The term food intolerance describes an abnormal
physiological response to an ingested food component, constituent or additive.
Such a reaction can include immunologic, idiosyncratic, metabolic, pharmacologic
or toxic response.
A food allergy adverse reaction to foods
involving an immune mechanism is a pathogenetic process that can include one
or more types of response: Type I IgE mediated immediate hypersensitivity;
Type II complement mediated cell injury; type III antigen-antibody complexes;
Type IV T-cell dependent delayed hypersensitivity. Variables include genetic
predisposition, age, gestation and weight at birth, prevalent mode of infant
feeding and age of introduction to solids, presence of primary immunodeficiency
(or excess), adjuvant effect of gut microflora, and cultural factors. Immunoglobulins
(Ig) can switch class instantly. This switch in class from IgG to IgE or IgA
can occur instantly in response to NK cytokine activity. All people (with
very rare exception) manufacture Ig antibodies to food peptides. Elevated
levels (above the normal range) are found in some people with autism to a
wide variety of vaccines, viruses and foods.
The risk of developing allergic disease
is considered to be largely inherited. In about 70% of patients documented
with allergic symptoms, a history of one or more first and second degree relatives
can be elicited. Food macromolecules absorbed intact incite both systemic
and mucosal immune response. Antibodies against food antigens are present
in serum of a large percentage of the ‘normal’ population and are not diagnostic
of food allergy. The mucosal immune response consists primarily of secretory
IgA against a particular antigen and retards the further absorption of the
antigen. It is suspected that T-cells produce a tolerance response to these
antigens and suppress the cell-mediated immune response in the gut.
Type I hypersensitivity is mediated
by IgE. Exposure of a sensitized individual to the appropriate antigen may
induce a metabolic response and the histopathologic picture may be normal.
Type II hypersensitivity is the result
of complement fixing antibodies combining with antigens. i.e. Leukopenia and
thrombocytopenia.
Type III hypersensitivity consists of
interaction between food antigen, antibody and complement components which
results in the formation of immune complexes. In healthy subjects these complexes
consist mainly of IgA; in food-allergic persons, IgG and IgE may also be found.
The IgA complexes can be rapidly cleared; other complexes may be deposited
in the bowel walls and other parts of the body where they can activate complement
responses. Immune complex in the gut leads to the accumulation of polymorphonuclear
leukocytes, generation of anaphylatoxin and enhancement of bowel wall permeability.
Activation of complement by IgG against food antigen, shown in patients with
egg white and fish allergy, results in acute or chronic diarrhea, asthma and
uticaria.
Type IV hypersensitivity is mediated
by T-lymphocytes and release of the lymphokines.
Type ‘V’ hypersensitivity
As you can see none of these adequately describe
what is happening in the autistic metabolism. The immune response in autism
is immunologic, idiosyncratic, metabolic and response to pharmacological agent
or toxin with signs and symptoms of food allergy both intensified and hidden.
I therefore postulate that an additional classification is overdue and could
be called Type V hypersensitivity, initiated and mediated by complement
activity and complement receptor activity. This type of immune response is
very variable and relative to the immune phenomena associated with mitochondrial
gene region activity. In the autist this results in specific phenomena that
may include binding of the Complement Receptor (CR) fragments (CRf) to macrophage
cells which in effect ‘hitch a ride’ as they locate food fragments often
containing sulphur. The CRf use ‘thiol’ (sulphur) to ‘mark’ the food
fragment, like placing a quil (sulphur) onto the surface of the food fragment
in a process called opsonization. The CR’s can also mark the toxin
(food fragment) without being bound to the macrophage and this can result
in ‘innocent bystander immune phenomena’ reactions, particularly in persons
with autism who are ingesting or who are exposed to large amounts of environmental
or food pathogens. I postulate that these immune activities result in the
biochemical changes seen in autism which include inhibition of sulphating
enzyme activity as a protective device regulated by immune activity at the
basic level of immune-gene (IoGc) interaction, occurring in the mitochondrial
DNA region already identified as altered in the autistic population without
knowledge of why this occurs.
The Alternative Pathway Activation
Pathway (APAP) has been studied in relation to Cobra venom factor (CoVF).
Consequences of APAP activity include the formation of C5 convertase which
results in rapid changes and increases the difficulty in finding consistent
patterns of immune activity in the autistic population, but which have been
found already with some degree of success, and the information consistently
identifies this type of immune system activity. Factors which result in Convertase
(C35 to C5a) activity within the Major attack complex, terminal complement
pathway (MAC-TCP) are regulated by individual IoGc factors and can include
cell lysis, influence virus receptor activity, opsonization, chemotaxis (seen
in the increased immune activity to damaged gut lining in the autistic population)
as well as neutrophil and monocyte activities which increase adherence of
cells, resulting in degranulation and release of intracellular enzymes, toxic
oxygen radicals and initiate other cellular events. These may include the
formation of cathepsins (immune system enzymes) which act and react as ‘normal
enzymes’. This pathway (APAP) in the autist allows for the immune system to
control digestion and digestive activity beginning at the point of ingestion.
This activity may begin with activated enzymes (cathepsins) and thoracic duct
response and/or mediated release of these enzymes and immune activation whereby
some foods are degraded immediately without ever reaching the digestive tract,
and the immediate breakdown of some substances (toxins), particularly those
which can be degraded to gases. Preventing the free radical gases from being
degraded in the liver is also a ‘protective’ factor of the immune system.
This can impact the individual’s ability to make fatty acids and a reduced
ability to make long chain fatty acids has been observed in this population.
It can result in free-radical activity in the brain and this too has been
found to occur in autism.
At the basic level of understanding
this is a ‘fight or flight’ immune response. The response is to food rather
than to external stimuli, or it is in addition to external stimuli. In order
to treat the autist we must remove the food pathogen as well as environmental
substances which for some have become immune triggering substances by association
(fumes from nail polish, petrol, pine oil and in the classroom oil based paints,
cleaning products and dry erase markers). If we do not intend to support
a ‘life long disability’ then we must address the cause of autism and take
action to produce changes in the diets and environment which allow the autistic
individuals to meet their potential. I suggest to you that many of these
people are gifted and we are depriving ourselves of the strange and extraordinary
people who like Warhol, Einstein and Mozart contribute to society as a direct
result of their desire to understand music, art, science and math in minute
detail.
