Talk:Causes of autism

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This is an old revision of this page, as edited by Miradre (talk | contribs) at 17:40, 18 October 2011 (→‎Removed for discussion). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

questionable statements

This article has many questionable statements.

First, heritability of autism being 90% is far from universally accepted. Research into non-genetic causes, such as maternal antibodies to fetal brain, in utero maternal immune activation, autoantibodies to brain in some autistics, make 90% far too high. The usual basis for claiming very high heritability is identical twin concordance, but identical twins were in the same mother at the same time, so they are very likely to be effected by similar in utero effects, assuming the concordance is all due to genetics is not logical. Furthermore, concordance for fraternal twins is MUCH higher than for siblings, which should not be the case if only genetics are the cause.

Heritability of 90% is far from universally accepted. —Preceding unsigned comment added by 75.61.137.185 (talk) 01:35, 8 February 2011 (UTC)[reply]

A new study from UCSF and Stanford reported in yesterday's paper has found more environmental than genetic cause for autism over all. This should be included in this article. This study was no surprise to me, note I was talking about 90% heritability being too high here back in February, but really it's been known for a couple of years that 90% was too high. The editors who make this article so bad, who ironically are the most active, kept out all this stuff. They are being proved wrong. Does anyone want to keep defending this stuff? — Preceding unsigned comment added by 76.232.8.239 (talk) 12:25, 5 July 2011 (UTC)[reply]

I just want to follow policy, something you ought to consider. Dbrodbeck (talk) 12:27, 5 July 2011 (UTC)[reply]

The first four lines of this article do not live up to the scientific state-of-the-art of 2011.

(1) "Heritability contributes about 90% of the risk of a child developing autism". This claim is based on one study, is not consensus, and at odds with many studies showing that environmental factors are necessary to explain the massive rise in ASD cases, which had a changing point in 1988-1989. See e.g. the recent status report by McDonald, M. E.; Paul, J. F. Environ. Sci. Technol. 2010, 44, 2112-2118. For an overview of the topic of incidence and environmental background, see e.g. Bernard, S.; Enayati, A.; Redwood, L.; Roger, H.; Binstock, T. Med. Hyp. 2001, 56, 462-471.

One of the key candidates is mercury (Hg, incidentally found also in thimoseral) which is well known to be highly neurotoxic. (i) Counter, S. A.; Buchanan, L. H. Toxicol. Appl. Pharmacol. 2004, 198, 209-230. (ii) Clarkson, T. W.; Magos, L. Crit. Rev. Toxicol. 2006, 36, 609-662. (iii) WHO. Elemental Mercury and Inorganic Mercury Compounds: Human Health Aspects, Concise International Chemical Assessment Document 50 2003, Geneva.

Several studies published 2008-2011, after the wiki-referenced papers, link Hg to ASD. See e.g.: (i) Geier, D. A.; King, P. G.; Sykes, L. K.; Geier, M. R. Indian J. Med. Res. 2008, 128, 383-411.) (ii) Leslie, K. E.; Koger, S. M. J. Dev. Phys. Disabil. 2011, 23, 313–324. Impaired social behavior has been found in animals subject to Cd and Hg in drinking water: (iii) Curtis, J. T.; Hood, A. N.; Chen, Y.; Cobb, G. P.; Wallace, D. R. Behav. Brain Res. 2010, 213, 42-49.

During pregnancy, Hg(0) vapor penetrates the placenta barrier and damages fetal organs including the brain, as observed in rats. (Yoshida, M.; Satoh, M.; Shimada, A.; Yamamoto, E.; Yasutake, A.; Tohyama, C. Toxicol. 2002, 175, 215-222.)


(2) Regarding the statement in the first four lines of the article: "numerous clinical studies have shown no scientific evidence supporting any link between vaccinations and autism". This is true, but the opposite is also true, and therefore modulation of this sentence is required. See e.g. (i) Blaxill, M. F.; Redwood, Bernard, S. Med. Hyp. 2004, 62, 788-794. (ii) Lewandowski, T. A.; Simeonov, L. I.; Kochubovski, M. V.; Simeonova, B. G. NATO Science for Peace and Security Series C 2010, 65-84. (iii) Schultz, S. T. Acta Neurobiol. Exp. 2010, 70, 187-195.


