There is evidence that the process leading to type 1 diabetes may start in early infancy or already in utero. Even though
diabetes-associated antibodies can be detected in up to half of the pregnancies of mothers with type 1 diabetes, pregnancy
itself has no major effect on these antibodies. If such antibodies are present in the mother, they are transferred to the
fetal circulation and are detectable in cord blood. Most of the transplacentally transferred antibodies disappear by 6 months
of age, but may persist even longer. Antibodies present in cord blood may represent true induction of β-cell autoimmunity,
but such a phenomenon is extremely rare.
The offspring of affected mothers have a 2% to 3% risk of type 1 diabetes, which is about one third of that in the offspring
of affected fathers. A novel conceivable explanation is that exogenous insulin transplacentally transferred in immune complexes
might lead to the induction of tolerance to insulin, which may be the primary autoantigen in type 1 diabetes. The possible
protective or predisposing effect of diabetes-associated antibodies detectable at birth on progression to clinical type 1
diabetes later will be assessed in ongoing prospective birth cohort studies.