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Early introduction of root vegetables in infancy associated with advanced ß-cell autoimmunity in young children with human leukocyte antigen-conferred susceptibility to Type 1 diabetes

Authors


Suvi M. Virtanen, National Institute for Health and Welfare, Department of Lifestyle and Participation, Nutrition Unit, PO Box 30, 00271 Helsinki, Finland. E-mail: suvi.virtanen@thl.fi

Abstract

Diabet. Med. 28, 965–971 (2011)

Abstract

Aims  Early introduction of supplementary foods has been implicated to play a role in the development of ß-cell autoimmunity. We set out to study the effects of breastfeeding and age at introduction of supplementary foods on the development of ß-cell autoimmunity.

Methods  A prospective birth cohort of 6069 infants with HLA-DQB-conferred susceptibility to Type 1 diabetes was recruited between 1996 and 2004. Antibodies against islet cells, insulin, glutamate dehydroxylase and islet antigen 2 were measured at 3- to 12-month intervals. The families recorded at home the age at introduction of new foods and, for each visit, completed a structured dietary questionnaire. The endpoint was repeated positivity for islet cell antibodies plus at least one other antibody and/or clinical Type 1 diabetes (n = 265).

Results  Early introduction of root vegetables (by the age of 4 months) was related to increased risk of developing positivity for the endpoint [hazard ratio (95% CI) for the earliest third 1.75 (1.11–2.75) and for the middle third 1.79 (1.22–2.62) compared with the last third (> 4 months), likelihood ratio test P = 0.006], independently of the introduction of other foods and of several putative socio-demographic and perinatal confounding factors. Introducing wheat, rye, oats and/or barley cereals (P = 0.013) and egg (P = 0.031) early was related to an increased risk of the endpoint, but only during the first 3 years of life.

Conclusions  Early introduction of root vegetables during infancy is independently associated with increased risk of ß-cell autoimmunity among Finnish children with increased genetic susceptibility to Type 1 diabetes.

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