http://www.jorsm.com/~binstock/
AUTISM RESEARCH MONOGRAPHS
of Teresa Binstock
last updated on August 14, 2000
New: Several documents about vaccinal ethylmercury and autism are now
available.
vaccinations, thimerosal,
ethylmercury: autism, ADHD, anorexia
Each of the papers and idea-collections on this web page reflects not only a
goodly amount of medical research but also reflects the wonderful determination
of autism-children's parents who are seeking to find answers and, in so doing,
are willing to share anecdotes amidst which patterns prompted each of the
monographs presented here.
New page: intra-monocyte infections, an autism subgroup
Mild immune impairments such as null alleles of complement C4b gene are
associated with autism and appear to be etiologically significant; reduced
IgA is also associated with the autism spectrum (Reed Warren et al; Mary
Megson et al). Reed Warren's findings were specific to the assays and methods
his lab used; that he found specific immune impairments suggests that others
exist if they can be identified and tested. A hypothesis based upon lab-test
data from autism-spectrum children offers that intra-monocyte infections (eg,
by CMV, HHV6, Yersinia enterocolitica) induce a different kind of mild immune
impairment and also lead to inflammatory and other pathologies along the
blood-brain barrier.
Infected
monocytes & autism
Related pages about Yersinia enterocolitica
Various intracellular pathogens often persist as chronic infections within
monocytes and impair hematopoiesis, immunity, and blood-brain "barrier"
function. Yersinia enterocolitica antibodies in an autism-spectrum
child prompted the research reflected on three webpages.
Yersinia, CMV, HHV6, and other
intra-monocyte pathogens
Yersinia cross-reactivities and
thyroid-related autoimmunity
Background
and intentions for this webpage
For
most of the 1990s I conducted Independent Research at the University of
Colorado
Health Sciences Center in Denver. During these years, my work led to
a
paper about molecular genetics, neuroanatomy, and the amygdala in fragile
X
syndrome (published in Developmental Brain Dysfunction) and to a
co-authored
paper about human sexuality, wherein my contributions focused
upon
immunology, neurosteroids, imprinting, and molecular genetics (published
in
Hormones and Behavior). Also, my autism-list writings led to the finding
of
two possibly significant viruses in the CNS and periphery of a child who
had
experienced an autistic-like deterioration (3). However, I am diagnosed
with
Asperger's Syndrome and am neither an MD nor a PhD, and I was never paid
for
my research, even though some parents make donations from time to time;
and
such grants as were offered to me always included the stipulation that I
discontinue
my research, which I chose not to do. Making progress in
autism-research
is too important.
Most
of these monographs and collections of ideas were originally posted
to
the Autism-List hosted by St. Johns University and here contain some minor
modifications.
Many of the original postings can be retrieved from
bit.listserv.autism.
My writings do not constitute medical advice.
Instead, they represent seeking to understand autism-spectrum disorders
and their causes and associated traits.
A
List of the Monographs:
My research writings in 1997, 1998, and 1999 reflect a deepening interest in
biologic aspects of causation in autism. The question "what is the cause of
autism?" is erroneous; ie, there are various causes (and do note the plural:
causes) already known to be capable of inducing a child to have traits worthy
of the diagnosis "autistic". Some such causes are genetic -- eg, fragile X
syndrome; but a goodly amount of evidence points towards non-genetic causes
in a large subgroup of autism-spectrum children, with fungal, bacterial, and
viral infections as important factors. Furthermore, recent evidence indicates
that specific alleles of certain genes create endogenous proteins that serve
as binding sites for certain infectious agents, thereby creating a complexity
of genetic/environmental interactions as causally significant.
A
short list of monographs is presented first, and an expanded list that
includes
brief descriptions of each topic can be found further down this
page.
A recent paper about vaccination-induced pathologies:
A letter to US Congressional
Representative Dan Burton, R-Indiana, providing numerous citations which
delineate mechanisms by which vaccination-related processes can induce or
exacerbate various pathologies.
