Finding common ground at the IACC

1 May

The Interagency Autism Coordinating Committee (IACC) met Friday. New members were introduced, including Ari Ne’eman of the Autistic Self Advocacy Network.

The autism communities are far from unanimous in goals and methods. Given the makeup of the IACC, consisting as it does of governmental agencies plus public members of organizations that have been highly critical of each other, one might wonder if it anything could get accomplished.

But, in the end, most groups have more than a single goal. And, if you remember back to your set theory lessons, that leads to intersections–overlap–common ground.

I was reminded of this watching the IACC meeting. I could only watch bits and pieces during the day. One standout part of the morning came when Jim Moody of the National Autism Association gave a public comment talking about issues of safety, elopement, drownings–preventable deaths of autistics young and old.

Towards the end of the meeting I listened to a number of people refer back to this presentation. Amongst these commenters was Ari Ne’eman. Mr. Ne’eman obviously took the idea seriously and was calling for serious consideration of how this could be implemented into the Strategic Plan, calling for input from the services subcommittee.

I know the idea of safety are not new to Mr. Ne’eman. I contacted him recently when I was preparing a piece, Search and Rescue and autistics.

The members of the IACC span a wide diversity of ideas and viewpoints. Diversity, that’s a good thing.

But, working together for the common good: that’s common ground. Ideas that span diverse organizations and viewpoints. That is a very good thing.

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3 Responses to “Finding common ground at the IACC”

  1. Kerry Scott Lane MD June 8, 2010 at 01:27 #

    PUBLIC SUBMISSION As of: July 28, 2009
    Tracking No. 809c7480
    Comments Due: June 08, 2009
    Late comments are accepted

    Docket: FDA-2009-N-0138
    Joint Meeting of the Drug Safety and Risk Management Advisory Committee, Nonprescription Drugs Advisory Committee, and the Anesthetic and Life Support Drugs Advisory Committee; Notice of Meeting.

    Comment On: FDA-2009-N-0138-0001
    Joint Meeting of the Drug Safety and Risk Management Advisory Committee, Nonprescription Drugs Advisory Committee, and the Anesthetic and Life Support Drugs Advisory Committee; Notice of Meeting – Notice of Meeting

    Document: FDA-2009-N-0138-0005
    Kerry Scott Lane MD – Comment

    ——————————————————————————–

    Submitter Information
    Organization: St. Mary’s Medical Center, W. Palm Beach, FL

    ——————————————————————————–

    General Comment
    Acetaminophen, Glutathione Depletion, and Regressive Autism

    Acetaminophen toxicity in the liver is well established. One of the known toxic
    effects of this commonly used drug is depletion of the most important antioxidant,
    glutathione. Disease states linked to depletion of glutathione and excessive
    amounts of oxidized glutathione, versus reduced glutathione, include Diabetes,
    Atherosclerosis, AIDS, Alzheimer’s, Pregnancy Induced Hypertension (PIH), and
    others.
    Regressive Autism is a condition that has defied a definitive pathobiology to
    date. The attachments enclosed reveal that acetaminophen, by exacerbating an
    already depleted glutathione antioxidant system due to a preexisting condition,
    triggers autism in the peri-vaccination period by reducing glutathione levels to
    below a critical level. Adequate glutathione levels are crucial to the effective
    functioning of the Metallothionein (MT) System. The MT system is involved in
    metabolism of metals, as is glutathione. However, the MT system is especially
    critical to the metabolism of Zinc in the brain. In states of depleted glutathione and
    excess oxidized glutathione, free Zinc is released in brain cells. This free zinc is
    toxic to the mitochondria, causing cellular hypoxia and a generalized neurological
    malfunctioning that we now recognize as Autism.
    It appears acetaminophen alone is not enough to cause Autism. The co-morbid
    pathobiology is due to the creation of a state of abnormal gastrointestinal biology
    due to antibiotic administration to the infant. This allows the replacement of the
    normal GI flora with yeast overgrowth by Candida species and others. Many
    yeasts and fungi produce mycotoxins which have been shown to be pathological
    to man and animal alike.
    Recently interest has focused on a mycotoxin known as Gliotoxin which has
    been shown to be immunosuppressive, by killing CD4 cells, along with a multitude
    of other deleterious effects. Gliotoxin has been shown to form adducts with
    glutathione, essentially removing it from the pool of bioavailable antioxidants. Over
    fifty per cent of Candida species have been shown to produce Gliotoxin.
    If we envision a sequence of events that results in an undesirable yeast in the GI
    tract, causing a depletion of glutathione and generalized oxidative stress, followed
    by a vaccination that includes a metal adjuvant (mercury or aluminum), followed
    by the administration of acetaminophen (antipyretic) to an infant- at a critical
    period of neurodevelopment- we can envision the pathobiology of Autism.
    The enclosed attachments from peer-reviewed articles are a roadmap to the
    above described pathobiology. I suggest the FDA act with all due haste to make
    this material public so the autism epidemic can be properly managed. Additional
    focus should be directed to the AIDS syndrome, which also involves depletion of
    glutathione. It would seem acetaminophen is inappropriate in this setting, and
    possibly in most settings.

    Kerry Scott Lane MD
    St. Mary’s Medical Center
    June 6, 2009

  2. Chris June 8, 2010 at 03:36 #

    It looks like your Spam is a year out of date.

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