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    « Autism Yesterday at Motherbaby Int'l Film Festival | Main | Holly Robinson Peete Defends her Autism Vaccines Position »

    October 14, 2008

    1986: AP Article "The Immune Systems of Many Autistics may be Attacking Brain Tissue."

    1986It was 22 Years Ago Today…

    By J.B. Handley

    In doing research for the background to the story I wrote about Henry Waxman and the National Childhood Vaccine Injury Act from the 1980s, I actually had to do some research offline, because its hard to find newspaper articles from the time before Internet.

    Not surprisingly, there wasn't a lot of press in general on autism in the mid-1980s, but I did find some. This Associated Press article, written 22 years ago, certainly caught my attention, I have reprinted it in full:

    Possible link between autism, immune abnormalities found

    October 7, 1986
    SALT LAKE CITY (AP) - For new parents, autism is a word tinged with dread. It can mean a child who doesn't cuddle, may be mute and, in many cases, is retarded.

    Only four or five children out of each 10,000 born in the United States are autistic, but treating them causes significant problems for doctors. Dr. Reed Warren, a Utah State University immunologist, said he hopes that a three-year study he has conducted will lead to effective treatment for autism.

    What the scientist has found, assisted by colleagues and students at USU's Developmental Center for Handicapped Persons in Logan, is that about half of 35 autistic patients tested since 1983 have malfunctioning immune systems. Warren also has found that the mothers of the autistic children he's studied have the same kind of immune abnormalities, leading him to believe "there's a genetic component to this thing, too."

    Warren's interest in autism research has roots in the death four years ago of his 5-year-old son, Spencer, who suffered from the disorder. "I was doing research in cancer at the time and we happened to look at his immune system and found the disorders," he said.

    The immune system is the body's complex network of organs and cells that fights off invading germs. A $30,000 grant from the Sylvester Stallone Fund — established by the film actor, who himself has an autistic son — has helped Warren pursue his research.

    The fund, founded in 19&3, has awarded 26 grants totaling $580,000. Autism is "an umbrella term for many medical and neurological defects." said Dr. Bernard Rimland, founder of the National Society for Children and Adults with Autism and director of the Institute for Child Behavior Research in San Diego. He praised Warren as a "systematic, thorough" scientist and said his research may someday lead to effective treatment.

    Rimland, executive secretary for the Stallone Fund's research funding committee, said it wasn't until about 1978 that psychiatrists and other doctors began to move away from the belief that autism was an emotional disorder. In addition to Warren's work, Rimland said, there has been some experimentation in treatment with high doses of vitamin B-6 and magnesium, which has resulted in some improvement in autistic children's behavior.

    Warren said blood samples from patients have confirmed his contention that the immune systems of many autistics may be attacking brain tissue. "You've heard that when you're tired or feeling bad that you're "coming down with the flu,"' he explained- "Well, it's possible these kids are going through that kind of feeling all the time.

    "It's similar in that regard to multiple sclerosis," Warren said. "The immune system interacts wit the brain tissues. We see the same kinds of immune abnormalities." Those abnormalities include low numbers of "Helper T" white blood cells, which play a critical regulatory role in activating the body's defenses. "The key thing is that we do see the immune abnormalities in about half the kids. It's one of the first biological markers for autism. Now we want to carry it on." Warren said. Although Warren stresses that the results are not conclusive, tests conducted on 10 mothers of autistic children have shown they lack the normal number of special "blocking factors" that prevent the maternal antibodies from attacking the fetus.

    Warren theorizes that in some cases a mother's bodily defenses, perhaps activated to battle an invading virus, may release proteins which damage portions of the baby's brain. Also, he said, the fetus may acquire the same virus and further brain damage could result as his own immune system fights the infection after birth.

    Many mothers of autistic children report having contracted the rubella virus during pregnancy, or that their child had a viral infection soon after birth, Warren said.

    The apparent linkage of immune deficiencies in mothers and their autistic children will be the primary focus of Warren's future research. Besides seeking additional funds from the Stallone Fund, Warren has applied for a three year, $250,000 grant from the National Institutes of Health.

    J.B. Handley is co-founder of Generation Rescue and a contributor to Age of Autism.

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    Comments

    I have 3 boys with autism. Being a disabled veteran, I find autism frustrating. If there is a cause, please find the cure. If it is the chemicals, please stop using them! If it is mercury mixed with the chemicals we spray on our foods(apples, cherries, potatoes, etc), Please, I beg of you stop. Studies backfire sometimes, and now the payment is steep. If this is accurate, just stop....

    Is there any followup to this study?

    Andres:

    They are PDF files, so you have to ensure
    you've got Adobe Reader installed. Or could be a browser security setting. You can also right click on those pdf links to save to your harddrive use the "save target as" menu option upon right clicking on link.

    if none of that works, send me an email and I can forward them to you.

    trophyfish at hotmail.com

    The Terbutaline/Autism connection is important to the Thimerosal theory is because it shows that infant exposure to a drug causing neuroinflammation can lead to autism. This neuroinflammation is the same mechanism, it's thought, by which Thimerosal can cause autism.