— Preceding unsigned comment added by Kpje (talkcontribs) 14:16, 8 October 2011 (UTC)[reply]


I suggest the following addition after the first four lines, to reflect objectivity currently absent:

However, a later, large study from 2008 of 278,624 subjects from the Vaccine Safety Datalink born 1990–1996 showed consistent and significant correlations between incidences of autism spectrum disorders, tics, attention deficit disorder, and emotional disturbances with thimerosal-containg vaccines, and no such correlation in controls.[1]

This is the largest study done, and recent compared to other, old, and one-sided references.


--Kpje (talk) 14:20, 12 October 2011 (UTC)[reply]

Neanderthal Admixture Hypothesis

Per WP:TPG this page is for discussion of how to improve the article. Until there are sources discussing autism directly, this is off-topic and should stay collapsed
The following discussion has been closed. Please do not modify it.

My only request is that you read before you delete:

The Journal of Evolutionary Psychology just published a paper that supports the hypothesis that the confirmed neanderthal admixture event(s) provided cognitive variations that were subsequently selected for, sometimes causing a locus of deleterious recombinations in the genomes of children with parents who selected one another for those characteristics: http://www.epjournal.net/filestore/EP09207238.pdf

  • "People on the autism spectrum are conceptualized here as ecologically competent individuals that could have been adept at learning and implementing hunting and gathering skills in the ancestral environment."
  • "The autism continuum could represent a remnant of genetic introgression that took place before humans were the lone species in our genus. Perhaps some of the genes for autism evolved not in our direct ancestral line but in a solitary subspecies which later merged genetically with our line of descent through gene flow."
  • "This article emphasizes that individuals on the autism spectrum may have only been partially solitary, that natural selection may have only favored subclinical autistic traits and that the most severe cases of autism may be due to assortative mating. "
  • "A portion of this complexity and uncertainty arises from the relatively large number of distinct susceptibility genes that have been identified, many of which can be completely absent even in pronounced autism (Freitag, 2007). This genetic heterogeneity may be responsible for the clinical heterogeneity..."
  • "1. isolated pockets of humans can remain reproductively insulated for long enough to evolve discrepant ecological strategies; 2. such populations can quickly (less than 40,000 years in the South American and Asian pygmies; Cavalli-Sforza, 1986) develop features that vary markedly from the norm; 3. these traits can involve multiple genes at different loci; and 4. interbreeding can result in either continuous or polymorphic variation in subsequent generations. It is interesting to note that, as these indigenous people become assimilated into other gene pools, the genes for short stature will persist and may affect phenotypic variability in sporadic and unpredictable ways for a long time to come."
  • "Like other polygenic, continuous traits, the mutations responsible for autism could have been maintained by “environmental heterogeneity,” a form of balancing selection. In other words, the genes responsible for autism may have remained in our gene pool because as social-environmental conditions fluctuated in the past, discrepant genetic polymorphisms, or “multiple alternate alleles,” were favored."

Here are some peer reviewed sources that imply a link between the genes garnered via neanderthal admixture and the genes that code for ASDs:

"The development of cognitive abilities during individual growth is linked to the maturation of the underlying neural circuitry: in humans, major internal brain reorganization has been documented until adolescence, and even subtle alterations of pre- and perinatal brain development have been linked to changes of the neural wiring pattern that affect behavior and cognition [9]. The uniquely modern human pattern of early brain development is particularly interesting in the light of the recent breakthroughs in the Neanderthal genome project [10], which identified genes relevant to cognition that are derived in living humans. We speculate that a shift away from the ancestral pattern of brain development occurring in early Homo sapiens underlies brain reorganization and that the associated cognitive differences made this growth pattern a target for positive selection in modern humans."
"Mutations in CADPS2 have been implicated in autism (67), as have mutations in AUTS2 (68)."

The fact that the male side of the admixture(s) was/were strictly neanderthal would mean that we share none of their mtDNA. This explains the lack of mtDNA abnormality and the existence of mitochondrial dysfunction in people with ASDs: http://www.biomedcentral.com/1471-2350/12/50

  • "the frequent observation of concomitant mitochondrial dysfunction and ASD could be due to nuclear factors influencing mitochondrion functions or to a more complex interplay between the nucleus and the mitochondrion/mtDNA."

