I am not sure what the relevance of this topic in this group is but I can clarify this as much as it can be clarified. I come at wheat glutens from an immunological perspective and so this discussion will tilt into its immune system biochemistry.
Scientific words often have two meanings For example human can mean specifically members of the species Homo sapiens sapiens (as to be distinguished from Neanderthals and other archaic homo sapiens), or in a more general sense any member of the taxa called homo. As to be distinguished from Neandertals and other Archaic homo sapiens. Gluten should be treated the same. Where does gluten come from? In the specific sense gluten refers to the sticky protein content that is derived from the hexaploid wheat species Triticum aestivum and some closely related subspecies (durum wheat as another example). However, it is only the hexaploid species that derives gliadins from three species, T. monococcum (ancestral-A), Aegilops speltoides (ancestral-B), and Aegilops tauschi strangulatum (ancestral-D) carry the full breath of properties associated with gluten (BTW, last 2 species are goat grasses). Each of these contribute unique protein components to the properties of gluten. Bread wheat is not of natural origin, the pollard wheat (AB) was used in Europe up until recently. Bread wheat evolved about 8000 years ago in Anatolia, it followed other wheat crops into Europe after the Early Neolithic and could not be grown in many areas because of its sensitivity to cold weather and poor soils. During the Bronze and Iron age wheat was increasingly cultivated in Western Europe. Up until r! ecently wheat was not grown in Ireland and parts of Scandinavia, where the primary grains grown were Barley, millet and Oats. Barley was preferred because of the ability to make alcohol, and to make storable products over the winter. Wheat is the preferred cereal crop where it can be grown because it has the highest protein content, around 5% which compares to much lower content for all related cereals. Definitions: Gluten as defined by culinary industry (a.k.a. bread making quality of wheat) Gluten as medically defined (a.k.a. gluten-free, DQ2.5/DQ8, tTG reactive gluten). 'Gluten' as a food additive (a.k.a deamidated gluten) 'Glutens' and gluten-like proteins (a.k.a. seed-prolamins from non-Triticeae plants) Gluten as defined by culinary industry. Wheat gluten is a seed storage protein but has several other functions. It is composed of two types of proteins known as prolamins and glutelins. Glutelins are almost entirely restricted to the grass tribe Triticeae. In the specific sense of the word wheat prolamins are called gliadins. Gliadins composed of repeating elements that are characterized by a 4 residue length polypeptide sequence that is a transglutaminase (TG) substrate. The binding and crosslinking capabilities of wheat gluten allow wheat to make elastic complexes (covelantly bound) that allow rising bread to trap carbon dioxide released from the yeast, that allow it to harden and keep its form when dried. This is also the definition of gluten used by the Roman Catholic Church in defining what is a 'host'. Gluten as medically defined. Because of this TG, gliadins can be cross-linked to other proteins in the presence of transglutaminase activity of human tissue TG (tTG). Of particular chemical interest is the alpha-2 gliadin (A contributed by the A components of the genome). This particular gliadin contains a 32 residue heavily overlapping HLA-DQ2.5 restricted T-cell recognition domain. This region has IIRC 4 transglutaminase substrate sites. Complete deamidation of the 32mer increases the T-cell recognition by an order of magnitude, and probably explains why late onset celiac disease (once very rare) is increasing along with the rate of deamidates gluten used in the last 50 years (whole wheat bread, imitation crab meat, etc.). [Just to note, it is the crosslinking of prolamin to tissue transglutaminase in the human gut that results in both and autoimmune disease and villus atrophy. Tissue TG is both a cause, by crosslinking and an autoimmune target, but there are no-known genetic differences between GSE a! nd normal individuals with TTG gene. IOW gliadin is a proxy for a unsuppressed T-cell recognition site that tTG does not have] The region in and of itself can cause gluten sensitive enteropathy (GSE; later stages known as Celiac Disease). Two other regions of wheat gliadin (alpha-9) are capable of circumventing the mono- and di-peptide limiting exclusion barrier around the gut, this can then alter CXC elements