observations that exist as isolated anecdotes in the literature, even the academically peer-reviewed literature. (Where you mention audience members with a variety of experiences, it could be WP:OR for us to imply that a particular reader's experience is explained by a particular case-study in the literature.) The academic peer-reviewed literature includes multiple review articles, and it would be better to shorten the page by largely deleting material that is not cited there. --Tryptofish (talk) 17:02, 22 July 2009 (UTC)

I am with you wholeheartedly on the "undue weight" issue. Extended remarks on hypoxia and more than a paragraph on cannabis seem way out of line, just to take a couple instances. I have my own reservations about a number of issues, but those are properly with the sources and not the article itself, but I do think the article format could generally be improved in the way that any thesis can be improved, by an overarching topic paragraph, solid outline, and a reasonable conclusion. It is an article for general reading and an introduction to the subject and should parse in those terms, rather than have the look and style of a research paper. Of course, you do want it to be even-handed and not have the appearance of an introduction to the subject, and yet be an advocate of a certain position under the surface, as is, for instance, NIMH's position paper on schizophrenia, a different example of how it ought not to be done.Uniquerman (talk) 17:49, 23 July 2009 (UTC) In addition, more emphasis might be placed on the issue whether schizophrenia is a primary disease or a symptomography. In the end this is the pole around which the whole subject turns.Uniquerman (talk) 19:25, 23 July 2009 (UTC)

Hi Tryptofish, I have transferred two sections of the article to a new article on Schizophrenia Symptoms, where editors can make a comprehensive list of symptoms. It needs an introduction. I was the author of both sections so I feel comfortable doing this. What do you think? Notpayingthepsychiatrist (talk) 17:58, 22 July 2009 (UTC)

I couldn't use the article Schizophrenia signs and symptoms as this seems to be as unspecific as the current articleNotpayingthepsychiatrist (talk) 18:06, 22 July 2009 (UTC)

Sorry, I guess I don't understand your question. The link you provided goes to Schizophrenia. Did you also create a new page? Where you say "transfer," does that mean you deleted parts of the page here? I don't see anything deleted. --Tryptofish (talk) 18:42, 22 July 2009 (UTC)

Yes, I thought I deleted the sections 'Childhood antecedants' and 'speccific delusions' as these describe symptoms, and I thought I created a new article 'Schizophrenia: symptoms' incorporating these. But apparently I must have done something wrong. I think this is the right thing to do, as authors can then relay some detail about specific symptoms - and being an encyclopaedia for the people, with the ability to form endless articles, I think that's what we should aim at. Can you give it a go, if you want to? Notpayingthepsychiatrist (talk) 19:39, 22 July 2009 (UTC)

My advice would be to try to incorporate any relevant material that is not specifically about causes into Schizophrenia; no need to fork off a lot of new pages. I agree with you that shortening this page by limiting it to causes only, would be a good idea, but it doesn't really address the issue that I raised. --Tryptofish (talk) 20:12, 22 July 2009 (UTC)
The reason this page exists is the size of the schizophrenia article itself. Having an article focussing on this topic, allows for greater depth and more hypothetical theories to be discussed. Also, a treatment of schizophrenia article exists for the same reason. I have not looked at this page in a while and at may be that some copyediting for flow and clarity is needed. This is almost always the case in medical and technical articles that some balance between jargon, accuracy and clarity needs to be struck. Casliber (talk · contribs) 20:20, 22 July 2009 (UTC)

I also found this article confusing - not because of the number of causes but because their explanations often lacked clear meaning (to a layman). I mean, doctors aren't going to be reading any wikipedia article for information about medical conditions (or so I hope!) and patients aren't going to be able to understand the majority of the information on this page. Just keep the audience in mind when editing. I especially liked the section on marijuana because of its applicability for a schizophrenic trying (almost anything) to avoid relapse. Also just the use of the word, 'disorder,' or, ya know, 'illness,' should be replaced in general by words like, 'condition,' or, 'diagnosis,' since the former two can be rather disheartening to read whereas the latter two are more neutral. I feel strongly about this. Ya know, recovery does depend on a positive outlook on the self and its capabilities...Makeswell (talk) 20:19, 14 September 2009 (UTC)

