The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Emily Sonestedt

Emily Sonestedt

Associate senior lecturer

Emily Sonestedt

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

Author

  • Shunming Zhang
  • Anna Stubbendorff
  • Kjell Olsson
  • Ulrika Ericson
  • Kaijun Niu
  • Lu Qi
  • Yan Borné
  • Emily Sonestedt

Summary, in English

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.

Department/s

  • Nutrition Epidemiology
  • EpiHealth: Epidemiology for Health
  • EXODIAB: Excellence of Diabetes Research in Sweden
  • Diabetes - Cardiovascular Disease

Publishing year

2023-01-19

Language

English

Pages

155401-155401

Publication/Series

Metabolism: Clinical and Experimental

Document type

Journal article

Publisher

Elsevier

Topic

  • Endocrinology and Diabetes
  • Public Health, Global Health, Social Medicine and Epidemiology

Status

Epub

Research group

  • Nutrition Epidemiology
  • Diabetes - Cardiovascular Disease

ISBN/ISSN/Other

  • ISSN: 1532-8600