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Homeopathy is controversial and hotly debated. The conclusions of systematic reviews of randomised controlled trials of homeopathy vary from 'comparable to conventional medicine' to 'no evidence of effects beyond placebo'. It is claimed that homeopathy conflicts with scientific laws and that homoeopaths reject the naturalistic outlook, but no evidence has been cited. We are homeopathic physicians and researchers who do not reject the scientific outlook; we believe that examination of the prior beliefs underlying this enduring stand-off can advance the debate. We show that interpretations of the same set of evidence--for homeopathy and for conventional medicine--can diverge. Prior disbelief in homeopathy is rooted in the perceived implausibility of any conceivable mechanism of action. Using the 'crossword analogy', we demonstrate that plausibility bias impedes assessment of the clinical evidence. Sweeping statements about the scientific impossibility of homeopathy are themselves unscientific: scientific statements must be precise and testable. There is growing evidence that homeopathic preparations can exert biological effects; due consideration of such research would reduce the influence of prior beliefs on the assessment of systematic review evidence.

OBJECTIVE: The aim of this study is to look at the influence of metformin intake and duration, on urinary bladder cancer (UBC) risk, with sulfonylurea (SU) only users as control using a new-user design (inception cohort). METHODS: We conducted a retrospective cohort study using data from the UK Clinical Practice Research Datalink (CPRD) including all patients with at least one prescription of oral anti-diabetic drugs (ADD) and/or insulin. The risk of UBC in different groups of ADD users (metformin alone (1), metformin in combination (2) with other ADD medication (glinides, glitazones, DPP-4-inhibitors, SUs, insulin or more than one combination), all metformin users (1 + 2) was compared with SU only users using Cox proportional hazards models. The estimates were adjusted for age, gender, smoking status, BMI and diabetes duration. RESULTS: The inception cohort included 165,398 participants of which 132,960 metformin users and 32,438 SU only users. During a mean follow-up time of more than five years 693 patients developed UBC, 124 of the control group and 461 of the all metformin users. There was no association between metformin use and UBC risk (HR = 1.12 (95% CI 0.90-1.40)) compared to SU only users, even after adjustment for diabetes duration (HR = 1.13 (95% CI 0.90-1.40)). We found a pattern of decreasing risk of UBC with increasing duration of metformin intake, which was statistically not significant. CONCLUSION: Metformin has no influence on the risk of UBC compared to SU in type 2 diabetes patients using a new-user design. This article is protected by copyright. All rights reserved.