Revision as of 15:18, 15 April 2013 editDbrodbeck (talk | contribs)Extended confirmed users, Pending changes reviewers, Rollbackers13,171 edits →Is there any rational objection to the maternal antibody related autism theory being included?: This is going nowhere, WP:IDIDNTHEARTHAT← Previous edit | Revision as of 04:23, 16 April 2013 edit undo76.245.46.174 (talk) →Most common likely single cause of autism is maternal antibodies to fetal brainNext edit → | ||
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So, that is a review paper endorsing this theory pretty clearly, in as definite a tone as you get with the many other causes suggested. <span style="font-size: smaller;" class="autosigned">— Preceding ] comment added by ] (]) 01:19, 19 February 2013 (UTC)</span><!-- Template:Unsigned IP --> <!--Autosigned by SineBot--> | So, that is a review paper endorsing this theory pretty clearly, in as definite a tone as you get with the many other causes suggested. <span style="font-size: smaller;" class="autosigned">— Preceding ] comment added by ] (]) 01:19, 19 February 2013 (UTC)</span><!-- Template:Unsigned IP --> <!--Autosigned by SineBot--> | ||
VERY IMPORTANT UPDATE :: | |||
A presentation at the INSAR annual meeting in 2012 in Toronto indicates the four most important targets of maternal antibodies to fetal brain have been identified. I have cut and pasted a summary of the paper below: | |||
Background: Previous observations of fetal-brain reactive maternal IgG antibodies in a subset of mothers of children with autism spectrum disorder (ASD), and an association between presence of these antibodies and severe behavioral manifestations led us to undertake identification of the protein targets of these antibodies. Fetal exposure during gestation to brain-reactive maternal IgG may be the underlying cause of the behavioral symptoms noted in some ASD cases and unraveling the molecular interactions between these antibodies and their targets may open new avenues for treatment and prevention. | |||
Objectives: The focus of this project was to identify the molecular targets of ASD associated, fetal-brain reactive maternal IgG antibodies. | |||
Methods: A protein extract derived from fetal Rhesus macaque brain (152 day gestation) was fractionated by molecular weight and individual fractions were probed with diluted plasma from mothers of children with ASD. Fractions containing antigenic proteins were subjected to duplicate 2-dimensional gel electrophoresis, with one gel being transferred to nitrocellulose and probed with diluted maternal plasma to pinpoint the antigen location, and the other used for spot picking and tandem MS/MS analysis. Verification of mass spectrometric results was carried out using commercially available purified or recombinant proteins, and further confirmed using blocking studies. Reactivity to the identified protein antigens was determined in a sample of 169 mothers of children with ASD and 149 mothers of typically developing children. | |||
Results: Four proteins were identified and confirmed to be the primary antigenic targets of ASD-associated maternal IgG. The 37kDa antigen is an essential metabolic enzyme with well characterized functions in neurogenesis. The 39kDa antigen is an enzyme known to regulate post-synaptic targeting. Two proteins were identified as 73kDa antigens – one that is critical for neuronal growth cone collapse and another that functions as a chaperone for several heat-shock proteins. Confirmed reactivity to the 37kDa and both of the 73kDa proteins is observed exclusively among mothers of children with ASD with a prevalence of approximately 8%, yielding an odds ratio of 26 (95% CI: 1.5-438) | |||
Conclusions: Maternal IgG reactivity to the protein antigens identified in this study constitutes the most significant biomarker of ASD risk identified to date. In our study sample, reactivity to the 37kDa and 73kDa proteins was observed in approximately 8% of mothers of children with ASD and absent in mothers of typically developing children yielding a highly significant association with ASD (p=0.0003). Furthermore, previous findings from our group and others indicate that such maternal antibodies are often present during pregnancy, supporting the hypothesis that they could play a causal role in precipitating the behavioral outcomes noted in some cases of ASD. | |||
== Maternal trans fat consumption link? == | == Maternal trans fat consumption link? == |
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Pyrethrin
The article currently states, "It has been suggested that exposure during pregnancy to pyrethrin, a common ingredient in antiflea and antitick pet shampoos, can cause autism in the child. One retrospective study suggesting an association has been conducted, but has not been published." If there is only one study that has been conducted and it has never been published, I don't think there is sufficient evidence to include this. It seems to violate WP:MEDRS. Also, there is a discrepancy between the statement that the study finds an "association", but the previous statement uses the term "cause". Association and cause are two very different concepts which seem to be conflated here. — Preceding unsigned comment added by 148.177.1.210 (talk) 17:27, 10 August 2012 (UTC)
- Agree, and removed that section, as well as others sourced to non MEDRS. Yobol (talk) 17:32, 10 August 2012 (UTC)
As you please ...