Thanks. I hear you. I'm planning to work on it soon. --Tryptofish (talk) 20:25, 14 September 2009 (UTC)

I deleted the confusing tag (which has been there since July 2009) as whether the article gives undue weight to one or another cause is a subjective judgement; since 2009 it has been refined and there is not a large number of suggestions under this heading. Notpayingthepsychiatrist (talk) 17:23, 7 October 2010 (UTC)

That's fine with me. (Also, thank you for leaving a message about it at my talk.) As it happens, my concerns have not been addressed, but I think that's 100% my own fault. I'm afraid that my list of edits that I need to get around to working on has gotten way longer than what I can keep up with, alas. My apologies for that. Eventually, I'll give this page a major overhaul, but until that time, it does our readers no good to leave the tag there, so I'm fine with removing it. Best, --Tryptofish (talk) 20:58, 7 October 2010 (UTC)

Specific examples[edit]

On thinking about it, tryptofish, can you point out the most difficult ones? I had a bit of a look but it is hard to know where to start. Also, I am a doctor so I use jargon all the time and might be a little blinded to some more obivous ones. Casliber (talk · contribs) 21:01, 22 July 2009 (UTC)

I'll try to give you a (too) short answer for now, because it would take me a lot of time to go through it all. I'm a Ph.D. so I know the jargon too, but jargon really isn't the issue for me. It's anecdotal case studies that, I think, do not rise to encyclopedic importance, especially given that we are writing for the general public. To be honest, my attention was drawn to the issue by recent edits to the page, and I was trying to gently suggest my concern to the editor who has been making them (so you could in part look at recent edit history). What I'd like to see is to take out the case studies of one or two individuals, and focus instead on theories about the cause that have been given notability by discussion in peer-reviewed review articles. --Tryptofish (talk) 21:16, 22 July 2009 (UTC)

If instead of calling the amphetamine examples 'anecdotal' we recognise them as 'primary evidence' - amphetamine being the motive for the dopamine hypothesis - and such evidence being the basis for any secondary source conclusions; would there be any problem with that? I should say that I have schizophrenia and have had the symptoms I describe. Encyclopedias vary on their use of technical explanations and as this is an encyclopaedia for the people I think we should consider first the patients and families, rather than the psychiatric profession. My status as a patient is why my edit history is so capricious. Notpayingthepsychiatrist (talk) 06:58, 23 July 2009 (UTC)

I must agree that there are many theories for which the evidence is very limited, but which gain some airing in popular media, and this is the best page to discuss them. I have been meaning to go through this article for some time, but have been busy all over the place....Casliber (talk · contribs) 11:11, 23 July 2009 (UTC)
I'm replying to you both. Casliber, you make good points both in that we can be helpful in providing an evidence-based context for confusing media reports, and in the issue of being busy -- me too on that. In that regard, when I have some time soon, I'm going to go through the article and try to pull out what I would suggest pruning, but I'll then rapidly self-revert my edit. That way, I won't change anything on the page, but hopefully it will be an efficient way for me to communicate what I would see as specific examples, and for other editors to react before we take any real action. I think that's fair. Notpaying, I've been deliberately trying not to frame my comments as only picking on your recent edits on amphetamine, because I do appreciate your very valuable input here, and I don't want to come across as criticizing. At the same time, it's important that we not let your self-observations as a patient become SYNTH or OR. I definitely agree that we are not writing the page primarily for the health care profession, but for the general public. The professional literature contains a lot of primary publications that are anecdotal case studies; these are useful because they provide a database for subsequent analysis. But when a site like ours presents these cases as encyclopedic, we risk misleading the public by implying that they are significant evidence, when in fact subsequent scientific analysis may (or may not!) demonstrate that an isolated observation was a false lead. Thus the value of subsequent (secondary) scientific review, and thus my suggestion that we cut back on some of the details. --Tryptofish (talk) 14:46, 23 July 2009 (UTC)

Hi again, I was thinking that one solution may be to leave the results of the study on HVA in tha article and move the anecdotal amphetamine psychosis information to the article on 'amphetamine psychosis'. Incidenally, that article contains the following sentence: "Although not common, these users offer some anecdotal evidence about the neurotoxicity of long-term methamphetamine use". Providing anecdotal evidence. What do you think?Notpayingthepsychiatrist (talk) 18:44, 23 July 2009 (UTC)