and basically open up the epithelium of the small intestine to the bidirectional transfer of proteins, and thus create inflammation. There are still other elements, for example omega-5 gliadin that can cause rare aspirin/exercise induced anaphylaxis (a property shared with certain shell fish antigens), therefore glutens can _also_ be allergenic. Thus wheat gluten specifically, has multiple inflammatory properties that most other cereals lack. But medical definition focuses particular on one aspect, the ability to perpetuate GSE in foods. To understand this we need to know that Gluten sensitivity has three areas: classically gluten sensitivity contains only celiac disease. The contentious area is neurological sensitivity. The final area is acute and idiopathic gluten allergies (that is to say an anaphylaxtic allergic reaction that is facilitated by other sensitivities and). Wheat allergy represents about 4% of people, celiac about 1%, Neuropathies (of no apparent cause Celiac or allergic) <0.001%, and induced anaphylaxis is equally rare. Because grasses seed all at once, they prevent single species from consuming all seeds for the coming year germination. Somewhere back in wheats evolution rodents began stockpiling seeds. The plants evolved to produced seeds with more toxic products. Wheat glutens are also toxic (celiac like disease) to mice and rats when fed in high quantities at a young age. GSE in older animals has not been noted, however, thus it appears that rodents coevolved some resistance. [Speculation on evolution] Wheat grass appear to prefer grazing animals as a preferential distributer of seeds. Humans that are susceptible to GSE appear to have evolved in areas where Triticeae did not evolve and that there were other selective pressures. DQ2.5 appears to have spread from N. Africa into Iberia where the AH8.1 haplotype (A1-B8-DR3-DQ2.5cis) evolved, this spread across Europe during the epipaleolithic but because of isolation remained concentrated in the islandic Gaelic speakers and Scandinavia, and! Serbia. Archaeological studies of their ancestors bones reveal that diet was estuarian, rich in shellfish and Bone carbon studies show that the diet was almost exclusively derived from marine species. The same is also true in the other DQ, DQ8.1 (DQA1*0301:DQB1*0302) is found globally but highest levels are in the Sea of Japan region of Asia and the isthmus of Central America. DQ8.1 appears to have been under strong, atypical positive selection in central America, and peoples in this regions with high levels of DQ8.1 have archaeological evidence of shell mound cultures. Therefore sensitivity to gluten appears to have evolved in a context of some sort of dietary pathogen protection. In DQ8.1 bearing individuals (a few percent of European celiacs) glutelins may be the causal dietary agent, or may contribute to disease. West and North Africa children who subsist on non-Triticeae diets are particularly susceptible to Celiac Disease, in these refuge feeding camps rates as high ! as 5% have been seen. Thus gluten is politically defined. Every edible seed, practically speaking contains gluten homologs, prolamins. Proteins in the grass tribe Triticeae have an abundance of TG sites and thus should be considered chemically active around deamidases and tranglutaminases. Grasses in this tribe include barley, rye, spelt, tritical, and many other plants species and genera. Oats, which are in Aveneae grass tribe (a sister tribe to wheat's tribe), do not have these qualities. A study of 150 celiacs on gluten free oats only found one individual with evidence of enteropathy on an otherwise gluten-free diet (this is about the recurrence rate of refractory disease). Therefore we have a third definition of gluten. As some of you saw on ABC (USA) NightLine last night a discussion about what defines gluten and gluten-free foods. The presenter is incorrect, there is a definition of gluten free, and that is defined by Codex-Alimentarius of the WHO. Essentially, if a food has more than 20 ppm of prolamin & glutalins from any Triticeae cereal it is not gluten-free. http://www.celiac.com/articles/206/1/Codex-Alimentarius-Explained---European-Gluten-Free-Standards-by-Frederik-Willem-Janssen/Page1.html [Other incorrect ABC statements, wheat free diet does not cause vitamin B deficiencies, per say, Celiacs have a problem adsorbing vitamins as a consequence of disease, and adsorption in late onset disease may not completely restore. As a consequence people who have maladsorption phenomena may need to consume more foods with fiber and vitamin B relative to a proto Celiac state. The other problem with gluten free foods is that they are rich in starch and low in fiber. Buckwheat however is not one of these, it is rich in fiber (12%) and thus is a good source of complex carbs. To correct what he said, all Americans should eat more whole foods (whole wheat bread is not a whole food) as these are both rich sources of vitamin B, complex carbohydrates and fiber.] 