Our study allowed us to address another important methodological issue: the adequacy, or otherwise, of using a common set of controls, rather than a sample recruited explicitly for use with a defined disease sample. It is often assumed that failure to match cases and controls for socio-demographic variables will lead to substantial inflation of the type I error rate. Our study demonstrates that, within the context of large-scale genetic association studies, for British populations at least, this concern has been overstated. A related argument against use of population controls relates to the perceived impact of misclassification bias when a proportion of controls meet the criteria used to define cases. However, the consequent loss of power is modest unless the trait of interest is very common6. Given the above, the present study provides a compelling case for both the suitability and efficiency of the common control design in Britain and warrants its serious consideration elsewhere. Further benefits can be expected from use of this common control genotype data set in future GWA studies in Britain. Finally, in failing to detect significant
