A database of blood group correlations to common diseases
Total number of records: 145 Matching records: 2
|Description:||Blood Type and Mucin|
The gut is covered by a protective film on the surface called mucin. Like the name implies, mucins are widely distributed in the mucous secretions liberally manufactured by the gut as a sort of 'selective insulation' against potentially hostile bugs and other foreign objects.
Mucin is composed of very large glyco-proteins molecules called mucopolysaccharides, which are liberally laced with sulfur. They have a feather-like shape which gives them the ability to bind water, and this function is what gives mucous its great variability; from the thin watery mucous of a bad head cold to the thick mucous of bronchitis, the amount of water is the only difference.
Mucin is quite variable from one person to another. Many of the glycoproteins of mucin are in fact ABO antigens and blood type is the single most significant influence on the structure of mucin.(3) Its composition can change dramatically in pathological situations. For example, by varying the amount of sulfate in mucin the body can limit the ability of certain bacteria to degrade (a nice word for eat) the glycoproteins in mucus, thereby 'starving' them out.
Whereas in earlier days mucins were only seen as water-binding molecules, protecting the underlying gut lining against harmful agents, the current picture of these molecules is characterized by the a much more selective interaction with their environment, sort of like a gatekeeper.
Sulfate residues on blood group structures can act as sites for selective interaction with gut bacteria and viruses such as Helicobacter pylori. Accumulating data also suggests a very important role for mucin in what is called 'recognition phenomena;' the cellular 'homing' of lymphocytes (from areas such as the tonsils in the throat or Peyer's Patches in the intestines) towards local areas of infection.
Obviously, the body would like very much for whoever is growing in the gut to be immunologically friendly. Your blood type functions with these bacteria in an almost symbiotic (mutually profitable) manner, a sort of microbial 'win-win.' Many of the end products produced by these bacteria help keep the cells lining the digestive tract healthy, or enhance the metabolism of other bacteria, which cannot themselves degrade blood type antigens, but can metabolize the resulting chemicals. Of the common flora normally seen in the digestive tract the strains that degrade blood type antigens are typically the Bifidobacterium (which degrades B antigen but not A) and Ruminococcus species (which typically degrades A and B).
Mucins regulate a great number of biological processes in the gut and ABO blood type regulates mucin.
As we saw in our section on the immune there five classes of antibodies made by the immune system to help protect the body. Immunoglobulin A (the words 'antibody' and 'immunoglobulin' are essentially interchangeable) is most involved in the health of the digestive tract. Unlike most other antibodies which are found predominently in the blood stream, Immunoglobulin A (for short, IgA) has quite a big presence in the gut. It is the main antibody in a variety of secretions such as saliva, milk, and the mucus lining the airways and digestive tract. IgA antibodies drmatically increase increase in amount during infections of the mucus lining.
IgA is liberally embedded in the mucus lining of the gut. Usually, one end is attached to the wall, and the other 'business end' of the molecule projecting out into the gut cavity, on the lookout for trouble. The IgA antibodies bind to micro-organisms such as bacteria and protect us against infection by preventing them from attaching to the epithelial surface to gain entry. Also, once IgA binds to a foreign invader, terrible things happen. The combination of the antibody and the invader (now called an immune complex) trigger the release of a series of corrosive enzymes which essentially shoots holes in the bad guy.
IgA deficiency is the most common of all immune deficiencies, affecting upward of 9% of all Northern Europeans. Defects in IgA have been shown to predispose to a celiac-like disorder, lupus, pernicious anemia, Giardiasis, and even inflammatory bowel disease. In one Italian study, 8% of 56 children with low IgA had celiac disease of the small intestine, and all had antibodies to gluten and gliandin (two common proteins found in grains) in their serum.
Several dietary lectins have been shown to increase IgA. In one study 5 of 6 subjects had increases in the IgA of their saliva after a test meal which included several lectins, including peas and peanuts. Interestingly, although two common components of wheat, gliandin and gluten, have been shown in repeated studies to increase IgA, in this study wheat germ lectin was shown to have no effect.
In a study of 310 people, it was found, perhaps not surprisingly, blood type O tends to make higher amounts of IgA that other blood types. Higher levels of antibodies imply a greater risk of auto-immune disease, a situation in which the body makes antibodies that tend to inadvertently attack its own cells and tissues. Type O is associated with a higher rate of auto-immune diseases in general.
Perhaps this explains why a lot of type O's who fill out response forms on the website report improvements in auto immune disease of the thyroid (such as Hashimoto's Thyroiditis and Graves Disease) when they follow the O diet. When they cut wheat out of their diet; they reduce their production of IgA in the gut.
What's that got to do with the thyroid? You might ask. Well, it turns out that there is a similarity in the expression of blood type antigens between the intestines and the thyroid (20). Remove the provocation of the antibody in the gut, then the decrease in antibody halts the immune destruction of the thyroid.
|References:||1. Hoskins LC et al. Degradation of blood group antigens in human colon ecosystems. J. Clinical Invest. 1976; 57: 74-822. |
2.Hoskins LC. Et al. Mucin degradation in human colon ecosystems. Isolation and properties of fecal strains that degrade ABH blood group antigens and oligosaccharides from mucin glycoproteins.J. Clinical Invest. 1985:944-53
3. Lesuffleur, T., Zweibaum, A. and Real, F. X. (1994). Mucins in normal and neoplastic human gastrointestinal tissues. Crit Rev Oncol Hematol 17:153-80.
4.Nieuw Amerongen AV, Bolscher JG, Bloemena E, Veerman EC Sulfomucins in the human body.Biol Chem 1998 Jan;379(1):1-18
5.Meini A, Pillan NM, Villanacci V, Monafo V, Ugazio AG, Plebani A Prevalence and diagnosis of celiac disease in IgA-deficient children. Ann Allergy Asthma Immunol 1996 Oct;77(4):333-6
6.Gibbons RJ, Dankers I Immunosorbent assay of interactions between human parotid immunoglobulin A and dietary lectins Arch Oral Biol 1986;31(7):477-81
7. Prokop O, Kohler W, Rackwitz A, Paunova R, Barthold E[Secretory antibodies in saliva against group G streptococci]. Immunitatsforsch Immunobiol 1977 Dec;153(5):428-34
8. Mourant AE. Blood Relations. Oxford university Press 1985
9. Vowden P, et al Thyroid blood group isoantigen expression: a parallel with ABH isoantigen expression in the distal colon. Br J Cancer. 1986 Jun;53(6):721-5.
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