11 Hayes Avenue
Lexington, MA 02421-3521
November 24, 2002
President George W. Bush
The White House
Washington, DC 20500
Fax: 202-456-2461
Dear President Bush:
I am writing in support of Congressman Dan
Burton's request for a White House Conference on childhood autism and
how best to investigate its epidemic increase. As a parent seeking
answers for more than 35 years I would very much like to be a
participant.
Much research on autism overlooks the obvious:
Autism is the result of impairment within the brain. Well-known causes
of brain impairment must therefore be ruled out before theories of
genetic causation receive any more federal research funding.
Early detection of autism has proven to be
difficult. The majority of children with autism are physically perfect
and do not bear stigmata of genetic malformations. Exceptions are cases
of autistic disorder associated with medical conditions like fragile-X
syndrome or tuberous sclerosis.
A vulnerable brain system must be sought to
explain the finding of autism in children with diverse metabolic
disorders like phenylketonuria (PKU) and adenylosuccinate lyase defect.
Brain abnormalities are not evident in most
children with autism. However, visible defects seen in some cases of
autism involve the cerebellum, subcortical centers and brainstem nuclei.
The cerebellar, subcortical, and brainstem damage found in cases of
autism can be viewed as variants of Wernicke's encephalopathy.
Wernicke's encephalopathy is a well-known pattern
of damage affecting a rank-order of brainstem and subcortical centers.
Wernicke's encephalopathy is best known as the neuropathology that
results from alcohol intoxication; and prenatal exposure to alcohol has
been reported as one of many medical conditions associated with autism.
Prenatal exposure to valproic acid (an
anti-epileptic medication) is another condition associated with autism.
A Wernicke-like pattern of damage has been reported in laboratory rats
subjected to valproic acid exposure during gestation.
The highest rates of blood flow and aerobic
metabolism have been found in the brainstem centers affected by alcohol.
Circulatory arrest and asphyxia at birth also damage these brainstem
centers of high aerobic metabolism.
Hypoxic birth results in two patterns of brain
damage: (1) Damage of motor systems involved in cerebral palsy results
from prolonged partial oxygen insufficiency during gestation or labor.
(2) The brainstem centers of high aerobic metabolism are damaged by a
few minutes of total oxygen deprivation.
Protective mechanisms go into action to preserve function in the
brainstem nuclei of high aerobic metabolism under conditions of partial
oxygen insufficiency. Thus involvement of motor systems and cerebral
palsy are most commonly associated with difficult birth. Total asphyxia
is more likely to result in death of the infant.
However, immediate clamping of the umbilical cord
has been adopted as a standard obstetric practice during the last 20
years. This is the same period in which the dramatic rise in autism has
occurred. Immediate clamping of the umbilical cord merits investigation
as cause of the increased incidence of autism over the past 20 years.
Clamping of the umbilical cord before the lungs
function and the infant breathes on its own will cause at least a few
minutes of total asphyxia, and this will impair the brainstem nuclei of
high aerobic metabolism.
Visible lesions within the brainstem observed in some children with
autism serve as a warning: Asphyxia at birth following immediate
clamping of the umbilical cord needs to be investigated as cause of the
increased incidence of autism.
The umbilical cord should be left intact until the
newborn breathes on its own. This ought to be intuitive. The dangers of
clamping the umbilical cord too early should be widely publicized. The
practice of umbilical cord clamping at birth must be stopped!
The issue of mercury intoxication should be
pursued along with neonatal bilirubin intoxication. Research on neonatal
jaundice indicates bilirubin only enters neurons already compromised by
asphyxia and hypoxia at birth; the same is likely true when levels of
mercury in the blood are high.
I received a doctorate in biochemistry from the
Boston University School of Medicine in 1975. My dissertation was on the
long-term effects of neonatal asphyxia in albino rats. One of my main
findings was a greater vulnerability of male animals: Male rats suffered
immediate and noticeable growth retardation as result of asphyxia, and
after maturation I found permanent changes in serotonin metabolism in
the brain.
The brainstem nuclei of highest metabolic rate are
in the auditory pathway. I believe auditory system impairment is the
cause of language disorder, hypersensitivity to noise, and defects of
attention and general awareness in children with autism. I have
presented more of my views of autism on the website I setup in memory of
my son who was autistic,
http://conradsimon.org (See also
http://cordclamping.com )
Autism is a horrible tragic affliction. Neither
children and their families nor taxpayers who foot the bill for
life-long care can wait any longer for researchers who view autism
mainly as an interesting scientific problem.
Sincerely,
Eileen Nicole Simon, PhD, RN
Eileen_Simon@alum.barnard.edu
cc: Vice President Richard Cheney
Congressman Dan Burton
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