Chapter 3: Fasting

The chapter establishes glucose as the obligatory fuel for the central nervous system and erythrocytes while explaining how other tissues progressively shift toward fatty acid oxidation and ketone body utilization. As hepatic glycogen becomes depleted, gluconeogenesis emerges as the critical pathway sustaining blood glucose through substrates including lactate from anaerobic glycolysis, glycerol from triglyceride breakdown, and glucogenic amino acids from muscle proteolysis, with nitrogen disposal occurring through the urea cycle. During extended starvation, hepatic ketogenesis intensifies and the brain adapts metabolically to oxidize ketone bodies as a primary fuel source, thereby reducing the reliance on gluconeogenesis and significantly sparing muscle protein from catabolism. The chapter integrates clinical assessment of nutritional status through anthropometric measurements including mid-upper arm muscle circumference, triceps skinfold thickness, and the creatinine-height index, alongside biochemical markers such as serum albumin, prealbumin, creatinine, and blood urea nitrogen that reflect protein depletion and organ dysfunction. Protein-energy malnutrition is classified into severity grades based on body mass index and clinical presentation, with detailed case analyses demonstrating how psychological factors such as depression and eating disorders like anorexia nervosa trigger metabolic derangements including severe hypoglycemia, amenorrhea, and ketosis. The chapter concludes by emphasizing how metabolic adaptation extends survival during starvation but ultimately becomes unsustainable as fat and protein reserves approach depletion, illustrating the critical importance of nutritional rehabilitation through dietary intervention, psychological support, and medical monitoring.