Adherence to the EAT-Lancet diet, genetic susceptibility, and risk of type 2 diabetes in Swedish adults
(2023) In Metabolism: Clinical and Experimental 141.- Abstract
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... (More)
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.
(Less)
- author
- Zhang, Shunming
LU
; Stubbendorff, Anna
LU
; Olsson, Kjell LU
; Ericson, Ulrika LU ; Niu, Kaijun ; Qi, Lu ; Borné, Yan LU and Sonestedt, Emily LU
- organization
- publishing date
- 2023-01-19
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Metabolism: Clinical and Experimental
- volume
- 141
- article number
- 155401
- publisher
- Elsevier
- external identifiers
-
- pmid:36682448
- scopus:85147221821
- ISSN
- 1532-8600
- DOI
- 10.1016/j.metabol.2023.155401
- language
- English
- LU publication?
- yes
- additional info
- Copyright © 2023. Published by Elsevier Inc.
- id
- 96dffc77-e9d3-4951-8a1e-1cfb7d0ba56c
- date added to LUP
- 2023-01-24 15:19:29
- date last changed
- 2024-07-13 02:16:04
@article{96dffc77-e9d3-4951-8a1e-1cfb7d0ba56c, abstract = {{<p>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.</p><p>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.</p><p>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).</p><p>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.</p>}}, author = {{Zhang, Shunming and Stubbendorff, Anna and Olsson, Kjell and Ericson, Ulrika and Niu, Kaijun and Qi, Lu and Borné, Yan and Sonestedt, Emily}}, issn = {{1532-8600}}, language = {{eng}}, month = {{01}}, publisher = {{Elsevier}}, series = {{Metabolism: Clinical and Experimental}}, title = {{Adherence to the EAT-Lancet diet, genetic susceptibility, and risk of type 2 diabetes in Swedish adults}}, url = {{http://dx.doi.org/10.1016/j.metabol.2023.155401}}, doi = {{10.1016/j.metabol.2023.155401}}, volume = {{141}}, year = {{2023}}, }