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

被引:40
|
作者
Zhang, Shunming [1 ,2 ,7 ]
Stubbendorff, Anna [2 ]
Olsson, Kjell [2 ]
Ericson, Ulrika [3 ]
Niu, Kaijun [4 ]
Qi, Lu [5 ,6 ]
Borne, Yan [2 ]
Sonestedt, Emily [2 ,7 ]
机构
[1] Xi An Jiao Tong Univ, Sch Publ Hlth, Hlth Sci Ctr, Xian, Shaanxi, Peoples R China
[2] Lund Univ, Dept Clin Sci Malmo, Nutr Epidemiol, Malmo, Sweden
[3] Lund Univ, Dept Clin Sci Malmo, Diabet & Cardiovasc Dis Genet Epidemiol, Malmo, Sweden
[4] Tianjin Med Univ, Nutr Epidemiol Inst, Tianjin, Peoples R China
[5] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA USA
[6] Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA
[7] Lund Univ, Dept Clin Sci Malmo, Nutr Epidemiol, Jan Waldenstroms Gata 35, S-21428 Malmo, Sweden
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2023年 / 141卷
基金
瑞典研究理事会;
关键词
Type; 2; diabetes; EAT-lancet diet; Polygenic risk score; Sustainable diet; HISTORY METHOD; MALMO FOOD; REPRODUCIBILITY; QUESTIONNAIRE; INDEXES; PATTERN; TIME;
D O I
10.1016/j.metabol.2023.155401
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 Malmo & BULL; 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 (& LE;13 points), participants who had the highest adherence (& GE;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 EATLancet 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.
引用
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页数:8
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