As per your request I am here on the Talk page. I was merely expanding on a known side-effect of inclement weather resulting in increased time spent indoors in front of the "boob-toob", video games and other related electronic distractions and the resulting POSSIBLE link to SOME Autism reports in very young children? Your first objection, that the reference did not contain the actual word, Autism, was ... well, specious IMHO but in an attempt to assuage your buzz word checker, I reverted the deletion and included the Scientific American page that _is_ discussing Autism and _does_ contain the aforementioned link; ergo the connection was more clearly made. So, what seems to be the problem now? :-) JimScott (talk) 18:05, 27 August 2012 (UTC)
- Please find a MEDRS compliant source. Your original source did not include the word autism, so it was of no use here. Dbrodbeck (talk) 18:16, 27 August 2012 (UTC)
- Argh! WIA. I assume from your acronym you would prefer the the American Academy of Pediatrics (Illinois) publication on the subject? What is the next step? Do you revert the reverted revert and then change the references? Or is that process up to me? Does the inclusion of the pediatric publication allow one to include the Scientific American article link (since it actually discusses the weather and possible connections thereto)? Once one enters the jargon jungle and acronym alleys it becomes difficult to determine the appropriate way to state the simple in convoluted manner. :-) JimScott (talk) 18:58, 27 August 2012 (UTC)
- That link does not mention the word autism. As for Scientific American, please read WP:MEDRS. Dbrodbeck (talk) 19:03, 27 August 2012 (UTC)
- Wow. An article discussing Autism mentions a possible link between communications issues (a well known feature of Autism) and early exposure to electronic media. That article specifically lists a source documenting same. That same source is widely used in a published article from American Academy of Pediatrics on the exact same topic. But the buzz word filter fails so this _possible_ connection between weather patterns and a _possible_ causative for Autism can never be listed on the pages of Misplaced Pages. But the BBC article about rain causing Autism via genetics can stay. Wow. And to think our biggest arguments used to be over POV. LoL. Back to your consoles, children. Nothing to see here. 8-) (those are my eyes rolling back in my head FYI) JimScott (talk) 20:34, 27 August 2012 (UTC)
- I am sorry to disappoint you. The link you provided does not mention autism. I am just stating a fact, there is no need for the whining, and no need for calling anyone a child. Please read WP:AGF. Dbrodbeck (talk) 20:45, 27 August 2012 (UTC)
- Wow. An article discussing Autism mentions a possible link between communications issues (a well known feature of Autism) and early exposure to electronic media. That article specifically lists a source documenting same. That same source is widely used in a published article from American Academy of Pediatrics on the exact same topic. But the buzz word filter fails so this _possible_ connection between weather patterns and a _possible_ causative for Autism can never be listed on the pages of Misplaced Pages. But the BBC article about rain causing Autism via genetics can stay. Wow. And to think our biggest arguments used to be over POV. LoL. Back to your consoles, children. Nothing to see here. 8-) (those are my eyes rolling back in my head FYI) JimScott (talk) 20:34, 27 August 2012 (UTC)
- That link does not mention the word autism. As for Scientific American, please read WP:MEDRS. Dbrodbeck (talk) 19:03, 27 August 2012 (UTC)
- Argh! WIA. I assume from your acronym you would prefer the the American Academy of Pediatrics (Illinois) publication on the subject? What is the next step? Do you revert the reverted revert and then change the references? Or is that process up to me? Does the inclusion of the pediatric publication allow one to include the Scientific American article link (since it actually discusses the weather and possible connections thereto)? Once one enters the jargon jungle and acronym alleys it becomes difficult to determine the appropriate way to state the simple in convoluted manner. :-) JimScott (talk) 18:58, 27 August 2012 (UTC)
I am not sure he did that, I think you have misinterpreted his post. I would like to point out, the rules for exclusion have often been misstated by Mr. Rodbeck and others who simply seem to feel they should be different. I am not weighing in on this issue which I don't fully understand, some of the discussion seems to be missing, but a lot of content which is very informative and completely 'legal" is removed by the same cadre of people. — Preceding unsigned comment added by 107.198.86.10 (talk) 00:15, 28 August 2012 (UTC)
