Talk:Coeliac disease/Archive 4

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Do we need nasty images without warnings?

Would it be possible to show a simple drawn diagram, instead of an actual photograph of something that nasty? Or have a warning where people have to click on something before showing it. is the image I'm referring to. I personally would like to read the article, without having that image on the side grossing me out. Dream Focus (talk) 10:57, 8 October 2008 (UTC)

I asked my friend, who specializes in cuteness, to draw a more suitable picture of a colonoscopy for you. Image:Happycolon.png How does that rub you?--Perceive (talk) 03:39, 31 December 2010 (UTC)
I'm sorry, but... no and no. Please see Wikipedia:Options to not see an image for some options you can implement over at your end :) Fvasconcellos (t·c) 11:32, 8 October 2008 (UTC)
Sorry, Dream Focus, I don't really see what's nasty about a duodenum. If no caption had been provided, I'm sure you could have easily mistaken it for a tunnel in an underground network on another planet. JFW | T@lk 21:07, 9 October 2008 (UTC)
Well we need a better picture, the image shown is not classic. I will work on it -- Samir 04:51, 14 June 2009 (UTC)
1) This is mild (heck, compared to the really bad stuff we have, I think it doesn't even reach "mild level"). 2) Wikipedia:Perennial proposals#Censor_offensive_images also specifically discuss this. Circeus (talk) 15:29, 14 June 2009 (UTC)

Indo-europeans not are a biologic group

indo-europeans are a linguistic group with very races converted to the aryan culture(for example: indians and iberics) —Preceding unsigned comment added by (talk) 04:34, 27 December 2008 (UTC)

Please make comments on the talk page rather than inserting them in the lead (which I've removed). However, I would be interested to know which source uses the term "indo-european" for the 1% figure, and whether there is a better classification. Also, the term is not repeated in the Epidemiology section, and the lead should be a summary of the body. Colin°Talk 10:24, 27 December 2008 (UTC)
I know i am going to be two technical with this, but here goes. The gene(s) primarily responsible for celiac disease is DQ2.5, DQA1*0501:DQB1*0201 haplotype. There have been some recent discoveries concerning this type, however I will give the background, first. This haplotype is found in three nodes in Europe. 1. Irish, 2. Sardinians 3. Basque (1 and 3 and 2 and 3 have some haplotype similarities). With more detailed haplotype information is appears that the Basque and Irish ("AH8.1" extended haplotype) have descent from common ancestor in the Pleistocene epoch. The Sardinian node, while in Europe, may have been the result a more recent migration from Africa.
Irish DQ2.5 - A1-Cw7-B8-DR3-DQ2.5 ("AH 8.1" all DQ2.5 is found with DR3 and all DR3 is found with DQ2.5) closest "living ancestral population" Basque - Indoeuropean-No
Sardinian DQ2.5 - A30-Cw5-B18-DR3-DQ2.5 closest "living ancestral population" North Africa - Afroasiatic.
(Several papers have now been written on the natural history/evolution of AH8.1)
AH8.1 spread in Europe during the epipaleolithic period from NW spain or SW France (Iberian refuge) in a quadrant that extended to what is now the Ilses, Scandinavia, Switzerland. It re-spread prior to and during the Migration Age into Eastern Europe (Goths), Russia(Norse), Yugoslavia(Slavs), Northern Italy(Germanics). In the Industrial age it spread into North America(anglo), Latin America(Basque), Australia(Anglo), South Africa(Anglo and Futch). 57% of people in these regions that have A1-Cw7, B8, or DR3-DQ2.5 also have the entire haplotype HLA A1-B8-DR3-DQ2 haplotype. It is said to be in selective linkage disequilibrium and spread from a recent common european ancestor. That ancestor did not likely speak European language (20 to 30 kya). Previously AH8.1 was believed to have been carried by Anglos into India, however, a recent study of Indian AH8.1 shows that only the DR3-DQ2.5 haplotype are linked to Irish AH8.1. The genes in the class III region (between HLA-B and HLA-DR) are all dissimilar, indicating that AH8.1-india is a fortuitous recombination, likely of Dravidian ancestral origin. I personally have spent an alot of time trying to determine precise origin of AH8.1 and basically the trail goes 'dry' in Northern Spain. West Africa has both A1-B8 haplotype and DR3-DQ2.5 but no evidence that AH8.1 formed in West Africa. Morocco has B8-DR3-DQ2.5 but the A1 bearing haplotype is not obviously present. I suspect that the components in Iberia come from West Africa, more than likely we are talking about a Berber origin and language placement is an issue. (Most berbers now speak a hamito-semetic language). A recent paper on these two variants suggest a common ancestor 80,000 years ago.
Finally there is an Asiatic version of DR3-DQ2.5. It is frequently found with a minority of DRB1*0302 (likely of African origin). The haplotype in which it is found more commonly is A33-B58 haplotype. There is no cohesive publication on this material. It is found in West Africa, Sudan, Western Pakistan, Central Asia, China, Thailand. Trace amounts of DQ2.5 are found in Korea, none in Japan. Given the Yayoi migration (2nd Mil BC to 4th century AD) and generally close alignment of Korean and Japanese HLA, I infer that almost all of the DQ2.5 in Korea came from the Asian interior after Yayoi migration, probably with the Mongol invasion of the previous millenium. This appears to be how much of DQ2.5 spread in the east, it is almost always found in cultures with a rich Chinese ancestry. Asian DQ2.5 peaks in Kazakhstan - However the most probable origin in Asia is from the Balochi peoples in SW Pakistan and these people probably arrived at this from W. Africa from a concurrent Sub-saharan/sahul language. This haplotype likely arrived in the holocene and may explain how African cereals spread through Asia.
Contribution of Indoeuropean language to early spread of DQ2.5 -none. Haplotypes common in Anatolia and proximal Europe are at highest frequencies in Europe (Paris basin, Belgium, parts of germany) where Ancestral European haplotypes are at there lowest frequencies. HOWEVER, with Indoeuropean language came advanced wheat cultivation, and this is the major risk factor for celiac disease. Because it is now clear that neolithization was largely non-genetic, it largely failed to displace genes adapted to the mesolithic lifestyle. In Europe, beyond where early neolithization stopped its advance north, or into highlands, the frequency of DQ2.5 is highest. This indicates the role of environment for wheat cultivation, genetics of migration and/or selection. The last peoples to enter the neolithic phase were the Irish, they have they highest level of AH8.1, so that we cannot 'unlink' IE from celiacs either. West Africa has very high DQ2.5 levels and yet CD is low in most areas in which African cereals are exclusively grown. So that the Indoeuropean language spread over a backdrop of preexisting DQ2.5 frequencies in Europe, Sardinia, India, parts of Pakistan and Central Asia but is more associated with the agricultural process of Westeurasian Neolithization.
Statistical concerns.
Risk and associated Risk.
DQ2.5/x risk is 65/100
DQ2.5/DQ2.5 homozygote ~12/100
DQ2.5/DQ2.2 homozygote ~17/100 cases
As frequency increases for DQ2.5 or DQ2.2
  • disease frequency will increase more rapidly
  • the proportion of DQ2 homozygotes in disease will increase.
  • threshold levels of wheat consumption and age of onset will lower.
Here is an example. DQ2.5 spread into northern Mexico with the basque, the combination DQ2.5/DQ8 heterozygotes (highest risk factor for type 1 diabetes) is second highest in Jalisco, Mexico. And yet type 1 diabetes is typically only found in peoples who identify themselves with European culture and virtually absent in people who identify more with mestizo or other native american peoples. In fact, within the indigenous populations of Mexico, where DQ8 (highest single gene risk factor for T1D) can run as high as 95% in gene frequency, inflammatory abnormalities of the immune system are very low. In the Andes of South America, when celiac disease is identified it is more commonly found with DQ8 and almost always found in people transitioning toward a more western lifestyle. Celiac disease is mediated by HLA-DQ variants, however, as these instances show it really is a disease of culture (affluence) that has resulted from peoples in transition from indigenous lifestyles into more Westeurasian cultural patterns in the last 2000 years this frequently was accompanied by a shift to an IE language. Indoeuropean speakers brought about the largest spread of western culture, including wheat, into indigeonous populations. Wheat culture has reached, however, beyond this group into cultures of Asia, and with this disconcerted spread comes the spread of celiac disease (e.g. Japan - DQ8, No DQ2.5). PB666 yap 15:07, 31 December 2008 (UTC)

The funny thing is that the Basque and the Irish speak, or spoke originally, bastards of Celtic. I am too lazy to look up whether these technically fall under IE languages but I do assure you that their structure is completely different and weird. Look at Basque or Gaelic, the helloworld sentences suffice, they are about as far away from the Western IE languages as Finnish is. -- (talk) 17:58, 11 September 2009 (UTC)
Basque isn't usually considered a 'Celtic' language. In fact, it appears to be a 'language isolate', with no obvious relationship to any other language or group of languages, including Celtic. Celtic languages do fall under IE languages. And 'weird' is a rather subjective judgement. Irish certainly has a lot of commonalities with other IE languages. Have a look at the numbers, they're a better indicator than greetings. ANB (talk) 11:03, 12 April 2011 (UTC)

What does this line mean in the opener?

1/3rd of the below sentence doesn't seem to convey meaning very well (the quoted part).

Symptoms include chronic diarrhoea, failure to thrive (in children), and fatigue, but these may be absent "...and symptoms in all other organ systems have been described."

Maybe it's a common phrasing I'm just unfamiliar with?Xetxo (talk) 01:06, 7 February 2009 (UTC)

Maybe the quoted part should be changed to "symptoms in all other organ systems have been reported." —Preceding unsigned comment added by (talk) 23:51, 16 April 2009 (UTC)

The point is that it's possible to have coeliac disease affecting only the skin, nervous system etc. JFW | T@lk 17:58, 17 April 2009 (UTC)

Van Weel is back - recent advances in the genetics of coeliac disease. May end up being useful. JFW | T@lk 01:31, 14 April 2009 (UTC)

There is a new Lancet review, doi:10.1016/S0140-6736(09)60254-3. Work to do, I reckon. Perhaps time we get rid of the BSG references and update them with this article, given its advantages. JFW | T@lk 23:46, 25 April 2009 (UTC)
Thanks Jeff I will look at both as soon as I have a chance.PB666 yap 23:54, 21 June 2009 (UTC)
With regard to Van Heel, I am not going to comment about his review per say, but the discussion of the major 'other' gene 4q27. Its actually associated with 6 diseases all of which show an increased prevelance in coeliac disease patients, and frequently a clinical prelude to CeD diagnosis. These diseases are
  • type 1 diabetes -Linked to DR4-DQ8 and DR3-DQ2.5
  • rheumatoid arthritis - Linked to DR4 and DR1
  • juvenile idiopathic arthritis
  • ulcerative colitis
  • graves disease
  • SLE
  • psoarasis
  • psoarasis arthritis
The problem arises in how are the tested individuals drawn into the study, if they are not drawn in randomly (for example random biopsy or random DQ/ATA screening) then all they are doing is picking up common autoimmune disease risk factor, possible increased in CeD, but also possibly drawn in because of the diagnosis process. Or to rephase, what percent of diagnoses celiacs have one or more of the above 6 diseases before showing up in the clinic?
There is a reference to DQ2.5cis, DQ2.5 and the semi-homozygote DQ2.5cis/DQB1*02 (As I said, this oblique terminology was starting to get around) on page 474.
The question we have to ask ourselves here since we have posted information on genetic associations and that information later needed to removed, do we want to add updated information on genetics now, that later will have to be removed when new studies reveal the inadequacies of the past approached. I quote from Van Heel because I think we align on this issue

MISSING HERITABILITY:SOMEWHAT PUZZLING... We estimate that the current coeliac disease risk SNPs account for only 3-4% of disease genetic heritability, with HLA accounting for a further 30%. So where is the rest [>75%] of the heritability of coeliac disease, known from twin and family studies? First we suggest many other associations are still to be found. Odds ratios (ORs) for the newly associated variants, are in the range of 0.7-1.4.

::and most of those are between .85 and 1.15 such that if we accumulated all the risk we still could not explain more than 30% of disease, at best. My opinion which does not account for much here, is that Coeliac disease outside of HLA is quasi-inherited and that there is a fascinating blend of environmental and genetic predispositions, possibly epi-genetic contributions. For example, in NW Europe almost no disease is associated with DQ2.2 and in Italy a surprising proportion is associated with DQ2.2, why should there be such a geographic distinction? There is a basic problem in these studies, early studies showed one locus was associated in place A and in place B not associated. That lead many to believe that the locus associated in place A was just a random association, what if they are not, what if place specific associations are the modus operandus for celiac disease genetics, and by doing genome-wide studies in wide samplings of the population we are simply diluting all the various regional associations and thus picking up diagnosis bias making the these regional susceptibility factors even harder to find. Two of the last two projects of this same kind I have worked on, when one narrowed the clinical subset (parsed according to strict clinical presentation), what appearred to be normal suddenly became significantly different. What Van Heel is saying is that 'we' have to do much better with the genetics.PB666 yap 01:29, 22 June 2009 (UTC) BTW I could not download the Lancet article.

Here are two recent papers discussion both issues:

  • Tissue Antigens. 2009 Mar;73(3):225-35. Variants within protectin (CD59) and CD44 genes linked to an inherited haplotype in a family with coeliac disease.
  • Celiac Disease Revealed in 3% of Swedish 12-year-olds Born During an Epidemic. J Pediatr Gastroenterol Nutr. 2009 May 25.
  • BMC Microbiol. 2008 Dec 22;8:232.Imbalances in faecal and duodenal Bifidobacterium species composition in active and non-active coeliac disease.

There is a paper out also on the Genetic Structure of Europeans: A view from the North-East:

Compounding by population stratification [because few regional cohorts of disease exceed 10,000 in number] heterogeneity between studies samples can give false positive results in association studies, as the association with the trait may be the result of the systematic ancestry difference in allele frequencies between groups.

