We
have been retrospectively examining data obtained from parents of children who
have autism/developmental delay, to see if there is any basic differences in the
Biochemistry between countries. We have separated out the Hair Metals Test
Analysis (HMTA) data and Organic Acids Test (OAT) data, and present the findings
in graphical form below.
Previous data has shown that in Modern Day Autism, the major precipitating
factor is functional B2 deficiency due to deficiencies in Iodine, Selenium
and/or Molybdenum, all of which are required to activate vitamin B12. We present
this data below. As can be seen all of the children were deficient in one or
more of Iodine (<1.0 ppm : 15/18), Selenium (<1.0 ppm 14/19), or Molybdenum
(<0.08 ppm: 13/19), with dual deficiencies being common. Hence, the data would
suggest that these children would have functional vitamin B2 deficiency. The
observation of Iodine deficiency in the children is consistent with data on the
known Iodine deficiency in USA. It is becoming increasingly obvious that
deficiency of Selenium and/or Molybdenum is now more common, with resultant lack
of activation of vitamin B2. Hence deficiency of any of I/Se/Mo in the soil or
diet is causing functional B2 in mothers or children resulting in functional B12
deficiency with developmental delay being the consequence.
Previous data has shown that in Modern Day Autism, the major precipitating
factor is functional B2 deficiency due to deficiencies in Iodine, Selenium
and/or Molybdenum, all of which are required to activate vitamin B12. This in
turn can be seen in alterred metabolism in OAT. We
present this data below.
All children had
functional deficiency in Adenosyl vitamin B12, with elevated MMA being common
and elevated methylsuccinate universal.
Functional vitamin
B2 deficiency was seen in all the children, with various levels of elevated
oxalate, lactate, and succinate.
Consistent with data
from many other countries, children in USA, generally were iron deficient,
suggesting that the observed functional B12 deficiencies seen were a combination
of low dietary intake of iron by the mothers as well as functional B2 deficiency.
Elevated citrate occurs due to uncoupling of aconitase when ferritin is below 60
ug/L.
Vitamin B1
deficiency was common (9 of 10), as judged by elevated AKG, and elevated pyruvic
acid. This is commensurate with a gluten-free diet, which was common in the
children.
All children were
functionally deficient in Methyl B12 as judged by VMA, HVA, 5HIAA, QA, and KA,
with elevated pyroglutamic acid being common. Data suggests that
in deficiency of Iodine and/or Molybdenum QA:KA ratio increases, succinate
increases, as too pyroglutamate, due to lack of formation of FMN from
riboflavin.
All children showed
some degree of vitamin D deficiency as judged by elevated phosphoric acid.
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