'Gluten' as a food Additive Gluten thus has another meaning. Gluten is also the deamidated extract from T. turgidum, a dry climate variety with lower protein content used to make modified food starch. The extraction with alcohol removes the glutens, but gluten is not resuspendable without alcohol or deamidation. There are two forms of deamidation, acid and enzymatic. Acid deamidation randomly converts some glutamine to glutamic acid. Enzymatic deamidation specifically targets the 4 amino-acid TG substrate sites. Enzymatic deamidation is preferentially used in the food industry and poisonous to anyone with any form of GSE, a high risk food for anyone with DQ2.5cis/DQ2.5cis genotype, not be fed to children below 1 year of age, and is particularly dangerous to children with DQ2.5 when fed less than 6 mos of age. 'Glutens' as a gluten-like substance in other cereals and edible seeds. So........... that now leaves us with the last definition which when correctly used is gluten-like seed storage proteins. Practically speaking, all seeds (pinto beans, buckwheat, etc) have seed storage proteins which activate when water is added to both provide amino-acids and certain activities to sprouting plants. The qualities of these seed storage proteins differ greatly, many are sticky but lack the cohesive properties of wheat. That is why wheat gluten is added to many of these to make breads. Authors in some papers may colloquially refer to these proteins as glutens others may call them gluten-like. But gluten is really defined by the sticky yeast-risen bread making qualities of cereals. All of this information is available on Wikipedia, you can read pages and follow the links from celiac disease. OK, so clarified but not simple. I should point out, I am a strong advocate that everyone be HLA DR-DQ typed at birth. While being a DQ2.5 hz does not mean you will have GSE, it increases risk 1000 fold over persons without DQ2.5 or DQ8. These two loci are responsible for the greatest number of inheritable diseases, and yet is not routinely typed. Typing of these loci could protect individuals (about 10% of the population) from autoimmune disease. Celiac disease (DQ2.5, DQ8.1) is present in about 1% of Europeans, and this lowers life expectancy by 5 years (mainly due to cancer risks). Type 1 diabetes (DR3, DR4-DQ8.1) is also at risk by age of wheat consumption commencement, meat consumption and coxsackie 4B virus (about 1/500, life expectancy has improved but still around 30-35 in less developed areas). Rheumatoid Arthritis (DR4,DR1, DR11) is at risk when consuming meat (arachidonic acid), smoking cigarettes, and wheat (death occurs as a consequence of morbitiy, type II diabetes and CAD). With these three d! iseases, most preventable if risk are removed early cover about 6% of Caucasian disease. Other autoimmune diseases included multiple sclerosis, systemic sclerosis (scleroderma), Addison's disease, Sjodgren's syndrome, ankylosing spondylitis, Grave's disease, Hashimoto's thyroiditis, psoriasis, primary biliary cirrhosis, and a list of about 50 more diseases confirmed and suspected. All have strong links to HLA DR and DQ. -----Original Message----- From: [email protected] [mailto:[email protected]] On Behalf Of Cathal Garvey Sent: Thursday, July 28, 2011 11:58 AM To: Yair Heimer Cc: [email protected] Subject: Re: buckwheat and gluten It does, although less so than wheat. The sequence of the gluten in terms of amino acids may also be different, though that mightn't be relevant. On 28 July 2011 14:44, Yair Heimer <[email protected]> wrote: > Hi, > Goes any one know if buckwheat contains gluten? > Thanks, > Yair. > > ______________________________**_________________ > Methods mailing list > [email protected] > http://www.bio.net/biomail/**listinfo/methods<http://www.bio.net/biomail/listinfo/methods> > -- letters.cunningprojects.com twitter.com/onetruecathal http://www.indiebiotech.com _______________________________________________ Methods mailing list [email protected] http://www.bio.net/biomail/listinfo/methods _______________________________________________ Methods mailing list [email protected] http://www.bio.net/biomail/listinfo/methods