The neanderthal haplotype described in this 2011 paper is x-linked: http://mbe.oxfordjournals.org/content/early/2011/01/25/molbev.msr024.full.pdf+html

The abstract finishes by saying: "It indicates a very early admixture between expanding African migrants and Neandertals prior to or very early on the route of the out-of-Africa expansion that led to the successful colonization of the planet." [On a side note: This could also explain the unique, cyclical pattern of brutal invasion, cultural assimilation, and intermarriage that is so common in the written history of human civilization. Evidence of mostly patrilineal migrations among early AMHs is just coming out: http://www.pnas.org/content/early/2011/05/24/1100723108 "Ancient DNA reveals male diffusion through the Neolithic Mediterranean route" (May 2, 2011)]

More evidence is cited in this wrongplanet thread: http://www.wrongplanet.net/postp3696657.html#3696657 Slartibartfastibast (talk) 20:06, 9 June 2011 (UTC)[reply]

I haven't had a chance to read through everything, but a few comments from the outset: 1) any claims need to be made explicitly by the source to include; in other words, the source must directly make the claim that Neanderthal admixture leads to autism - we can't piece together several articles that make different parts of that claim to make a new claim none of the sources make themselves individually (see WP:SYNTH); 2) any claims made about the causes of autism should be compliant with our guideline on making medical claims - preferably reviews in medical literature, rather than primary (original) articles. I'll look through the material in a few days, but I get the sense we will be having a problem with #1. Yobol (talk) 22:01, 10 June 2011 (UTC)[reply]
not if you title the section "Archaic Hominid Admixture Hypothesis" Slartibartfastibast (talk) 22:17, 10 June 2011 (UTC)[reply]
Someone who believes people with severe autism (or even mild) would make good hunter-gatherer's cannot know much about either autism or hunting-gathering.·ʍaunus·snunɐw· 22:33, 10 June 2011 (UTC)[reply]
Someone who makes a comment like that is either incapable of comprehending the evidence given, or simply didn't take the time to read it. Slartibartfastibast (talk) 23:04, 10 June 2011 (UTC)[reply]
There is absolutely no evidence in the Reser article, only very liberal amounts of speculation. Even as Evolutionary Psychology goes this is poorly argued.·ʍaunus·snunɐw· 00:27, 11 June 2011 (UTC)[reply]
Your scrollbar, use it. There's more evidence immediately below the quotes from the speculative article. There's a great deal more evidence at the wrongplanet thread. Slartibartfastibast (talk) 00:43, 11 June 2011 (UTC)[reply]
That is not evidence it is also speculation - and a completely wrongheaded understanding of what it means when geneticists say that x gene is "implicated in autism" or that it is found in the neanderthal genome. We have one source that autisim might eb an evolutionary adaptation - another source saying for the neanderthal link. There is no reliable source making the Neanderthal - autism link - it is merely SYNTHesis. While the "lone forager hypothesis" is published in a reliable source I don't think the hypothesis has achieved sufficient attention in reliable sources to merit inclusion here. When reliable secondary sources start mentioning it then we can think about adding it.·ʍaunus·snunɐw· 01:30, 11 June 2011 (UTC)[reply]
That is not a rebuttal it is also silly - and a completely wrongheaded understanding of what is meant by "a remnant of genetic introgression that took place before humans were the lone species in our genus" or "supports the hypothesis." We have one source that directly speculates about an admixture from a relative of homo sapiens - another source saying that we received neanderthal DNA (that regulates cognitive development and immune function) from a sex-asymmetrical, highly bottlenecked admixture. I think the "Archaic Hominid Admixture Hypothesis" might have enough supporting evidence at this point to warrant placement on a page that at one point contained a section that tried to push MMR vaccines as a possible culprit [correction: I meant the "Autism" page, not this one]. Slartibartfastibast (talk) 01:49, 11 June 2011 (UTC)[reply]
What decides whether to include is not the amount of evidence but the amount of attention in reliable sources. The MMR hypothesis generated lots of attention - that is why we have to include that one and describe its current state. The Archaic Homonid Admixture Hypothesis seems to not even have been published in that form, and certainly hasn't generated any significant attention yet. It may yet, then we discuss it.·ʍaunus·snunɐw· 14:11, 11 June 2011 (UTC)[reply]
Fair enough. Slartibartfastibast (talk) 21:47, 11 June 2011 (UTC)[reply]