- "Back to your consoles children" seems pretty clear to me. Again, THERE IS NO MENTION OF AUTISM IN THE LINK HE ADDED. Oh and I have no idea who in the hell Mr. Rodbeck is. Dbrodbeck (talk) 00:48, 28 August 2012 (UTC)
I think you misinterpreted that phrase. To me, it sounds like "there's nothing to see here folks" of course said sarcastically. Not that YOU are the child, or anyone is, just that you are treating readers like children by denying them what he thinks is good information. — Preceding unsigned comment added by 107.198.86.208 (talk) 19:31, 28 August 2012 (UTC)
- Oh so it is insulting in another way then, how lovely. Dbrodbeck (talk) 19:36, 28 August 2012 (UTC)
I have redacted a section heading here which unnecessarily singles out one editor; please read Misplaced Pages talk page guidelines and avoid personalizing discussions. Also, please use WP:MEDRS compliant sources. SandyGeorgia (Talk) 03:52, 2 September 2012 (UTC)
- A significant aspect of Autism (communication issues) was discussed in a Scientific American article (MEDRS-compliant under Popular Press, paragraph 3) which included, as a supporting device, a reference to a study involving communication issues caused by excessive media exposure, published by the American Academy of Pediatrics (MEDRS-compliant under Biomedical Journals). Ergo one might be led to think that MEDRS requirements have been met. Dr. Brodbeck kept mentioning MEDRS but these two sources seem to fit MEDRS criteria. Thus we are left with the "it doesn't mention Autism" argument. The original article discusses a specific, possible trigger for a well-documented aspect of Autism: communication issues. The article then references a study that correlates a specific mechanism (excessive media exposure) and communication issues. In other words, we have a MEDRS-compliant source discussing Autism and citing the work of another MEDRS-compliant source in support of their conclusion. Why Dr. Brodbeck continues to object is not entirely clear to me. The primary source is about Autism. The connective element (excessive media exposure) is clearly identified in both sources. Is there a neutral party assignable to review and rule upon these kinds of issues, or is it just up to whichever combatant :p has the most accolades (ergo, editorial clout)? P.S. There are plenty of AGF and PDNBTN issues earlier in this discussion and I apologize for my exacerbating contributions. JimScott (talk) 19:37, 23 December 2012 (UTC)
- The article is not about autism. If you want a second opinion as to whether it can be used as a reliable source for this article on autism, you can raise that question at WP:RSN. SandyGeorgia (Talk) 21:56, 23 December 2012 (UTC)
Most common likely single cause of autism is maternal antibodies to fetal brain
Roughly 15% of the mothers of autistics have antibodies to fetal brain in patterns not found in typicallly developing children.
This information should be in the article. It's very valuable for mothers of one autistic child, as they could be tested for the antibody before beginning another pregnancy.
Pediatric Bioscience is working on developing and commercially marketing a test.
All this info shouild be in the article. — Preceding unsigned comment added by 75.61.129.155 (talk) 00:36, 22 December 2012 (UTC)
- Just in case anyone else wanted to know what "unsigned is talking about", two articles from a quick Google:
- JimScott (talk) 20:25, 23 December 2012 (UTC)
- Those are not secondary reviews that meet WP:MEDRS; one is an advocacy organization blog, and the other is news and opinion. This discussion has already been had at Talk:Autism (see here) and will no longer be entertained here unless reliable secondary reviews are provided. Further posts that do not provide a secondary review article that meets WP:MEDRS and is independent from the source, or that repeat discussion that has been held for almost four years, will be deleted per this discussion. SandyGeorgia (Talk) 21:33, 23 December 2012 (UTC)
Throw it down the memory hole if you must Sandy, but in fact Misplaced Pages rules do not prohibit primary sources. As far as sources go, this work has been published in the Proceeding of the National Acadamy of Science, so while those two links above might not meet Misplaced Pages standards, the work itself was good enough for the editors of PNAS. — Preceding unsigned comment added by 75.61.130.19 (talk) 03:05, 14 February 2013 (UTC)
I'm not very good at this but I am going to cut and paste several paper titles from listingsin Pubmed.gov where the findings where the maternal antibodies were correlated with autism. As far as I know, there are NO papers refuting these findings. Although I cna not read all papers found, if they had found to the contrary it would say so in the abstract typically.