The paper goes onto detail the 3 pole 2 component plots of Europeans. Notably in this image the Irish/Anglo pole in missing.PB666 yap 03:28, 22 June 2009 (UTC)

Reliable sources

A user added this source, and it was added back in by another user after reversion: Spersud, Erik and Jennifer (January 3, 2008). Everything You Want To Know About Recipes And Restaurants And Much More. USA: Authorhouse. p. 144. doi:10.1007/b62130. ISBN 9781434360342.. The book is self-published; Authorhouse is a self-publishing company. This book does not meet WP:MEDRS, so it cannot be used as a source for the statement: "Other cereals, such as maize (corn), quinoa, millet, sorghum, chia seed, and rice, are safe for patients to consume". Fences and windows (talk) 15:14, 17 April 2009 (UTC)

There must be better sources for that claim. JFW | T@lk 17:58, 17 April 2009 (UTC)

NICE guideline

The NICE guideline is out. It focuses mainly on diagnosis and not so much on follow-up, JFW | T@lk 20:58, 1 June 2009 (UTC)

Section Order

I notice that a recent edit has moved Screening down to its proper place, as per WP:MEDMOS#Sections, which is great. While even MEDMOS identifies it as a minor concern, I'm wondering if we should change the rest of the sections to match that standard as well (they're close, but a couple are switched around) least in my mind, consistency is a good thing. Does anybody else have any opinions?

Also, as part of this, consider whether Screening should be bumped back up (and how far back up), following the guideline in MEDMOS that suggests leaving more-technical sections till lower.

I have no particular opinion on this, so in the absence of any other feedback, I'll switch the ordering to MEDMOS standard in a couple of days. But if there's consensus to use a different order, I'll happily switch it to that. --Rob (talk) 21:26, 13 June 2009 (UTC)

I'm cool either way -- Samir 04:51, 14 June 2009 (UTC)

Endo pic

Need a better one! -- Samir 04:51, 14 June 2009 (UTC)

Antioxidant study

I've reverted the addition of a claim that an in vitro study of macrophages "suggests that the natural antioxidants lycopene, quercetin and tyrosol may help to control the inflammation of coeliac disease." For starters, it doesn't belong in a section on "treatment". Nor does it belong in the "experimental treatments" since it isn't an experimental treatment (in humans). If the article has a section on basic research then this sort of thing might belong, but per WP:MEDRS, we should citing reliable literature reviews to get a balanced picture of the current state of research in this field. All basic-life-science articles (with positive results) conclude that their study on X "suggests" something "may help". This is standard boasting of researchers drumming up funds for future research in the field. It has no significance beyond the intended readership (other researchers). It certainly isn't significant enough to warrant space in a general encyclopaedia. Colin°Talk 09:11, 19 July 2009 (UTC)

This was the reason I originally removed this study. WP:MEDRS is very clear about including primary studies, especially when they are lightyears removed from being replicated in man. I can already hear the complaint: "But these are natural treatments and therefore no drug company cash will be available to conduct these expensive studies in people..." JFW | T@lk 10:10, 19 July 2009 (UTC)
Agree, and the other problem here is that getting something in a natural dose may have positive or neutral benefits but taking a supplement may have a negative benefit. Two of the compounds are aromatics, and certain aromatic compounds have been identified as sensitizing agents in some people for allergic disorders. WP should not be in a position of making medical recommendations (implied or otherwise).PB666 yap 15:38, 31 July 2009 (UTC)

you are putting up straw men, making arguments that have nothing to do with what I wrote, or with why I wrote it. this is a peer-reviewed paper, Scopus shows 11 other peer-reviewed papers that cite it. does it occur to you that the authors may have a deeper understanding of coeliac disease than you do? macrophage activation is at the core of the pathogenesis of coeliac disease, in vitro research has always been essential to learning about this disease and to understanding what is observed in vivo. —Preceding unsigned comment added by (talk) 16:31, 21 July 2009 (UTC)

Please don't make personal attacks. They distract from the subject under discussion. JFW | T@lk 21:58, 21 July 2009 (UTC)

Coeliacs/Celiacs vs Coeliac Disease

Can someone please fix this article by not calling people who suffer from coeliac disease coeliacs (or celiacs for the Americans). It is incorrect to call someone a coeliac. They have coeliac disease, it does not define their person and it is, IMHO, quite offensive and gramatically incorrect to call someone a coeliac. We don't call people with Chron's disease Chronies... Well at least not to their face or in an encyclopedia. —Preceding unsigned comment added by (talk) 15:59, 14 August 2009 (UTC)

I'd be happy to go through the article and make the required changes, provided that we have consensus to do so. I'm just thinking, though, that this may not be an open-and-shut case - after all, we regularly refer to people with several other conditions or attributes by one-word terms: diabetics, paraplegics, disabled (more often "the disabled" or "disabled people, I'll grant), brunettes, lesbians, etc. Oh and contrary to your assertion about Crohnies, around here we do call at least one person a Crohnie: this one. ;) --RobinHood70 (talk) 20:38, 14 August 2009 (UTC)
See WP:MEDMOS and People-first language. Generally, I support people-first terminology. Just because people regularly do something doesn't make it right. However, some medical conditions seem to carry no or little stigma or implications that one is disabled as a person. Both diabetes and coeliac disease could be in that category, and I note that regularly uses the term "coeliacs" and uses the term "celiacs". However, NICE is careful to only use "people with coeliac disease" in their guidelines. I find the over-use of the word "patients" in this article to be more problematic: this is not a medical textbook (the word is fine when discussing people actively interacting with healthcare professionals, such as during diagnosis or treatment). Colin°Talk 22:38, 14 August 2009 (UTC)


Not to annoy anyone, but it should be noted that by the numbers, more people will recognize Celiac versus Coeliac (mostly beacuse there are more people who use Wikipedia who speak American English than British English.) Of course there is the redirect, but if Coleiac is seen on another page, it may not be recognized, thus causing signifigant confusion. Now, I don't have a problem with the usage of British English on pages pertaining to the UK and commonwealth nations, but on an international page, the most used spelling would be appropriate. —Preceding unsigned comment added by (talk) 23:32, 26 August 2009 (UTC)

See WP:ENGVAR. JFW | T@lk 21:49, 16 September 2009 (UTC)
Also have a look at the discussion mentioned at the top of this page. Here's a copy of the link to save you time. —RobinHood70 (talkcontribs) 23:59, 16 September 2009 (UTC)

Should be Celiac - recognized as such around the world, including jolly England. And should be changed. I've never seen this screwed-up spelling before Ever. Confusing for someone new doing research. —Preceding unsigned comment added by (talk) 20:17, 26 July 2010 (UTC)

Please moderate your language. There are plenty of redirects that make the content easy to find, and in England the spelling is coeliac. In fact, if you Google "celiac disease", this article comes up second despite the commonwealth spelling. JFW | T@lk 08:16, 27 July 2010 (UTC)
I'll second that. I've read several European articles that use the spelling "Coeliac". There is no pressing reason to change the spelling to Celiac other than to cater to us North Americans. :) —RobinHood70 (talkcontribs) 15:53, 30 July 2010 (UTC)

False positive serology

False Positive Serology results? Is it possible to receive a false positive blood test result? Forgive me for bad formatting or for placing this in the wrong section. I am new at this, but would suggest information about false positive blood test results be placed in the main article. Thank youTunalucy (talk) 19:15, 2 September 2009 (UTC)

This is not discussed in the sources, so probably not that much of a problem. Serology is pretty specific. JFW | T@lk 19:56, 2 September 2009 (UTC)

Re: False positive serology

It would seem that the following information would be helpful to get accurate (rather than false positive) results, but when I added it to the article it was removed on the grounds that by posting the portion I linked to the original place I found the information was 'incorrect' formatting. That I should put it 'in my own words' then have a link with the vital information below. I honestly do not feel that something this exact should be 'put in my own words'. I do not break any copyright law as I am quoting directly with a link to it's source at the bottom. Following is the information I attempted to add, exactly as I added it. Please suggest changes more specifically (if that is possible) that can be made to my contribution that would not step on copyright law and still be scientifically as well as clinically correct:

Blood tests

Blood Tests for Celiac Disease

There are a total of 6 tests that can be run for Celiac disease. (1) Anti-Gliadin (AGA) IgA (2) Anti-Gliadin (AGA) IgG (3) Anti-Tissue Transglutamise (tTg) IgA (4) Total Serum IgA

(5) Anti-Tissue Transglutamise (tTg) IgG (6) Endomesial Antiobody (EMA) IgA

Note that AGA is simply the abbreviation for Anti-Gliadin antibody, tTg is for Tissue transglutimase and EMA for Endomeisial antibody. Sometimes you see the letters instead, because writing and saying the words is a pain. The tests with IgA test for the IgA antibody in the system. The IgG tests test for IgG antibodies in the system. The most indicative tests of Celiac are the tTg-IgA (number 3 above) and the EMA (number 6 above).

What is often referred to as the “Celiac Disease Panel” consists of the first 4 tests above. These are the “standard” tests that should always be run to test for Celiac disease. Number 4 - Total Serum IgA is critical to include. This will tell you if the body is able to produce IgA antibodies. Some people (10% of the population) can’t produce the IgA antibodies and are considered IgA deficient. If you cannot produce IgA antibodies, the IgA tests above (number 1, 3, and 6) will never come back positive for Celiac disease, even if you have Celiac disease. Therefore, you have to have the IgG numbers. They usually only run #5 if Total Serum IgA indicates a deficiency and/or if the AGA IgG (number 2 above) is the only one that is abnormally high.

The EMA (number 6) is very sensitive for CD. However, it is a test that is more difficult to read – meaning that you have to have an experienced lab tech reading the results or there could be an error. The tTg-IgA test is more “idiot proof” in the lab and cheaper to do, so it has become more of the standard instead of the EMA. You can have both done, but it isn’t necessary.

Special note for young children: The total IgA is not really considered accurate until the age of 4 or so (at least that is what I have read), so when those results come back, a diagnosis of IgA deficiency would not be made if the child was under the age of 4.


Nobodyz (talk) 12:54, 20 October 2009 (UTC)

Latent coeliac

A mortality study from Sweden that will need to be mentioned: JFW | T@lk 21:48, 16 September 2009 (UTC)

Am I reading this right

The absolute mortality rate was 10.4 (95% CI, 10.0-10.8) per 1000 person-years in celiac disease, 25.9 (95% CI, 25.0-26.8) in inflammation, and 6.7 (95% CI, 5.7-7.6) in latent celiac disease. Excess mortality was 2.9 per 1000 person-years in celiac disease, 10.8 in inflammation, and 1.7 in latent celiac disease. This risk increase was also seen in children. Excluding the first year of follow-up, HRs decreased somewhat.


10.4 per 1000 person years is not that bad, 6.7 sounds like a really low mortality risk, what is the risk in person-years for the normal population.PB666 yap 21:39, 20 October 2009 (UTC)
Great question! Where's the control group?
"Excess mortality" is a non-scientific (non-neutral) phrase that tends to overstate risk of dying. Think of it this way: Your odds of winning the lottery triple if you buy three different lottery tickets. Sounds like a great idea when that's all you consider, except we all know that three lottery tickets still only give us a one-in-a-gajillion chance of winning. Not so great.
This type of reporting contains that fundamental flaw, an over-emphasis on the differences between groups when in the big picture they are hardly distinguishable. Research articles written by MDs in medical journals tend to use that sort of language when a more neutral (and scientifically appropriate) way of reporting the data would be in the form of a risk ratio (sometimes odds ratio) over a given period (say ten years), separated by age group, which in this case would be a relatively low number. (No one lives 1,000 years.) Average age at death would also be a more neutral endpoint to report. "Excess mortality" (or excess anything) is sometimes used as a way of rearranging the data to achieve statistical significance when it wasn't originally achieved by more widely accepted methods, or (probably more often) as a way of overstating the problem when the relative contribution of the variable being studied is low. It also ignores the possible unforeseen protective effect some conditions can have against other diseases (i.e., sickle cells can prevent malaria, obese people have a lower risk of lung cancer, etc.). "Excess" implies a fundamental assumption that the norm is understood, though it rarely is.
This statistical manipulation is often the result of people reporting scientific research who have not been properly trained. Medical schools in the US do not train physicians to design experiments, perform research, report their findings, or evaluate scientific evidence, though physicians often do research anyway, and it's common practice for many of them to employ statisticians to go over their data in multiple ways until they find something statistically significant (which scientists call post hoc analysis without correction, a scientific no-no) while completely ignoring whether the finding was clinically significant. Some US physicians receive research training after medical school, so I'm not saying MDs as a whole don't know what they're doing. (I've worked with exceptionally gifted MD researchers.) What I'm saying is that the data above was reported in a dubious manner, and it's difficult for non-scientists to recognize that. The physician peer-reviewers of this medical journal didn't recognize it. This is an excellent example of why it's not a good idea to use primary research as source material in Wikipedia. Professional journalists don't know how to interpret this stuff. How could WP readers be expected to understand these issues?
For the record, I have not read the above article, so I can't comment specifically on what that team of researchers did, only that their choice of statistical reporting raises alarm bells. Also, the team reporting the research is apparently Swedish, not American, though for some reason they published their work in an American medical journal, specifically one with a bad reputation for its reporting of original research and poor quality peer review. JAMA does many things well, but reporting research isn't one of them. Dcs002 (talk) 09:05, 26 August 2011 (UTC)

CD and DH severity by autoantibody levels

Dahlbom I, Korponay-Szabó IR, Kovács JB, Szalai Z, Mäki M, Hansson T (2009). "Prediction of Clinical and Mucosal Severity of Coeliac Disease and Dermatitis Herpetiformis by Quantification of IgA/IgG Serum Antibodies to Tissue Transglutaminase". J. Pediatr. Gastroenterol. Nutr. ([Epub ahead of print]). doi:10.1097/MPG.0b013e3181a81384. PMID 19841593. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)PB666 yap 13:41, 24 October 2009 (UTC)

CD in MG

Freeman HJ, Gillett HR, Gillett PM, Oger J (2009). "Adult celiac disease with acetylcholine receptor antibody positive myasthenia gravis". World J. Gastroenterol. 15 (38): 4741–4. PMC 2761549. PMID 19824105. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

I did an unpublished study of patients with MG and anti-gliadin antibodies, I looked strictly at patients with DQ2.5 or DQ8 haplotypes and found 2 of 20 with high levels, which indicates that >1 in 25 had elevated levels of anti-gliadin (aplha/beta/gamma). I am going to add this citation to the secondary conditions page, by MEDRES its too premature for this page.PB666 yap 13:57, 24 October 2009 (UTC)

Ciclitira's guideline

Colin correctly pointed out that the British Society of Gastroenterology has removed links to its "interim guideline" from its website (link). I totally agree that 7 years is very long for an "interim" guideline, and I must admit that for a medical featured article it has many drawbacks as a WP:MEDRS.

