Comment on “Lifestyle, genetic susceptibility, and risk of diverticular disease: a prospective cohort study”

To the Editor, Guo et al leverage the scale and follow-up depth of UK Biobank to address a practical prevention question in diverticular disease: how do modifiable lifestyle factors and inherited susceptibility jointly shape risk – particularly for complicated diverticulitis?1 Their analysis of 472 612 participants (median follow-up 13.6 years) provides a clear, clinically useful message: risk is cumulative and strongly patterned by behaviors that are, in principle, modifiable. This commentary was prepared in accordance with the TITAN 2025 guideline to support transparent and responsible reporting2. Two findings are especially actionable for surgical prevention. First, smoking stands out as a consistent and high-magnitude risk factor, including for perforation/abscess – an association that is well supported by prior population data1,3. Second, the dietary signal – higher fruit/whole-grain patterns and lower red meat/refined grains – fits with prospective evidence that greater dietary fiber intake (and fiber source) is associated with lower diverticular disease incidence1,4. Importantly, Guo et al extend these prevention signals to the harder endpoint of complicated diverticulitis, not only “any diverticular disease,” which strengthens relevance to surgeons and emergency services1. The gene–environment framing is also valuable, but the authors’ caution should be foregrounded in translation: most interaction tests did not survive false-discovery-rate correction1. In other words, the strongest inference is not “precision prevention” by PRS subgroup, but that a healthier lifestyle profile is likely beneficial across genetic strata – consistent with recent prospective work showing lifestyle scores reduce diverticulitis risk regardless of genetic susceptibility5. Several limitations temper immediate deployment as a clinical risk tool. UK Biobank’s selection and ancestry composition may affect calibration; lifestyle measures are self-reported and mostly baseline-only (regression dilution and time-varying misclassification); and ICD-coded inpatient ascertainment may under-capture outpatient uncomplicated disease while enriching severe phenotypes1. These constraints do not negate the signals, but they argue for replication with repeated exposure measures and clinically adjudicated phenotypes. Overall, Guo et al provide strong population-level evidence to support a prevention narrative that surgeons can credibly amplify: smoking cessation, sleep health, and diet quality may meaningfully reduce diverticular disease burden, even before genetics is ready for routine risk-directed imaging or prophylaxis1.