The gastrointestinal tract in normal circumstances learns to tolerate foods that are presented regularly. Oral tolerance to food is learned by infants as solid foods are introduced. In the best case, tolerance to regularly eaten food endures throughout the life of the individual. Most immune cells live and die in a resting state. Activation of cells can be specific by antigens that alert only cells armed with specific antibody or, activation can be non-specific with whole populations of cells turned-on by a super-antigen or overabundance of cell-stimulating mediators, such as interleukins and cytokines.
Patients often report the onset of new hypersensitivity symptoms after an acute illness, an anaphylactic reaction to drugs of injected antigen, and following childbirth or injury; this always suggests non-specific activation of immune networks. An infectious gastroenteritis may leave the gastrointestinal tract in a hypersensitivity state and the patient reports decreased tolerance to many foods. This post-infectious hypersensitivity may lead to chronic "irritable bowel" symptoms.
Tolerance may be mediated by the expansion of clones of supressor T- cells that act against activator mechanisms. It is likely that different cell populations in the gut respond differently to the same signal. Sometimes they are activated by antigen stimulus. At other times, they are turned off. Several signals can act on cells simultaneously, selecting a variety of non-linear responses. Antibody production has the most curious form and does not stop with the simple logic of making one antibody to attack one antigen. Once the primary antibody exists, it stimulates the production of a second line antibody that attacks the primary antibody and has some of the characteristics of the original antigen. Tertiary and possibly fourth and fifth generation antibodies create a complex, reverberating network. Stable immune networks exist in a state of balance between activation and inhibition.
The idea of oral tolerance has been exploited by some researchers in an attempt to suppress system immune responses to self-antigens. For example, administration of porcine insulin to diabetes-prone mice lowered the frequency and delayed the time of onset of insulin dependent diabetes. Oral administration of bovine myelin reduced symptoms in patients with MS. These are brief experiments that do not mean that tolerance will be long-lived, nor that hypersensitivity will not erupt at some point in the future. Oral-tolerance balances tenuously with immune activation.
Loss of oral tolerance in an immunological sense would mean that food antigens activate defensive responses and cause symptoms and disease. Tolerance is an unstable, constantly varying variable of the gastrointestinal tract. Selective tolerance is a phenomenon of chronic illness; acute responses to food antigens such as pain, and vomiting are turned off so that the patient has no warning of delayed onset symptoms which come-on gradually, often many hours after eating the offending food. Because of the delay, the patient does not recognize the food factors in their disease.
Selective tolerance is deceptive; the apparent hypersensitivity following abstinence seems to be a more "normal" state - certainly a more informative state. Patients report enhanced awareness of more immediate and/or more dramatic symptoms after they have gone through a clearing period on a low allergy diet or elemental nutrient formula. Some patients present with progressively increasing symptoms from many foods appear to be losing tolerance generally. If the loss of tolerance is bona fide, symptoms remit when the patient is fed an elemental nutrient formula and recur with re-feeding.