PMID 19394538 in the review by Di Sabatino and Corazza in the Lancet this year. It seems pretty good and certainly separates chaff from corn (no pun at all intended) with regards to some of the data about CD. Does everyone agree that this source should be used as much as possible to replace the "interim guideline" as much as possible. JFW | T@lk 11:50, 29 November 2009 (UTC)

This is the UK paediatric guideline. JFW | T@lk 11:51, 29 November 2009 (UTC)
PMID 18431060 is the first reference of Lancet2009, a historical review of coeliac disease. I will need to find the fulltext, but I reckon it can replace the website that we are currently using for much of the historical context. JFW | T@lk 14:39, 29 November 2009 (UTC)

Great, having removed Ciclitira's guideline I have now found a number of other documents that we definitely need to refer to, such as the NASPGHAN guideline (USA) and the NICE CG86 (UK, diagnosis only). The AGA review is still fairly topical, and of course much of what needs to be cited can still be traced to VanHeelWest and Lancet. The following two claims currently are uncited, and I will need to look for replacements:

  • Need for osteoporosis investigations - which patients?
  • Bloods to be monitored at follow-up. Not only to monitor for malabsorption, but also are patients having micronutrient deficiencies due to a restrictive diet? JFW | T@lk 12:40, 13 December 2009 (UTC)


In regards to the recent addition, I'm noticing that the wording of the study implies that only those who were gluten-consuming were studied, since they mention those with Marsh stages 1-3 and for Marsh stage 0, they refer to it as "latent Celiac Disease" and mention a positive serology (which I believe becomes negative when you're gluten-free). If someone can confirm my understanding of it, I think we should change the wording to "active coeliac disease" or something to that effect...I'm not sure what the best way of saying that is. —RobinHood70 (talkcontribs) 07:39, 1 December 2009 (UTC)

I have temporarily removed the addition. It was in the wrong section (should be in "prognosis" beause death is not a symptom) and needs some qualifiers without sounding alarmist. JFW | T@lk 00:20, 8 December 2009 (UTC)

Update tracker

Right then, I've finally managed to bring myself to update this article. There's a fair amount of crud that has accumulated since the FA drive in 2007, much of which is WP:MEDRS-incompatible material. As stated above, there are a number of excellent sources available (and more in the bag if needed), and hence no excuse to source stuff to small papers in borderline impact factor journals.

  1. Signs and symptoms   Done
  2. Diagnosis   Done
  3. Pathophysiology
  4. Screening   Done
    Major update with Lancet and NICE now possible
  5. Treatment
  6. Epidemiology
  7. Social and religious issues
    Could do with some tightening and scrubbing
  8. History   Done
  9. References
  10. External links
    Could be reduced in size and ported to DMOZ

Anyone willing to help along is more than welcome. JFW | T@lk 20:41, 13 December 2009 (UTC)

This material seems dated. Under the heading DIET, it reads, " GF products are usually more expensive and harder to find than common gluten-containing foods. This is not the case. Gluten free foods are widely available in supermarkets and restaurants now offer gluten free menus. I don't have a refernce for thias but will look for one.Cableknitpower (talk) 11:45, 24 September 2011 (UTC)

Blood test table

In regards to the Blood test table, I'm noticing that it talks about the HLA DQ2 and DQ8 tests, but these aren't actually mentioned in the Blood test section. Does this table actually make sense to be where it is, or should it be moved down to the Pathophysiology section (or a sub-section thereof)? I don't understand the medicine involved, so I'm completely clueless here. If it does make sense to stay where it is, I'm thinking that perhaps we should move it to the top of the section and let the text wrap around it, to remove the white-space that it causes now. —RobinHood70 (talkcontribs) 01:22, 15 December 2009 (UTC)

I think "pathophysiology" may need to be moved up for the "diagnosis" section to make sense. The table could be reformatted in the process. JFW | T@lk 20:09, 15 December 2009 (UTC)

"Patients with coeliac"

One issue I'm noticing in some places in this article, which I've noticed in many Coeliac articles from various sources, is the question of whether the phrase "patients with coeliac (disease)" applies in context to patients with coeliac who aren't gluten-free, those who are gluten-free, or both. (And just to complicate matters, those who have recently become gluten-free may still be suffering from the effects of not having been for a long period of time, so may apply to different groups, depending on context.) The specific context may not be available much of the time, but wherever possible, we should try to differentiate. —RobinHood70 (talkcontribs) 02:04, 15 December 2009 (UTC)

There was some debate as to whether you're allowed to refer to a person as a "coeliac" to begin with. Once that label has been applied, one is always at risk of relapse unless on GFD and therefore the condition is still regarded as chronic even though the changes may have healed. JFW | T@lk 20:11, 15 December 2009 (UTC)
It seems to me that that would be an important distinction to make, regardless of how you label them. While there are many people with coeliac who ignore the GFD completely (or whenever they're tempted, at least), there are a great many who are extremely strict about it, for whom a relapse is, for all intents, an impossibility. I would tend to think that for that group, many of the statements broadly applied to "coeliacs" would not apply to them. On the flip side, I know some statements still do apply to all of us — for example, I remember coming across a report some time ago that suggested that deficiencies in some of the B-complex vitamins were still a concern, even for GF-compliant individuals, where other vitamin/nutrient deficiencies (I don't remember which) were not. But I suppose in many cases, this will be a concern to be dealt with in the original studies, not necessarily with the article. Nevertheless, where identified in the studies, I think it makes sense to identify whether the GFD or lack thereof was taken into consideration in the results. —RobinHood70 (talkcontribs) 00:42, 16 December 2009 (UTC)
Please use "people with coeliac," not "patients with coeliac," unless specifically referring to the actions of health care professionals concerning their patients. "Patient" refers to a relationship between a care provider and one receiving care. (e.g., "Physicians generally prescribe a gluten-free diet to their patients with coeliac.") Whether someone is actually following a GFD is irrelevant. Whether someone is actually receiving professional care is also irrelevant unless the use of the word "patient" is used to refer specifically to an interaction between someone providing care and someone receiving care.
Consider this example: A person with coeliac is also presumably someone's son or daughter, and it would be equally ridiculous to refer to "patients with coeliac" as it would be to refer to "sons & daughters with coeliac" unless we're talking specifically about how the disease is relevant to those specific relationships. This also extends to using the phrase "patients with coeliac" rather than "coeliac patients" when the word "patients" is appropriate. People first, disease second. Dcs002 (talk) 10:12, 26 August 2011 (UTC)
Since I was talking about it in the context of the article's wording, which mostly uses the phrase in the context of medical studies, it was entirely appropriate phrasing. As for whether it matters if someone is on a GFD or not, if a study reports something that applies only to those who aren't gluten-compliant, it's extremely relevant. That was the thrust of my point, not whether we should be using "patient" or "people" in any given context. Since I'm not a doctor, but rather someone with Coeliac myself, I wouldn't use the term "patient" or mention the GFD unless it was relevant to my point. RobinHood70 talk 22:37, 26 August 2011 (UTC)

Reviews, reviews

Gastroenterology this month carried this review doi:10.1053/j.gastro.2009.09.008. No need for any primary sources now! JFW | T@lk 22:18, 22 December 2009 (UTC)

It's free as well. Expect me to quote it a lot when I finally rewrite "pathophysiology", thus also eliminating lots of the primary research that crept in. JFW | T@lk 22:51, 26 December 2009 (UTC)

Liver damage and Coeliac disease

I have been reading about the disease and I came across this issue which was not mentioned in our article, so how about we add a section about that, there is this free review that can help allot :-) MaenK.A.Talk 18:09, 27 April 2010 (UTC)

Abnormal liver enzymes are discussed, as are some related autoimmune liver conditions. Also, your review is in Spanish and hence less ideal as a source for an English article. JFW | T@lk 18:59, 27 April 2010 (UTC)

Genetics, Again

Well, folken, its that time again where somehow we decide what to do about the genetics. Van heel has published a new study on Celiac Disease (Nature genetics 42:295-302. It is not a review, but it does cover many of the problems presented in the previous paper. Other than HLA-DQ there appears to be no common genetic ('weak evidnece') association that appears consistent across all populations (12) in their study. In addition it would appear that if you are a DQ2.5cis homozygote (which they expressly mention by name) all other associations appear to be weak, possibly unneccesary. IOW DQ2.5cis homozygosity by its 'genetic' self, may be sufficient with environmental factors to cause Celiac Disease. They describe the faults in the previous studies, which I mentioned here as a reason for removing the non HLA portion of the genetics, and appear to have redressed the problems. The wording they use is not exactly clear, so some aspect of their conclusions may not be worthy of the main article. The following loci are positively associated with very low random probabilities.

[pra = probability of random association mag = magnitude of the probability, less that -9 is considered to be an association with celiac disease as these probabilities are not corrected for the size of the SNP database]

LPP - 3q28 - Lipoma-preferred partner - OR = (1.25-1.34, positive association) pra <-39 Mag. The protein is involved in cell adhesion and extracellular matrix formation. Note a potent target of gliadin-tTG reactive Eosinophiles and Killer Cells is the extracellular matrix, where tTG becomes localized in the villi. LPP and IL1R genetically interact in celiac Disease according to the paper.

IL12A- 3p12-q13.2 - Interleukin 12 alpha chain, OR = 1.36 (1.29-1.44, positive association) pra <-27 mag. This gene encodes a subunit of a cytokine that acts on T and natural killer cells, and has a broad array of biological activities.

IL2, IL21 - Because of haplotype linkage at this locus delineation of the involved locus is not clear - Interleukin 2 and Interleukin 21 - the minor allele is negatively associated. (OR = 0.74) pra < -27.

These three associations can be added to the genetics section as the differential random probabilities are less than 10E-18. Adding these three would not clutter up the genetics section.

SH2B3 - 12q24 - Alias lymphocyte adaptor protein; LNK. LNK Mediates the interaction between the extracellular receptors and intracellular signaling pathways for T-cell activation. - OR ~ 1.2 and pra = -21 corrected = -11.

TNFAIP3 - 6q23 - Several SNP at this locus have been found involved in autoimmune disorders. locus associates strongly with rhuematoid arthritis and type 1 diabetes, it is an inflammatory, disregulation fails to dampen inflammatory immune responses. OR ~1.2 pra = -18, corrected = -9

CCRx loci - 3p21.3 - Chemokine receptor - Different receptors of this class respond to different stimuli, can produce innate response to superantigens, like LPS. Different CCR are found in different T-cells types. The G protein-coupled receptor encoding RNA was isolated from human eosinophils. Eosinophils also expressed a much lower level of a second chemokine receptor, CC CKR1, which appeared to be responsible for the effects of MIP-1-alpha; see CMKBR1 According to Dubois CCRx act synergistically with HLA-DQ genes (figure 1).

These are 6 loci with unquestionable involvement in Celiac Disease susceptibility. However if the patients are not randomly draft other autoimmune diseases may associate with testing. So that the really outstanding loci are those that have no other autoimmune association.

LPP has the highest association is not currently associated with any other autoimmune disease. It has a high odds ratio, a very low corrected probability, and its function appears to be a potential a target of degradation caused by tTG reactive Eosinophiles. IL12A is also a T1D association however, its OR is fairly high, much higher than the percentage of CD who have T1D and therefore part of its risk should be independent of T1D. IL2/IL21 contains a third gene that is not mentioned in this paper, causative function is ambiguous at best. SH2B3 is found in association with a half dozen autoimmune diseases. TNFAIP3 is associated with rheumatoid arthritis, coronary artery disease, psoriasis, celiac disease, type 1 diabetes, inflammatory bowel disease, and systemic lupus erythematosus. CCR loci individually are involved in different diseases.

Conclusions: I do not have a problem adding information concerning Lipoma-preferred partner (LLP) since its highly positively associated with CD, and it appears not to be enriched as a consequence of autoimmune pathways toward celiac disease clinical detection. We can discuss the value of adding IL12A to the main page, if someone believes or has reason to suggest it is of particular mention at this point. PB666 yap 22:31, 20 July 2010 (UTC)

Malabsorption-related list is very incomplete

The list is missing many problems related to malabsorption. I frequent the Celiac's forums and find that it is common for us to have Rickets, Scurvy, and severe fatigue. The severe fatigue I believe is really just unrecognized BeriBeri from vitamin B1 deficiency. I had all 3 of these which are now nearly all gone due to my Gluten free diet. My mother has also just gotten diagnosed properly(due to my demanding the doctors to test her for it. Sad hey.) Anyway she has had it a lot longer and the evidence of Rickets is so obvious in her hands it's not even funny. Her fingers are all very crooked especially her thumbs, and her legs too. Yet the docs called it Arthritis before she was diagnosed with celiac's properly. So ya lets get this list corrected to include what everybody on the forums knows to be true already. That is, Rickets, Scurvy, and probably BeriBeri too, are all likely complications due to Celiac's. —Preceding unsigned comment added by (talk) 17:59, 3 September 2010 (UTC)

I wrote much of the content, and in none of the review articles that I used did experienced doctors mention either low thiamine or ascorbate. Rickets are a consequence of low vitamin D (mentioned in the article) but adults who have not suffered rickets in childhood would experience osteomalacia rather than rickets. Neither thiamine nor ascorbate are fat-soluble vitamins, so villous atrophy is less likely to interfere with their absorption.
We have to be very careful and distinguish between self-diagnosis (which may be incorrect) and clinical diagnosis (which is sometimes incorrect but probably less so on the basis of the doctor's training and experience). Self-diagnoses in internet forums can be completely incorrect and based on misperceptions, and sometimes even intended to mislead (especially when then mentioning the name of an expensive supplement product).
Please provide us will a reliable source with regards to thiamine and ascorbate deficiency, and we can review the matter. JFW | T@lk 18:07, 3 September 2010 (UTC)

Fix the spelling

Can someone please fix the spelling of "diarrhea" in the first paragraph? I don't think the spelling given (with an "o") is proper in any variation of English.

