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 reporting[2]. 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 data[1,3]. 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 incidence[1,4]. 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 services[1]. 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 correction[1]. 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 susceptibility[5]. 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 phenotypes[1]. 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 prophylaxis[1].