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A parent of an autistic child wrote:
‘Normal pregnancy. Excretion of dark greenish fluid by mother
prior to delivery.’
Reply:
‘Amniotic fluid is normally clear, a pigmented amniotic fluid was used
as an indication of possible/probable problems prior to the use of the
amniocentesis. Once amniocentesis became the primary medical test to determine
potential problems, measuring the pigments in the amniotic fluid virtually
has become extinct. However, with the newer amber colored tubes for drawing
fluid this test is again becoming a much needed medical tool. In the meantime
years of statistics have been lost at a time when autism spectrum
disorders began to increase. The pigmentation in the amniotic fluid is
actually the expired respiratory pigments from the developing baby. It
has been my experience that the primary pigment producing a hapten type
immune responce is lutein - widely dispersed among foods. At the time when
the babies immune system is beginning to develop the first mechanism
is for the cytokine to identify a substance which is nonself. Lutein has
no obvious function at this point in development although later in 'normal'
metabolism lutein regulates 'pineal' function, protects the eyes from UV
light and has additional biochemical contributions to the endocrine system.
When the genetic information from both parents is similar, such as same
race, same hair color, etc. it is more likely that the diagnosis is autism
with less chance of a co-occuring disorder unless the co-occuring disorder
is one that is more prominent for that race based on my data.’
It has been indicated that neurofilament antibody is a consistent marker for autism. From Dorland’s 28th edition: ‘Neuroglia: The supporting structure of the nervous tissue consists of a fine web of tissue made up of modified ectodermal elements, in which are enclosed peculiar branched cells known as neuroglial cells or glial cells. The neuroglial cells are of three types: astrocytes and oligodendrocytes (astroglia and oligodendroglia), which appear to play a role in myelin formation, transport of material to neurons, and microcytes (microglia), which phagocytize waste products of nerve tissue. Called also glia.’ (1)So, if the types of neuroglial cells associated with myelin formation are not effected, as can be indicated by CSF testing, then we are left with the neuroglial cells which are associated with phagocytosis. One type of phagocyte cell is the macrophage. In the brain this is called myelinophage, in the liver kupffer cells. The primary function of these cells are to break down and remove substances the immune system marks as ‘non-self’. In studies dating back to 1952 (2) carotenes, bilirubin, methemoglobin and the levels of these and other pigment wastes in amniotic fluid have been used as a marker to determine the fetal environment. High or toxic levels of pigment wastes in the amniotic fluid are still used as a rationale for inducing labor. The color of the amniotic fluid at birth gives clinical evidence for determining the potential for newborn distress factors. Elevated bilirubin is a consistent marker in infants later diagnosed with neurological impairment.(3) Bilirubin is said to remain in the brain once it has reached this destination. However, I believe that with the autist, the immune trigger is pigment and that the phagocytosis is the immune system’s attempt to remove the hapten from the brain through the Cerebral Spinal Fluid, thus the lack of evidence for brain deposits of bilirubin in the autopsied brains of autists who have as a marker high bilirubin levels at, or shortly after, birth. This area of investigation has been tragically overlooked as scientists search for the genetic cause. Research into the phagocytosis of the pigment metabolites (pterins, carotenoids) and the improvement for many using dietary intervention removing the pigments from their diet leading to improvement and ‘symptom free’ results has certainly not been given funding although the latter has produced some of the most dramatic case histories available. (4)
Sandra & Max Desorgher c. 1999
references
1. Dorland’s 28th edition
2. Amniocentesis in Rh Incompatibilities; Bevis; 1952.
(from: Gradwohl’s 7th edition, Clinical laboratory methods and diagnosis,
Vol. 1 1970, The C.V.Mosby Company)
3. Hyperbilirubinemia in preterm infants and neurodevelopmental
outcome at 2 years of age: results of a national collaborative survey;
van de Bor, M., et al.; Pediatrics 83(6):915-20, 1989 Jun.
4. Pigment-restricted diets alleviate the symptoms of
autism – some case histories; Johnson, S.A., Desorgher, M.E.; 1999.