In the UK it is spelled "diarrhoea", consistent with the remainder of the article, which is written in British English. See WP:ENGVAR. JFW | T@lk 23:54, 12 January 2011 (UTC)
We also sometimes use "diarrhoea" in Canada, though "diarrhea" is more common, I think, probably due to the US influence. RobinHood70 talk 01:18, 13 January 2011 (UTC)

Only 1 in 10

Only 1 in 10 Celiacs have stomach pain, diarrhea or fail to thrive. That is why it is known as the "ice berg disease." Only 10% of Celiacs have obvious symptoms. The other 90% can have many seemingly unrelated symptoms such as mood swings, crying spells, iratability, inability to lose weight, loss of apetite for weeks at a time, elevated liver enzymes, depression within 2 hours of eating gluten, neurological changes. So the three symptoms listed in the first paragraph are misleading. Those three symptoms listed are the RARE symptoms. Common symptoms include depression and mood swings. I suggest you do some research about the MOST COMMON CELIAC SYMPTOMS. Later in life the most common symptom is osteoporosis and arthritis.

Also, wikipedia should provide a link to the 300 symptoms of Celiac Disease: (Search Google for "300 symptoms of Celiac Disease.")

Please, correct the first paragraph!!! —Preceding unsigned comment added by (talk) 23:07, 14 January 2011 (UTC)

Wikipedia medical articles work primarily on the basis of peer-reviewed medical studies. Due to the preponderance of self-serving medical information out there, it cannot be based on the opinions expressed in a book unless that book has been peer-reviewed (and testimonials don't really count as peer-reviewed). You may wish to read WP:MEDRS for more information. RobinHood70 talk 23:30, 14 January 2011 (UTC)

Footnote #3 doesn't support

Footnote #3 doesn't support an incidence range of 1/1750 to 1/105 as indicated. I'm not sure why this footnote is connected with this text - the nih document shows a very low level of certainty. (talk) 02:05, 5 June 2011 (UTC) (forgot to sign)

Article name should be the common spelling -- Celiac; not the rare "coeliac"

In common use, more than 6 to 1:

"Coeliac disease" hits in Google: 1,090,000

"Celiac disease" hits in Google: 6,650,000

In scientific use, more than 10 to 1:

A PubMed search for "(coeliac) NOT celiac" hits returned: 1,563

A PubMed search for "(coeliac) NOT celiac" hits returned: 17,226

For the 6 out of 7 general readers, and 9 out of 10 medical readers, it is disconcerting at best and unhelpful at worst to be searching for celiac disease, see that wikipedia has an article on "coeliac" disease, and have to wonder if it is the same thing.

Articles should be named in a way that is helpful to searchers and readers. — Preceding unsigned comment added by (talk) 00:49, 11 July 2011‎

The article has the 4th spot when Googling celiac diesease, so it is not a problem. "Celiac disease" directs to the article. We avoid changing names (see MOS:ENGVAR). Novangelis (talk) 01:04, 11 July 2011 (UTC)
Actually from a scientific point of view it is increasingly called Gluten-sensitive enteropathy in the literature. So if any name changing is in order . . . . .PB666 yap 22:10, 6 September 2011 (UTC)
No, practically all recent high-quality reviews use the term "coeliac disease". No change needed. JFW | T@lk 23:49, 8 September 2011 (UTC)
Of course it is a more common spelling. It is an Ameican spelling, and American English will dominate many areas due to its dominance of the Internet, science funding, and sheer economic output. As such most media will likely use "celiac disease". And I agree with Pdeitiker/PB666, in that it is often termed gluten-sensitivity, probably to both avoid differrences in spell-forking and since it is becoming apparent doctors really haven't known the whole story, that there is a range of sensitivity with celiac disease being the most severe. And on that matter it seems to me most people have gluten-sensitivity than celiac disease. In any event, it has been agreed long ago by the original editors that the UK common version should be used, which will always override WP:COMMON until UK English overtakes American English worldwide and on the Internet and/or Wikipedia, which is unlikely in the near future. Int21h (talk) 23:08, 20 November 2011 (UTC)

Natural selection

It's not a single source. There were two references just in the section that was removed. See also doi:10.1016/j.mehy.2011.07.034.--Itinerant1 (talk) 05:43, 15 September 2011 (UTC)


Should Celiac Disease be capitalized? What about Type 1 Diabetes? — Preceding unsigned comment added by Cableknitpower (talkcontribs) 01:29, 21 September 2011 (UTC)

No, Wikipedia is fairly minimalist with capital letters (see:Wikipedia:Manual of Style/Capital letters). Thank you for asking before editing. In general, these talk pages are used for article specific edits. There are several venues for more general help.Novangelis (talk) 03:38, 21 September 2011 (UTC)


Celiac Disease is spelled "coeliac" ONLY in the UK. The vast majority of other English-speaking countries spell it "celiac." Jimmy Wales, the founder of Wikipedia, is from North America, and we spell it "celiac" here. ALL of the medical journals referenced spell it "celiac." When spell-checkers see it, they flag "coeliac" as being incorrect. Hence the upcoming change.

I and many other English-speaking people around the world are sick and tired of one country's imperialistic attempts to get everyone else to bow down to their point of view. Sorry, Brits - ain't gonna happen. Barring any CREDIBLE argument to the contrary, the changes will occur in a week. — Preceding unsigned comment added by (talk) 23:38, 16 November 2011 (UTC)

Please read the many other discussions on this topic above (Requested move, Coeliac/Celiac, Article name...). As a general rule, articles are written in either the appropriate version of English for the subject (i.e., The Beatles would be in British English, Elvis would be in American English), or if there is no particular nationality for the subject, then whatever the existing variant is should be retained. Unless you can garner consensus from other editors, any changes that are solely to switch from one language variant to another will be reverted, according to policy.
I'm sorry, but "consensus among editors" is not Wikipedia's policy. Accuracy and correctness is Wikipedia's policy. As the preceding entry entitled "Article name should be" very clearly describes, "coeliac" is NEITHER the most common spelling among the general public (6:1 AGAINST "coeliac") NOR is it the more common spelling among medical professionals (10:1 against "coeliac"). I repeat, unless you can show good cause for why it should remain in it's current, mostly incorrect spelling, it will soon be changed. 03:59, 22 November 2011 (UTC)
WP:Consensus You were saying? The article is both accurate and correct, so that argument is moot. Also, by all means, feel free to try to change the spelling against consensus. Be aware, however, that this will get reverted, and if you continue to change it without consensus or adequate justification based on Wikipedia's policies, it will lead to repercussions against you, possibly ending in a block. Which spelling is popular is irrelevant on Wikipedia, the existing policies and guidelines that have already been pointed out to you govern how things are spelled. If you feel that there are too many articles with non-American spellings, please feel free to preemptively create new articles that use the spellings you prefer. For existing articles, however, spellings stand as they are, as is Wikipedia's policy. RobinHood70 talk 05:12, 22 November 2011 (UTC)
Also, contrary to your assertion, outside of North America, "coeliac" is the more common spelling. This includes many of the European countries, as well as Australia, and undoubtedly several others.
Horsehocky. This is your assertion. You present it without proof. It runs contrary to the aforementioned facts. It is without merit.03:59, 22 November 2011 (UTC)
Very well, here's the proof, though as pointed out, the proof is irrelevant given the various Wikipedia policies that come into play here.
Finally, please use talk pages for discussions about the article itself. Rants about a specific country are inappropriate. RobinHood70 talk 00:36, 17 November 2011 (UTC)
Have you any clue as to how many Wikipedia entries are presented in the LEAST common spelling simply because British editors gang together and try to force everyone else around the globe to do things their way? (rolls eyes) 03:59, 22 November 2011 (UTC)
Yeh! Let's replace WP:ENGVAR with "How would Jimbo spell it?" :-) -- Colin°Talk 08:38, 17 November 2011 (UTC)
One of my first editing disputes on Wikipedia (in 2004) was about ENGVAR. I figured that because Wikipedia was based in the US, the spelling had to be American. But How would Jimbo spell it, no.
Also loving the firm language, the ultimatum and the threats. This exclusive club might invite you for membership,! JFW | T@lk 10:50, 17 November 2011 (UTC)
I appreciate your humor.  :) My goal, however, isn't to try and force North America's spelling on others. That's precisely the problem, but on the British end. It's to change the spelling to "celiac," as is used by 5 out of 6 English-speaking people around the world and 9 out of 10 English-speaking medical professionals around the world. You want consensus? That's consensus. As an entry in the High Importance Medical Articles, the least that Wikipedians could do is accept the spelling used by 9 out of 10 medical professionals. Keeping it's current, British-only spelling is insanely asinine. 03:59, 22 November 2011 (UTC)
There is little logic to spelling in English. This is the International English version of WP, not the US version of WP. In order to prevent pointless per-article debates on spelling, we come up with arbitrary house rules like WP:ENGVAR or defer to international standards bodies. Colin°Talk 08:58, 22 November 2011 (UTC)

Genetics Update (2011)

Since the last time I reported here on the Genetics there has been significant changes behind the scenes of the genome-wide associations. To give a background: several of the early genome wide results differed from the latest and most recent results outside of the HLA superlocus. Studies looked at different peoples in different regions, they used different markers, etc. Since these studies in the last 2 years there has been a general realization of the certain deficiencies in GWAS (see referenced paper below for an example of 'missing' associations).

  1. The markers in different studies are different.
  2. Different regional studies can give markedly different results
  3. Peak random probability is frequently, in fact, most often overestimated. Many associations are marginal simply because of the selection of markers used in the GWAS (one source of markers versus another)
  4. Haplotype associations that are present are often not resolved.
  5. In general, no effort was made to deduce SNPs that were not part of the marker set but are more enriched in patients. In other words, markers in general were drafted from the control patient studies, not from sequencing affected cohort.

These specific problems were not exclusive to Gluten-sensitive enteropathy, as they have been observed in other autoimmune diseases. The aspect that came under critique here is that very few candidate genes were unique to GSE, that most were shared by other AID.

So what has changed and why. First, the "why". In some AID, familial studies continued to progress despite GWAS, these studies began detecting 'defect' alleles that ran in disease-enriched families that were not observed in GWAS which cover the same region. Other studies used family trios (1 unaffected parent, 1 affected parent, and 1 affected offspring) in a genome-wide set-up and they also found associations that are not obvious in GWAS. In addition, different studies have done the following to see what has been missing.

  1. To draft affected individuals into genomic sequencing efforts to look for high risk rare variants (e.g. that may run in families) that are enriched in affected individuals but are inadequate to be drafted into a GWAS (one-size-fits-all) marker set.
  2. To focus studies on genomic regions, not just regions that showed up as significant after correction in GWAS, but to focus on marginal genes that are suspicious. The effort here was to find better markers, and thus improve the association of marginally associated regions.
  3. To examine haplotypes and to parse haplotypes according to specific risk
  4. To pay more attention to what is going on in families with a history of disease not explained by the major genetic determinants (e.g. not DQ2/DQ2 homozygotes).
  5. To split certain autoimmune diseases up into subgroups according to clinical parameters (e.g. serotypes, clinical manifestations, etc)

The latest installment by Van Heel:

Dense genotyping identifies and localizes multiple common and rare variant association signals in celiac disease. Trynka [100 authors snipped]. van Heel. Nature Genetics 43: 1193-1203

This paper goes a long way towards pointing a new direction in the GSE genetics, something we should feel more comfortable about the results, but anguished as how to present these.

Based on GWAS association signals are marked, represented, by SNPs that cover haplotypes. Causal signals generally occur in adjacent territory, however the causal allele may not be marked best by the representative SNP. That allele may lie on a specific and unidentified haplotype. So when scientist talk about gene sharing by autoimmune disease (AID), in may mean that two AID share risk for a specific causal variant or more likely (since we often dont know the causal variant) share risk for a region.

Trynka and company have broken some of these associations down (i.e. parsed them) into their component risks. Examples are CTLA4 and STAT4 genes. Some of these risk are shared with other AID, and some of the risk are specific to GSE. TNFAIP3 (Tumor necrosis factor alpha interacting protein 3) gene encodes A20. Despite its genes name, the protein is known to interact in multiple pathways, some papers claim in acts through apoptosis mediators (e.g. TNF superfamily) others claim it acts through different internal signalling. This recent paper shows that different mutations in the protein may alter where the 'affected' protein are interacting. Regulatory defect (quantitative trait loci, QTL) may alter expression in many cells or may affect expession in specific cells, this in turn can determine a protein greatest variant role. The problem however is that they focused on regions in patients that have already been tagged as autoimmune or immune genes. As a consequence 10 of 13 newly discovered GSE association loci are immmune function related. From this they found 57 celiac disease association signals from 39 different gene regions, 32% were not effectively tagged in the previous GWAS. This story is not over yet, I'm afraid to say that these results underscore the need to do more family-based studies. In addition many of their new markers were not capable of resolving causal variants (only to the level of haplotypes) and these haplotype overlay several adjacent 'genes'.

As exemplified above, the various haplotypes that bear highly associated alleles can subdivide the genetic associations into those that are most meaningful to celiac disease, In most cases we cannot identify a specific variant that we can note causality as we currently note for DQ2.5cis haplotype. By subdividing risk and finding alleles that act uniquely in celiac disease one is on the road to finding those disease causing variants. In other words, using these types of studies it is possible to separate rank-and-file autoimmune disease risk variants from very close by celiac disease specific variants. The basic problem here with GWAS as we currently understand the results, the overwhelming majority of mutations affect expression levels. There are examples of these QTL that can alter gene expression 1/2 million nucleotide distance, and it is not clear how or why this is occurring. Consequently finding a peak allele or peak haplotype is not the end-result. Other studies need to assess expression levels in different cell lineages to determine the 'affected' gene, and thus to understand the nature of the genetic defect. A widely touted example of this is CTLA4, but CTLA4 lies in a region with haplotypes that cover CD28, CTLA4 and ICOS. Another example is IL2, IL21, within its region of linkage disequilibrium their are 4 genes, 3 of which are expressed in immune cells, 2 of which have known involvement in autoimmune disease.

