title: Why diabetes incidence increases--a unifying theory.
abstract: There is a wide spectrum within the diabetes syndrome. Type 1 diabetes may have a slow progression with good residual insulin secretion and without autoantibodies, while phenotypic type 2 diabetes may have autoantibodies. A single patient may have traits of both types of diabetes. Their incidence increases in parallel. The etiology is mainly unknown, but environmental factors play an important role in genetically predisposed individuals. The search for just one single cause of manifest diabetes may be confusing. Different mechanism may be important in different parts of the world. Furthermore, certain mechanisms may lead to islet inflammation while other/additional mechanisms may increase insulin demand and cause insulin deficiency with manifestation of clinical diabetes. Several hypothesis of etiology may fit different parts of the disease process. Thus, increased hygiene may contribute to an imbalance of the immune system, facilitating autoimmune reactions when virus infections, or proteins like cow's milk or gluten, provoke. Increased insulin demand because of rapid growth, or insulin resistance caused by stress, infections, puberty, etc., lead to beta cell stress, antigen presentation and may cause both an autoimmune reaction in genetically predisposed individuals, and insulin deficiency leading to manifest diabetes in individuals who have lost beta cell function. Vitamins may modulate the immune process, but we know too little to give vitamin substitution. However, we do know that low physical exercise, obesity, and stress, increases insulin demand resulting in insulin deficiency. Now we can therefore intervene to prevent the diabetic syndrome.
authors.affiliation: Division of Pediatrics, and Diabetes Research Centre, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, SE-581 85 Linköping, Sweden. johnny.ludvigsson@lio.se
authors.forename: Johnny
authors.initials: J
authors.lastname: Ludvigsson
mesh_terms: D015551:Autoimmunity / Q000276:immunology*; D003920:Diabetes Mellitus / Q000453:epidemiology* / Q000209:etiology* / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000209:etiology / Q000235:genetics / Q000276:immunology; D006801:Humans; D015994:Incidence; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D007333:Insulin Resistance / Q000235:genetics; D007515:Islets of Langerhans / Q000276:immunology / Q000473:pathology; D008954:Models, Biological; D011236:Prediabetic State / Q000235:genetics / Q000517:prevention & control