I copied the genes from page 111 of the supplemental pdf for the neanderthal draft sequence to a gene list on autworks: http://tools.autworks.hms.harvard.edu/gene_sets/7035

You can view and manipulate its disease network here: http://tools.autworks.hms.harvard.edu/gene_sets/7035/networks

This is a network of relationships between neanderthal genes and 699 genes linked to autism (blue = neanderthal, orange = autism-linked): Mirror: http://i.imgur.com/N5ObG.png

It shows 173 genes with 358 interactions (using the lenient settings in the screenshot)

  • The cluster in the bottom left is of genes that code for olfactory receptors. Neanderthals seem to have had smell-related genes that were important.

This is the reverse (blue = autism-linked, orange = neanderthal): Mirror: http://i.imgur.com/kBXYM.png

It shows 264 genes with 624 interactions (using the lenient settings in the screenshot)

  • PITX3 "is involved in lens formation during eye development."
  • SRD5A2 "catalyzes the conversion of the male sex hormone testosterone into the more potent androgen, dihydrotestosterone."
  • CADPS2 is already implicated in autism.
  • GABRA2 "is the major inhibitory neurotransmitter in the mammalian brain"
  • BDNF "acts on certain neurons of the central nervous system and the peripheral nervous system, helping to support the survival of existing neurons, and encourage the growth and differentiation of new neurons and synapses."
  • ROBO1 "was implicated in communication disorder based on a Finnish pedigree with severe dyslexia. Analyses revealed a translocation had occurred disrupting ROBO1. Study of the phonological memory component of the language acquisition system suggests that ROBO1 polymorphisms are associated with functioning in this system."
  • MY01D codes for the tails of spermatozoa.
  • STK3 "presumably allows cells to resist unfavorable environmental conditions."
  • SND1 "plays an important role in miRNA function"
  • OTX1 "may play a role in brain and sensory organ development" is a "dyslexia susceptibility locus candidate gene" and "is important in neuronal cell development and differentiation"

Slartibartfastibast (talk) 01:18, 30 June 2011 (UTC)[reply]

With some different settings:

Mirror: http://i.imgur.com/GhbQ7.png

  • EHBP1 Has a role in insulin regulation: http://www.ncbi.nlm.nih.gov/pubmed/15247266
  • The HOXD family seems to have something to do with limb development.
  • FOXP1 "expression patterns in human fetal brain are strikingly similar to those in the songbird, including localization to subcortical structures that function in sensorimotor integration and the control of skilled, coordinated movement"
  • AUTS2 is directly implicated in autism.

Slartibartfastibast (talk) 18:26, 30 June 2011 (UTC)[reply]

Figure S34: http://i.imgur.com/S4wgx.png "Selective sweep screen region of top S score. This region of chromosome 7 contains the gene AUTS2. The red line shows the log-ratio of the number of observed Neandertal derived alleles versus the number of expected Neandertal derived alleles, within a 100 kilobase window. Above the panel, in blue is the position of each human polymorphic site. Green indicates polymorphic position where the Neandertal carries derived alleles. The region identified by the selective sweep screen is shown highlighted in pink."

From page 121 of the supplemental pdf of the neanderthal draft sequence: http://www.sciencemag.org/content/suppl/2010/05/05/328.5979.710.DC1/Green_SOM.pdf Slartibartfastibast (talk) 14:38, 3 July 2011 (UTC)[reply]


  • To the fellow who added the "Wikipedia is not a place to discuss your ideas"

It's not my idea. I found this in the journal of evolutionary psychology: "The autism continuum could represent a remnant of genetic introgression that took place before humans were the lone species in our genus. Perhaps some of the genes for autism evolved not in our direct ancestral line but in a solitary subspecies which later merged genetically with our line of descent through gene flow." - http://www.epjournal.net/filestore/EP09207238.pdf Slartibartfastibast (talk) 22:02, 3 July 2011 (UTC)[reply]