Hi Tryptofish, just on the Synthesis of Ideas - I don't believe the amphetamine examples introduce new ideas, as it says they confirm the HVA experiment; and I don't think it's Original Research as I didn't find the subjects myself. However, if for the sake of academic honesty you want to delete them, Wikipedia does encourage us to be bold in doing so.Notpayingthepsychiatrist (talk) 18:26, 25 July 2009 (UTC)

Thanks for being so generous about that. For myself, I really need more time to think about it. --Tryptofish (talk) 19:15, 25 July 2009 (UTC)
I'll look into this some more, but I think the recent edits by another editor have gone a long way towards addressing the concerns that I raised. --Tryptofish (talk) 22:20, 26 July 2009 (UTC)

The only problem is, if a schizophrenic were to wonder why he/she was experiencing particular delusions so that the patient had the confidence not to trust them, what information does the article supply, or the article on delusions? When I started to have delusions my gender was changing the doctor couldn't help me, and I said 'I bet this is a side effect of the medication' so I looked it up, but it wasn't the medication. Notpayingthepsychiatrist (talk) 05:05, 27 July 2009 (UTC)

As much as I feel very sympathetic to what you have gone through, I think we need to be careful about what kind of a role we take on. It is worth reading WP:NOTGUIDE, which is very relevant to all of this discussion, in part because of what it says about medical advice, and in part because of what it says about the writing style appropriate to this page generally. --Tryptofish (talk) 16:04, 27 July 2009 (UTC)

Yes, I see what you mean about 'scientific theories' which have not yet had their day. It seems that 'amphetamine psychosis' is a type of 'cause specific delusion' though; I suppose what was missing was a link made by the original author. Sorry about that. Notpayingthepsychiatrist (talk) 09:25, 29 July 2009 (UTC) Notpayingthepsychiatrist (talk) 09:53, 29 July 2009 (UTC) Notpayingthepsychiatrist (talk) 10:17, 29 July 2009 (UTC)

Tryptofish, hi, while waiting for your revision, I thought it best to mention in the introduction the feelings we have here about an incoherent and technical article. So I included the description of the 'medical model' and scientific language. I actually don't believe any revision could do the vast amount of literature on the subject justice; which is why it is important to keep these caveats in the introduction. The article may be unreadable as a whole, but I think if we use the table of contents properly a reader will be able to locate the information he/she is interested in.Notpayingthepsychiatrist (talk) 12:08, 4 October 2009 (UTC)

Thanks. Sorry to keep you waiting! Oh well, I'm overextended and WP:There is no deadline. I appreciate your patience. --Tryptofish (talk) 20:00, 4 October 2009 (UTC)

Hey Tryptofish - when you get around to doing your review, remember the introduction says the factors are part of a scientific debate, so please represent as many arguments as possible and give arguments for and against Notpayingthepsychiatrist (talk) 13:48, 13 October 2009 (UTC)

Hi, we should move 'Childhood antecedants' to Schizophrenia/Prognosis/Course as it is not a cause. (Except the motor skills mentioned have been called by Mary Cannon a genetic marker - I personally believe they show hypoxia).Notpayingthepsychiatrist (talk) 23:00, 28 December 2009 (UTC)

Syd Barrett[edit]

Appropriate? I thought I'd try this experimentally.

user / professional movement to change the name of schizophrenia[edit]

Several academics support the abandonment of the term schizophrenia which is outmoded. i propose that the reason that this article is so confusing is that the term schizophrenia itself means so many different things to so many different professionals. There is a movement amongst both users and professionals to change the name to something more modern than the outmoded term with its derivative connotations of jekyl and hyde split personality - the campaign page is here : - I think it would be important to recognise this user movement either on the main page or in 'disambiguation' from the wiki subset on schizophrenia ? What are others thoughts on this ? Darwinerasmus (talk) 23:29, 6 December 2009 (UTC)

