Consumption of red meat, genetic susceptibility, and risk of LADA and type 2 diabetes.


Journal

European journal of nutrition
ISSN: 1436-6215
Titre abrégé: Eur J Nutr
Pays: Germany
ID NLM: 100888704

Informations de publication

Date de publication:
Mar 2021
Historique:
received: 26 02 2020
accepted: 11 05 2020
pubmed: 24 5 2020
medline: 1 6 2021
entrez: 24 5 2020
Statut: ppublish

Résumé

Red meat consumption is positively associated with type 1 (T1D) and type 2 (T2D) diabetes. We investigated if red meat consumption increases the risk of latent autoimmune diabetes in adults (LADA) and T2D, and potential interaction with family history of diabetes (FHD), HLA and TCF7L2 genotypes. Analyses were based on Swedish case-control data comprising incident cases of LADA (n = 465) and T2D (n = 1528) with matched, population-based controls (n = 1789; n = 1553 in genetic analyses). Multivariable-adjusted ORs in relation to self-reported processed and unprocessed red meat intake were estimated by conditional logistic regression models. Attributable proportion (AP) due to interaction was used to assess departure from additivity of effects. Consumption of processed red meat was associated with increased risk of LADA (per one servings/day OR 1.27, 95% CI 1.07-1.52), whereas no association was observed for unprocessed red meat. For T2D, there was no association with red meat intake once BMI was taken into account. The combination of high (> 0.3 servings/day vs. less) processed red meat intake and high-risk HLA-DQB1 and -DRB1 genotypes yielded OR 8.05 (95% CI 4.86-13.34) for LADA, with indications of significant interaction (AP 0.53, 95% CI 0.32-0.73). Results were similar for the combination of FHD-T1D and processed red meat. No interaction between processed red meat intake and FHD-T2D or risk variants of TCF7L2 was seen in relation to LADA or T2D. Consumption of processed but not unprocessed red meat may increase the risk of LADA, especially in individuals with FHD-T1D or high-risk HLA genotypes.

Identifiants

pubmed: 32444887
doi: 10.1007/s00394-020-02285-2
pii: 10.1007/s00394-020-02285-2
pmc: PMC7900036
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

769-779

Subventions

Organisme : Vetenskapsrådet
ID : GA 2018-03035
Organisme : Forskningsrådet om Hälsa, Arbetsliv och Välfärd
ID : GA 2018-00337
Organisme : European Research Council Advanced Researcher grant
ID : GA 269045

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Auteurs

Josefin E Löfvenborg (JE)

Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden. josefin.lofvenborg@ki.se.

Emma Ahlqvist (E)

Department of Clinical Sciences, Lund University, Malmö, Sweden.

Lars Alfredsson (L)

Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden.

Tomas Andersson (T)

Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden.
Center for Occupational and Environmental Medicine, Stockholm County Council, Stockholm, Sweden.

Leif Groop (L)

Department of Clinical Sciences, Lund University, Malmö, Sweden.
Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland.

Tiinamaija Tuomi (T)

Department of Clinical Sciences, Lund University, Malmö, Sweden.
Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland.
Division of Endocrinology, Abdominal Centre, Helsinki University Hospital, Helsinki, Finland.
Folkhälsan Research Center, Helsinki, Finland.

Alicja Wolk (A)

Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden.

Sofia Carlsson (S)

Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden.

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