Finally with previously identified loci being subdivided by risk haplotypes, some of which shared GWAS markers, we are seeing some decline in risk variance for some markers, but increases in the number of markers that elevate risk variance for a region. This speaks to the importance of regional genetics and family-based genetics. An example of this is the elevation of PTPN2 association with dual variant risk imm_18_12833137(T) + ccc-18-12847758-G-A(A) (~10E-14, OR = 0.84, protective). As they state shortly thereafter, their new study was able to pinpoint certain genes, but still unable to resolve other clusters. For similar papers on these matters also see: Nature genetics 11:1066-1076 use similar methods to examine inflammatory bowel disease.

From the WP perspective, I will review this works supplimentary material to see what their pinpoint results are and see if this achieves a prosperities-sake level for inclusion. Currently the material is much too complicated to add to this article in its current form (57 associations, 39 loci, ....); however some of the results may value selective inclusion. PB666 yap 15:49, 6 December 2011 (UTC)

It is a primary source. JFW | T@lk 00:21, 7 December 2011 (UTC)

"British" English

Why are there so many articles with different spellings or names using the rarer spellings or names that are said to be "British English"? Is this an attempt for Wikipedia to be more formal? I'm not complaining, just pointing out this this has happened many times (see the spelling of Caesium). Thylacinus cynocephalus (talk) 23:19, 18 December 2011 (UTC)

Not an issue for this talk page, really. Try reading WP:ENGVAR. JFW | T@lk 23:43, 18 December 2011 (UTC)

More emphasis needed on how this is not an allergy

At the start of the article, we are told that this is not the same as wheat allergy, but could there not be more emphasis on how coeliac disease is not, strictly speaking, an allergy? I know that lots of people who put labels on foods seem unaware of this - one often reads on food packets "allergy advice - contains gluten" - but that does not make them right! ACEOREVIVED (talk) 21:45, 1 February 2012 (UTC)

That is mainly because the general population has a lot of misconceptions about allergy in general.
We can only elaborate on this question with the use of secondary sources. Can you think of any? JFW | T@lk 23:36, 1 February 2012 (UTC)

A redirect for discussion

I was rather unhappy about how, for a long time, typing in gluten intolerance got one redirected to this article (coeliac disease). As mentioned on "Inside Health", the Radio Four programme presented by Mark Porter, the term "gluten intolerance" is often used interchangeably with the term gluten sensitivity; the programme did point out that these terms refer to something other than coeliac disease. This has now gone to an entry at Wikipedia: Redirects for discussion. ACEOREVIVED (talk) 21:08, 8 February 2012 (UTC)

Gluten intolerance incorporates a much wider group of problems. Coeliac disease has distinct immunological and histological features. I would be happy for the redirect to point somewhere else. JFW | T@lk 22:37, 8 February 2012 (UTC)

This did get to "Redirect for Discussion", and it now appears to be settled - gluten intolerance now redirects to gluten sensitivity. ACEOREVIVED (talk) 09:26, 9 February 2012 (UTC)

Please refer to discussion here to see papers I provided MaenK.A.Talk 09:11, 10 February 2012 (UTC)


I added the following information to the Interleukin 15 which may be useful for inclusion here. This is certainly only a potential avenue of treatment, so I leave it to those with more connection to the article to determine how best to include it. Phil (talk) 09:06, 24 April 2012 (UTC)

There have been recent studies suggesting that suppression of IL-15 may be a potential treatment for celiac disease and even presents the possibility of preventing its development. In one study with mice blocking IL-15 with an antibody led to the reversal of autoimmune intestinal damage. [2] In another study mice used were able to eat gluten without developing symptoms. [3]

Please only add content supported by high-quality secondary sources (e.g. reviews). In this case, the fact that it works in mice is absolutely no indication that it will work in people. Let's avoid WP:CRYSTAL here. JFW | T@lk 09:34, 24 April 2012 (UTC)
I didn't suggest mentioning this as a current treatment, the word potential means just that, potential. The information is quite relevant to those interested in celiac disease and developments regarding it. This is certainly a notable one which received significant medical news coverage as such. Feel free to select higher quality sources if you have concerns about the legitimacy of the medical journal referenced or WebMD Health News, there was plenty of coverage of both studies most of which quote doctors stating basically that this look like a very promising potential avenue for treatment although you are correct that human studies need to be done. Anyway I'm not adding it myself as I think maybe someone could do a better job than me of putting it properly but I don't think concerns about the sources are well-founded and the content is definitely relevant and notable regarding celiac disease the only thing needed is to present it properly to avoid your other concern. If you really are that concerned about crystal ball gazing then on a separate note the several other experimental treatments mentioned in the article, some of which are entirely unsourced currently certainly deserve some review. (talk) 16:24, 5 May 2012 (UTC)
I don't think my points need to be restated. There are several "promising" treatment modalities that are supported with better data. A secondary source (e.g. review) is needed to determine whether this therapeutic approach is indeed considered promising by those in the field. People are more helped by discussion about treatment that is currently known to be effective. JFW | T@lk 02:22, 6 May 2012 (UTC)


To my horror I discovered that the article had somehow grown a section on neurological syndromes in coeliac disease, mostly based on the poorest of sources and generally not reflecting the immense controversy that surrounds these associations. When I removed it, (talk · contribs) came along and reinserted it without an edit summary.

For those who care, the association with coeliac disease and neurological symptoms has been reported almost exclusively by one centre (Sheffield, UK) with a fair number of other researchers showing no evidence that coeliac disease specifically increases the risk of any of those phenomena (ataxia, neuropathy). In some cases, specific coeliac serology is negative but the more outdated assays (e.g. anti-gliadin) are positive, and there may not be any evidence of villous atrophy.

I don't think the section should be returned in its current form. Strong WP:MEDRS-compliant secondary sources are required to reflect the current thinking about neurocoeliac. JFW | T@lk 19:32, 17 May 2012 (UTC)

I wasn't previously aware of any such possible association, but I do find it intriguing, since I developed many of these symptoms (which I later came to believe was CFS) one year after significant Celiac symptoms manifested; five months after starting on a gluten-free diet. (I had been symptomatic for CD since childhood, it was just never properly diagnosed until symptoms become overwhelming.) I was also diagnosed with mild absence via EEG when I was 20, which faded notably after starting a GF diet. However, a random set of occurrences in my life obviously doesn't make a larger pattern, so I browsed around quickly on PubMed to see if there was anything there. I think there's enough that we can't dismiss the possibility entirely out of hand. This isn't exhaustive by any means, but a quick list of the ones that caught my attention:

Some of these were more tenuous while others were more definitive, but nothing ruled out an association by any means. That said, the fact that both studies quoted in the newly added text were from the same author makes me a little wary of a possible COI. Any text we do add needs to be based on a wide array of sources. If there are counter claims, then of course we need factor those in as well for appropriate balance. RobinHood70 talk 14:13, 18 May 2012 (UTC)

Epidemiology in the United Kingdom


Emily Maitlis said on Newsnight on May 24 2012 that in the United Kingdom, one in a hundred people had coeliac disease. However, the newsnight website, which can be found at:

says that the one in a hundred figure applies to gluten intolerance. If any one knows the correct figure for the United Kingdom, and knows better sources than the Newsnight report, it could be added to the "Epidemiology" section. ACEOREVIVED (talk) 23:32, 24 May 2012 (UTC)

It would be better to have a WP:MEDRS-compatible secondary source. JFW | T@lk 23:43, 24 May 2012 (UTC)

This website:

does say that prevalence of people with coeliac disease in the United Kingdom is approximately one in a hundred. ACEOREVIVED (talk) 09:06, 25 May 2012 (UTC)

This website:

says that the prevalence in Western Europe is about one in one hundred and fifty, and at least it is based on an article in the British Medical Journal. ACEOREVIVED (talk) 09:13, 25 May 2012 (UTC)

The BMJ article is a primary source. How about you have a look at WP:MEDRS, which provides some support in selecting sources. JFW | T@lk 11:56, 29 May 2012 (UTC)

More common in females

This looks as if it is a good source:

and it does say that coeliac disease is more common in females. Perhaps this should go in the article. ACEOREVIVED (talk) 09:20, 25 May 2012 (UTC)

It is a secondary source, which is good, but it is 13 years old. It would be preferable to have a more recent source. JFW | T@lk 11:56, 29 May 2012 (UTC)


One of the studies cited to claim that incidence of undiagnosed celiacs is increasing is a study of 1950s-era Air Force personal. I think it's likely problematic to compare military cohorts with civilian cohorts for a disease that can affect development and general health. People suffering from celiacs would be less likely to be in proper physical condition for the military, hence incidence among military cohorts can rationally be assumed to be lower than in the general civilian population. — Preceding unsigned comment added by (talk) 22:19, 2 June 2012 (UTC)

Which study are you referring to? JFW | T@lk 23:00, 2 June 2012 (UTC)
If it was doi:10.1053/j.gastro.2009.03.059, this is a very interesting study that uses serology samples from the 1950s to determine how many people (in retrospect) had undiagnosed CD, and to determine whether a lack of a diagnosis conferred harm. The results are suggestive of several important points: case-finding of CD is appropriate, and the prevalence of CD has increased markedly provided you consider the methodological disadvantage of having a selected cohort.
I have removed the study only because it is a primary source, the kind that we avoid in encyclopedia articles. JFW | T@lk 23:05, 2 June 2012 (UTC)


Just to better explain my edit summary, while the ligatures are a bit of a nuisance to type, I have no overwhelming objections to them. The reason I reverted was that numerous inappropriate "oe" replacements were made, such as in "gastroenterology" and several interwiki and off-wiki links. In addition, the spelling used in citation titles should match that of the source itself.

Also, if ligatures are to be used for words like "coeliac" and "diarrhoea" in the article body itself, that should probably be discussed here on the talk page first. RobinHood70 talk 21:12, 4 June 2012 (UTC)

The editor Tea and a lump o' cake (talk · contribs) is invited to explain here why this was thought to be necessary. It's archaic spelling and should not be used except when listing different spellings. JFW | T@lk 23:05, 4 June 2012 (UTC)

Is this still FA standard?

A relative has been diagnosed with CD. I notice it's been 5 years since this was promoted to Featured Article status. Do any regulars here have an opinion on it's up-to-dateness and accuracy, before I point her to this article? --Anthonyhcole (talk) 15:42, 24 July 2012 (UTC)

Sorry to hear about your relative. Some parts of the article are up-to-date, particularly those on the signs and symptoms and treatment (gluten free diet remains the only real treatment in almost all cases). There have been some developments in the understanding of the pathophysiology that are a bit too complicated for this bear of little brain.
If you find the article below par, please feel free to send it to WP:FAR.
In 2007 a professor of medicine went on the record comparing this article favourably with a recently released textbook of gastroenterology (doi:10.1136/gut.2007.121533). JFW | T@lk 20:10, 24 July 2012 (UTC)
Thanks JFW. I shall point her to the article and your comment. --Anthonyhcole (talk) 05:18, 25 July 2012 (UTC)

Atopic dermatitis

Not sure about this "Atopic dermatitis, a type of eczema, has been linked to coeliac disease patients and their relatives, although this has been disputed.[4]" While it may be more common this is far from definitive.Doc James (talk · contribs · email) (if I write on your page reply on mine) 04:31, 26 May 2013 (UTC)