Your point is clearly a good one in the sense that there must be a plethora of causes for a condition that is not a single entity. On the other hand, readers will tend to come looking for this familiar word, so we really shouldn't rename this article at this time. I think, for now, it's best to continue to treat this as something that does not have a single cause. --Tryptofish (talk) 23:49, 6 December 2009 (UTC)

Iwasn't aware of this movement, but think it is a very good idea and other people should be made aware of it too - it doesn't take away the legitimacy of illnesses such as delusions and explains why scientists have had such trouble finding one schizophrenia.Notpayingthepsychiatrist (talk) 21:55, 27 August 2010 (UTC)

environmental interpretation of genetic evidence[edit]

Just incase there are any problems - I included the sentence on shared placenta in the section on 'Genetics' first thinking the report in Schizophrenia Bulletin was a longitudinal study of placenta number at birth and following concordance of monozygotic twins with schizophrenia. However the technique of finger print analysis stands unreplicated and is not 100% certain as it is not longitudinal. But the statistical inference of some genetic influence in monozygotic twins has some remaining doubt because of the mono/dichorionic theory, which was included in the Molecular Psychiatry review, so I think one sentence is appropriate? Notpayingthepsychiatrist (talk) 03:31, 26 January 2010 (UTC)

Caption to sz graph[edit]

Hi, I have spoken to Dr Seeman about this graph and he still supports it, so the research is still relevant; however, the caption includes a lot of information which gives a proper perpective on the dopamine hypothesis, and the possible monomer explanation, which is why it is so long. As this is a team effort, feel free to adjust the length. Notpayingthepsychiatrist (talk) 06:10, 14 February 2010 (UTC)

variety of causes[edit]

I think the variety of causes demonstrated in this article is excelent testimony to the state of schizophrenia research. Especially the last contributor who emphasised a behavioural aspect to dopamine conditioning. Notpayingthepsychiatrist (talk) 10:35, 12 August 2010 (UTC) However, for any new-diagnosed patient, excessive sexual activity used to be thought of as a cause of schizophrenia (by Thomas Coulston) and there are higher rates of this activity amongst schizophrenia, however it has been discounted as many people who do this do not get schizophrenia and some schizophrenics don't do it ('A very brief introduction to Schizophrenia' Chris Frith, Eve Johnstone, Oxford) and excess dopamine such as by amphetamine can increase sex drive.Notpayingthepsychiatrist (talk) 22:56, 12 August 2010 (UTC). This is why I put the OR tag on the dopamine addiction entry.Notpayingthepsychiatrist (talk) 21:46, 27 August 2010 (UTC)

original research tag.

I have tried to find a journal or book which substantiates the claim that innab made that some schizophrenics are abusing their reward circuitry. I thought I remembered from about a decade ago Kaplan and Saddock's Synopsis of Psychiatry saying the habit circuit was possibly causal in schizophrenia but can't find the quote on line. Notpayingthepsychiatrist (talk) 17:05, 1 September 2010 (UTC)

dangerous original research tag[edit]

I have tried to find a journal or book which substantiates the claim that innab made that some schizophrenics are abusing their reward circuitry. I thought I remembered from about a decade ago Kaplan and Saddock's Synopsis of Psychiatry saying the habit circuit was possibly causal in schizophrenia but can't find the quote on line. Notpayingthepsychiatrist (talk) 17:05, 1 September 2010 (UTC) Notpayingthepsychiatrist (talk) 17:09, 1 September 2010 (UTC) Innab actually causes the schizophrenic an abuser, so I deleted the section Notpayingthepsychiatrist (talk) 19:05, 1 September 2010 (UTC)

Cause of schizophrenia[edit]

(Crosspost from Talk:Schizophrenia) Today's papers have a study from Nature Genetics that needs to be in the article. It's called Exome sequencing supports a de novo mutational paradigm for schizophrenia by Bin Xu, Maria Karayiorgou and several others. It costs $18. Can anybody who is actively working on this article afford to buy it? There are high level summaries in WebMD, Ars Technica and elsewhere. Thanks. -SusanLesch (talk) 02:34, 9 August 2011 (UTC)

Striking comment here because the question has been answered at Talk:Schizophrenia. Thanks. -SusanLesch (talk) 18:39, 9 August 2011 (UTC)


