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  1. Ian Forgacs, Associate Editor

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YOU ARE WHAT YOU EAT

The concept that what we eat might be an important cause of human disease would not surprise most of the world’s population. However, the fact that infected food is such a significant problem in the West causes distress—especially to governments who, in the UK, have pledged to reduce the problem by 20% in 4 years. Clearly reliable data on the burden of foodborne disease would be helpful in evaluating such targets. Adak and colleagues have used a number of data sources and applied corrections. Since 1992, there are fewer foodborne infections and related deaths, but the number of hospitalisations has changed little. Campylobacter is by far the most significant problem which must be tackled if the government’s targets are to be met. See page 832

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See page 832. Credit: AJHD/DHD

A SOLLID VIEW ON INTRODUCING SOLIDS

A Swedish study of infants starting to ingest gluten showed that continuing breast feeding had a beneficial effect on preventing coeliac disease. The paper was published in the American Journal of Clinical Nutrition and is featured in Clinical @lert. In a brilliant essay, Sollid highlights the limitations of proving causality using epidemiology. He considers the case for continuing to breast feed as being unproven but concludes that it is reasonable to do so as it may be beneficial and is most unlikely to be harmful. Hard to argue with that. See page 767

DON’T BE A NERD

Apparently major car manufacturers, such as Volkswagen, invest much effort in ensuring that the names of their models, such as “Polo” do not mean something offensive, derogatory or lewd in Urdu, Japanese, Sanskrit, or indeed any other language. NERD may mean non-erosive reflux disease but it has unsatisfactory connotations for anglophones. The problem of functional heartburn stimulates clinical investigation and puzzles clinicians and patients. Responses to anti-secretory treatment is unsatisfactory—a finding which somehow undermines further that gallant (but diminishing) band of clinicians who feel therapeutic trials are acceptable surrogates for proper investigation. See page 885

THERE’S NO DOUBT, CHOP IT OUT

Many teachers used to tell me that, where possible, surgery should be avoided in patients with inflammatory bowel disease. They were probably thinking about operating (or not) on the gut, but if you are going to develop ulcerative colitis (UC) there is another intra-abdominal organ it is best to be without—the appendix. We know that appendicectomy lowers the risk of developing UC but two papers in this month’s Gut extend that observation. A prior appendicectomy delays disease onset and confers a milder course in patients with UC. See pages 763, 803, and 808

LET THERE BE LIGHT

Advances in understanding the role of NF-kappaB in cancer and inflammation are being made at light speed. Mann’s piece in Science @lert highlights and illuminates an original paper in Journal of Immunology that describes luminescence as an indicator of NF-kappaB activation. Such work shines brightly in the firmament of transcription factor research. The NH-kappaB luciferase transgenic mouse model experiments are not always easy to follow—maybe the devil does lie in the detail. See page 769

CHRONIC PANCREATITIS: A HIGH RISK CONDITION?

Few human diseases are in greater need of a breakthrough than pancreatic cancer. Even its aetiology is more obscure than for most common tumours. Hereditary pancreatitis is a recognised, powerful but uncommon premalignant condition. In the past 15 years chronic pancreatitis has emerged as a potentially significant risk factor but the magnitude of the association is unclear as case series are often retrospective and ascertainment is ill-defined. Malka and co-workers followed 373 patients with chronic pancreatitis between 1973 and 1997. The standardised incidence ratio (observed v expected) for pancreatic cancer was 26.7. Useful information but note that there were only 4 cases and the confidence intervals are not small. See pages 765 and 849

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