Abstract of "Diabetes, diet and denervation"

Contemporary theories to explain the autoimmune aetiology of type 1 diabetes mellitus (T1DM) include the "hygiene", "accelerator" and "thrifty phenotype" hypotheses though none accounts for its natural history, or, epidemiology. Early-onset, T1DM is epidemic in Western countries and shares features of its epidemiology with other major childhood diseases.

In the autonomic denervation view, early-onset, T1DM results from injury to autonomic nerves supplying the pancreas through persistent physical efforts during defaecation in infancy. Pancreatic denervation results in loss of islets of Langerhans and reduced insulin production that may present in infancy or later life. Early introduction of cows milk and solids to the infants' diet cause increased rates of bowel problems whereas exclusive breastfeeding in non-Western countries, protects the infant from both constipation and diarrhoea.

What about the extended MHC haplotypes that link to T1DM and other diseases ? Then the question arises as to what is an "autoimmune" disease ? Criteria for an "autoimmune" disease were set out by Witebsky and Rose in 1957. Few, if any, diseases meet those stringent criteria. Over the decades many different conditions have been added to the "autoimmune" dustbin - largely on the basis that their immunohistopathology includes CD4 and CD8 lymphocytes, or, there are MHC associations.

Other important Western diseases may result from the varying effects of injuries to nerves at different sites in the autonomic nervous system.