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As individuals living a Western lifestyle age, the prevalence of diverticulosis steadily rises reaching around 50% over the age of 75 years.1 While for most this is a harmless ageing change reflecting weakening of colonic connective tissue, around 30% suffer recurrent abdominal pain, often with diarrhoea,2 and 1–4% will be hospitalised with diverticulitis.3 As our population steadily ages this represents a substantial health burden, however, we know surprisingly little about the underlying mechanisms of this disease.
Heritability of symptomatic diverticular disease is around 40%,4 however, studies of immigrants from low-risk areas to high-risk countries show that environmental factors are equally important.3 Once hospitalised with diverticulitis the risk of further hospitalisation is around 1% per year but the majority continue to suffer pain or bowel disturbance, at least for the 1st year after discharge.5 Diverticulitis is associated with inflammation, tissue destruction and remodelling which includes striking muscular hypertrophy and morphological abnormalities of the enteric nerves thought to be responsible for symptoms.6 However the mechanisms whereby diverticulosis leads to diverticulitis remains unclear though dietary factors such as meat eating, obesity and low fibre intake play a role. One way these could act is by altering the microbiota.7 This might also account for reports that antibiotics8 probiotics9 or the anti-inflammatory agent mesalazine10 can reduce symptoms, though in most cases the number needed to treat is high.
The current paper11 represents a start in our attempts to understand this phenomenon. The authors hypothesised that the presence of diverticula creates a unique environment which leads to important changes in microbiota with potential effects on the gut immune system and hence symptoms. Controls (n=14) and 16 patients with asymptomatic diverticulosis (termed ‘diverticulosis’) were compared with 8 patients with …
Contributors RCS and TJS are joint authors.
Funding RCS is supported by the NIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and the University of Nottingham.
Disclaimer The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.
Competing interests RCS has acted on Advisory Boards for Allergan, Commonwealth Diagnostics and Ipsen, and received speaker's fees from Menarini.
Provenance and peer review Commissioned; internally peer reviewed.
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