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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Italian pediatric data support hypothesis that simultaneous epidemics of type 1 diabetes and type 2 diabetes/metabolic syndrome/obesity are polar opposite responses (i.e., symptoms) to a primary inflammatory condition.

We previously postulated that iatrogenic inflammation caused epidemics of type 2 diabetes/metabolic syndrome/obesity by activating an immune suppressive cortisol response which protects against type 1 diabetes and other autoimmune diseases. In the current study, data on the incidence of obesity in different Italian provinces was compared with the incidence of type 1 diabetes in the same region. The association between obesity and type 1 diabetes was analyzed using Wilcoxon rank analysis. Results showed an inverse relationship; the regions with the highest rate of obesity (Campania and Lazia) were associated with a protective effect against type 1 diabetes. However, regions with the lowest rates of obesity were associated with the highest rate of type 1 diabetes. These results are consistent with previous analysis across different racial groups; races with high cortisol activity had an increased rate of type 2 diabetes but were protected from type 1 diabetes.[1]

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