It is just a claim of a link. There is no claim, as I understand it, that it is a symptom, but the section heading clearly begins "Coeliac disease has been linked", not that these are symptoms of the disease. Nor is the claim that it is "occasional". The fact that your not sure is not really a reason to revert or remove the material.
I noticed you re-added the material under dermatitis herpetiformis, but this is incorrect, or at least less correct. Dermatitis herpetiformis is actually listed under a different category of ICD-10, under the "Bullous disorders" (L10-L14) section, whereas atopic dermatitis is a specific form of eczema, which is under the ICD-10 section for "Dermatitis and eczema" (L20-L30). I do not think Dermatitis herpetiformis is a type of eczema, which is usually classified as more of a allergy, with atopic dermatitis being a more acute, clinical manifestation, as I understand it.
I think atopic dermatitis should be clearly differentiated from dermatitis herpetiformis, even though they are both classified under chapter XII of the ICD-10 "Diseases of the skin and subcutaneous tissue". Int21h (talk) 04:48, 26 May 2013 (UTC)
Well, OK, they are clearly differentiated, and both being in chapter XII, with AD being a "weak" link, I think the current setup is fine. As long as the AD link is in the CD article somewhere. Int21h (talk) 04:59, 26 May 2013 (UTC)
I think we're at risk of falling into a large trap here. Both CD and atopic dermatitis are common, and a number of secondary sources (doi:10.1155/2012/952753 and PMID 16436335, for starters) list a number of other dermatological conditions that are seemingly associated with coeliac disease and/or gluten intolerance. These papers state that the association is by no means proven, and that there are important pathophysiological differences between the disease states. I don't think I can support inclusion of this association at the moment, especially if we're not also going to discuss all those other cutaneous conditions discussed in our sources.
As an aside, "Celiac Disease and Dermatologic Manifestations: Many Skin Clue to Unfold Gluten-Sensitive Enteropathy" - what kind of editorial process finds a title like this acceptable? JFW | T@lk 10:52, 26 May 2013 (UTC)
This position poses some big problems IMO. First, it does not need to be "proven" to a group of editor's satisfaction; that is not the standard of review here as I understand it, and any claim to the contrary, even as part of some particular subject matter policies (e.g. WP:MEDRS), would violate some core Wikipedia philosophies about the inclusiveness of allowed material. There are some big reasons why, mainly because this moving standard of review is subject to abuse and subjective interpretation, again going against the spirit of Wikipedia.
Second, there are "a number of other dermatological conditions that are seemingly associated with coeliac disease", but they are not in this article? What are they exactly? What else isn't meeting your collective expectations? Is there a reason other than they haven't been "proven" or they aren't "definitive"? As in can somebody link some WP standards here? I did not think I would need to bring up philosophy here, but "proven" and "definitive" are way too subjective to use as standards for WIkipedia. I think we literally need to get a list of information that has been removed because they don't meet some editor's worldview or standard of relevance. And don't tell me "its already been decided", as that is nonsense I hear way too often. This is not the German Wikipedia. A discussion by 5 people a couple several years ago is not a reason to ignore the (English) Wikipedia policies.
Information about relationships, no matter how strenuous, are not "traps", they are "beachheads" for further research, a sign that there may be more information waiting for the would-be editor to add to Wikipedia, a sign that an article is not complete.
I think the "trap" we are getting into here is the trap when editors view the article as relatively complete, or view themselves as the guardians of the article, and wish to keep it static to the detriment of new edits and editors. Remember, Wikipedia is an evolving beast, and the status quo cannot be used as an excuse to keep the status quo from changing. I have been there, I have cringed when someone makes a big edit in an article I care about (or created) that does not meet my expectations. It is a particular effort of mine to let the article change regardless. (I obviously have problems when information is removed, though.) Only years later do I reap the rewards when the article has grown into something I did not intend.
As to the research article title, it is simple: they are Italian doctors. English language usage is exceptionally not widespread in Italy, I understand. (Read: not many Italians speak English in Italy.) They have spent their time learning medicine, not English, I assume. But again, this is not the standard of review. Int21h (talk) 18:52, 26 May 2013 (UTC) Int21h (talk) 18:55, 26 May 2013 (UTC)
Not everything mentioned in the literature needs to be included in this article. It boils down to an editorial decision whether to include one skin disease from the long lists in the two secondary sources I listed in my post above. My editorial perspective is that the link currently is not of sufficient strength to mention it here in a very broad article on coeliac disease.
If you feel strongly that atopic eczema needs to be included, I think we would be obliged to list the other cutaneous conditions as well. Again, there is only a weak association, and my view is that we would fall foul of WP:WEIGHT by including it. JFW | T@lk 20:25, 26 May 2013 (UTC)
I definitely think the other conditions that have links with CD (and possibly GI if it is used interchangeably with CD) should be mentioned as well. There are multiple (presumptively) reliable secondary sources. Requiring every person to do their own research (like me), whilst simultaneously preventing all those people from adding it to this article, defeats the purpose of Wikipedia. If there are many conditions etc with only weak links, a single paragraph (or possibly even a sentence if they are all for example skin conditions) will do. Yes, this article can deal with "long lists"; they do not need to be in bullet (long) form, but can simply be given a sentence or two. Again, just a mention will do, there is no need to go into great detail. This is in line with WP:WEIGHT/WP:UNDUE. But I reiterate my position that, if there is literature out there, such facts should be here for further research by interested parties, without regard to other editors' opinions about their veracity or "definitive" relevance. Int21h (talk) 21:23, 26 May 2013 (UTC) Int21h (talk) 21:35, 26 May 2013 (UTC)
And just to clarify, the link to these conditions is not a "minority viewpoint" per WP:UNDUE, as there is no "majority viewpoint" that there is no link. Which is to say, there is no majority/minority viewpoint split regarding this topic. This is why I think my proposal is in line with these policies. There is merely discussion in the scientific literature about primary sources concerning possible links, which has been reviewed by multiple secondary sources, which is the classic type of material for inclusion in Wikipedia. To say they are, or are not, correct or definitive or relevant (against claims in the sources vis-a-vis relevance) is WP:OR. We are not here to discuss the merits of the research (which claim there is a link and it is relevant to CD), but to simply reference the existence of such research. I also note this is why I oppose such policies as WP:UNDUE, as people start to use their own OR (or just opinions) as a reason for exclusion, in contravention of clear standards (reliable secondary sources, mainly) for inclusion (that have been met IMO.) Int21h (talk) 21:59, 26 May 2013 (UTC) Int21h (talk) 22:16, 26 May 2013 (UTC) Int21h (talk) 22:29, 26 May 2013 (UTC)
I think you're veering off topic. It is a matter of editorial judgement whether to discuss reports of a possible association with other skin conditions, and I think that doing so would be premature and place excessive emphasis on something that is not yet fully established. JFW | T@lk 22:51, 26 May 2013 (UTC)
Obviously I don't think I'm off-topic, given that the reasons for reverting my edit have gone from "lack of secondary source" to "WP:UNDUE" all the way to "editorial judgement". This is important because "editorial judgement" is not a blanket reason for reverting others' edits that meet inclusion criteria. I think we should all admit that my edit is not against any WP policy, that the reason for reverting me is something else. I would have preferred to have started the discussion at this point, but I don't think people thought I would get so technical over a sentence. WP inclusion standards are literally intended to force the debate to this point, where an editor reverting another is forced to increasingly refer to ever-ambiguous reasons until it ultimately comes down to what its really about: personal opinions, a.k.a. bias.
So yes, I think this is about a judgement call. But what is the criteria for this material? Your judgement? Based on what? Your experience? This is the whole point of WP policies, to preclude such nonsense. I think what we have here is a classic "I don't believe it" situation. This is the "not fully established" phrase you use. It is really not our place, neither mine nor yours, to decide such things; it is enough that literature (sources) assert there is a potential link, and our job is to, at a minimum, report that such assertions exists. This is not an assertion, like the example in WP:UNDUE, which contradicts majority views. This is not an assertion from a primary source. This is not an assertion from an unreliable source. If there are other similar conditions that meet this criteria, as you say, go ahead and add them too (or don't), but this has no bearing on my edit, and certainly not reason to revert me.
These journal articles are not "reports"; these are reviews of medical studies (that were probably started because of multiple reports; funding studies ain't easy). Not one medical study, but multiple medical studies, with secondary sources discussing and hypothesizing on their meaning and importance, etc.
This is an edit mentioning studies asserting potential links between CD and a specific dermatological condition, backed by multiple reliable, secondary sources. As such, it is simply incorrect to revert my edits. Int21h (talk) 01:59, 27 May 2013 (UTC) Int21h (talk) 02:04, 27 May 2013 (UTC)
Please propose a way in which you are going to address my concerns. JFW | T@lk 17:37, 27 May 2013 (UTC)
Per WP:BRD it is the person who wishes to add new content who is required to get consensus before the addition. Doc James (talk · contribs · email) (if I write on your page reply on mine) 17:59, 27 May 2013 (UTC)
No. WP:BRD is not a policy and does not impose requirements. It in particular does not change any burdens of proof; consensus building is not an excuse for editors imposing additional and intractable requirements. I actually think WP:BRD hints at what is happening here though: "not for reverting changes .. to protect your preferred version or ideas". It is merely a guideline to encourage discussion, which we are doing. Int21h (talk) 01:32, 28 May 2013 (UTC)


OK, I think I should summarize (note this is a large section and someone will inevitably point out errors so it will probably have to be modified as the discussion progresses.) I wanted to add the following sentence and was reverted:

There is also some evidence of a link to [[atopic dermatitis]], a type of [[eczema]].

I believe I should elucidate on my conversion process, i.e. how I turned the sources' claim(s) into that sentence. Throughout the numerous sources, there are various strengths of claims, from strong claims ("significantly more common") to weak claims ("linked"). I have chose to pick the lowest common denominator, to wit, that there is a "some evidence of a link", as such a claim can be support by all sources. We should also think about diluting it even more like "assertions of evidence of a link" or "claims of a link" or similar, or the even weaker "disputed assertions of a link".

This was added under the section "Miscellaneous" that begins:

Coeliac disease has been linked with a number of conditions. In many cases, it is unclear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition.

I note the section does not begin (emphasis added):

Coeliac disease has been conclusively linked with a number of conditions. In many cases, it is unclear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition.


Coeliac disease has been definitively linked with a number of conditions. In many cases, it is unclear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition.


Coeliac disease has been linked with a number of conditions. In many cases, it is clear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition.

This actually logically forms part of what my added material claims, given that my added sentence is after this one but in the same section. What is not claimed is important to consider: the current article does not list the current claims of a "link" as either conclusive or definitive but leaves the type of link as unqualified.

So on to a survey of the research. I begin with a selection of references, themselves often secondary sources reviewing other secondary and primary sources:

  • Hodgson, Davies, Gent, and Hodson. "Atopic disorders and adult coeliac disease", Lancet 1 (7951), pp. 115–117, 1976. (Hereinafter "Hodgson 1976".)
  • Cooper, Holmes, Cooke. "Coeliac disease and immunological disorders", British Medical Journal 1 (6112), pp. 537–539, 1978. (Hereinafter "Cooper 1978".)
  • Williams. "Coeliac disease and allergic manifestations", Lancet 1 (808), 1987. (hereinafter "Williams 1987".)
  • Kelly, O'Shea, Kelly, Feighery, Weir. "Atopy in childhood coeliac disease", Lancet 2 (109), 1987. (Hereinafter "Kelly 1987".)
  • Greco, De Seta, D'Adamo et al. "Atopy and coeliac disease: bias or true relation?", Acta Paediatrica Scandinavica 79 (6-7), pp. 670–674, 1990. (Hereinafer "Greco 1990".)
  • Ciacci, Cavallaro, Iovino et al. "Allergy prevalence in adult celiac disease", Journal of Allergy and Clinical Immunology 113 (6), pp. 1199–1203, 2004. (Hereinafter "Ciacci 2004".)
  • Caproni, Bonciolini, D'Errico, Antiga, Fabbri. "Celiac Disease and Dermatologic Manifestations: Many Skin Clue to Unfold Gluten-Sensitive Enteropathy", Gastroenterology Research and Practice 2012, 2012. (Hereinafter "Caproni 2012".)

Now I turn to what the references say:

  • Hodgson 1976 states "flexural eczema was significantly more common in patients with adult coeliac disease" in its abstract. This is a primary source.
  • Cooper 1978 reviews Hodgson 1976 as a secondary source stating (considering both this research combined with Hodgson 1976) "suggests that .. eczema [is] more common in patients with coeliac disease than in the normal population." This is both a primary source and a secondary source.
  • Greco 1990 states "Several reports have suggested a relationship between atopy and coeliac disease". This is both a primary source and a secondary source.
  • Ciacci 2004 states "atopic dermatitis was about 3 times more frequent in patients with celiac disease". This is a primary source in that is conducted a medical study, but it is also a secondary source as it also surveys the literature saying "some reports have suggested that allergy manifestations are more frequent in patients with celiac disease" citing Williams 1987, "Atopic disorders were more frequently found in children" citing Kelly 1987, and "Atopic disorders were more frequently found in .. adult patients with celiac disease and their relatives than in normal control subjects" citing Hodgson 1976 and Cooper 1978. This is both a primary source and a secondary source.
  • Caproni 2012 reviews all of the above literature reiterating the same as given above. This is secondary source.

I note there are also criticisms and counter-criticisms of the criticisms. This does not refute the fact that there is evidence of a link, or my weaker proposal, assertions of a link or disputed assertions of a link.

Terminology should also be discussed. The sources above give 3 related terms: flexural eczema, atopy, eczema, and atopic eczema. This actually poses a considerable problem in my view that must be addressed. There are several options here depending on how one views the relationship between the terms. Cooper 1978 refers to Hodgson 1976's claim of "flexural eczema" as evidencing a link to "eczema". The ICD-10 uses "atopic dermatitis" and "eczema" interchangeably in L20-L30 per its section introduction, with eczema (from what I can tell) being considered the generic term. We may consider just using eczema in my proposed addition instead of atopic dermatitis. Caproni 2012 also states "[Dermatitis herpetiformis] must be differentiated from atopic dermatitis ... in children, whereas eczema ... should be considered in adults."

The concerns I have seen thus far read that have not been alleviated are thus:

  1. "excessive emphasis on something that is not yet fully established";
  2. "the link currently is not of sufficient strength";
  3. "I don't think I can support inclusion of this association at the moment, especially if we're not also going to discuss all those other cutaneous conditions discussed in our sources."

Unfortunately, the concerns are unreasonable (reasons were not given, they were impliedly reasonable):

  1. I believe I must conduct OR and convert the sources' claim(s) of a "link" to that of something stronger like a "fully established" link, which is most often found in the form of a causality claim or similar, but since all (or even most) of the sources do not make such a claim I do not think this can be done per WP:OR combined with WP:MEDRS. The sentence is not "excessive emphasis" in such a large article, especially given the section heading of "linked to" that lists a multitude of other claims. (Again I reiterated that I think the sentence can be shortened as long as the keywords are included.) This concern contradicts the current state of the article, as stated above, as well. It is not reasonable, nor is such a WP policy requirement. Hence I reject this concern as invalid.
  2. The concern that the sources are "not of sufficient strength" falls in the realm of ambiguous requirements; since I do not know what "sufficient" is defined as, I cannot meet such a standard. It is not reasonable, nor is such a WP policy requirement. So I also reject this concern as invalid.
  3. The concern implies I should expand (and hence combine or consolidate) my claim to include other "cutaneous conditions", which I have no idea about (I did not bring them up) and cannot support with references per WP:MEDRS/WP:RS. Whether or not others' claims regarding "cutaneous conditions" can be included have no bearing on the current claim(s) I wish to have included, and such a requirement that I prove others' claims to prove my own is improper. It is not reasonable, nor is such a WP policy requirement. So I reject this concern as well as invalid.

