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Having been awarded the 2019 British Nutrition Foundation Annual Prize I had looked forward to delivering a lecture to assembled guests at the BNF Annual Day at the Royal College of Physicians in London, in 2020. Unfortunately, this was not to be; the COVID‐19 global pandemic prevented a face‐to‐face meeting, and my talk was delivered remotely. In the paper, I shall summarise some of the research that I have carried out during my career as a nutrition scientist. I shall not dwell in much detail on any single aspect of my work but rather I shall attempt to show how my research interests developed over the decades, how one thing led to another, so to speak. The elements of my work that I have selected, in order to make this short walk together, commence with vitamin B2, riboflavin and a consideration of two particular aspects of function. I then move on to folate in the context of homocysteine metabolism and cardiovascular disease and finally consider the role of this vitamin and other methyl donors in cancer risk and outcome. [ABSTRACT FROM AUTHOR]

We have previously reported that supplementation with folic acid (1.2 mg day(-1) for 12 week) elicited a significant improvement in the folate status of 61 healthy volunteers. We have examined effects of this supplement on markers of genomic stability. Little is known about the effect of folate supplementation on DNA stability in a cohort, which is not folate deficient. Preintervention, there was a significant inverse association between uracil misincorporation in lymphocyte DNA and red cell folate (P < 0.05). In contrast, there were no associations between folate status and DNA strand breakage, global DNA methylation or DNA base excision repair (measured as the capacity of the lymphocyte extract to repair 8-oxoGua ex vivo). Folate supplementation elicited a significant reduction in uracil misincorporation (P < 0.05), while DNA strand breakage and global DNA methylation remained unchanged. Increasing folate status significantly decreased the base excision repair capacity in those volunteers with the lowest preintervention folate status (P < 0.05). Uracil misincorporation was more sensitive to changes in folate status than other measures of DNA stability and therefore could be considered a specific and functional marker of folate status, which may also be relevant to cancer risk in healthy people. [ABSTRACT FROM AUTHOR]