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
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.