Cow's milk contains many proteins that are antigenic - they excite immune responses. Patients of all ages with gastrointestinal tract disease may have difficulty digesting these proteins and may absorb them as antigens. Milk problems may be attributed to lactose intolerance and the milk-sugar enzyme, lactase, may be prescribed.

Milk allergy is a protein problem and is not improved by changing the milk sugar - often the diagnosis of "lactose intolerance" is incomplete or wrong and symptoms persist with only lactose exclusion. Often, infant milk allergy is thought to be a specific and limited condition which children "outgrow." This idea can be misleading many children continue to have chronic symptoms from milk, although the original problem may disappear, the pattern of illness changes and confuses parents and physicians.

At the very least, we can say that some children have an allergic diathesis that persists and evolves with different manifestations. In a follow-up study of children with immediate anaphylactic reactions to cows milk as infants, a prolonged pattern of hypersensitivity was noted with the development of multiple food and inhalant allergies, multiple hospitalizations and frequent episodes of drug reactions. These children may continue to manifest hypersensitivity and grow into adults with immune-mediated diseases. Although there are few studies which focus on milk-induced disease if adults, there is enough suggestive evidence to suspect that milk proteins play a major role in human disease at all ages.

There are at least 30 antigenic primary proteins in milk. Casein is the most commonly used milk protein in the food industry; lactalbumin, lactoglobulin, bovine albumin, and gamma globulin are other protein groups within the milk. Digestion probably increases the number of possible antigens to over 100.

Milk proteins tend to stay intact as milk is converted to dairy products of all types. While lactose intolerance may not be an issue with yogurt ingestion, for example, milk protein allergy remains. Many patients have been fooled by health claims for lactose-free or lactaid-fixed milk and continue to have symptoms from milk allergy when they ingest these products. Digested fractions of each of the milk proteins may induce the production of IgE, IgA, and IgG antibodies and may trigger complex, variable immune responses. Skin tests with whole milk proteins are, therefore, misleading - type 1 responses do appear regularly on skin tests showing IgE activity against intact proteins, but secondary antigens are not detected.

Furthermore, milk antigens tend to get through the GIT mucosa intact and are therefore responsible for a host of delayed immune responses which do not depend on IgE and do not show up on skin tests. The role of milk proteins in triggering the most serious pathology usually goes undetected.

Evidence of a pathogenic role of cows milk in many disorders has been presented - asthma, rhinitis, eczema, urticaria, serous otitis media, pulmonary alveolitis (hemosiderosis), milk-induced enteropathy in infants, eosinophilic gastroenteritis, gastrointestinal bleeding with iron deficiency anemia, migraine headaches, attention deficit hyperactivity disorder, Crohn's disease, rheumatoid arthritis, and insulin dependent diabetes mellitus.

A major effort has been made by companies manufacturing infant formulas to produce "hypoallergenic" milk products by various methods of protein hydrolysis. One study showed whey hydrolysate formula reduced the incidence of atopy in the first year of life in infants at risk; 21.8% of infants on whey hydrolysate presented atopic symptoms compared with 48.6%.

Formulas with partially hydrolyzed protein have not been as 'safe" as manufacturers had hoped and promised as Carnation found out after they marketed their "Good Start" infant formula and many allergic reactions including anaphylaxis were reported. In animal models, Jarret had demonstrated that small doses of cow's milk antigens are more sensitizing than large doses.

The IgE model of allergy is attractive to researchers, because of its simplicity and the ease of testing for sensitization; but, it selects only a special population of people with Type 1, IgE-mediated allergy. While this is an important reaction pattern, some physicians have claimed it is the only valid form of allergic reactions to food. Their opinion is not acceptable. A distinction between immediate, obvious allergic reactions and delayed, less obvious, chronic immune injury is useful.

Because of evidence that cow's milk intake can trigger diabetes in rodents, a study of diabetic children showed that antibodies 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). 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" They go on to describe "... a slow inefficient process, consistent with the fact that clinical disease develops in only about 5 to 6 % of hosts with the relevant genetic predisposition."

The diabetes model of food-antigen triggered disease is a potentially important immunological model of many unsolved diseases which appear to be "autoimmune". A long-term, inefficient pathogenesis which may produce target-organ damage, especially if the antigen is provided by a common food and intake continues over many years. Alternative explanations suggest that beta cells are attacked by cytotoxic T-cells after they are infected by a virus, or by T-cells originally targeted on other cells infected by virus whose cell-surface antigens happen to resemble beta cell antigens.

An Australian study of children who developed diabetes found that children given cows 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.