Dietary intake shapes the growth of organisms, enables organ development and maintenance, affects immune system function and ultimately influences health and lifespan. Although diet has an enormous impact on health, consensus about how what we eat affects our biology remains largely elusive. However, there is consensus that our diet has a much more pervasive role than previously thought in modulating molecular mechanisms governing susceptibility to diseases such as type 2 diabetes, cardiovascular disease and cancer. The biological mechanisms linking diet to disease however remain unclear.
To address the gap in our knowledge, we established the FastBio (religious Fasting Biology) study which explores the biological impact of a dietary pattern involving periodic dietary restriction (DR) of animal products. We carried out in-depth molecular characterisation of a unique group of individuals from Greece who alternate between omnivory and animal product DR for religious reasons. These individuals abstain from meat, fish, dairy products and eggs for ~190 days annually, in a consistent and highly structured pattern involving four extended periods of DR throughout the year, and DR on Wednesdays and Fridays. We compared findings to a continuously omnivorous group of individuals studied in parallel. Participants were profiled at two timepoints: T1 (autumn), covering a period of omnivory for both groups, and T2 (spring), covering a 3-4-week period of DR, during Lent.
We aimed to investigate how animal product DR affects:
1) Health-related clinical chemistry biomarkers and complete blood counts
2) Molecular traits (blood metabolites, gene expression and protein levels, the gut microbiome) and how our genetic makeup can influence their levels
3) Immune system cells and their function
We found that short-term DR can reprogram biological pathways resulting in substantial metabolic, immune and molecular changes with predominantly positive effects on health. However, further investigation is needed to clarify both positive and potentially negative consequences and to better understand how genetic and environmental factors, such as diet and seasonal variation, interact to influence disease risk. Importantly, our results indicate that dietary recommendations may not have uniform effects across individuals due to differences in genetic background. These insights have important implications for clinical practice, supporting the development of precision nutrition and personalised strategies for disease prevention. Additionally, we have identified promising molecular candidates for therapeutic evaluation, including targets for drugs designed to mimic diet-associated molecular responses that support healthy aging. Finally, our data reveal diet-driven changes in the abundance of potentially druggable targets, suggesting that dietary interventions could be leveraged to optimise pharmacological outcomes.
