T. Kimpimaki et al., Short-term exclusive breastfeeding predisposes young children with increased genetic risk of Type I diabetes to progressive beta-cell autoimmunity, DIABETOLOG, 44(1), 2001, pp. 63-69
Aims/hypothesis. This study aimed to establish the relation between early i
nfant nutrition and signs of beta-cell autoimmunity in young children.
Methods. We identified and observed from birth 2949 infants with increased
genetic risk of Type I (insulin-dependent) diabetes mellitus (HLA DQB1*02/
*0302 or DQB1*03021x, x = other than *02, *0301 or *0602) and monitored the
m for islet cell antibodies at 3 to 6 month intervals. If an infant serocon
verted to islet cell antibody positivity, all of his or her samples were al
so analysed for autoantibodies to insulin, GAD65 (GADA) and to the protein
tyrosine phosphatase related IA-2 molecule (IA-2A). Our case-control study
comprises the first 65 children who seroconverted to islet cell antibody po
sitivity before the age of 4 years and 390 control children who were islet
cell antibody-negative (six control children/case). We monitored the durati
on of exclusive and total breastfeeding and the age at which cows' milk was
introduced.
Results. Infants who had been breastfed exclusively for at least 4 months h
ad lower risk of seroconversion to positivity for IA-2A or all four autoant
ibodies [odds ratio (OR) 0.24; 95% CI 0.06-0.94 and OR 0.17; 95 % CI 0.03-0
.86, respectively] than those infants who had been breastfed exclusively fo
r less than 2 months. The risk of seroconversion to positivity for IA-2A or
all four autoantibodies was higher in those younger than 2 months (OR 4.37
; 95% CI 1.33-14.42 and OR 5.02; 95 % CI 1.27-19.89) or aged 2 to 3.9 month
s (OR 5.50; 95 % CI 1.21-25.04 and 6.19; 95% CI 1.10-34.84) when they first
received cows' milk than in those aged 4 months or older.
Conclusions/interpretation. These observations suggest that short-term brea
stfeeding and the early introduction of cows' milk-based infant formula pre
dispose young children who are genetically susceptible to Type I diabetes t
o progressive signs of beta-cell autoimmunity.