Chronic kidney disease (CKD) is a growing concern, affecting a significant portion of the global adult population. In a recent study published in CMAJ, researchers explored the link between the EAT-Lancet planetary health diet and its potential to reduce the risk of CKD.
Unveiling the Power of Diet: A Game-Changer for Kidney Health?
Diet quality has emerged as a crucial factor in preventing CKD, and various diet plans have been scrutinized for their impact on kidney health. Common healthy diet approaches, such as DASH, aMed, AHEI-2010, and hPDI, all promote anti-inflammatory foods like fresh fruits and vegetables while limiting pro-inflammatory red meat. The EAT-Lancet diet takes this a step further by restricting added sugars and fats, which are also known to cause inflammation.
While the EAT-Lancet diet has been associated with improved health outcomes for diabetes, cancer, and overall mortality, its impact on CKD has been less clear. This study aimed to fill that knowledge gap and explore how genetic and environmental factors might influence the relationship between diet and CKD risk.
Unraveling the Mystery: UK Biobank Data Provides Insights
The study utilized data from the UK Biobank, a large-scale longitudinal study encompassing England, Scotland, and Wales. The data was collected from 179,508 participants who were free of CKD at the study's onset. Adherence to the EAT-Lancet diet was assessed using four scoring methods, with the Kesse-Guyot score standing out for its ability to capture individual variation.
Over a median follow-up period of 12.1 years, 4,819 participants developed new-onset CKD. The average age of participants was approximately 56 years, with a predominantly White (96%) and female (55%) cohort.
At baseline, individuals who later developed CKD were older, more likely to be smokers, had a higher BMI, were less physically active, and reported lower alcohol consumption compared to those without CKD. They also had lower dietary scores on the EAT-Lancet diet and were more likely to have high blood pressure, high cholesterol, and diabetes mellitus.
The Role of Genetics and Environment: Uncovering the Complex Relationship
After adjusting for various confounders, higher adherence to the EAT-Lancet diet was associated with a slightly lower CKD risk, regardless of the scoring method used. The strongest association was observed with the Kesse-Guyot score, which showed a dose-response relationship, indicating the greatest risk reduction in the highest score quartile.
Sensitivity analyses further supported these findings, and an incident CKD definition based on biochemical measures of kidney function showed a similar inverse association. Other healthy diet plans, such as DASH, aMed, hPDI, and AHEI-2010, also demonstrated inverse correlations between diet adherence and CKD risk.
The negative association was particularly strong in the presence of the rs2010352 GG genotype, but it was not influenced by the CKD genetic risk score. This variant may impact adenosine signaling pathways, which play a role in modulating dietary inflammation.
Lower exposure to green spaces also predicted a stronger inverse association, suggesting that environmental factors play a role in the diet's impact on CKD risk. Interestingly, other sociodemographic factors, physical activity levels, and diabetes status did not affect the association.
Unraveling the Diet's Impact: Metabolic and Proteomic Signatures
The metabolic profile of the EAT-Lancet diet, consisting of 122 metabolites, was inversely associated with CKD risk. Participants with higher metabolic signature scores had an 11% decrease in risk per 1 standard deviation increase in the score. This was primarily driven by the degree of unsaturation in fatty acids and glycoprotein acetyls.
The proteomic diet signature, comprising 143 proteins, showed an even stronger trend, with CKD risk declining by 20% per 1-SD increase in the 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. These changes partially mediated the diet's impact on CKD risk by 18% and 27%, respectively.
The Promise of Personalized Nutrition: Tailoring Diets for Optimal Kidney Health
The study identified multiple biomarkers common to all healthy diets, which may explain their similar protective associations. However, the EAT-Lancet diet was also associated with 23 unique biomarkers, offering potential tools for monitoring dietary adherence.
The use of multi-omics tools highlights the wide-ranging effects of diet on CKD risk. The study encourages the integration of genetic, environmental, and multi-omics data to develop tailored nutrition plans that can effectively reduce CKD risk.
Despite its strengths, the study has limitations, including potential bias from self-reported data and a predominantly White cohort from the UK, which limits its generalizability.
Final Thoughts: A Step Towards Personalized Kidney Care
Participants who adhered more closely to the EAT-Lancet diet experienced a modest reduction in new CKD risk, which could have a significant population-level impact. Further research is needed to explore the benefits of this diet in individuals living in non-green neighborhoods or carrying the genetic variant rs2010352. The study's findings also highlight the role of metabolites and proteins influenced by the diet in mediating its effect on CKD risk.
These insights support the adoption of planetary health diets in CKD prevention and emphasize the value of personalized nutrition strategies that consider genetic, environmental, and molecular profiling. With further research, we can continue to unlock the potential of diet as a powerful tool for kidney health.
