Fasting-Caloric Restriction

The folk admonition to starve a fever may have a scientific basis. Fevers due to infectious organisms that produce neuraminidase (sialidase) may contribute to the pathophysiology of autoimmune conditions. Neuraminidase unmasks host cellular lectins that interact with food lectins and can induce human leukocyte antigen type II (HLA II) expression. HLA II can then bind food lectins and serve as targets for antibody production. Some of these antibodies can then cross-react and attack healthy tissue, inducing disease. The example of insulin-dependent diabetes mellitus is discussed, helping to explain why infectious organisms and dairy product ingestion appear to be linked to some cases of this disease. Genetic variants and other factors may contribute to disease pathogenesis, so this model does not explain all instances of autoimmune disease. Fasting as a way to avoid the process by not introducing food lectins is briefly reviewed. Neuraminidase inhibitors might be useful in preventing genesis of autoimmunity during infection, although this possibility has not been formally tested.