Commentary: Understanding sources of complexity in chronic diseases—the importance of integration of genetics and epidemiology

Abstract

Progress in identifying genes for nearly all known Mendelian diseases spurred by mapping of the human genome generated a nearly universal expectation that the same research strategies would eventually be successful in identifying genes for complex diseases, such as heart disease, obesity, cancer, diabetes, and many common psychiatric conditions. As the failure to identify and replicate genes for complex disorders has become increasingly apparent, enthusiasm for rapid success has waned. In ‘Dissecting Complex Disease: The Quest for the Philosopher’s Stone?’ Buchanan et al. 1 admonish geneticists and epidemiologists who are engaged in searching for either genetic or environmental risk factors for complex diseases that there may be no gold at the end of the rainbow (or that the philosopher’s stone will generate base metals rather than gold; or that there is no ‘fountain of youth’.) 2