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NY Times' Sins Of Omission In Autism Article: Commentary by Binstock

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FEAT DAILY ONLINE NEWSLETTER http://www.feat.org

Letters Editor: FEAT@... Archive: http://www.feat.org/listarchive/

M.I.N.D.*: http://mindinstitute.ucdmc.ucdavis.edu

" Healing Autism: No Finer a Cause on the Planet "

____________________________________________________________

NY Times' Sins Of Omission In Autism Article: Commentary by Binstock

Thursday, December 30, 1999

[This open letter is addressed to Blakeslee writer for Science

Times of the The New York Times. It is in response to " New Theories Help

Explain Mysteries of Autism " , published in that paper and this newsletter

last Thursday, December 28. It is an authored opinion of autism researcher

Binstock.]

Science Times articles often achieve a level of excellence beyond that

of articles in scientific journals. Your recent article about autism was an

exception. Instead of presenting diverse sides of an important issue, you

focused upon a single model summarized as " it must be genetic and must occur

in utero " . Increasing data indicate that this model of causation and timing

is relevant only to a subgroup of children within the autism-spectrum.

In support of the genetic-autism theory, you presented opinions of

Marie Bristol-Power and Leventhall; regarding in-utero timing, you

presented speculations from Rodier and Margaret Bauman.

The flaw in your article arises from its omissions. You did not

mention the immune-atypicality findings of Warren, VK Singh, HH

Fudenberg, S Gupta, AV Plioplys, and others (e.g., 3-24). Nor did you

present the autoimmune and infection-related ramifications of these

researchers' findings.

You did not present ideas from the Autism Research Institute's Bernie

Rimland (2), long credited as the person who removed autism from the tainted

" science " of Bruno Bettelheim; nor did you mention or interview any of the

physicians who are treating etiologically significant immune and/or

infection-related processes in specific autism-spectrum children, some of

whom improve sufficiently so as to lose their diagnosis, some of whom

advance to inclusion within mainstream classes.

At least you offered Courchesne's statements indicating he no

longer accepts Bauman's " autism must occur in-utero " model. I myself came to

a similar position several years ago as I perused Dr. Bauman's articles and

primary citations along with newer articles unavailable as she was forming

her theory of in-utero timing (1).

Many parents and professionals within the autism community believe

that Dr. Bristol-Powers and her " it must be genetic and must occur in-utero "

cohorts constitute a primary stumbling block to advances in diagnostics,

research, and treatment regarding children of the autism-spectrum.

In contrast to the one-sided, paradigm-enforcing nature of your

article, Science Times recently presented a summary of human migrations into

North, Central, and South America (11.9.1999). The article presented

traditional theories alongside newer data showing that the older theories

are in need of revision.

A similarly structured autism article would have been consistent with

Science Times' usual level of excellence and would have done justice to the

research and clinic-based findings offering new models of causation,

diagnostics, and treatment of autism-spectrum children.

In my opinion, now that the " autism must be genetic and in-utero "

clique has had its say, Science Times ought prepare and publish another

autism article, wherein the " necessarily in-utero " model is more thoroughly

challenged and wherein the immune-atypicality and infection-related data and

researchers are fairly presented.

Sincerely,

Binstock

Researcher in Developmental & Behavioral Neuroanatomy

aspergerian@...

References

1. http://www.jorsm.com/~binstock/bk.htm

2. http://www.autism.com/ari

3. Serological association of measles virus and human herpesvirus-6 with

brain autoantibodies in autism. Singh VK et al. Clin Immunol

Immunopathol 1998 Oct;89(1):105-8.

4. Dialysable lymphocyte extract (DLyE) in infantile onset autism: a

pilot study. Fudenberg HH. Biotherapy 1996;9(1-3):143-7.

5. Immunodiagnosis and immunotherapy in autistic children. Singh VK,

Fudenberg HH et al. Ann N Y Acad Sci 1988;540:602-4.

6. Th1- and Th2-like cytokines in CD4+ and CD8+ T cells in autism.

Gupta S et al. J Neuroimmunol 1998 May 1;85(1):106-9.

7. Lymphocyte function in autism and Rett syndrome. Plioplys AV et al.

Neuropsychobiology 29.1.12-6 1994.

8. Brief report: immunoglobulin A deficiency in a subset of autistic

subjects. Warren RP et al. J Autism Dev Disord 1997 Apr;27(2):187-92.

9. Hyperserotoninemia and serotonin receptor antibodies in children with

autism but not mental retardation. Singh VK et al. Biol Psychiatry 1997

Mar 15;41(6):753-5.

10. Strong association of the third hypervariable region of HLA-DR beta

1 with autism. Warren RP et al. J Neuroimmunol 1996 Jul;67(2):97-102.

11. Immunogenetic studies in autism and related disorders. Warren RP et

al. Mol Chem Neuropathol 1996 May-Aug;28(1-3):77-81.

12. Elevated serotonin levels in autism: association with the major

histocompatibility complex. Warren RP, Singh VK. Neuropsychobiology

1996;34(2):72-5.

13. Increased frequency of the extended or ancestral haplotype

B44-SC30-DR4 in autism. s WW et al. Neuropsychobiology

1995;32(3):120-3.

14. DR-positive T cells in autism: association with decreased plasma

levels of the complement C4B protein. Warren RP et al. Neuropsychobiology

1995;31(2):53-7.

15. Decreased plasma concentrations of the C4B complement protein in

autism. Warren RP et al. Arch Pediatr Adolesc Med 1994 Feb;148(2):180-3.

16. Antibodies to myelin basic protein in children with autistic

behavior. Singh VK et al. Brain Behav Immun 1993 Mar;7(1):97-103.

17. Possible association of the extended MHC haplotype B44-SC30-DR4 with

autism. Warren RP et al. Immunogenetics 1992;36(4):203-7.

18. Changes of soluble interleukin-2, interleukin-2 receptor, T8 ntigen,

and interleukin-1 in the serum of autistic children. Singh VK et al.

Clin Immunol Immunopathol 1991 Dec;61(3):448-55.

19. Increased frequency of the null allele at the complement C4b locus

in autism. Warren RP et al. Clin Exp Immunol 1991 Mar;83(3):438-40.

20. Detection of maternal antibodies in infantile autism. Warren RP et

al. J Am Acad Child Adolesc Psychiatry 1990 Nov;29(6):873-7.

21. CD4+ helper T cell depression in autism. Yonk LJ et al. Immunol

Lett 1990 Sep;25(4):341-5.

22. Deficiency of suppressor-inducer (CD4+CD45RA+) T cells in autism.

Warren RP et al. Immunol Invest 1990 Jun;19(3):245-51.

23. Reduced natural killer cell activity in autism. Warren RP et al. J

Am Acad Child Adolesc Psychiatry 1987 May;26(3):333-5.

24. Immune abnormalities in patients with autism. Warren RP et al. J

Autism Dev Disord 1986 Jun;16(2):189-97.

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