Autophagy is a promising therapeutic target as preclinical studies show that it slows biological ageing, and age-related disease. Further, in preclinical models, autophagy is modifiable; in cell models, autophagy is increased by removal of amino acids, and in mice it can be stimulated by fasting for 24-48 hours. However, very little is known about how autophagy behaves in living human beings. Therefore, we have optimised an autophagic flux assay for use in intact human blood to reflect physiological autophagy. This is important as we know removing cells from whole blood and culturing them in standard culture media changes autophagy dramatically. One major barrier to investment in the field is a lack of demonstration of autophagy modification in humans. To address this gap, we have used our blood assay to measure human autophagy in response to nutrient restriction. We have generated autophagy-related data from over 240 people from four different interventional human studies that have explored different kinds of nutrient restriction. Across these interventions, we have found mixed results that have deviated from hypotheses. I will discuss these results, the limitations of this work, and current work that will focus on improving our human autophagy measurement systems.