Introduction : The importance of ketone body metabolism in diabetic patients has been known since the 1970s, but recently β-hydroxybutyrate (βHB) has been identified as a key component of a metabolic signaling pathway. However, many questions remain unanswered about individual differences in the production and excretion of ketone bodies. Objectives: Fourteen healthy subjects were admitted in the ARSOA Wellness Fasting program. During a 4-day fasting period, they received a combination of very low-energy vegetarian diet, physical exercise, meditation, and lectures about healthy lifestyles. Methods: Every morning, participants measured their body composition, blood glucose, and β-hydroxybutyrate (βHB). The first urine of the day was analyzed for βHB, glucose, pH and 7 other elements. Ten milliliters of urine were deep frozen for further quantitative analysis. Peripheral blood was collected on days 1 and 4 for routine biochemical analyses and for the determination of serum levels of hormones. All data were collated in an Microsoft Excel ® file, and transferred to SPSS for statistical analysis. Results: Ketone bodies in the blood increased from 0.3±0.2 mM at day 1 to 1.8±0.9 mM at day 4 of fasting, while the glucose level decreased from 5.8±1.9 mM to 4.5±1.5 mM. Increases in peripheral blood βHB were assigned to 3 groups (0.8-1.2 mM, 1.3-1.8 mM, 1.8-4.8 mM). Pass analysis suggested that decreased insulin and glucose levels under 4.5 mM both seemed to trigger ketogenesis. The βHB/Acetoacetate (AcAc) ratio in blood was about 5, regardless of the βHB concentration, but the range varied from 0.56 to 3.36 in the urine. The highest excreted concentration of βHB was 597 mmol/g creatinine. These values returned to normal ranges on the 14 th day (10 days after fasting). Changes in blood ketone bodies significantly correlated with total thyroxin, while urinary epinephrine changes correlated with urinary ketone bodies. Ketone body production seemed to cause hepatic and renal damage, as indicated by a slight alteration in markers of hepatic function and a 12% decrease in eGFR. Conclusions: Four days of fasting induces hyperketosis with some metabolic changes. The magnitude of changes in ketone body concentrations correlates with the levels of insulin, glucose, triacylglycerol and several hormones. The urinary excretion of βHB abruptly increased in group 3 (more than 1.8 mM). It was 100 times higher than the blood βHB concentration. Further studies are necessary to establish the safety of fasting as a way to induce hyperketosis for therapeutic needs. Our observations of a slight decrease in hepatic function and a 12% decrease in eGFR call for caution.