Since primary sources ARE allowed when not contradicted by secondary sources these are all allowed. Since the article contains mention of several theories with far less evidence (one or two papers instead of around a dozen) there is no reason to keep this out.
Biol Psychiatry. 2008 Oct 1;64(7):583-8. doi: 10.1016/j.biopsych.2008.05.006. Epub 2008 Jun 20. Maternal mid-pregnancy autoantibodies to fetal brain protein: the early markers for autism study.
J Neuroimmunol. 2008 Feb;194(1-2):165-72. Epub 2008 Feb 21. Antibodies against fetal brain in sera of mothers with autistic children.
xicology. 2008 Mar;29(2):226-31. Epub 2007 Nov 6. Autism: maternally derived antibodies specific for fetal brain proteins. Braunschweig D, Ashwood P, Krakowiak P, Hertz-Picciotto I, Hansen R, Croen LA, Pessah IN, Van de Water J. Source Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, CA, USA. Brain Behav Immun. 2007 Mar;21(3):351-7. Epub 2006 Oct 6. Maternal antibrain antibodies in autism. Zimmerman AW, Connors SL, Matteson KJ, Lee LC, Singer HS, Castaneda JA, Pearce DA. Source Department of Neurology and Developmental Medicine, Kennedy Krieger Institute, 707 North Broadway, Baltimore, MD 21205, USA. Ann Neurol. 2003 Apr;53(4):533-7. Maternal neuronal antibodies associated with autism and a language disorder. Dalton P, Deacon R, Blamire A, Pike M, McKinlay I, Stein J, Styles P, Vincent A. Source Neurosciences Group, Department of Clinical Neurology, University of Oxford, Oxford, United Kingdom. J Am Acad Child Adolesc Psychiatry. 1990 Nov;29(6):873-7. Detection of maternal antibodies in infantile autism. Warren RP, Cole P, Odell JD, Pingree CB, Warren WL, White E, Yonk J, Singh VK. Source Developmental Center for Handicapped Persons, Utah State University, Logan 84322. — Preceding unsigned comment added by 75.61.130.19 (talk • contribs)
- Please see http://en.wikipedia.org/Talk:Autism/FAQ and stop spamming. Dbrodbeck (talk) 12:10, 14 February 2013 (UTC)
Professor Brodbeck: I have brought in for discussion, in an article entitled "Causes of Autisnm" which already contatins theories for causes of autism for which far less peer reviewed research can be found in support, papers which have nverr been cited before directly, or if they were are not in the current "Talk" session, and which meet the criteria for sources, as long as the caveats for primary sources are followed. How is that "spamming"? I really don't understand that. Because there are so MANY papers in support? I would like to point out, the papers are from peer reviewed journals with fiarly high impact factors by researchers at Oxford, Johns Hopkins, and UC Davis MIND Institute, and coauthored in some case by the Past President of INSAR, International Society for Autism Research which is by far the largest organization of scientists doing autism research. Certainly this theory should be included in an article which already includes many theories for which there is only one source cited. — Preceding unsigned comment added by 75.61.132.77 (talk) 18:24, 14 February 2013 (UTC)
- Please go read this, again, and stop your disruptive editing. http://en.wikipedia.org/search/?title=Misplaced Pages:Administrators%27_noticeboard/Incidents&oldid=529496007#Persistent_dynamic_IP_at_Talk:Autism Dbrodbeck (talk) 20:10, 14 February 2013 (UTC)
This article includes many theories, presented as theories, with only one primary citation. Go check the links, some are reviews, many are not. — Preceding unsigned comment added by 75.61.132.77 (talk) 04:14, 17 February 2013 (UTC) Here is the abstract of a review paper on this subject with the citation:
Dev Neurobiol. 2012 Oct;72(10):1327-34. doi: 10.1002/dneu.22052. Epub 2012 Sep 4.
Maternal and fetal antibrain antibodies in development and disease.
Fox E, Amaral D, Van de Water J.
Source
Department of Internal Medicine, University of California, Davis, Davis, California 95616, USA.
