liu.seSearch for publications in DiVA
Change search
ReferencesLink to record
Permanent link

Direct link
Why diabetes incidence inereases- A unifying theory
Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Pediatrics . Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
2006 (English)In: Annals of the New York Academy of Sciences, ISSN 0077-8923, Vol. 1079, 374-382 p.Article in journal (Refereed) Published
Abstract [en]

There is a wide spectrum within the diabetes syndrome. Type I 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.

Place, publisher, year, edition, pages
2006. Vol. 1079, 374-382 p.
Keyword [en]
islet inflammation, preclinical diabetes, type 1 diabetes, type 2 diabetes, LADA, etiology, hypothesis, autoimmunity, insulin resistance
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-45974DOI: 10.1196/annals.1375.058OAI: diva2:266870
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2011-01-11

Open Access in DiVA

No full text

Other links

Publisher's full text

Search in DiVA

By author/editor
Ludvigsson, Johnny
By organisation
Faculty of Health SciencesPediatrics Department of Paediatrics in Linköping
In the same journal
Annals of the New York Academy of Sciences
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 104 hits
ReferencesLink to record
Permanent link

Direct link