EAT-Lancet diet pattern, genetic risk, and risk of colorectal cancer: a prospective study from the UK Biobank

Feb 24, 2025The American journal of clinical nutrition

EAT-Lancet Diet, Genetic Risk, and Colorectal Cancer Risk in UK Adults

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Abstract

During a median follow-up of 13.05 years, 2,016 participants developed colorectal cancer (CRC).

A higher EAT-Lancet Diet Index (ELD-I) is associated with a reduced risk of CRC, with a hazard ratio of 0.87 for those with the highest versus the lowest ELD-I.
There is a significant additive interaction between genetic risk, measured by a polygenic risk score (PRS), and ELD-I on CRC risk.
The ELD-I is linked to reduced CRC risk primarily in individuals with moderate genetic risk, showing hazard ratios of 0.76 for moderate risk compared to 0.84 for low risk and 0.96 for high risk.
Participants with lower genetic risk and higher ELD-I experienced a 75% reduction in CRC risk compared to those with higher genetic risk and lower ELD-I.
The ELD-I could contribute to a 13% reduction in CRC risk, particularly for individuals with moderate genetic risk.

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BACKGROUND: Diet and genetic risk are risk factors for colorectal cancer (CRC). The interaction between the EAT (Lancet Commission on healthy diets from sustainable food systems)-Lancet diet and genetic variants on CRC risk remains unclear.

OBJECTIVES: We aim to investigate the association between EAT-Lancet diet and CRC risk and to evaluate its combined effect with genetic risk on CRC risk.

METHODS: We conducted a prospective cohort study involving 177,441 participants from the UK Biobank who completed 24-h food recall questionnaires at least once. The EAT-Lancet Diet Index (ELD-I) was calculated using the dietary recall data to assess EAT-Lancet diet, and a polygenic risk score (PRS) was constructed by using 197 single-nucleotide polymorphisms to evaluate genetic risk. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards regression models to assess the associations.

RESULTS: During a median follow-up of 13.05 y, 2,016 participants developed CRC. Higher ELD-I was significantly associated with a reduced CRC risk (the highest compared with the lowest HR: 0.87, 95% CI: 0.76-0.99). A significant additive interaction between PRS and ELD-I was identified on CRC risk (relative excess risk due to interaction: 0.142, 95% CI: 0.058, 0.225). The ELD-I was significantly associated with reduced CRC risk in individuals with moderate but not low and high genetic risk, with HRs (95% CIs) of 0.76 (0.63, 0.92), 0.84 (0.53, 1.33), and 0.96 (0.76, 1.20), respectively. Compared with participants with higher PRS and lower ELD-I, those with lower PRS and higher ELD-I showed a 75% reduction in CRC risk (HR: 0.25; 95% CI: 0.17, 0.36).

CONCLUSIONS: The ELD-I could reduce 13% of CRC risk, especially in individuals with a moderate genetic risk. Individuals with high ELD-I and low PRS had the lowest CRC risk than those with low ELD-I and high PRS. These findings underscore the potential role of EAT-Lancet Diet in CRC prevention.

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EAT-Lancet diet pattern, genetic risk, and risk of colorectal cancer: a prospective study from the UK Biobank

Abstract

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