Abstract
Recent evidence has emerged indicating that the maternal immune response can have a substantial deleterious impact on prenatal development (Croen et al., : Biol Psychiatry 64:583-588). The maternal immune response is largely sequestered from the fetus. Maternal antibodies, specifically immunoglobulin G (IgG), are passed to the fetus to provide passive immunity throughout much of pregnancy. However, both protective and pathogenic autoantibodies have equal access to the fetus (Goines and Van de Water : Curr Opin Neurol 23:111-117). If the mother has an underlying autoimmune disease or has reactivity to fetal antigens, autoantibodies produced before or during pregnancy can target tissues in the developing fetus. One such tissue is the fetal brain. The blood brainbarrier (BBB) is developing during the fetal period allowing maternal antibodies to have direct access to the brain during gestation (Diamond et al. : Nat Rev Immunol; Braunschweig et al. ; Neurotoxicology 29:226-231). It has been proposed that brain injury by circulating brain-specific maternal autoantibodies might underlie multiple congenital, developmental disorders (Lee et al. : Nat Med 15:91-96). In this review, we will discuss the current state of research in the area of maternal autoantibodies and the development of autism. — Preceding unsigned comment added by 75.61.132.77 (talk) 01:10, 19 February 2013 (UTC)
One more quote from a review paper in BMC Pediatrics 2012 July 2:::
"The presence of circulating auto-antibodies against fetal brain proteins in mothers is associated with higher risk of autism and suggests disruption of the blood-brain-barrier (BBB). "
So, that is a review paper endorsing this theory pretty clearly, in as definite a tone as you get with the many other causes suggested. — Preceding unsigned comment added by 75.61.132.77 (talk) 01:19, 19 February 2013 (UTC)
VERY IMPORTANT UPDATE ::
A presentation at the INSAR annual meeting in 2012 in Toronto indicates the four most important targets of maternal antibodies to fetal brain have been identified. I have cut and pasted a summary of the paper below:
Background: Previous observations of fetal-brain reactive maternal IgG antibodies in a subset of mothers of children with autism spectrum disorder (ASD), and an association between presence of these antibodies and severe behavioral manifestations led us to undertake identification of the protein targets of these antibodies. Fetal exposure during gestation to brain-reactive maternal IgG may be the underlying cause of the behavioral symptoms noted in some ASD cases and unraveling the molecular interactions between these antibodies and their targets may open new avenues for treatment and prevention. Objectives: The focus of this project was to identify the molecular targets of ASD associated, fetal-brain reactive maternal IgG antibodies.
Methods: A protein extract derived from fetal Rhesus macaque brain (152 day gestation) was fractionated by molecular weight and individual fractions were probed with diluted plasma from mothers of children with ASD. Fractions containing antigenic proteins were subjected to duplicate 2-dimensional gel electrophoresis, with one gel being transferred to nitrocellulose and probed with diluted maternal plasma to pinpoint the antigen location, and the other used for spot picking and tandem MS/MS analysis. Verification of mass spectrometric results was carried out using commercially available purified or recombinant proteins, and further confirmed using blocking studies. Reactivity to the identified protein antigens was determined in a sample of 169 mothers of children with ASD and 149 mothers of typically developing children.
Results: Four proteins were identified and confirmed to be the primary antigenic targets of ASD-associated maternal IgG. The 37kDa antigen is an essential metabolic enzyme with well characterized functions in neurogenesis. The 39kDa antigen is an enzyme known to regulate post-synaptic targeting. Two proteins were identified as 73kDa antigens – one that is critical for neuronal growth cone collapse and another that functions as a chaperone for several heat-shock proteins. Confirmed reactivity to the 37kDa and both of the 73kDa proteins is observed exclusively among mothers of children with ASD with a prevalence of approximately 8%, yielding an odds ratio of 26 (95% CI: 1.5-438)
Conclusions: Maternal IgG reactivity to the protein antigens identified in this study constitutes the most significant biomarker of ASD risk identified to date. In our study sample, reactivity to the 37kDa and 73kDa proteins was observed in approximately 8% of mothers of children with ASD and absent in mothers of typically developing children yielding a highly significant association with ASD (p=0.0003). Furthermore, previous findings from our group and others indicate that such maternal antibodies are often present during pregnancy, supporting the hypothesis that they could play a causal role in precipitating the behavioral outcomes noted in some cases of ASD.
Maternal trans fat consumption link?
Has anyone else heard about a link between trans fats consumption and autism babies? Seems to make sense on the basis of brain cell membrane formation etc. If this is true, then the current phasing out of trans fats in most countries (interestingly not in Japan which has the highest rate of new autism diagnoses) will correct the problem with no further regulatory action.
