April 6, 2000

Mr. Chairman, Honorable Dan Burton and members of the committee;

My name is Mary Norfleet Megson. I am a board-certified pediatrician, Fellowship trained in Child Development, a member of the American Academy of Pediatrics and Assistant Professor of Pediatrics at Medical College of Virginia. I have practiced pediatrics for twenty-two years, the last fifteen years seeing only children with Developmental Disabilities, which include learning disabilities, attention deficit hyperactivity disorder, cerebral palsy, mental retardation and autism.

In 1978, I learned as a resident at Boston Floating Hospital that the incidence of autism was one in 10,000 children. Over the last ten years I have watched the incidence of autism skyrocket to 1/300-1/600 children.1 Over the last nine months, I have treated over 1,200 children in my office. Ninety percent of these children are autistic and from the Richmond area alone. The State Department of Education reports that there are only 1522 autistic students in the state of Virginia.

MHMR agencies have created local infant intervention programs, and have had a hard time keeping up with the numbers of delayed infants and toddlers. I have served as advisor to the City of Richmond and the surrounding counties as they have established entire programs for autistic children that fill multiple classes in several schools in each district. The segment of children with "regressive autism," the form where children develop normally for a period of time then lose skills and sink into autism most commonly at 18-24 months of age, is increasing at a phenomenal rate. I am seeing multiple children in the same family affected, including in the last week four cases of "autistic regression" developing in four-year-old children after their MMR and DPT vaccination. In the past, this was unheard of.

In the vast majority of these cases, one parent reports night blindness2 or other rarer disorders which are caused by a genetic defect in a G protein,3 where they join cell membrane receptors, which are activated by retinoids, neurotransmitters, hormones, secretin and other protein messengers. G proteins are cellular proteins that upgrade or downgrade signals in sensory organs that regulate touch, taste, smell, hearing and vision. They are found all over the body, in high concentration in the gut and the brain:4 and turn on or off multiple metabolic pathways including those for glucose, lipid, protein metabolism5 and cell growth and survival.6 Close to the age of "autistic regression," we add pertussis toxin, which completely disrupts G Alpha signals.7 The opposite G proteins are on without inhibition leading to:8


    1. Glycogen breakdown or gluconeogenesis. Many of these children have elevated blood sugars. There is sixty-eight percent incidence of diabetes in parents and grandparents of these children.
    2. Lipid breakdown which increases blood fats that lead to hyperlipidemia. One-third of families has either a parent or grandparent who died from myocardial infarction at less than 55 years of age and was diagnosed with hyperlipidemia.
    3. Cell growth differentiation and survival which leads to uncontrolled cell growth. There are 62 cases of malignancies associated with ras-oncogene in 60 families of these autistic children.9 The measles antibody cross reacts with intermediate filaments which are the glue that hold cells together in the gut wall.10 The loss of cell to cell connection interrupts aproptosis or the ability of neighboring cells to kill off abnormal cells. The MMR vaccine at 15 months precedes the DPT at 18 months, which turns on uncontrolled cell growth differentiation and survival.

Most families report cancer in the parents or grandparents, the most common being colon cancer.10The genetic defect, found in 30-50% of adult cancers, is a cancer gene (ras-oncogene). It is the same defect as that for congenital stationary night blindness.11

G protein defects cause severe loss of rod function in most autistic children.12 They lose night vision, and light to dark shading on objects in the daylight. They sink into a "magic eye puzzle," seeing only color and shape in all of their visual field, except for a "box" in the middle, the only place they get the impression of the three dimensional nature of objects. Only when they look at television or a computer do they predictably hear the right language for what they see. They try to make sense of the world around them by lining up toys, sorting by color. They have to "see" objects by adding boxes together, thus "thinking in pictures." Their avoidance of eye contact is an attempt to get light to land off center in the retina where they have some rod function. Suddenly mothers touch feels like sandpaper on their skin. Common sounds become like nails scraped on a blackboard. We think they cannot abstract, but we are sinking these children into an abstract painting at 18 months of age and they are left trying to figure out if the language they are hearing is connected to what they are looking at, at the same time.

The defect for congenital stationary night blindness on the short arm of the X chromosome affects cell membrane calcium channels13 which, if not functioning, block NMDA/glutamate receptors in the hippocampus,14 where pathways connect the left and right brain with the frontal lobe. Margaret Bauman has described a lack of cell growth and differentiation in the hippocampus seen on autopsy in autistic children.15 The frontal lobe is the seat of attention, inhibition of impulse, social judgement and all executive function.

When stimulated, these NMDA receptors, through G proteins stimulate nuclear Vitamin A receptors discovered by Ron Evans, et al Dec 1998.16 When blocked, in the animal model, mice are unable to learn and remember changes in their environment. They act as if they have significant visual perceptual problems and have spatial learning deficits.17

Of concern the Hepatitis B virus protein sequence was originally isolated in the gene for a similar retinoid receptor (RAR beta),18 which is the critical receptor important for brain plasticity and retinoid signaling in the hippocampus.19 After the mercury is removed, I understand we will restart Hepatitis B vaccine at day one of life. Studies need to be done to determine if this plays an additive roll in the marked increase in autism.

I am using natural lipid soluble concentrated cis form of Vitamin A in cod liver oil to bypass blocked G protein pathways and turn on these central retinoid receptors. In a few days, most of these children regain eye contact and some say their "box" of clear vision grows. After two months on Vitamin A treatment some of these children, when given a single dose of bethanechol to stimulate pathways in the parasympathetic system in the gut, focus, laugh, concentrate, show a sense of humor, and talk after 30 minutes as if reconnected.20

This improves cognition, but they are still physically ill. When these children get the MMR vaccine, their Vitamin A stores are depleted; they can not compensate for blocked pathways. Lack of Vitamin A which has been called "the anti-infective agent," leaves them immuno-suppressed. They lack cell-mediated immunity. T cell activation, important for long term immune memory, requires 14-hydroxy retro-retinol. On cod liver oil, the only natural source of this natural substance, the children get well. The parasympathetic nervous system is blocked by the second G protein defect. These children are unable to relax, focus and digest their food. Instead, they are in sympathetic overdrive with a constant outpouring of adrenaline and stress hormones. They are anxious, pace, have dilated pupils, high blood pressure and heart rate. These and other symptoms of attention deficit hyperactivity disorder are part of this constant "fright or flight" response. These symptoms improve on bethanechol.