Bacteria of food and human intestine are the most possible sources of the gad-trigger of type 1 diabetes.
Type 1 diabetes incidence increases at about 3% per year in the Western world. From genetically predisposed people only 20-50% develop the disease. To unravel these mysteries, literature was searched to determine the disease background and to find suggestions for research and prevention. A promising hypothesis was found: the enzyme glutamic acid decarboxylase (GAD) in bacteria may be the source of type 1 diabetes. Epidemiological data can be accounted for this possibility. GAD-containing bacteria can originate from raw foods, especially salted or dried or smoked raw meat and fish products or from proliferation in the ileum of the human small intestine. Proliferation of GAD-containing bacteria in the ileum is probably the most frequent causation of type 1 diabetes. This proliferation is stimulated by the consumption of nitrate-containing ingredients such as vegetables, fruits or nitrate-polluted water and by sugars dissolved in liquids, for example lactose in milk or sugars in juicy fruits and fruit-juices. In the ileum GAD is released from bacteria by endocrine enzymes of the small intestine. Released GAD enters Peyer's patches (PP) in the ileum wall, where it is bound or enclosed by immune cells. These cells move GAD by the lymph- and bloodstream to the immune system for priming and elimination. In case of type 1 diabetes, however, malfunction of PP causes GAD freely move in the lymph stream where it settles on vascular endothelial cells and pancreatic beta-cells. GAD-settlement on beta-cells gives an inflammatory immune response, leading to destruction of the beta-cells and to type 1 diabetes. A perspective for prevention of the disease in predisposed individuals is discussed. It is concluded that GAD-containing bacteria and malfunction of PP should be taken into account in future type 1 diabetes research.
Mulder
Sieger Jeen
SJ
Tussen de Dennen 12, 3708 BJ Zeist, The Netherlands. sjmulder@planet.nl
D003922:Diabetes Mellitus, Type 1 / Q000209:etiology* / Q000382:microbiology*; D005516:Food Microbiology; D020022:Genetic Predisposition to Disease; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006801:Humans; D007082:Ileum / Q000382:microbiology; D007249:Inflammation; D007422:Intestines / Q000382:microbiology*; D007515:Islets of Langerhans / Q000378:metabolism; D008962:Models, Theoretical
D005968:Glutamate Decarboxylase