Power of Exile

The Power of Exile -
 Autism, A journey to recovery


Introduction: Sara’s Diet
and the IDEA


  1. Sara
  2. Sandra
  3. The Journey begins
  4. Sara joins our Family
  5. Journal Notes
  6. Impressions
  7. Influential People
  8. Center Stage
  9. I believe in Miracles
  10. Miracles in Abundance
  11. A Second Rainbow
  12. Widening Horizons
  1. World travel on a Wing and a Prayer
  2. Asperger Syndrome (Sam’s story)
  3. Autism: a Causal Theory and Treatment Option
  4. A Change in the Weather
  1. Second Timothy
  2. Turning Blue
  3. Food Intolerance in autism
  4. Sara’s Diet
    1. Introduction to the restricted diet
    2. Essential nutrients from foods
    3. Practical help with implementing a diet program
  5. What is Lutein?
  6. Autism, Pigments and the Immune System
  7. South Africa, World Community Autism Program
  8. Eating disorder in autism
  9. Autism, Origin – A Plausible Theory
  10. Autism, putting it all together

From: Food intolerance in autism
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.