Diabetologia

pp 1–11

Fatty acid status in infancy is associated with the risk of type 1 diabetes-associated autoimmunity

  • Sari Niinistö
  • Hanna-Mari Takkinen
  • Iris Erlund
  • Suvi Ahonen
  • Jorma Toppari
  • Jorma Ilonen
  • Riitta Veijola
  • Mikael Knip
  • Outi Vaarala
  • Suvi M. Virtanen
Article

DOI: 10.1007/s00125-017-4280-9

Cite this article as:
Niinistö, S., Takkinen, HM., Erlund, I. et al. Diabetologia (2017). doi:10.1007/s00125-017-4280-9

Abstract

Aims/hypothesis

We investigated the association of early serum fatty acid composition with the risk of type 1 diabetes-associated autoimmunity. Our hypothesis was that fatty acid status during infancy is related to type 1 diabetes-associated autoimmunity and that long-chain n-3 fatty acids, in particular, are associated with decreased risk.

Methods

We performed a nested case–control analysis within the Finnish Type 1 Diabetes Prediction and Prevention Study birth cohort, carrying HLA-conferred susceptibility to type 1 diabetes (n = 7782). Serum total fatty acid composition was analysed by gas chromatography in 240 infants with islet autoimmunity and 480 control infants at the age of 3 and 6 months. Islet autoimmunity was defined as repeated positivity for islet cell autoantibodies in combination with at least one of three selected autoantibodies. In addition, a subset of 43 infants with primary insulin autoimmunity (i.e. those with insulin autoantibodies as the first autoantibody with no concomitant other autoantibodies) and a control group (n = 86) were analysed. A third endpoint was primary GAD autoimmunity defined as GAD autoantibody appearing as the first antibody without other concomitant autoantibodies (22 infants with GAD autoimmunity; 42 infants in control group). Conditional logistic regression was applied, considering multiple comparisons by false discovery rate <0.05.

Results

Serum fatty acid composition differed between breastfed and non-breastfed infants, reflecting differences in the fatty acid composition of the milk. Fatty acids were associated with islet autoimmunity (higher serum pentadecanoic, palmitic, palmitoleic and docosahexaenoic acids decreased risk; higher arachidonic:docosahexaenoic and n-6:n-3 acid ratios increased risk). Furthermore, fatty acids were associated with primary insulin autoimmunity, these associations being stronger (higher palmitoleic acid, cis-vaccenic, arachidonic, docosapentaenoic and docosahexaenoic acids decreased risk; higher α-linoleic acid and arachidonic:docosahexaenoic and n-6:n-3 acid ratios increased risk). Moreover, the quantity of breast milk consumed per day was inversely associated with primary insulin autoimmunity, while the quantity of cow’s milk consumed per day was directly associated.

Conclusions/interpretation

Fatty acid status may play a role in the development of type 1 diabetes-associated autoimmunity. Fish-derived fatty acids may be protective, particularly during infancy. Furthermore, fatty acids consumed during breastfeeding may provide protection against type 1 diabetes-associated autoimmunity. Further studies are warranted to clarify the independent role of fatty acids in the development of type 1 diabetes.

Keywords

Autoimmunity Breast milk Fatty acid status Infant n-3 fatty acids Type 1 diabetes 

Abbreviations

AA

Arachidonic acid

ALA

α-Linolenic acid

CLA

Conjugated linoleic acid

DIPP

Type 1 diabetes prediction and prevention study

DHA

Docosahexaenoic acid

DPA

Docosapentaenoic acid

EPA

Eicosapentaenoic acid

FDR

False discovery rate

GADA

Autoantibodies to 65 kDa isoform of GAD

GLA

γ-Linolenic acid

IAA

Insulin autoantibodies

IA-2A

Antibodies to tyrosine phosphatase-related islet antigen 2

ICA

Islet cell autoantibodies

LA

Linoleic acid

MUFA

Monounsaturated fatty acid

PUFA

Polyunsaturated fatty acid

SFA

Saturated fatty acid

Supplementary material

125_2017_4280_MOESM1_ESM.pdf (121 kb)
ESM Table 1(PDF 120 kb)
125_2017_4280_MOESM2_ESM.pdf (106 kb)
ESM Table 2(PDF 105 kb)
125_2017_4280_MOESM3_ESM.pdf (130 kb)
ESM Fig. 1(PDF 130 kb)

Copyright information

© Springer-Verlag Berlin Heidelberg 2017

Authors and Affiliations

  • Sari Niinistö
    • 1
  • Hanna-Mari Takkinen
    • 1
    • 2
  • Iris Erlund
    • 1
  • Suvi Ahonen
    • 1
    • 2
    • 3
  • Jorma Toppari
    • 4
    • 5
  • Jorma Ilonen
    • 6
  • Riitta Veijola
    • 7
  • Mikael Knip
    • 8
    • 9
    • 10
    • 11
  • Outi Vaarala
    • 9
  • Suvi M. Virtanen
    • 1
    • 2
    • 3
    • 11
  1. 1.Department of Public Health SolutionsNational Institute for Health and WelfareHelsinkiFinland
  2. 2.The Faculty of Social SciencesUniversity of TampereTampereFinland
  3. 3.Science CenterTampere University HospitalTampereFinland
  4. 4.Department of Physiology, Institute of BiomedicineUniversity of TurkuTurkuFinland
  5. 5.Department of PediatricsTurku University HospitalTurkuFinland
  6. 6.Immunogenetics LaboratoryUniversity of TurkuTurkuFinland
  7. 7.Department of Pediatrics, PEDEGO Research Unit, Medical Research CenterOulu University Hospital and University of OuluOuluFinland
  8. 8.Children’s HospitalUniversity of Helsinki and Helsinki University Central HospitalHelsinkiFinland
  9. 9.Research Programs Unit, Diabetes and ObesityUniversity of HelsinkiHelsinkiFinland
  10. 10.Folkhälsan Research CenterHelsinkiFinland
  11. 11.Center for Child Health ResearchUniversity of Tampere and Tampere University HospitalTampereFinland

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