    Does anyone know why the .pdf links to the transcripts do not open?
    ftp://autism.uscfc.uscourts.gov/autism/thimerosal.html
    Very interested in Terbulatine references
    Thank you.

    FYI: Thimerosal transcripts have finally been posted. Of special interest are all the references to Terbutaline causing autism.

    Terbutaline references (note: page numbers refer to Adobe page number not document page number)

    ftp://autism.uscfc.uscourts.gov/autism/thimerosal.html

    Day 1 - pages 42, 43, 44, 139, 140, 231, 232, 234
    Day 10 – pages 21, 22, 23, 24, 25
    Day 12 – pages 165, 166
    Day 13 – pages 192, 282
    Day 2 – page 131
    Day 3 – pages 52, 144
    Day 4 – page 116
    Day 5 – page 214
    Day 6 – page 177, 178, 179, 180, 181, 185, 189
    Day 8 – page 229

    This is a recent manuscript on the HepB vaccine
    Neurology. 2008 Oct 8.
    Hepatitis B vaccine and the risk of CNS inflammatory demyelination in childhood.Mikaeloff Y, Caridade G, Suissa S, Tardieu M.
    BACKGROUND: The risk of CNS inflammatory demyelination associated with hepatitis B (HB) vaccine is debated, with studies reporting conflicting findings. METHODS: We conducted a population-based case-control study where the cases were children with a first episode of acute CNS inflammatory demyelination in France (1994-2003). Each case was matched on age, sex, and geographic location to up to 12 controls, randomly selected from the general population. Information on vaccinations was confirmed by a copy of the vaccination certificate. The odds ratios (ORs) of CNS inflammatory demyelination associated with HB vaccination were estimated using conditional logistic regression. RESULTS: The rates of HB vaccination in the 3 years before the index date were 24.4% for the 349 cases and 27.3% for their 2,941 matched controls. HB vaccination within this period was not associated with an increase in the rate of CNS inflammatory demyelination (adjusted OR, 0.74; 0.54-1.02), neither >3 years nor as a function of the number of injections or brand type. When the analysis was restricted to subjects compliant with vaccination, HB vaccine exposure >3 years before index date was associated with an increased trend (1.50; 0.93-2.43), essentially from the Engerix B vaccine (1.74; 1.03-2.95). The OR was particularly elevated for this brand in patients with confirmed multiple sclerosis (2.77; 1.23-6.24). CONCLUSIONS: Hepatitis B vaccination does not generally increase the risk of CNS inflammatory demyelination in childhood. However, the Engerix B vaccine appears to increase this risk, particularly for confirmed multiple sclerosis, in the longer term. Our results require confirmation in future studies.

    More studies to the left
    http://www.ncbi.nlm.nih.gov/pubmed/17276994?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=3&log$=relatedarticles&logdbfrom=pubmed
    and

    Clin Dev Immunol. 2005 Sep;12(3):217-24.
    A study of molecular mimicry and immunological cross-reactivity between hepatitis B surface antigen and myelin mimics.Bogdanos DP, Smith H, Ma Y, Baum H, Mieli-Vergani G, Vergani D.
    Institute of Liver Studies, London School Medicine at King's College Hospital, UK.

    On the basis of the reported association between hepatitis B vaccination (HBvacc) and autoimmune demyelinating complications such as multiple sclerosis (MS), we have looked for aminoacid similarities between the small hepatitis B virus surface antigen (SHBsAg), and the MS-autoantigens myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG) that could serve as targets of immunological cross-reactivity. Twenty-mer peptides spanning 4 SHBsAg/MOG and 1 SHBsAg/MBP mimicking pairs, were constructed and tested by ELISA as targets of cross-reactive responses. A total of 147 samples from 58 adults were collected before HBvacc (58/58), and post-HBvacc (48/58 before the second and 41/58 before the third boost). Eighty-seven sera from anti-SHBsAg antibody negative patients with various diseases were tested as pathological controls. Reactivity to at least one of the SHBsAg peptides was found in 8 (14%) pre-HBvacc subjects; amongst the remaining 50, reactivity to at least one of the SHBsAg peptides appeared in 47 (94%) post-HBvacc. Reactivity to at least one of the MOG mimics was present in 4 (8%) pre-HBvacc and in 30 (60%) post-HBvacc (p < 0.001). Overall 30/50 (60%) vaccinees had SHBsAg/MOG double reactivity on at least one occasion compared to none before-vaccination and in 2 (2%) of the pathological controls (p < 0.001 for both). SHBsAg/MOG double reactivity was cross-reactive as confirmed by inhibition studies. At 6 months post-vaccination, 3 of the 4 anti-MOG reactive cases before vaccination and 7 of the 24 (29%) of the anti-MOG reactive cases at 3 months post-vaccination had lost their reactivity to MOG5-24. There was no reactivity to the SHBsAg/MBP mimics. None of the vaccinees reported symptoms of demyelinating disorders. In view of the observed SHBsAg/MOG cross-reactivity, the vaccine's possible role as an immunomodulator of viral/self cross-reactivity must be further investigated.

    Why these kind of studies are not done on vaccinated children with HepB vaccine- at birth?


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