I also note who has announced opposition to my edit:

I assert this is an attempt to hold my edit to unreasonable and unsustained policies, and the reverts should be rejected and my edits re-added. I think I have met my burden to show that "Coeliac disease has been linked with .. [atopic dermatitis]" and all the requisite WP policies. I think the main hangup is the inappropriate (and plain incorrect) interpretation that all the links given in the miscellaneous section are "definitive" and/or "conclusive" or that they are required to be (such that a weaker claim cannot and should not be made, as in the current form of the article.) So with that, what say you all? Int21h (talk) 01:32, 28 May 2013 (UTC)

On a less technical level, the only editorial discretion really is how the wording should go, not reverting (deleting) all references to properly sourced material entirely based on subjective and ambiguous standards (a fatal combination.) On Wikipedia, nobody cares that you're a dog. You could maybe attack the material by saying the Journal of Allergy and Clinical Immunology is not reliable or that it cannot be considered a secondary source but not such an ambiguous and subjective standard as has been proposed. Because otherwise all editors will be forced to play such subjective decisions by the numbers (e.g. just get enough other editors that think it is of sufficient strength and that its not excessive emphasis; this is the Internet, not medical school, it will be easier than you think), but I'll drag this out for a while before I go there because of the destructive effect that would have (to accept that standard of review.) Int21h (talk) 07:59, 29 May 2013 (UTC)


... has been reviewed in an international forum doi:10.1136/gutjnl-2011-301346 JFW | T@lk 21:31, 11 December 2012 (UTC)

NEJM review

doi:10.1056/NEJMcp1113994 ("Clinical practice") JFW | T@lk 11:28, 21 December 2012 (UTC)

RfC: Claims of link between medical conditions and WP:WEIGHT

Does a simple (single sentence) claim of a link between medical conditions, in a large article, need to be "fully established" or "definitive" to not run afoul of WP:WEIGHT or any other policy? (Assuming it meets the requirements of WP:MEDRS.) Int21h (talk) 05:17, 9 June 2013 (UTC)

  • Coeliac disease has been associated with a very large number of conditions. Int21h has decided to emphasise one (atopic dermatitis) of many associated skin conditions in their edits. I don't think that is the right way of going about it. The only classically associated skin condition is dermatitis herpetiformis. JFW | T@lk 22:12, 10 June 2013 (UTC)
    • So am I to understand you assert an association must be a "classic association" to be mentioned on Wikipedia? Int21h (talk) 04:17, 11 June 2013 (UTC)
      • You are twisting my words. Please don't do that. JFW | T@lk 20:48, 24 June 2013 (UTC)
  • if a link between conditions is to be mentioned, then there must be a good reason why other linked conditions are *not* mentioned. So if there are multiple conditions of at least as certain association as the one currently mentioned, we should either mention all or none. Quantum Burrito (talk) 23:21, 20 June 2013 (UTC)
This is a tentative link at best as discussed above. Maybe if we had a subpage these less significant details could be discussed there. Doc James (talk · contribs · email) (if I write on your page reply on mine) 20:53, 24 June 2013 (UTC)
  • If this article can get into very technical details about tissue transglutaminase and epitopes which go way over the head of over 99.9% of readers, I don't see why it can't discuss things which are much more relevant to the average reader such as associated medical conditions. The proposed edit adds stuff about eczema; however, the cited review by Caproni et al 2012 discusses psoriasis after DH and says "among the inflammatory skin diseases improved by gluten-free diet, psoriasis is one of the most important". It follows with overviews of alopecia areata, chronic uticaria, hereditary angioneurotic edema, cutaneous vasculitis, and finally atopic dermatitis. I suggest citing Caproni et al with a more balanced overview of the skin conditions the reviewers feel are noteworthy. At the same time, Wikipedia articles improve iteratively. For example, someone probably didn't try to keep out the details on prolamins on the basis that, say, the diet section lacked details. II | (t - c) 03:32, 25 June 2013 (UTC)
The article is in need of simplification. Doc James (talk · contribs · email) (if I write on your page reply on mine) 05:38, 19 August 2013 (UTC)

2013 clinical guideline Doc James (talk · contribs · email) (if I write on your page reply on mine) 05:38, 19 August 2013 (UTC)

doi:10.1038/ajg.2013.79 is the DOI. It's behind a paywall on the Am J Gastroenterol website, always a great idea with guidelines. JFW | T@lk 08:37, 26 August 2013 (UTC)

External links

I don't know where to put this comment so I'll put it here. In the history section there's a brief reference to the diet proposed in 1924 by Sydney Haas with the comment: "This diet remained in vogue until the actual cause of coeliac disease was determined." But the diet is still very much 'in vogue' in a more developed form referred to by Haas as the Specific Carbohydrate Diet. It was presented by Haas in 1951 in his medical textbook 'The Management of Celiac Disease'. So I'm suggesting that a link should be provided to the Wiki article 'Specifi Carbohydrate Diet' which discusses this form of the diet and also discusses a 1987 book for laypeople which is still in print and which lists thirteen web sites devoted to the issue. This 1987 book had been translated as of 2005 into seven languages, a good indication that many people have found the diet useful. In fact the diet addresses a whole range of digestive problems, not just coeliac disease.

Until recently, the article had several useful external links to reliable, professionally-written websites with relevant extra information that could be useful to interested readers and future editors (e.g. the US NIH). This has been removed and replaced with a link to "DMOZ", which appears to be a vague web directory of oddly chosen non-professional websites. I tried to restore the professional medical links, but they were removed and the DMOZ link replaced, with the claim that this is in line with WPMED consensus. Can someone enlighten me as to where WPMED stipulates we must replace reliable medical resources with strange web directories? Arripay (talk) 00:48, 22 September 2013 (UTC)

WP:NOT states we are not a collection of external links. The great think about DMOZ is that one can go there and help improve the links they have if you deem they are not professional. Doc James (talk · contribs · email) (if I write on your page reply on mine) 11:35, 22 September 2013 (UTC)
Let me get this straight - this is not a collection of external links, so we should link to a collection of external links. We can then edit the other site's collection of links, but we can't do that directly on wikipedia - the website on which I am actually an editor. Nope, still making no sense to me I'm afraid. The manual of style for medicine-related pages says of external links: "Disease-related organisations and government health departments sometimes produce web pages containing substantial information that would be of interest to readers wishing to further study the topic. Such links are chosen for the information content, not because the organisation is particularly worthy or helpful." This perfectly describes the links that were there (NIH etc). That's been changed to link to a bunch of irrelevant stuff. It baffles me that anyone could see that as an improvement. Arripay (talk) 23:27, 22 September 2013 (UTC)
None of the links really contains anything our article does not already discuss. Doc James (talk · contribs · email) (if I write on your page reply on mine) 12:31, 23 September 2013 (UTC)
May as well delete all of them, then. Arripay (talk) 19:21, 24 September 2013 (UTC)

Updates in Genetics in reference to Evolutionary History

I would like to make the following changes to the final paragraph in the Genetics subsection so the paragraph reads:

The prevalence of CD genotypes in the modern population is not completely understood. Given the characteristics of the disease and its apparent strong heritability, it would normally be expected that the genotypes would undergo negative selection and to be absent in societies where agriculture has been practised the longest (compare with a similar condition, Lactose intolerance, which has been negatively selected so strongly that its prevalence went from ~100% in ancestral populations to less than 5% in some European countries). This expectation was first proposed by Simoons (1981).[5] By now, however, it is apparent that this is not the case; on the contrary, there is evidence of positive selection in CD genotypes. The DQ2.5 haplotype, in certain tests did not show a preference for positive selection but, 4 out of the network of 40 CD related genes showed a positive selection.[6] The four genes are also risk factors for other diseases such as Crohn’s, Type 1 diabetes, and other autoimmune/inflammatory diseases.[6] It is suspected that some of them may have been beneficial by providing protection against bacterial infections.[7][8] One particular loci, SH2B3 when in a homozygous patient, allows for a higher concentration of cytokines responsible for inflammatory responses. This observation further suggests that the four loci with a positive selection may play a role in fighting infection but makes individuals more susceptible to autoimmune diseases like coeliac.[6]

End of edit

My reasoning for this change is to update the proposed cause of coeliac. What was present in the article wasn't completely correct and I believe this expands on why this disease is still prevalent despite its negative effects. Please let me know what changes you would suggest either here or on my talk page. Thanks.

Note: The reference numbers should changed once the edit is made. If I messed that up, please let me know.

Tcs46 (talk) 02:04, 31 October 2013 (UTC)

Per WP:MEDRS we typically use secondary sources rather than primary sources. This is a primary source [1]]. Can you make these changes? Thanks Doc James (talk · contribs · email) (if I write on your page reply on mine) 12:42, 31 October 2013 (UTC)
The article you linked to is already present in the article and was not added by me. Tcs46 (talk) 15:14, 31 October 2013 (UTC)
I'm not finding it. It would be helpful if you would use PMIDs (and add them to your suggested text to make it easier to review your sources). For example, I do not see PMID 19805228 in the current article. SandyGeorgia (Talk) 19:03, 31 October 2013 (UTC)
OK, I found and tried to fix the problem, and failed so I archived the old sections. That primary source was not in the article-- but it was being pulled into the ref list here on talk because it was discussed elsewhere on this talk page. I fixed it by changing the reflist parameter in this talk section and archiving the old talk sections. There is a reference template that will pull only from the current section on talk, but I don't know where to find it-- perhaps someone else will fix it. SandyGeorgia (Talk) 19:16, 31 October 2013 (UTC)

Proposed change

So, you've included the entire current para above with your changes. Is it correct that your proposed change is adding these two sentences (for which I have corrected your citation of Abadie to the style used in the article):

  • The DQ2.5 haplotype, in certain tests did not show a preference for positive selection but, 4 out of the network of 40 CD related genes showed a positive selection.[9] The four genes are also risk factors for other diseases such as Crohn’s, Type 1 diabetes, and other autoimmune/inflammatory diseases.[9]
  • One particular loci, SH2B3 when in a homozygous patient, allows for a higher concentration of cytokines responsible for inflammatory responses. This observation further suggests that the four loci with a positive selection may play a role in fighting infection but makes individuals more susceptible to autoimmune diseases like coeliac.[9]


  1. ^ source:
  2. ^ Mann, Denise (9 February 2011). "New Treatment for Celiac Disease?: Research Shows Blocking a Protein May Reverse Celiac Disease Symptoms". WebMD Health News. Retrieved 24 April 2012.
  3. ^ Yokoyama, S (Sep 15 2009). "Antibody-mediated blockade of IL-15 reverses the autoimmune intestinal damage in transgenic mice that overexpress IL-15 in enterocytes". PNAS. 106 (37): 15849–15854. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: extra punctuation (link)
  4. ^ Caproni, M; Bonciolini, V; D'Errico, A; Antiga, E; Fabbri, P. "Celiac Disease and Dermatologic Manifestations: Many Skin Clue to Unfold Gluten-Sensitive Enteropathy". Gastroenterol Res Pract. Hindawi Publishing Corporation. 2012. doi:10.1155/2012/952753. PMID 22693492.
  5. ^ Walcher, Dwain N. and Kretchmer, Norman (1981). Food, nutrition, and evolution: food as an environmental factor in the genesis of human variability. Papers presented at the International Congress of the International Organization for the Study of Human Development, Masson Pub. USA. pp. 179–199. ISBN 0893521582.{{cite book}}: CS1 maint: multiple names: authors list (link)
  6. ^ a b c [Abadie, V., Sollid, L., Barreiro, L., & Jabri, B. (2011). Integration of Genetic and Immunological Insights into a model of Celiac Disease Pathogenesis. Annual Review of Immunology, 493-525.], PMC 21219178.
  7. ^ Catassi, Carlo (2005). "Where Is Celiac Disease Coming From and Why?". Journal of Pediatric Gastroenterology & Nutrition. 40 (3): 279. doi:10.1097/01.MPG.0000151650.03929.D5.
  8. ^ Zhernakova A; et al. (2010). "Evolutionary and Functional Analysis of Celiac Risk Loci Reveals SH2B3 as a Protective Factor against Bacterial Infection". The American Journal of Human Genetics. 86 (6): 970. doi:10.1016/j.ajhg.2010.05.004. {{cite journal}}: Explicit use of et al. in: |author= (help)
  9. ^ a b c Abadie V, Sollid L, Barreiro L, Jabri B (2011). "Integration of genetic and immunological insights into a model of Celiac Disease pathogenesis". Annual Review of Immunology: 493–525. doi:10.1146/annurev-immunol-040210-092915. PMID 21219178.{{cite journal}}: CS1 maint: multiple names: authors list (link)

I am not following why you want to add these two sentences, but perhaps DocJames or Jdfwolff will. SandyGeorgia (Talk) 19:31, 31 October 2013 (UTC)

They add clarification to the genetic history. The paragraph before the change made it seem that the haplotype was positively selected for. This is incorrect. 4 other genes within the network are positively selected for and this change gives an example to show their significance in other diseases related to coeliac. Tcs46 (talk) 18:46, 1 November 2013 (UTC)
If clarification was the intent, perhaps one of the other editors here can reword in such a way that that is achieved. SandyGeorgia (Talk) 18:48, 1 November 2013 (UTC)

Selenium and thyroid disease

3AlarmLampscooter added a discussion about doi:10.4415/ANN_10_04_06. This seems to pose a number of theories about why autoimmune thyroiditis is linked with coeliac disease, and places hyposelenaemia at the centre of the hypothesis. As SandyGeorgia suggests, this is not something that has made its way into the major reviews on coeliac disease. The theory is probably too obscure to discuss here with such certainty (WP:WEIGHT is the relevant policy). If stronger sources can be provided, this can be revisited. JFW | T@lk 20:50, 17 December 2013 (UTC)

  • The link between coeliac disease and low selenium levels was published in the BMJ all the way back in 1985. Nature Endocrinology published a review last year calling selenium deficiency "likely to constitute a risk factor for a feedforward derangement of the immune system". While benefits of actually supplementing selenium in either case is still a very controversial topic and perhaps should be left out, I think it's pretty clear selenium is a legitimate factor in the diseases, and all the explained pathways between selenium, coeliac and thyroiditis in the 2010 review I cited checked out fine to me. 3AlarmLampscooter (talk) 14:13, 18 December 2013 (UTC)
PMID 22009156 is a recent review; Jfdwolff may have better information about the journal. SandyGeorgia (Talk) 17:36, 18 December 2013 (UTC)
My concern is that the recent reviews don't mention this link directly. The only source that unequivocally claims that in coeliac disease, the predisposition to thyroid disease is mediated by hyposelenaemia is the obscure review in Ann Ist Super Sanità. Selenium status may be abnormal in coeliac disease, but can we say with confidence that it is a causal relationship? I think the fact that this hypothesis is not followed by any other reviewer is sufficient to exclude it from this very broad article.
Unfortunately I have no access to the Nat Rev Endocr review (doi:10.1038/nrendo.2011.174), but if it does not mention coeliac disease explicitly I don't think it's going to help us much. JFW | T@lk 19:30, 18 December 2013 (UTC)
Funny how fast things can progress, the new version of Clinical Gastroenterology just came out a few days ago, now citing the Stazi and Trinti paper on the link to autoimmune thyroiditis. Highlights include "Micronutrient screening for zinc, copper, and selenium should be performed at least annually and sooner, if deficiency is suspected" and "CD patients deficient in selenium may complain of generalized fatigue and muscle weakness. Physical exam and labwork may reveal low serum selenium levels, hypertension, cardiomyopathy, elevated transaminases, autoimmune thyroid disease, and perhaps even psychiatric manifestations (schizophrenia)". I'd say at this point we should update the article to reflect this. Any objections 3AlarmLampscooter (talk) 17:17, 20 December 2013 (UTC)
I am happy to mention selenium deficiency with doi:10.1007/978-1-4614-8560-5_11 as a reference, but it doesn't seem that this source says that hyposelenaemia is the cause of the thyroid disease, so I don't think I can support any claims to that effect. JFW | T@lk 23:14, 21 December 2013 (UTC)
I've re-added the content with some more reserved wording on possible causation versus correlation, in addition to copper and zinc deficiency. Other evidence of selenium's beneficial effects for some patients continues to grow: 3AlarmLampscooter (talk) 20:21, 24 October 2014 (UTC)
3AlarmLampscooter The points about trace element deficiencies are reasonable and the source is good, but the fringe theory about the association with thyroid disease needs to stay out. We would need a much stronger source than what you've presented so far. JFW | T@lk 22:00, 26 October 2014 (UTC)
Incidence of Selenium deficiency in thyroid disease, Celiac Disease and Autoimmune Thyroid Disease. 3AlarmLampscooter (talk) 20:47, 1 December 2014 (UTC)

Hwp1 proposed to be included in the transglutaminase section

Hwp1 should be added to the Coeliac Disease transglutaminase section page.

