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Coffee consumption, genetic susceptibility and risk of latent autoimmune diabetes in adults: A population-based case-control study.
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2018 (engelsk)Inngår i: Diabetes & Metabolism, ISSN 1262-3636, E-ISSN 1878-1780, Vol. 44, nr 4, s. 354-360, artikkel-id S1262-3636(18)30087-9Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

AIM: Coffee consumption is inversely related to risk of type 2 diabetes (T2D). In contrast, an increased risk of latent autoimmune diabetes in adults (LADA) has been reported in heavy coffee consumers, primarily in a subgroup with stronger autoimmune characteristics. Our study aimed to investigate whether coffee consumption interacts with HLA genotypes in relation to risk of LADA.

METHODS: This population-based study comprised incident cases of LADA (n=484) and T2D (n=1609), and also 885 healthy controls. Information on coffee consumption was collected by food frequency questionnaire. Odds ratios (ORs) with 95% CIs of diabetes were calculated and adjusted for age, gender, BMI, education level, smoking and alcohol intake. Potential interactions between coffee consumption and high-risk HLA genotypes were calculated by attributable proportion (AP) due to interaction.

RESULTS: Coffee intake was positively associated with LADA in carriers of high-risk HLA genotypes (OR: 1.14 per cup/day, 95% CI: 1.02-1.28), whereas no association was observed in non-carriers (OR: 1.04, 95% CI: 0.93-1.17). Subjects with both heavy coffee consumption (≥4 cups/day) and high-risk HLA genotypes had an OR of 5.74 (95% CI: 3.34-9.88) with an estimated AP of 0.36 (95% CI: 0.01-0.71; P=0.04370).

CONCLUSION: Our findings suggest that coffee consumption interacts with HLA to promote LADA.

sted, utgiver, år, opplag, sider
2018. Vol. 44, nr 4, s. 354-360, artikkel-id S1262-3636(18)30087-9
Emneord [en]
Autoimmune diabetes, Coffee consumption, Gene–environmental interaction, LADA, Latent autoimmune diabetes in adults, Type 2 diabetes
HSV kategori
Identifikatorer
URN: urn:nbn:se:uu:diva-368173DOI: 10.1016/j.diabet.2018.05.002ISI: 000447960300007PubMedID: 29861145OAI: oai:DiVA.org:uu-368173DiVA, id: diva2:1267913
Tilgjengelig fra: 2018-12-04 Laget: 2018-12-04 Sist oppdatert: 2018-12-10bibliografisk kontrollert

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Carlsson, Per-OlaMartinell, MatsWolk, Alicja

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