Please read WP:OR and remember, this is not a forum, and finally, don't remove others' talk page comments. Dbrodbeck (talk) 22:35, 3 July 2011 (UTC)[reply]
Apologies. I was under the impression I had only removed the strange minimizing bracket that someone had placed here under the false assumption that I was discussing my own ideas. Slartibartfastibast (talk) 22:42, 3 July 2011 (UTC)[reply]
Also, WP:OR applies to articles. This is a talk page, where I have presented another scientist's opinion published in a peer-reviewed journal, as well as stuff that could be considered supporting evidence.Slartibartfastibast (talk) 22:46, 3 July 2011 (UTC)[reply]
Talkpages are for discussing improvemnts to the article, not general forums for discussion. That is why Dbrodbeck assumed you were suggesting to insert the suggestion of neanderthal admixture related to autism in mo0dern populations which is in obvious violation of WP:OR, and therefore cannot be inserted in any form untill published in reliable sources.·ʍaunus·snunɐw· 02:20, 25 August 2011 (UTC)[reply]
The paper from the JEP isn't reliable? Slartibartfastibast (talk) 16:28, 25 August 2011 (UTC)[reply]
THE JEP paper does not even mention the word neanderthal at all - so it can not be used to suggest anything about neanderthal admixture. Furthermore it is basically pure speculation, and a primary source and it would have to be mentioned by other writers in order to qualify for inclusion under WP:UNDUE.·ʍaunus·snunɐw· 17:45, 25 August 2011 (UTC)[reply]
From this Guardian article:
  • "Paul Norman, a co-author on the paper, put it like this: 'There's enormous genetic variation in people's immune systems and that can control how different people fight different diseases. This could go some way to explaining why some people are better at fighting some infections than others, but we think it also goes some way to explaining why some people are susceptible to autoimmune diseases...'"
"The vast majority of autoimmune diseases have been shown by genome-wide association studies to be associated with particular HLA alleles and we find a couple of those in Denisovans," Norman added. "So it looks to me like modern humans have acquired these alleles, but we weren't kind of prepared for them, we hadn't grown up with them, and in some circumstances, they can start to attack us as well as the viruses and other pathogens."

How many times do I have to explain to you that this has to be mentioned in a secondary source? We have no idea how this relates AT ALL to autism in the eyes of the experts. This is a rather clear case of WP:IDIDNTHEARTHAT and is becoming quite disruptive. Dbrodbeck (talk) 13:30, 28 August 2011 (UTC)[reply]

Disruptive? How so? Slartibartfastibast (talk) 15:33, 28 August 2011 (UTC)[reply]
Talk pages are for discussion of how to improve the article, not about a general discussion on the topic. Until secondary sources tie this particular theory to autism, it has no place on this talk page. I will collapse this section as inappropriate for the talk page, which can be reversed once appropriate secondary sources are found. Yobol (talk) 15:43, 28 August 2011 (UTC)[reply]

I'll keep this list updated:

Legitimate source(s) that propose hominid admixture is behind autism:

Non-legitimate source(s) that propose hominid admixture is behind autism:

Sources that mention neanderthal genes implicated in autism (via mutation or otherwise):

"There are some interesting tantalizing clues littered about; some genes implicated in autism seem to exhibit Neandertal vs. modern human differences (with the Neandertals carrying the autism-implicated variants)." Note: Razib Khan’s degrees are in biochemistry and biology.
"Mutations in CADPS2 have been implicated in autism (67), as have mutations in AUTS2 (68)."

Slartibartfastibast (talk) 17:49, 17 October 2011 (UTC)[reply]

Heritability is not the same as genetic

I take issue with this statement:

Early studies of twins estimated heritability to be over 90%, in other words, that genetics explains over 90% of whether a child will develop autism.

