What the evidence actually shows about food, fasting and infection — and how narrow it is.
What the evidence says
- The effect of feeding during infection depends on the PATHOGEN TYPE, and the two directions are opposite. In bacterial inflammation (Listeria, LPS), fasting was protective and nutritional supplementation was detrimental. In viral inflammation (influenza, Poly(I:C)), glucose supplementation protected against mortality while blocking glucose utilisation was uniformly lethal[1]
- These opposing effects were largely independent of pathogen burden and of the magnitude of inflammation — they reflect distinct cellular stress-adaptation pathways rather than differences in how hard the infection hit[1]
- The mechanisms differ by direction: in bacterial inflammation, ketone bodies from fasting metabolism acted as histone deacetylase inhibitors, enabling adaptation to reactive-oxygen-species damage in the brain; in viral inflammation, glucose utilisation prevented ER-stress-induced apoptosis through CHOP regulation[1]
- This is mouse work. Neuronal dysfunction was the proximal cause of death in both scenarios, with autonomic control defects in body temperature, heart rate and respiratory rate[1]
- Chicken soup inhibits neutrophil migration IN VITRO — a concentration-dependent effect measured in a Boyden blindwell chemotaxis chamber, with two different chemoattractants, suggesting a broad anti-inflammatory mechanism in the assay[2]
- The active component was nonparticulate: clarified supernatant retained most of the inhibitory activity after centrifugation[2]
- All individual vegetables (onion, sweet potato, parsnip, turnip, carrot, celery, parsley) and the chicken each inhibited chemotaxis on their own — but chicken broth before the vegetables were added was NOT active, and the soup acquired maximal activity shortly after the first vegetables went in[2]