The EAT-Lancet diet, genetic susceptibility and risk of atrial fibrillation in a population-based cohort.
Atrial fibrillation
EAT-Lancet diet
Genetic risk score
Sustainable diet
Journal
BMC medicine
ISSN: 1741-7015
Titre abrégé: BMC Med
Pays: England
ID NLM: 101190723
Informations de publication
Date de publication:
28 07 2023
28 07 2023
Historique:
received:
12
01
2023
accepted:
19
07
2023
medline:
31
7
2023
pubmed:
29
7
2023
entrez:
28
7
2023
Statut:
epublish
Résumé
The EAT-Lancet Commission proposed a global reference diet with both human health benefits and environmental sustainability in 2019. However, evidence regarding the association of such a diet with the risk of atrial fibrillation (AF) is lacking. In addition, whether the genetic risk of AF can modify the effect of diet on AF remains unclear. This study aimed to assess the association of the EAT-Lancet diet with the risk of incident AF and examine the interaction between the EAT-Lancet diet and genetic susceptibility of AF. This prospective study included 24,713 Swedish adults who were free of AF, coronary events, and stroke at baseline. Dietary habits were estimated with a modified diet history method, and an EAT-Lancet diet index was constructed to measure the EAT-Lancet reference diet. A weighted genetic risk score was constructed using 134 variants associated with AF. Cox proportional hazards regression models were applied to estimate the hazard ratio (HR) and 95% confidence interval (CI). During a median follow-up of 22.9 years, 4617 (18.7%) participants were diagnosed with AF. The multivariable HR (95% CI) of AF for the highest versus the lowest group for the EAT-Lancet diet index was 0.84 (0.73, 0.98) (P for trend < 0.01). The HR (95% CI) of AF per one SD increment of the EAT-Lancet diet index for high genetic risk was 0.92 (0.87, 0.98) (P for interaction = 0.15). Greater adherence to the EAT-Lancet diet index was significantly associated with a lower risk of incident AF. Such association tended to be stronger in participants with higher genetic risk, though gene-diet interaction was not significant.
Sections du résumé
BACKGROUND
The EAT-Lancet Commission proposed a global reference diet with both human health benefits and environmental sustainability in 2019. However, evidence regarding the association of such a diet with the risk of atrial fibrillation (AF) is lacking. In addition, whether the genetic risk of AF can modify the effect of diet on AF remains unclear. This study aimed to assess the association of the EAT-Lancet diet with the risk of incident AF and examine the interaction between the EAT-Lancet diet and genetic susceptibility of AF.
METHODS
This prospective study included 24,713 Swedish adults who were free of AF, coronary events, and stroke at baseline. Dietary habits were estimated with a modified diet history method, and an EAT-Lancet diet index was constructed to measure the EAT-Lancet reference diet. A weighted genetic risk score was constructed using 134 variants associated with AF. Cox proportional hazards regression models were applied to estimate the hazard ratio (HR) and 95% confidence interval (CI).
RESULTS
During a median follow-up of 22.9 years, 4617 (18.7%) participants were diagnosed with AF. The multivariable HR (95% CI) of AF for the highest versus the lowest group for the EAT-Lancet diet index was 0.84 (0.73, 0.98) (P for trend < 0.01). The HR (95% CI) of AF per one SD increment of the EAT-Lancet diet index for high genetic risk was 0.92 (0.87, 0.98) (P for interaction = 0.15).
CONCLUSIONS
Greater adherence to the EAT-Lancet diet index was significantly associated with a lower risk of incident AF. Such association tended to be stronger in participants with higher genetic risk, though gene-diet interaction was not significant.
Identifiants
pubmed: 37507726
doi: 10.1186/s12916-023-02985-6
pii: 10.1186/s12916-023-02985-6
pmc: PMC10386230
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
280Informations de copyright
© 2023. The Author(s).
Références
J Am Heart Assoc. 2018 Apr 12;7(8):
pubmed: 29650711
Lancet. 2019 Jul 20;394(10194):213-214
pubmed: 31235280
PLoS Med. 2016 Jun 07;13(6):e1002036
pubmed: 27270749
BMJ. 2018 Jan 10;360:j5644
pubmed: 29321156
Atherosclerosis. 2018 Aug;275:174-181
pubmed: 29920438
Eur J Cancer Prev. 2001 Dec;10(6):489-99
pubmed: 11916347
J Am Coll Cardiol. 2014 Dec 2;64(21):e1-76
pubmed: 24685669
J Am Heart Assoc. 2019 May 7;8(9):e011955
pubmed: 31020911
Nutr J. 2002 Nov 19;1:3
pubmed: 12537595
Am J Cardiol. 2018 Jan 15;121(2):199-204
pubmed: 29153246
Diabetes Care. 2021 Nov;44(11):2470-2479
pubmed: 34433621
J Am Coll Cardiol. 2021 Sep 21;78(12):1197-1207
pubmed: 34531019
J Am Coll Cardiol. 2008 Feb 26;51(8):779-86
pubmed: 18294560
Adv Nutr. 2020 Sep 1;11(5):1255-1281
pubmed: 32298420
Clin Epidemiol. 2017 Jan 24;9:53-62
pubmed: 28182159
Eur J Clin Nutr. 1996 Mar;50(3):134-42
pubmed: 8654326
Eur J Clin Nutr. 1996 Mar;50(3):143-51
pubmed: 8654327
Arterioscler Thromb Vasc Biol. 2020 Nov;40(11):2738-2746
pubmed: 32957805
Stroke. 2022 Jan;53(1):154-163
pubmed: 34872335
Nat Genet. 2018 Sep;50(9):1225-1233
pubmed: 29892015
Circ Res. 2020 Jun 19;127(1):4-20
pubmed: 32716709
Front Nutr. 2022 Jan 14;8:784018
pubmed: 35096931
Nutrients. 2021 Nov 05;13(11):
pubmed: 34836209
Nutr Metab Cardiovasc Dis. 2013 Feb;23(2):115-21
pubmed: 21798731
Metabolism. 2023 Apr;141:155401
pubmed: 36682448
Nutrients. 2022 Sep 01;14(17):
pubmed: 36079872
Eur Heart J. 2021 Feb 1;42(5):373-498
pubmed: 32860505
J Arrhythm. 2019 Nov 06;35(6):781-788
pubmed: 31844466
Int J Surg. 2014 Dec;12(12):1500-24
pubmed: 25046751
Eur J Epidemiol. 2010 Feb;25(2):95-102
pubmed: 19936945
Eur J Prev Cardiol. 2017 Sep;24(14):1555-1566
pubmed: 28617620
Am J Clin Nutr. 2023 May;117(5):903-909
pubmed: 36841443
J Am Heart Assoc. 2021 Aug 17;10(16):e021515
pubmed: 34346245
J Am Coll Cardiol. 2017 Jul 25;70(4):411-422
pubmed: 28728684
Am J Clin Nutr. 2022 Mar 4;115(3):705-716
pubmed: 34791011
Lancet. 2019 Feb 2;393(10170):447-492
pubmed: 30660336