Many
people are not aware of an extremely threatening incidence
of an appalling disease affecting our very young children.
Although the disease known as Autism was described many years
ago, the manifestations of it that are appearing in virtually
epidemic form are associated with environmental factors. The
exact mechanisms are still not clear but a number of important
medical articles have provided evidence that intoxication
with heavy metals, including mercury used in some inoculations
as a preservative, and possibly antibiotic abuse, all might
be behaving as triggers in genetically sensitive individuals.
Since it is reported that there are 8 new cases a day in California
alone, it is very unlikely that this is a purely genetically
determined disease.
The only treatments so far acceptable, most of which sometimes
give symptomatic relief, are various nutritional supplements
and a diet free from wheat gluten and casein, the peptide
found in milk. Drugs are of no value except to modify symptoms
and do nothing for the ultimate causes. Also, their effect
is unpredictable. To date, the only phenomena that can be
used for diagnosis are the diverse symptoms that apply to
the developmental and behavioral characteristics observed
in the children, including serious disturbances of the gastro-intestinal
tract. There is no known biologic test to guarantee the diagnosis.
In
the August issue of Neuroendocrinology Letters, Lonsdale and
associates report on the use of a supplemental nutrient know
as thiamine (vitamin B1) tetrahydrofurfuryl disulfide (TTFD)
in treating 10 autistic spectrum children between the ages
of 3 and 8 years. This synthetic disulfide derivative of the
vitamin is manufactured in Japan where the original naturally
occurring substance was discovered in garlic. Since it has
never been approved for use in the U.S.A. Dr. Lonsdale holds
an Independent Investigator License from the FDA. The patent
in Japan expired years ago and no drug company in the U.S.
has undertaken the rigorous testing required for its use here.
Dr.
Bernard Rimland, head of the Autistic Research Institute in
San Diego, and his associates have constructed special forms
that give numerical value to the severity of symptoms, These
forms are filled in by the parents as treatment proceeds and
evaluated by computer, providing evidence of the trend in
symptom severity. The study reported by Lonsdale and associates
showed that 8 or the 10 children improved with two months
of continuous treatment with TTFD. There was evidence of biologic
disturbances that may be an important part of the environmental
factors involved. For example, it is known that it is not
uncommon for many of these autistic children to suffer from
various vitamin deficiencies and three of the children in
this study were shown to be deficient in vitamin B1. Since
TTFD provides high concentrations of this vitamin as part
of its metabolic action, later tests showed this deficiency
to be much improved. Six of the ten children had unusually
high concentrations of arsenic in their urine that increased
after 30 days of treatment with TTFD and decreased after 60
days, thus providing evidence that this toxic metal was being
removed from the child thus affected. There were also sporadic
appearances of mercury, cadmium, lead and nickel in the urine
of some of the children, all of which have the effect of damaging
important aspects of sulfur metabolism in the body.
An
important discovery made by Dr. Walsh of the Pfeiffer Treatment
Center in Illinois is that more than 90% of over 300 tested
children with autistic spectrum disorder had evidence of a
missing sulfur containing protein called metallothionein.
This is known to provide protection from the toxic effects
of some of the metals, referred to above, that attack sulfur
metabolism. It is therefore, an obvious strategy that removing
these metals from the child's body is mandatory if they are
responsible for detrimental metabolic changes. This Pilot
Study suggests that TTFD may be a valuable agent in carrying
out this role and further study will be required in order
to confirm this effect.
Scheduled
for publication in the August issue,
Vol. 23 No. 4, 2002
Neuroendocrinology Letters www.nel.edu
