Objective: We estimated the genetic and environmental components of type 1 diabetes susceptibility in a twin cohort of recent-onset cases to explore the sources of changing disease epidemiology.
Design: We linked the population-based Italian Twin Registry with 14803 type 1 diabetes records from 36 pediatric diabetes care centers throughout Italy, except Sardinia, and identified 173 diabetic twins. Patients were positive for at least one autoantibody to islet cell, glutamate decarboxylase, tyrosine phosphatase, insulin, or zinc transporter 8 and were insulin dependent since their diagnosis. Zygosity was determined by DNA genotyping or by questionnaire.
Outcome Measures: We estimated pro-band-wise concordance, co-twin recurrence risk with Kaplan-Meier method, and genetic and environmental proportions of susceptibility variance by structural equation models.
Results: We recruited 104 diabetic twins (53 males) from 88 pairs (34 monozygotic, 54 dizygotic) and one triplet. The mean age at diagnosis was 8.1 yr (range 1.1–20.5 yr), and the median year of diagnosis was 2002. Pro-band-wise concordances were 45.5 and 16.4% in monozygotic and dizygotic pairs. Recurrence risks in monozygotic and dizygotic co-twins were 37 and 12% after 10 yr from the proband’s diagnosis. Genetic contribution to type 1 diabetes susceptibility was 40% (95% confidence interval 8–78), and the shared and individual-specific environmental components were 51% (14–77) and 9% (4–19), respectively.
Conclusions: In addition to the moderate genetic effects on type 1 diabetes susceptibility, our results draw attention to the substantial shared environmental effects, suggesting that exposures in fetal or early postnatal life may contribute to the increasing incidence of the disease.
Health-e-Solutions comment: The study of environmental factors and epigenetics is really only beginning to emerge. As this study and others has revealed, the environmental contribution to type 1 diabetes development is substantial. We believe the most logical deduction would be that removing – as much as it is possible – those environmental factors can have a large and lasting impact on the development or progression of this autoimmune disease.
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