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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