Adherence to the EAT-Lancet diet, genetic susceptibility, and risk of type 2 diabetes in Swedish adults.


Journal

Metabolism: clinical and experimental
ISSN: 1532-8600
Titre abrégé: Metabolism
Pays: United States
ID NLM: 0375267

Informations de publication

Date de publication:
04 2023
Historique:
received: 02 11 2022
revised: 11 01 2023
accepted: 14 01 2023
pubmed: 23 1 2023
medline: 3 3 2023
entrez: 22 1 2023
Statut: ppublish

Résumé

In 2019, the EAT-Lancet Commission proposed a mainly plant-based diet that nurtures human health and supports environmental sustainability. However, its association with type 2 diabetes (T2D) has not been widely studied, and it remains unclear whether genetic susceptibility for T2D can modify this association. The aim was therefore to investigate the association between the EAT-Lancet diet and risk of T2D and assess whether the association differs by the genetic predisposition to T2D. A total of 24,494 participants from the Malmö Diet and Cancer study were analyzed. Dietary intake was assessed using a modified diet history methodology, and an EAT-Lancet diet index (range from 0 to 42 points) was constructed based on the EAT-Lancet reference diet. National and local registers were used to identify T2D cases during follow-up. Cox proportional hazards regression model was applied to estimate the association between the EAT-Lancet diet index and risk of T2D. Genetic predisposition to T2D was captured based on 116 single nucleotide polymorphisms. During a median of 24.3 years of follow-up, 4197 (17.1 %) T2D cases were documented. Compared with those with the lowest adherence to the EAT-Lancet diet (≤13 points), participants who had the highest adherence (≥23 points) showed an 18 % (95 % CI: 4 %-30 %) lower risk of T2D (P for trend <0.01). There was no significant multiplicative interaction between genetic predisposition to T2D and the EAT-Lancet diet index (P = 0.59). Also, no significant additive interaction between the genetic risk and the EAT-Lancet diet was seen (P = 0.44). The highest risk was observed among the 22.9 % of the individuals with high genetic risk and low EAT-Lancet diet score (HR = 1.79; 95 % CI: 1.63, 1.96). Our findings indicate that high adherence to the EAT-Lancet diet was associated with decreased risk of incident T2D among people with different genetic risks.

Sections du résumé

BACKGROUND AND AIMS
In 2019, the EAT-Lancet Commission proposed a mainly plant-based diet that nurtures human health and supports environmental sustainability. However, its association with type 2 diabetes (T2D) has not been widely studied, and it remains unclear whether genetic susceptibility for T2D can modify this association. The aim was therefore to investigate the association between the EAT-Lancet diet and risk of T2D and assess whether the association differs by the genetic predisposition to T2D.
METHODS
A total of 24,494 participants from the Malmö Diet and Cancer study were analyzed. Dietary intake was assessed using a modified diet history methodology, and an EAT-Lancet diet index (range from 0 to 42 points) was constructed based on the EAT-Lancet reference diet. National and local registers were used to identify T2D cases during follow-up. Cox proportional hazards regression model was applied to estimate the association between the EAT-Lancet diet index and risk of T2D. Genetic predisposition to T2D was captured based on 116 single nucleotide polymorphisms.
RESULTS
During a median of 24.3 years of follow-up, 4197 (17.1 %) T2D cases were documented. Compared with those with the lowest adherence to the EAT-Lancet diet (≤13 points), participants who had the highest adherence (≥23 points) showed an 18 % (95 % CI: 4 %-30 %) lower risk of T2D (P for trend <0.01). There was no significant multiplicative interaction between genetic predisposition to T2D and the EAT-Lancet diet index (P = 0.59). Also, no significant additive interaction between the genetic risk and the EAT-Lancet diet was seen (P = 0.44). The highest risk was observed among the 22.9 % of the individuals with high genetic risk and low EAT-Lancet diet score (HR = 1.79; 95 % CI: 1.63, 1.96).
CONCLUSIONS
Our findings indicate that high adherence to the EAT-Lancet diet was associated with decreased risk of incident T2D among people with different genetic risks.

Identifiants

pubmed: 36682448
pii: S0026-0495(23)00004-5
doi: 10.1016/j.metabol.2023.155401
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

155401

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest None.

Auteurs

Shunming Zhang (S)

School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China; Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden. Electronic address: shunming.zhang@med.lu.se.

Anna Stubbendorff (A)

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

Kjell Olsson (K)

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

Ulrika Ericson (U)

Diabetes and Cardiovascular Disease-Genetic Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.

Kaijun Niu (K)

Nutritional Epidemiology Institute and School of Public Health, Tianjin Medical University, Tianjin, China.

Lu Qi (L)

Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

Yan Borné (Y)

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

Emily Sonestedt (E)

Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden. Electronic address: emily.sonestedt@med.lu.se.

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