Talk:Triticeae

• It's good to see this subject expanding, but a lot of errors and inconsistencies are coming in too. If adding to this page, please ensure that the botanical names you use are consistent with other pages in wikpipedia, especially Hordeum and Triticum, and that biological terms are consistent with wider usage, eg tetraploid rather than quadriploid. This page needs a great deal more correction & I'll try and return to it. Mark Nesbitt 14:28, 8 October 2006 (UTC)

I have made a start on tidying this page. In particular:

• Creating a consistent list of genera that follows a cited, published, widely used scheme. That means deleting Critesion, for example.
• Removing some of the duplication of other articles. All the crop species covered here are covered in detail on their own page. So, I'm planning to retain handy summaries here, with an emphasis on genetics but not too much detail.
• Removing many minor errors, epecially in plant names.
• Removing non-information, e.g. that some wild Triticeae are edible (but never in fact eaten)
• Imposing NPOV on health aspects of Triticeae.
• Clarifying text.

I'll return to this article as there is more work to do on:

• More consistent info on human uses for food & fodder.
• Reworking text for clarity.
• Adding a very important element which is missing - explanation of genomes and their impact on classification.

Mark Nesbitt 20:58, 2 April 2007 (UTC)

I have moved much information out of this group into other groups, but I notice that a large amount of material on the domestication and cultivation of Triticeae cultivars in the Neolithic period was removed. I think the section is important and has been overly abbreviated. Pdeitiker 15:32, 1 July 2007 (UTC)

This is covered in detail (and much more accurately) under each crop. There is surely no need to repeat it in this article.Mark Nesbitt 20:41, 1 July 2007 (UTC)

In that case it is completely missing links to that coverage in those other pages Pdeitiker 03:16, 2 July 2007 (UTC)

There are links from the genera list. But I agree with your point that it is difficult to follow up more detailed accounts from this page. What the Triticeae page needs is a general discussion of the role of genomes, hybridisation and domestication in this tribe, with cross-references to the more detailed presentations found in each genus account. That will avoid repetition, and also lower the risk that one or more of multiple detailed discussions of the same topic will become out-of-date.Mark Nesbitt 08:08, 2 July 2007 (UTC)

Table for genomes has been created, many species to link to, few destinations. Before I created this page I found 2 cladograms for the diploid wheat strains they differed depending on the focus (mtDNA, etc). Aside from that, being a molecular anthropologist the manner of genome definition is basically from cultivars down, which is not very objective, and many genera lack inclusion. My access to info is via pubmedPdeitiker 22:38, 4 July 2007 (UTC)

Citation needed

Citation is needed for this sentence;

"Overlapping properties with regard to food preparation have made these proteins much more useful as cereal cultivars and a balanced perspective suggest a variable tolerance to Triticeae glutens reflects early childhood environment and genetic predisposition."

This contradicts the sentence right before it (which does have a citation).

That sentence was provided to show the extreme nature of the argument. As recently such extreme statements have been made, although I do not support that point of veiw. It is clear that HLA-DQ that are nodal where wheat was domesticated are protective against type I diabetes and while can (~2% of patients) independently mediate celiac disease, it is largely DQ2.5, DQ2.2 and DQ8 in reagions of europe that underwent Neolithization late that have the largest potential. DQ7.5 which is found in 64% of Lebanese shows no special increase as homozygotes in celiac disease, theoretically it should show the same risk as DQ2.2 because together they can form a mediating transhaplotype. But DQ2.2/DQ2.2 are enriched in the DQ2.2/X (X not eqaul to DQ2.5) population. DQ2.2 is at highest frequencies in iberias basque population. Therefore the genetics favors a hypothesis that DQs local to the site of wheat domestication have evolved gluten tolerance more so that DQs most distal and isolated from wheat culture in europe. The most isolated cultures for wheat cultivation are in central and south america. Only one known member of triticeae was routinely gathered. In central and south america the DQ8 gene reaches a 87% bearer frequency, obviously sensitivity played very little selective role there. IOW in some places (central america) or western ireland, the statement may have validity. But in other places it has very little validity. People(s) are not all the same. See HLA-DQ8 page and HLA DR3-DQ2 page. The reason we study HLA-DR and DQ is to assist people to better adapt to the environment they live in, if everyone were the same, there would be no need.

This really needs a citation, as it seems like it was pulled out of the air.

thank you for spotting this, it was a summarization of several opinions in the literature.

Actually it looks like astroturfing. If I do not see this sentence cited (preferably with something from this year) I am deleting it. -Nodekeeper 10:46, 29 August 2007 (UTC)

Frankly, if I was to remove a sentence it would have been the previous debating the safeness of wheat. I have heard arguments of this sort on discussion groups and frankly they are more or less a form of refractory ethnocentrism.

4 references have been provided, however with regard to the astroturfing suggestion, I don't think it fits the criteria, but probably it should be better written. Wikipedia ask for a neutral point of view, there are two camps, one camp that is growing (obsessing) that gliadins are simply poisons, and the other camp that thinks gluten sensitivity is hypochondria. Currently, there are those who are suggesting that the rate of gluten sensititivity is on the rise (certainly true in places like peru and Japan where the first cases of disease were reported in the mid 60s, are now seen at frequencies more consistent with DQ8.1 haplotype frequency ~21% genotype frequency). DQ2.5/DQ2 phenotype represents a new set of disease phenomena, not only is this phenotype more common in childhood disease, more common in type 1 diabetes with GSE, but DQ2.5 homozygotes are specifically associated with more serious disease and 60 to 80% of EATL patients have DQ2.5/DQ2 phenotype. So there is no doubt at the moment that some people will be more likely to get disease no matter the early environment. However, in one specific area of Europe, Western ireland, where barley use has been present for at least the last 3000 years, but wheat use and growth increased after WWII, DQ2.5 is at the highest frequency, and celiac disease incidence quickly in the late 20th century to the highest frequency in the western world. So it does seem true that wheat gliadins influence the threshold which, after crossed, grains like barley can maintain. If we look only at genetics 5 to 10% of DQ2.5/DQ2 will get celiac disease, CTLA4'X' gene may raise likelihood by another 30%, and a few other genes may raise it by 5%. There is nothing more than a 15% penetrance on the most highly associated gene sets for gluten sensitivity. IOW there are environmental factors other than wheat, much of the role currently unclear, that modulate early childhood risk (this is what you are refering to as astroturf?)

Independent evidence, other than the references provided, suggests that children given cow's milk instead of breast milk are more likely to develope cow's milk allergies and intolerances. Children given soy milk instead of breast milk are more likely to develope soy allergies. One of the references provided agrees with this, but suggest wheat may be specially treated, possibly related to its special toxicology. Other studies suggest the rotavirus infection after wheat consumption begins places susceptible (DQ2.5/DQ2?) children at elevated risk. The issue that remains unknown is whether these might develope sensitivity later on in life, for example, travelers enteropathy (rotavirus, enterovirus, dysentary).

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