Heritability is based on both genetics and environment. CartoonDiablo (talk) 02:10, 4 July 2011 (UTC)[reply]

The very first sentence of heritability defines it as "the proportion of phenotypic variation in a population that is due to genetic variation between individuals", and that's how the term is normally used within science, so there's nothing wrong with that statement. brtkrbzhnv 15:13, 14 July 2011 (UTC)[reply]

New Study from UCSF/Stanford shows much less role for genetics in Autism

A new study from USCF and Stanford shows much less role for genetics in autism than previously thought. This study should be included in "Causes of Autism" and "Autism" both. Does anyone object to it? The basic conclusion of the study is environmental factors, rather than genetic, are more important on average in causing autism. The main basis for this study was fraternal twin concordance which is much higher than sibling concordance, which should not be the case if autism is mostly genetic. — Preceding unsigned comment added by 76.232.8.239 (talk) 13:28, 5 July 2011 (UTC)[reply]

Here's the study: "Genetic Heritability and Shared Environmental Factors Among Twin Pairs With Autism" Slartibartfastibast (talk) 19:16, 5 July 2011 (UTC)[reply]
It's pretty clear that environment plays a significant role: "A large proportion of the variance in liability can be explained by shared environmental factors (55%; 95% CI, 9%-81% for autism and 58%; 95% CI, 30%-80% for ASD) in addition to moderate genetic heritability (37%; 95% CI, 8%-84% for autism and 38%; 95% CI, 14%-67% for ASD)." Slartibartfastibast (talk) 19:20, 5 July 2011 (UTC)[reply]
This is being discussed over at Talk:Autism and that is an article that I figure more people watch, so let us continue the discussion there. Dbrodbeck (talk) 20:48, 5 July 2011 (UTC)[reply]

Prenatal Environment, 3RR and 'Medical Hypotheses' journal

Two IPs (perhaps the same user) have added, 3 times, a citation to an article from Medical Hypotheses. I have reverted twice, but do not want to get into 3RR territory. Anyway, I have left edit summaries noting that this journal does not meet WP:MEDRS. Thoughts? Dbrodbeck (talk) 15:12, 26 July 2011 (UTC)[reply]

Agreed. Medical Hypotheses is a horrible journal with a horrible reputation and I wouldn't call it a WP:RS, much less a WP:MEDRS. The other addition was a primary study that was being used to debunk a review, which is expressly prohibited by MEDRS and so therefore reverted. Yobol (talk) 17:30, 26 July 2011 (UTC)[reply]

Removed for discussion

The "imprinted brain" theory of autism is a related but not identical theory. It is based on the kinship theory of genomic imprinting which argues that in diploid organisms, such as humans, the maternal and paternal set of genes may have antagonistic reproductive interests. An extreme genomic imprinting in favor of paternal genes is argued to cause autism while an extreme genomic imprinting in favor of maternal genes is argued to cause schizoaffective disorders with schizotypal personality disorder being a less severe form that is analogous to Aspberger syndrome. Thus, while people with autism seem to be blind to the intentions of others, people with schizophrenia read too much into situations and see hidden intentions everywhere, causing delusions and paranoia. There are other contrasts such as single-mindedness versus ambivalence. The theory argues that since it is uncertain if a woman's other and future children have and will have the same father, as well as the father generally having lower parental investment, it may be in the father's reproductive interest for a child to maximize usage of the mother's resources while it may be in the mother's interest to limit this in order to have resources for her other and future children. Thus, a genomic imprinting with slight maternal bias would be associated with factors such as decreased suckling, decreased growth, more tractable behavior, and an empathizing and less self-centered personality causing less demands on the mother. A more extreme maternally biased imprinting would predispose to psychosis. The opposite would occur for paternally biased imprinting and autism. Empirical evidence is argued to support these patterns. Also, according to this theory there could be a mismatch and more severe problems when extreme genomic imprinting occurs in the opposite sex, which would explain why female autism (and male psychosis) is often particularly severe, which is a problem for the "extreme male brain" theory which predicts the opposite.[2][3][4]

Removed to talk for discussion. First, see WP:MEDRS; a New York Times article discussing a "novel theory" based on "two scientists work" does not meet MEDRS. Further, it's unclear which of this text is cited to what, and whether any of it is based on secondary peer reviewed sources, so discussion and clarification is needed. SandyGeorgia (Talk) 19:14, 28 August 2011 (UTC)[reply]

