Timothy Key - Biography#

Timothy Key graduated in Veterinary Medicine from Edinburgh University in 1978. Following veterinary hospital work in London he took up a Fellowship at the University of Bristol, where he recognized a new disease in cats subsequently named Key-Gaskell Syndrome/Feline Dysautonomia. He then took a Masters in Nutrition in London and subsequently moved to Oxford. As part of his DPhil he wrote a critical review and synthesis of the epidemiology of hormones and breast cancer (591 citations), predicting that exposure to exogenous progestagens would cause a higher risk of breast cancer than oestrogens alone, as subsequently confirmed by Key and others. He then established the Endogenous Hormones and Breast Cancer Collaborative Group, to harmonize the worldwide data on hormones from prospective studies and allow the reliable assessment of effects.

In 1993 Key established the EPIC-Oxford prospective cohort study, part of the EPIC-Europe consortium part-funded by the EU and co-ordinated by the World Health Organization. EPIC-Oxford is the largest study in the world with detailed information, a biobank and comprehensive health record linkage for a large number of vegetarians, vegans and others on plant-based diets. Key's group constitutes a centre of excellence on the long-term health impacts of vegetarian and other plant based diets, with landmark publications on major diseases including cancers, cardiovascular diseases, gastrointestinal disorders and bone health, as well as empirical research demonstrating the strikingly low environmental impact of contemporary plant-based diets in the UK.

Key developed prostate cancer research in the pan-European EPIC study, establishing a working group in 1999 which he chaired until 2020. He secured substantial funding and led a programme of research on hormones, nutritional biomarkers, genetics, metabolomics and proteomics, with collaborative research across Europe and with the US National Cancer Institute. Key's research on prostate cancer has shown that both insulin-like growth factor-I and free testosterone are associated with high risk, with confirmation in genetic analyses.