Following the EAT-Lancet diet lowers chronic kidney disease risk

By Dr. Liji Thomas, MDReviewed by Lauren HardakerJan 28 2026

Large-scale UK Biobank data show that the EAT-Lancet planetary health diet is associated with lower CKD risk, with genetics, green space, and molecular signatures shaping who benefits most.

Study: The EAT–Lancet planetary health diet and risk of incident chronic kidney disease. Image credit: monticello/Shutterstock.com

Chronic kidney disease (CKD) is a major issue among adults, affecting approximately 10 % of people worldwide. A recent paper in CMAJ explored the association of this disorder with the EAT-Lancet planetary health diet.

Diet quality emerges as modifiable CKD prevention factor

Scientists estimate that CKD will be the fifth leading cause of death by 2040. Dietary intake is a major potential risk factor, and various diet plans have been assessed for their associations with reduced CKD risk.

Commonly used healthy diet approaches include the Dietary Approaches to Stop Hypertension (DASH), the Alternate Mediterranean diet (aMed), the Alternative Healthy Eating Index, 2010 (AHEI-2010), and the healthful Plant-Based Diet Index (hPDI). All promote anti-inflammatory fresh fruit and vegetable intake and limit pro-inflammatory red meat consumption, both of which are associated with lower CKD risk. In addition, the EAT-Lancet diet limits pro-inflammatory added sugars and fats.

The EAT-Lancet planetary health diet is framed to be both healthy and sustainable. While its associations with diabetes, cancer, and overall risk of death have been defined in prior research, not much is known about its correlation with CKD. Similarly, how genetic and environmental factors modify the relationship between diet and CKD risk remains unclear.

The proteomic and metabolomic profiles of a diet help define its actions on the biology of the human organism, modulated by genetic and environmental contexts. The current study sought to examine the association between the EAT-Lancet diet and new CKD risk and the role of these factors.

UK Biobank links diet patterns to long-term kidney outcomes

The study drew on the UK Biobank, a large-scale longitudinal study from England, Scotland, and Wales. The data were based on 24-hour food recall questionnaires from 179,508 participants who were free of CKD at baseline.

Adherence to the EAT-Lancet diet was scored using four methods: the Stubbendorff, Kesse-Guyot, Yi-Xiang, and Knuppel scores. Among these, the Kesse-Guyot score can describe individual variation due to its continuous nature. The Yi-Xiang score was originally developed in Asian populations.

Metabolic and proteomic signatures partially explain diet effects

The study had a follow-up period of 12.1 years (median), with new-onset CKD developing in 4,819 participants. The mean age of participants was approximately 56 years, with 96 % being White and 55 % female.

At baseline, individuals who later developed CKD were older and more likely to be smokers. They had a higher body mass index (BMI), were less physically active, and reported lower alcohol consumption than non-CKD patients. They also had lower dietary scores with the EAT-Lancet diet, and were more likely to have high blood pressure, high cholesterol, and diabetes mellitus.

After adjusting for multiple confounders, higher adherence to the EAT-Lancet diet was associated with a somewhat lower CKD risk with all scoring methods:

• Stubbendorff, 9 % decrease
• Kesse-Guyot, 8 % decrease
• Yi-Xiang, 6 % decrease
• Knuppel, 6 % decrease

Both the Stubbendorff and Kesse-Guyot scores began to show decreased CKD risk by the second quartile. The Kesse-Guyot score showed a dose-response relationship, the greatest risk reduction occurring in the highest score quartile versus the lowest. The other scores also showed the same trend.

These associations were supported by sensitivity analyses that included other food groups, early CKD exclusion, exclusion of those with only one dietary evaluation, and the use of complete-case records for analysis. An incident CKD definition based on biochemical measures of kidney function showed a similar inverse association, supporting the main findings.

Other healthy diet plans, such as DASH, aMed, hPDI, and AHEI-2010, also showed inverse correlations between diet adherence and CKD risk.

The negative association was strongest in the presence of the rs2010352 GG genotype, but was not affected by the CKD genetic risk score. The rs2010352 variant may influence adenosine signaling pathways, which modulate dietary inflammation.

Lower exposure to green spaces also predicted a stronger inverse association. No other sociodemographic factors affected the association, nor did physical activity or diabetes. These findings suggest the need to understand how the EAT-Lancet diet impacts certain groups.

The metabolic profile of the EAT-Lancet diet, comprising 122 metabolites, was inversely associated with CKD risk. There was an 11 % decrease in risk per 1 standard deviation (SD) increase in metabolic signature score. This comprised the degree of unsaturation in fatty acids and glycoprotein acetyls primarily.

The proteomic diet signature, comprising 143 proteins, showed a stronger trend, with CKD risk declining by 20 % per 1-SD increase in score. This involved the interleukin-18 receptor 1 and kidney injury molecule 1.

Participants with higher metabolic or proteomic signature scores were also less likely to have CKD, independent of and complementary to dietary adherence, compared to those with lower signature scores. These changes partly mediated the diet's impact on CKD risk by 18 % and 27 %, respectively.

Multiple biomarkers have been identified to be common to all healthy diets, possibly explaining their similar protective associations. However, the EAT-Lancet diet was associated with 23 unique biomarkers, which could aid in monitoring dietary adherence.

The use of multi-omics tools suggests that diet has wide-ranging effects on CKD risk. The study thus encourages the integration of genetic, environmental, and multi-omics data to frame and monitor adherence to tailored nutrition plans to reduce CKD risk.

Despite these strengths, the study has several limitations.

• The use of 24-hour recall questionnaires could introduce bias through faulty memory and short-term capture of dietary intake. This is less likely since the findings remained consistent with sensitivity analyses.
• Residual confounding could have affected the results.
• Self-reported drinking, smoking, and exercise habits may be inaccurate due to social biases.
• CKD diagnosis relied primarily on ICD-10 codes, which may have limited sensitivity.
• Non-diverse, mostly White cohort confined to the UK, limiting generalizability.

Planetary health diet shows promise for CKD prevention

Participants with higher adherence to the EAT-Lancet diet had a modest reduction in new CKD risk, though this may potentially have a large impact at the population level. Further research should examine the benefits among individuals living in non-green neighborhoods or who carry the genetic variant rs2010352. The results also indicate that metabolites and proteins influenced by the diet mediate the effect.

These findings support the adoption of planetary health diets in CKD prevention and underscore the value of personalized nutrition strategies that incorporate genetic, environmental, and molecular profiling.