The major monographs:
Atypical chronic infections
and other immune atypicalities, a new diagnostic subgroup:
Immune panels for
autism-spectrum children
Case study: cytopenia with
monocytosis and anemia
Case study: elevated
anti-EBV, HHV6, and Bell's Palsy
Case study: gastrointestinal
Klebsiella pneumoniae and hemolytic E. coli
Critique of Margaret Bauman's
in-utero timing theory
Suboptimality Factors and
Various Causations in Autism
Febrile Seizures, the
Amygdala, and Autism
Febrile Seizures: Human
Herpes Virus 6, Roseola
LKS and HSV: Landau-Kleffner
Syndrome and Herpes Simplex Virus
Neonatal gastroenterologic
events: immunity, IgA, CD5+ cells
CVID: common variable immune
deficiencies; hypogammaglobulinemia of infancy
Ganglioside Heterozygotes,
Impaired Immunity, NK cells
Ignaz Semmelweiss, the NIH,
and models of autism causation
HHV6 resource page
Vaccinations and possible sequelae:
Vaccination-induced
neuropathies
MMR and
interferon-gamma: gastrointestinal and neurologic effects
Some additional tidbits:
Contra-indications to
steroid therapy
EBV and atypical
mosquito bite reactions
Febrile Seizures: a
miscellany including somatostatin
Suboptimality and IgA
An IgA miscellany
infection-impaired
immunity, a new direction in autism research
Chronic active
infections of the Blood-Brain Barrier
Brief Summaries of the Monographs:
Atypical chronic
infections and other immune atypicalities, a new diagnostic subgroup:
The fact that most of the autism-spectrum immune-panels I've perused contain
either (a) signs of an immune irregularity, and/or (b) atypical elevations of
at least one and *usually several* anti-viral antibodies titres suggests that a
new subgroup in autism-spectrum diagnostics is becoming identified, with the
following characteristics: (i) Atypical elevations of common pathogens... (ii)
Many of these immune panels... also delineate a specific immune impairment
revealed by the absence of antibodies against a common antigen for which
antibodies ought be present... (iii) Regarding HSV and CMV, *seemingly* normal
peripheral-antibodies levels of HSV and CMV are difficult to interpret and may
represent false-negatives... (v) Generally -- and there are exceptions -- many
of these kids appear to have an immune shift in a Th2 direction...
Ramifications for diagnostics and treatments are preliminarily discussed.
Critique of Margaret
Bauman's in-utero timing theory
The research and writings of Margaret Bauman and a colleague are considered to
have established that virtually all autisms occur in-utero -- because, as Dr.
Bauman has argued, a lack of gliosis was observed during autopsy of a
neurological region affected in autism. However, recently published articles
have reported that gliosis need not be permanent. These newer findings indicate
that "lack of gliosis" does not necessarily mean that the brain
region being studied had its atypicality induced in-utero. This is extremely
important for models of autism causation, because many parents and physicians
report that the child's autism occurred months or, in many cases, even more
than a year subsequent to birth and after a long period of obvious normalcy. If
the recently published articles about gliosis are correct, then a "lack of
gliosis" does not necessarily imply "in-utero" causation; and,
as consistent with numerous parental and other reports, later timings for
autism causation are possible too.
Immune panels for
autism-spectrum children
Increasingly, parents of autism-spectrum children are purchasing thorough
immune panels as a way to gain insight into the child's atypical responses to
vaccinations and/or infections; in some cases, this kind of information has led
to effective treatments of specific children. This page offers one researcher's
opinion of what tests have been significant in the autism-spectrum immune
panels she has perused.
Contraindications
to steroid therapy
This page offers a comments and citations demonstrating the importance of
infections when contemplating steroid therapies in autism-spectrum children.
Febrile Seizures,
the Amygdala, and Autism
Febrile seizures are often said to be benign; however, what may be generally
true in most cases is not necessarily true in all cases. Recently published
studies delineate mechanisms by which atypical brain areas in a subgroup of
autism-spectrum children might have been caused by febrile seizures, eg, from
vaccinations, from HHV6, etc.
Febrile Seizures,
the Amygdala, Somatostatin
This page offers a miscellany of posts relating to febrile seizures, the
amygala, somatostatin, etc.
Febrile Seizures:
Human Herpes Virus 6, Roseola
Febrile seizures are not always benign. HHV6 does not always create symptoms of
roseola.
Suboptimality Factors
and Various Causations in Autism
Adverse events during pregnancy and birthing and during the neonatal and infant
periods provide clues as to possible causations among a large subgroup of
autism-spectrum children. Suboptimality refers to a numeric tally of adverse
events.
Suboptimality and
IgA
IgA atypicalities are statistically associated with autism. This page presents
a miscellany of IgA tidbits, some connected with adverse events relating to a
suboptimality score.
HHV6 resource page
Human herpesvirus 6 is ubiquitous; most children and adults are infected with
this virus and effectively immunosuppress it. However, individuals with
immune-impairments may have atypical responses to HHV6; and in the
autism-spectrum immune panels I've perused, many report atypical elevations of
anti-HHV6 antibodies, often along with other immune atypicalities.
An IgA miscellany
More about IgA, which is so crucial to immunity, including gastrointestinal
immunity.
LKS and HSV:
Landau-Kleffner Syndrome and Herpes Simplex Virus
Increasingly, new data show that HSV, in the absence of HSV encephalitis, is
present in neuronal tissues taken from a goodly percentage of epileptic sites.
