Autoimmune Diseases: Diabetes
Diabetes 1 Model
Diabetes 1 is caused by T-lymphocyte destruction of insulin-producing
pancreatic cells. Several triggers for this immune process have been
identified: viruses and food proteins lead the list. Because of evidence
that cow's milk intake can trigger diabetes in rodents, a study of diabetic
children showed that antibody to bovine serum albumin and a 17-amino-acid
bovine serum albumin peptide (ABBOS). These antibodies would bind to a
pancreatic beta-cell surface antigen. This study showed that diabetic
patients had high serum concentrations of anti-BSA antibodies (IgA and IgG).
Cow's Milk Triggers Diabetes
Because of evidence that cow's milk intake can trigger diabetes in
rodents, a study of diabetic children demonstrated antibodies to bovine
serum albumin and a 17-amino-acid bovine serum albumin peptide (ABBOS).
The presence of antibody (which means presence of antigen-specific B-cells)
may signal the concomitant presence of antigen-specific cytotoxic T-lymphocytes,
although these have not yet be demonstrated. The researchers suggest that ...
"relevant clones (of lymphocytes) are continuously transferred from immature
IgM-expressing B-cell compartments to pools of IgG-secreting or IgA secreting
cells.... a slow inefficient process, consistent with the fact that clinical
disease develops in only about 5 to 6 % of hosts with the relevant genetic
An Australian study of children who developed diabetes found that children
given cow’s milk formula in the first three months were 52% more likely to
develop diabetes than those not fed milk. Breast fed infants had a 34% lower
incidence of diabetes than formula fed infants. An Italian study showed that
exposure to beta casein produced proliferation of T- lymphocytes from the blood
of 51% of 41 insulin dependent diabetics.
The diabetes model of food-antigen triggered disease is an important
immunological model of many unsolved diseases that appear to be "autoimmune".
Food is an abundant source of protein antigens. A long-term, inefficient
pathogenesis can produce target-organ damage, especially if the antigen
challenge continues over many years.
Alternative explanations suggest that beta cells are attacked by cytotoxic
T-cells after a virus infects them or by T-cells originally targeted on other
cells infected by virus whose cell-surface antigens happen to resemble beta cell
antigens. Coxsackie B viruses, for example