In addition an article in Nature as well as a review was cited. Fulfill all criteria for notability and reliable sources. Miradre (talk) 19:49, 28 August 2011 (UTC)[reply]
  • Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1038/4541054a, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1038/4541054a instead.
  • Benedict Carey, In a Novel Theory of Mental Disorders, Parents’ Genes Are in Competition, The New York Times, November 11, 2008, http://www.nytimes.com/2008/11/11/health/research/11brain.html
  • Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1111/j.1469-185X.2008.00050.x, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1111/j.1469-185X.2008.00050.x instead. Miradre (talk) 19:52, 28 August 2011 (UTC)[reply]
On the other hand, you have restored a claim based on a source that did not mention autism and thus was OR.[1] Miradre (talk) 19:55, 28 August 2011 (UTC)[reply]
I see that the material has been removed again without further discussion here. See the arguments given above. I therefore propose restoring the material. Miradre (Talk E-mail) 07:12, 18 October 2011 (UTC)[reply]
This theory has had sufficient exposure in my opinion, to warrant inclusion in this article, and a fuller treatment in its own article. Can you make it a bit shorter and a bit more accessible to the general reader for this article, Miradre? And perhaps use the above as a starting point for a stand-alone article? --Anthonyhcole (talk) 07:55, 18 October 2011 (UTC)[reply]
Good ideas! A separate article would be better since the theory is also about schizoaffective disorders and not only autism. Would also allow a less compact style which may improve readability. I also agree that a shorter, more accessible summary here would be better. Miradre (Talk E-mail) 08:36, 18 October 2011 (UTC)[reply]
According to surveys like this, [2] which is very recent, there are no definitive findings or theories at present. There seem to be only tentative or speculative primary sources that have not been assimilated by the academic community: in other words there is an absence of proper review articles. That would make writing a wikipedia article on the subject almost impossible. If one of the experts in the field like Simon Baron-Cohen has commented, that might change matters. It might be worth looking for academic reviews of Badcock's 2009 book. "The Imprinted Brain - How Genes Set the Balance Between Autism and Psychosis". I found one here,[3] but it confirms that the theory is in an early and untested stage. Here is another, [4] (from PsycCRITIQUES, Vol 55(24), 2010, doi:10.1037/a0020160) where again the ideas are described as interesting but speculative. Mathsci (talk) 09:56, 18 October 2011 (UTC)[reply]
The first is a student journal. As such not a particularly reliable source. Neither does it find the theory to be wrong. Certainly does not invalidate the many other peer-reviewed papers supporting the theory, including literature review papers. I noted one literature review paper above. Likewise, book reviews does not overrule peer-reviewed papers and peer-reviewed literature reviews. Again they do not state that the theory is disproven. No one has said that the theory is proven. But I agree with Anthonyhcole that it has gained enough attention for an article of its own. Miradre (Talk E-mail) 10:55, 18 October 2011 (UTC)[reply]
All theories of autism etiology are flaky and speculative, including this one and all Baron-Cohen's various efforts. In my opinion, there is enough coverage of this one to warrant a stand-alone article summarising it, as well as a short mention here commensurate with its relative youth and lack of stature. --Anthonyhcole (talk) 11:05, 18 October 2011 (UTC)[reply]
We need to be using independent secondary reviews to establish WP:weight. Has this been discussed by independent experts in the field of autsim as a notable theory to be discussed? If not, then we should avoid discussion of it. If so, we give it as much weight as experts in the field give it, as documented in secondary independent reviews. Yobol (talk) 16:29, 18 October 2011 (UTC)[reply]
See sources above such as articles in Nature, the NYT, and literature reviews. A Google scholar search gives more than 50 hits: [5] Certainly better sources than almost all of the theories mentioned in this article which often only cites a single dubious source. Miradre (Talk E-mail) 16:51, 18 October 2011 (UTC)[reply]

I am writing a draft for an article on the theory. It is still by no mean finished but for example the empirical evidence supporting the theory may be interesting to examine: User:Miradre/sandbox3#Supporting_evidence Miradre (Talk E-mail) 17:40, 18 October 2011 (UTC)[reply]

  1. ^ H. A. Young, D. A. Geier, M. R. Geier, Journal of the Neurological Sciences 271 (2008) 110–118
  2. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1038/4541054a, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1038/4541054a instead.
  3. ^ Benedict Carey, In a Novel Theory of Mental Disorders, Parents’ Genes Are in Competition, The New York Times, November 11, 2008, http://www.nytimes.com/2008/11/11/health/research/11brain.html
  4. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1111/j.1469-185X.2008.00050.x, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1111/j.1469-185X.2008.00050.x instead.