Abstract
(1) Background: Iron requirement increases during pregnancy and iron supplementation is therefore recommended in many countries. However, excessive iron intake may lead to destruction of pancreatic β-cells. Therefore, we aim to test if higher neonatal iron content in blood is associated with the risk of developing type 1 diabetes mellitus (T1D) in childhood; (2) Methods: A case-control study was conducted, including 199 children diagnosed with T1D before the age of 16 years from 1991 to 2005 and 199 controls matched on date of birth. Information on confounders was available in 181 cases and 154 controls. Iron was measured on a neonatal single dried blood spot sample and was analyzed by laser ablation inductively coupled plasma mass spectrometry. Multivariate logistic regression was used to evaluate if iron content in whole blood was associated with the risk of T1D; (3) Results: A doubling of iron content increased the odds of developing T1D more than two-fold (odds ratio (95% CI), 2.55 (1.04; 6.24)). Iron content increased with maternal age (p = 0.04) and girls had higher content than boys (p = 0.01); (4) Conclusions: Higher neonatal iron content associates to an increased risk of developing T1D before the age of 16 years. Iron supplementation during early childhood needs further investigation, including the causes of high iron in neonates.
Highlights
The incidence of childhood type 1 diabetes mellitus (T1D) is increasing, especially in Western countries [1,2], the causes remain unknown
Iron values were measured for 199 cases and 199 controls
When iron was divided in quartiles we found a significant lower risk of developing T1D in those belonging to the lowest quartile compared to highest quartile (p = 0.04)
Summary
The incidence of childhood type 1 diabetes mellitus (T1D) is increasing, especially in Western countries [1,2], the causes remain unknown. When compared to earlier generations, the proportion of patients with high-risk human leukocyte antigen (HLA) alleles has not increased [4]. It seems likely that environmental factors play an important part in the etiology of T1D. Studies suggest that T1D may already have its origin in fetal life [5], e.g., through modification of epigenetic processes in the fetus [6]. The most abundant metal in the body, is an essential trace element and has numerous functions. The most important is oxygen transportation bound to hemoglobin. Iron is a key element in immune homeostasis, and studies have shown that iron deficiency and overload may affect
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