I would like to suggest that this article be updated to describe schizophrenia as a neurodevelopmental disease. I am reading the book The Origins of Schizophrenia, published 2012 by Columbia University Press, and chapter 1 (page 25) says:

In recent years, evidence has accumulated in support of a role for neurodevelopmental insults in the etiopathogenesis of schizophrenia (Brown, 2011). The dramatic changes in brain structure and function from conception to birth underscore the particular vulnerability to insults during this stage of development with regard to both short- and long-term disease outcomes (Tau & Peterson, 2010). Hence, the determinants of detal brain development- both genes and environmental factors- deserve consideration as potential risk factors for schizophrenia.
The Origins of Schizophrenia, published 2012 by Columbia University Press, and chapter 1 (page 25), source:

Thank you. (talk) 22:59, 29 January 2012 (UTC)

Hi, you may find it interesting to note that it is the prominence of hypoxic contribution to obstetric complications which gave rise to the neurodevelopmental model which the article says has now become the standard model. Best wishes.

Notpayingthepsychiatrist (talk) 09:47, 15 April 2012 (UTC)

Schizophrenia the norm?[edit]

"psychologist Julian Jaynes in his 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind; he proposed that until the beginning of historic times, schizophrenia or a similar condition was the normal state of human consciousness.[139"

Well, it couldn't have been schizophrenia. I don't care how expert Mr. Jayne is it's obvious he never knew someone with schizophrenia very well. Otherwise he'd have realized long ago that someone with this illness cannot carry on a coherent conversation with someone else for any length of time. They may hallucinate but so what? Since someone who's schizophrenic can't communicate their ideas w/ anyone else easily at all, I'd like to know how a schizophrenic person could ever become a shaman in any society. In fact, the idea is so ludicrous it gives one pause. There should be an accompanying statement that despite the guy's lofty wishes, people with schizophrenia frequently cannot organize their thoughts, have great difficulty communicating their thoughts, and at times can appear catatonic for long stretches. Which might sort of ruin their persuasive abilities. It makes this guy's statement seem ill informed at best. Case and point, Joan of Arc may have been pyschotic and experienced hallucinations but she was definitely NOT schizophrenic. — Preceding unsigned comment added by (talk) 07:33, 26 November 2012 (UTC)

I wonder.[edit]

Can make mice be schizophrenia?Manzzzz(talk) 06:51, 12 July 2013 (UTC)

good question difficult to answer I guess. I think that schizophrenia is not a mice diseases but, maybe some mice have symptoms close to schizophrenia but it's certainly not a wide disease like what we can see in humans... but what is interesting is that some physicians or biologist have modified the genome of mice, or have added drugs during the pregnancy or during the whole life of the mice to create schizophrenic's mice, they are not exactly schizophrenic but have some characteristics of schizophrenic people.--Nicobzz (talk) 22:02, 11 July 2014 (UTC)

A new article about schizophrenia and autophagy[edit]

Hi! I have found a new article about links between schizophrenia and autophagy, I added this link in french version of the shizophrenia article.

If you find it interesting, you can also add it: [1]

It says there is a significant lack of Beclin 1 protein, which promote autophagy in schizophreniac's hippocampus. And also an excess of other protein or RNA in blood's lymphocyte.

--Nicobzz (talk) 22:14, 8 January 2014 (UTC)

Genome wide association study and 129 SNP over 136 are located in mhc region[edit]

In September 2011, a meta-analyse of genome-wide association studies discovered that 129 over 136 single-nucleotide polymorphism (SNP) significantly associated with schizophrenia were located in Major histocompatibility complex region of the genome.[2]

I had just added this part in this article, as I'm not a specialist in this domain I'm not sure it tells exactly what I told in this article, but it seems that I didn't tell something wrong, don't hesitate to download the publication and check it and discuss here.--Nicobzz (talk) 22:06, 11 July 2014 (UTC)

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  1. ^ Golan, H. Kashtutsky, I. Hallack, M. Sorokin, Y. and Huleihel, M. (2004) "Maternal Hypoxia During Pregnancy. Delays of development of motor reflexes in newborn mice" Developmental Neurosicience 26, pp338-349
  2. ^ Genome-wide association study identifies five new schizophrenia loci.