I think Hwp1 (Candida Albicans protein) is as required to be cited in the Coeliac Disease page of Wikipedia as VP7 (Rotavirus protein). VP7 is greatly related to Coeliac disease, but Hwp1 too.

VP7 is cited in the Coeliac Disease Wikipedia page and Hwp1 is not.

Moreover, VP7 is cited in the transglutaminase section when VP7 is NOT so far defined as a transglutaminase substrate. Hwp1 has been proven as a transglutaminase substrate, It has also been clearly associated with celiac disease by the homology between Hwp1 and gliadin.

The three references below has been considered by Doc James as Not suitable to allow Hwp1 to be included.

1) Staab JF, et al. (1999) Adhesive and mammalian transglutaminase substrate properties of Candida albicans Hwp1. Science 283:1535-1538

2) Nieuwenhuizen WF, et al. (2003) Is Candida albicans a trigger in the onset of coeliac disease?. Lancet 361: 2152–54

3) Sakly W, Thomas V, Quash G, El AS. 2006. A role for tissue transglutaminase in alpha-gliadin peptide cytotoxicity. Clin. Exp. Immunol. 146:550–558

But these three references show that:

1) Hwp1 is a transglutaminase substrate.

2) Hwp1 share homology in primary sequence with gliadin.

3) Gliadin is a transglutaminase substrate.

4) Hwp1 and gliadin enter human body by the same route: oral route and transglutaminase acts on both gliadin and Hwp1 being this transglutaminase action related to associated diseases (Coeliac Disease and Candidiasis respectively)

5) Hwp1 and gliadin are cause of diseases in human oro-esapho-gastro-intestinal system.

6) Hwp1 (Candidiasis) and gliadin (Coeliac disease) related diseases share histophatological tissue damage characteristics.

7) Hwp1 is a Candida Albicans virulence factor in Candididasis disease and gliadin is the causative agent of coeliac disease.

8) Removing of Hwp1 (hwp1 knockout mice experiments) is related with significantly reduced virulence and removing of gluten

I think that the eight proven facts above do Hwp1 inclusion in the transglutaminase section of Coeliac Disease page of WIkipedia neccesary to have a complete understanding of the relationships in this disease.

The truth is I still do not understand why these references are invalid having been published in prestigious publications like Science or Lancet.

--FOTGCREN (talk) 13:47, 18 February 2014 (UTC)

The edit in question is this one [2] were the primary sources were removed and the review left.
This [3] is a primary source
This [4] is a primary source
And this [5] is a primary source
Per WP:MEDRS we should be using secondary sources such as review articles Doc James (talk · contribs · email) (if I write on your page reply on mine) 14:19, 18 February 2014 (UTC)
Indented line

--Ok. Thanks for the clarifications. I now can understand that my references are primary sources and they are not allowed as references in this type of medical pages of Wikipedia. I need Wikipedia reliable sources that acomplish with Wikipedia policies. I´ll try to find them. I request anybody to help me to do it. I think Hwp1 must be included in transglutaminase section of Coeliac Disease page. --FOTGCREN (talk) 15:12, 18 February 2014 (UTC)

Hello FOTGCREN, I think I need to clarify why I reverted your edit[6] despite your use of secondary sources. I think you might be falling foul of WP:NOR/WP:SYNTH, suggesting an association that can only be supported by sources if you extrapolate stuff from them. If I search PubMed with MeSH "MAJR" headings "celiac disease" and "candida albicans" only a single paper comes up (PMID 12826451). When I review citations to this paper in Scopus, it has received some citations but not in the core reviews of coeliac disease in any of the major journals. I think it is a theory that has not been sufficiently investigated to be suitable for inclusion on this page.
I am not at all clear whether "Alternative Medicine Review" is a WP:MEDRS, by the way. JFW | T@lk 11:43, 28 February 2014 (UTC)
Oh, and FOTGCREN, your personal website[7] seems to concede that this is still a hypothesis. It's not common for encyclopedia articles to discuss hypotheses that are awaiting proof, unless the proof has been elusive and the hypothesis has received extremely widespread attention (e.g. the Higgs boson). JFW | T@lk 11:54, 28 February 2014 (UTC)
First of all, thanks for the clarifications. I agree with almost everything you say. Anyway, there is a fact, two proteins, Hwp1 and gliadin, its primary sequences are available in UNIPROT.,, It is simple. Compare them. Protein structure define protein function and enzyme substrate ability. Primary sequence has its role in building structure of proteins. It is not a definitive proof but it is very suspicious. Maybe not so suspicious as the fact that after Nieuwenhuizen, research on these issues does not exist. Maybe does not interest that were to conclude that the cereals couln´t be a human food. I´ll try one last editting trying to accomplish all requirements about "WP:NOR" and "WP:PRIMARY" — Preceding unsigned comment added by FOTGCREN (talkcontribs) 13:38, 28 February 2014 (UTC)
Oh, and maybe the Higgs boson hypothesis, like searching what is the exactly number of stars in the universe be an hypothesis that has received extremely widespread attention. To me it has no interest compared with the minimun possibility of knowing how any food you eats everyday could be the cause of any disease that affects you in the future. Thats is important to me. Not the Higgs Bosson. I suppose I'm a rare guy. Thanks anyway for your time.
--FOTGCREN (talk) 17:41, 28 February 2014 (UTC)

Have reverted these edits [8] as:

1) This line was copied and pasted from this source "Nieuwenhuizen et al.9 demonstrated that the virulent factor of Candida albicans—hyphal wall protein 1—shares similar sequence homology of amino acids with gliadin." [9] 2) This source does not mention the disease in question [10] Doc James (talk · contribs · email) (if I write on your page reply on mine) 19:38, 28 February 2014 (UTC)

And this one? There were three paragraphs deleted.
The Candida albicans hyphal wall protein 1 (Hwp1) is homologous to T cell epitopes involved in celiac disease.
Wagner (2005) "Innate and Adaptive Immunity against Candida spp. Infections in the Gastrointestinal Tract". Fungal Immunology: 303–321.
--FOTGCREN (talk) 21:20, 28 February 2014 (UTC)
Yes you copied and pasted from this source to. Doc James (talk · contribs · email) (if I write on your page reply on mine) 21:41, 28 February 2014 (UTC)
Ok. Its true but there are few ways of saying the same. Last attempt in this Coeliac Disease page. I´ll try to do my best. Thanks. — Preceding unsigned comment added by FOTGCREN (talkcontribs) 22:51, 28 February 2014 (UTC)
Well, I better thought that I am going to leave the decission of adding these two references on you Doc,do what you think is best;
It was shown by the dutch Ph.D. Willem Nieuwenhuizen in the year 2003 that gliadin has homologous sequences of amino acids when it is compared to Candida albicans hyphal wall protein 1 (hwp1). This is indicated in the review: “New Insights in Celiac Disease”.
Branski D. New Insights in Celiac Disease. RMMJ 2012;3 (1):e0006. doi:10.5041/RMMJ.10073
T cell epitopes related to celiac disease were shown having homologies with aminoacids into the sequence of the Candida albicans hyphal wall protein 1 (hwp1). This is indicated in the review: “Innate and Adaptive Immunity against Candida spp. Infections in the Gastrointestinal Tract”
Wagner (2005). "Innate and Adaptive Immunity against Candida spp. Infections in the Gastrointestinal Tract". Fungal :Immunology: 303–321.
Put these links or not say it did not seem right not to add them with reference to the review of Williams 2013 indicating that Hwp1 is a substrate of transglutaminase.
Hyphal wall protein 1 (Hwp1; encoded for by the HWP1 gene) is a protein involved in Candida Albicans adhesion to epithelial cells and this protein is perhaps the most widely studied adhesin of C. albicans. Glutamine residues in the N-terminal domain of Hwp1 can be cross-linked to unidentified host proteins by host transglutaminase activity and this leads to covalent attachment of the yeast to host epithelial cells. This interaction has been shown to be important for Candida albicans colonisation within the oral cavity
Williams DW, Jordan RP, Wei XQ, Alves CT, Wise MP, Wilson MJ, Lewis MA (2013)."Interactions of Candida albicans with host epithelial surfaces". J Oral Microbiol.doi:10.3402/jom.v5i0.22434.
Yet when VP7 is not a transglutaminase substrate proved (to date). And VP7 is broadly cited in this page.
Thanks for all.
--FOTGCREN (talk) 23:56, 28 February 2014 (UTC)

FDA issued final regulation for gluten free

The FDA issued final regulation for gluten free last year [11]. The article should be updated to reflect that.Jasonhein1 (talk) 23:25, 20 February 2014 (UTC)

I have updated the citations for the final rule and added a citation to the codified regulations. The mention of the (proposed) regulations was already in the #Diet section next to the Codex Alimentarius mention. Int21h (talk) 17:34, 21 February 2014 (UTC)
I should also note that the Food Allergen Labeling and Consumer Protection Act of 2004 (the law requiring regulation of the term "gluten-free") also requires wheat to be identified prominently on labeling. The European Union also has some analogous regulations, somewhat explained here and here, which discusses the background of Commission Delegated Regulation (EU) No 1155/2013, which was published November 2013 and amends Regulation (EU) No 1169/2011, with implementing regulations to come later; "gluten-free" had been regulated in the EU since 2009 with Commission Regulation (EC) No 41/2009, which will be repealed by Regulation (EU) No 609/2013 effective July 2016. Int21h (talk) 19:26, 21 February 2014 (UTC)
Those are some interesting links. There should be more coverage on gluten-free labeling in the US given the market size for the product. Also, FALCPA said that gluten-free should have been finalized by 2008, but wasn't which perturbed the celiac community. Also, there's no mention of the CSA certification seal, or GFCO's GF seal.Jasonhein1 (talk) 22:27, 21 February 2014 (UTC)

Increasing incidence?

The article suggests that there may not be a real rise in prevalence, it was simply underdiagnosed in the past: Historically, coeliac disease was thought to be rare, with a prevalence of about 0.02%.[88] Recent increases in the number of reported cases may be due to changes in diagnostic practice.[89]
Recent studies seem to contradict that view.

How can you ensure that these are not the results of increased testing? JFW | T@lk 21:33, 23 February 2014 (UTC)

No studies quite "ensure" that yet that I know of, but the sources that Ssscienccce offered above are certainly reputable, and these more recent papers do speak directly to the question of underdiagnosis vs. real evidence for a real rise. The italicized portions included above are quoted from the "Conclusions" sections of the abstracts of these papers, and specifically use the terms "prevalence" and "incidence" to mean actual occurrence of CD -- as opposed to just a rise in number of diagnoses from better screening methods. Here are a few more related sources corroborating the involvement of external factors:

"'This tells us that whatever has happened with celiac disease has happened since 1950,' Dr. Murray says. 'This increase has affected young and old people. It suggests something has happened in a pervasive fashion from the environmental perspective.'"
“'Consumption of wheat has increased steadily over the past 50 years, but it still is less than what it was a century ago, so the issue is not simple consumption,' Murray noted. 'It more likely involves the wheat itself, which has undergone extensive hybridization as a crop and undergoes dramatic changes during processing that involves oxidizers, new methods of yeasting, and other chemical processes. We have no idea what effect these changes may have on the immune system.'”
"Dr. Alessio Fasano, MD, director of the Center for Celiac Research and chief of the division of pediatric gastroenterology and nutrition at Mass General Hospital for Children, was a co-author of that recent study about breast-feeding and timing of gluten introduction. He says he found the 'major, unpredictable results shocking. The lesson learned from these studies is that there is something other than gluten in the environment that can eventually tilt these people from tolerant to the immune response in gluten to developing celiac disease...We’ve been radically changing our lifestyle, particularly the way that we eat, too fast for our genes to adapt.'"

In any case, I think it's worth updating the article to mention the fact that more recent studies have provided strong evidence that the increase in CD incidence can't simply be explained by better screening methods. If no objections, I will do this. Dalfet (talk) 09:07, 18 October 2015 (UTC)

Found a BMJ review that says their is a 4.5 fold increase (despite taking into account changing diagnostic criteria). Have updated with that review. Doc James (talk · contribs · email) 09:06, 19 October 2015 (UTC)