I can't find much published evidence on this, but I'm still looking, so I'd appreciate anyone's opinions. Stepford chemist (talk) 16:12, 13 March 2013 (UTC)
Ambient noise
- "rv animal study, abstract does not mention autism"
Practically all human diseases are studied by means of a animal models, and finding an animal model is a crucial step in understanding the mechanisms behind a disease, so the successful development of an animal model places this theory on a much firmer scientific basis than many of the other theories mentioned on this page. The paper's abstract indeed does not mention autism directly, however the motivation of this research is to develop a neurological understanding of the causes of autism. Merzenich himself is one of the world's leading reseachers on autism and brain plasticity. I'd appreciate any suggestions on how I can rewrite this section to provide greater clarity.
Prime Entelechy (talk) 06:45, 16 March 2013 (UTC)
- Please see WP:MEDRS. Dbrodbeck (talk) 12:22, 16 March 2013 (UTC)
- The word 'autism' is nowhere in the article cited. Please bring the passage from the book here so we can discuss it. The article though is out, as I said, it has no mention of the word autism, and, is not about humans. Dbrodbeck (talk) 15:29, 16 March 2013 (UTC)
Is there any rational objection to the maternal antibody related autism theory being included?
Collapse per SOAP, NPA, and AGF violations |
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The following discussion has been closed. Please do not modify it. |
Within this section I've included the links to a few papers on certain maternal antibodies to fetal brain proteins being very highly linked to autism. Between 10 and 20 % of mothers of autistic children have the antibodies, they are practically unknown among mothers of typically developing controls. The p values for this are very high according to the published papers. The objection to this was the papers are primary sources not secondary sources. As I've pointed out again and again, primary sources are not allowed. I've also pointed out a leader in the research is a very respected scientist who was President of INSAR and it's been confirmed by more than two respected institutions, Kennedy Krieger in Baltimore and UCDavis MIND Institute in California, have lead the way I think it's fair to say but researchers at Imperial College and I think Washington U have also backed it up. There is nothing in any of these primary papers which refutes any secondary source as far as I know. None of the requested edit violates any Misplaced Pages rule, but if the edit is made it gets reverted. It seems like a power trip some editors are on. They either think the rules should be different, and are enforcing them as they wanted them to be, or just don't want anyone else to get to say anything. Can I please put the edits in so people with one autistic child will understand the high risk their next kid will be autistic if the mother has the antibodies? Or if no one cares about that, just let the edits be made because they are allowed? — Preceding unsigned comment added by 76.252.220.215 (talk) 15:09, 9 April 2013 (UTC)
Can you please answer the question? Again, the question is, is there any reason to not include the maternal antibody theory of autism? Let's break this down: 1. Does this info somehow not qualify under Misplaced Pages rules? Answer: No, it's allowed, primary sources are allowed but not all the papers are primary, some are reviews. 2. Is a primary source being used to rebut a secondary source? No, there is no secondary source disputing these findings. 3. Is the edit of some substantial value to the article? Yes. This requires some knowledge of the subject matter. If you look at genetic causes for example, the most common proven genetic causes of autism only account for about 2% of all cases (FMRP for example). This cause is suspected of accounting for over 10% of all cases. Please, if you are acting in good faith, give me a real objection to this. The links for it are already contained in the other post. Can you give any real valid reason for not including it? Did you SEE the rest of this article and some of the theories mentioned which have basically no body of literature in support? — Preceding unsigned comment added by 75.61.141.96 (talk) 20:04, 9 April 2013 (UTC)
But I've got new references. The objection was lack of secondary sources, which for the umpteenth time, are NOT forbidden, but I've included links to secondary sources now. You don't really care about the rules, do you? It's all about control. — Preceding unsigned comment added by 76.245.46.174 (talk) 12:37, 11 April 2013 (UTC)
No need to curse at me. It just seems to me there are many parts of this article you should remove if you are primarily concerned with following the rules you have made for yourself, which are not Misplaced Pages rules in any case. The quote you gave from Fox et al is not saying the theory is in doubt, just that t you can't experiment on humans to prove it. — Preceding unsigned comment added by 76.245.46.174 (talk) 05:01, 13 April 2013 (UTC)
I DID assume good faith, but you and several other editors proved that assumption was not warranted. Let's see if you are capable of good faith right now --- are primary sources allowed in a medical article? If you say no, then support that. If you say yes, then why are you telling people in other Talk sections to not use primary, and implying those are the rules? — Preceding unsigned comment added by 76.245.46.174 (talk) 13:56, 15 April 2013 (UTC) |
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