HSV is also known to migrate towards the temporal lobe and to be associated
with impairments in language. Given the anecdotal information about beneficial
effects of the anti-HSV drug acyclovir, the question arises, do some LKS or
autism-spectrum children have a subclinical CNS infection with HSV? Addressing
this concern is urgent not only because of the new data about HSV in seizure
foci but also because a traditional LKS-treatment (steroids) would augment the
infection even while generating initial improvements. These data and studies,
as well as the anecdotes, have ramifications for early diagnostics and initial
treatments of LKS-like children.
Prednisone
considerations
Prednisone therapy is often suggested to parents of autism-spectrum children
and appears to have beneficial results in some, and less than beneficial
results in others. Two webpages explore chronic infections and immune
atypicalities as possible contraindications to Prednisone therapy.
Vaccination-induced
neuropathies
That vaccinations can induce neurologic sequelae has been known for decades.
More recent medical literature provides more understanding about how CNS-damage
can occur and, given the neurologic locales affected, how autism- spectrum
disorders might arise therefrom.
MMR effects:
interferon-gamma, gastrointestinal, neurologic
Numerous parents of autistic children report the onset of symptoms within hours
or days after a vaccination. Contrastingly, the medical establishment
discourages this concept and thereby inhibits inquiries into how such
vaccination-related injuries might occur. This monograph presents information
about the MMR's inducing of interferon-gamma production and, for some children,
its potential role in the development of neurologic and/or gastrointestinal
symptoms as sequelae to the MMR.
Neonatal
gastroenterologic events: immunity, IgA, CD5+ cells
Many parents of autism-spectrum children report gastrointestinal symptoms
and/or altered profiles on immune-related lab-tests. New immunological data
about CD5+ cells indicate that during the neonatal period, infectious agents in
the gastrointestinal tract can alter immunity in long-lasting ways. Thus, the
neonate's developing immunity offers clues regarding (i) his or her subsequent
immune-panel profiles, as well as (ii) subsequent gastrointestinal problems
that occur in many autism-spectrum children.
CVID and pTHI
In some medical reviews, CVID (Common Variable Immune Deficienies) are presumed
to be genetic in origin, and many CVID do have a genetic basis. However,
various studies report CVID-like symptoms-patterns and immune-shifts in
response to lingering infections. Some of these symptoms-lists resemble many of
the anecdotes shared by parents of autism-spectrum children. Similarly, a
period of reduced immunity during infancy -- after the mother's
transferred-immunity has subsided and before the infant's immune system has
matured -- has been labeled "transient hypogammaglobulinemia of
infancy" (THI); and researchers have noticed that in some infants this
period is prolonged (pTHI). These various phenomena raise the possibility, at
least in a subgroup of autism-spectrum children, that the child's atypical
immune-panel results and various medical-history specifics may have
infection-related causations. Investigations in these areas -- often led by
parents purchasing lab-tests -- are beginning to yield clues regarding
treatment and/or causation in autism-spectrum disorders.
Ganglioside
Heterozygotes, Impaired Immunity, NK cells
Tay-Sachs, Gaucher's, and other ganglioside-related syndromes are the result of
a child's having two mutated genes (homozygous) whose protein-products, in the
absence of mutations, lead to enzymes needed for ongoing degradation of
gangliosides, and children with only one copy of the mutated gene do not
develop the ganglioside-related syndromes (often called Gangliosidoses).
Research has demonstrated that autism has a genetic linkage to at least one
ganglioside- enzyme gene; and recent studies reveal the even mildly elevated
levels of gangliosides -- as would occur if a child were heterozygous (only one
mutated gene) -- might impair the immune function of Natural Killer cells in
ways (i) remarkably consistent with some autistic children's atypical
immune-panel profiles; and (ii) conducive to increased neurologic sequelae from
various infectious agents -- be they viral, bacterial or fungal.
Ignaz Semmelweiss,
the NIH, and models of causation
The NIH's autism-research funding has supported a model wherein the cause of
autism is presumed to be genetic. This strategy has continued despite a goodly
amount of data and widespread patterns among parental anecdotes, ie, data and
anecdotes indicating that non-genetic areas of research ought be funded -- as a
way to advance autism-research more rapidly.. In medical history, the story of
Ignaz Semmelweiss illustrates of the extent to which new data can be ignored by
"the medical establishment", even if the new data and ramifications
thereof are found, after many years, to have been quite on-target.
a new direction in
autism research
Increasingly, my research was focusing upon infectious aspects of autism, not
only in regard to viruses in the CNS but also in regard (i) to how viruses,
bacteria, and fungi affect immunity, and (ii) to how certain viruses can
establish long-term residence in the gi- tract and/or bone marrow and/or CNS.
Many of the immune-panel atypicalities and neurologic effects seen in autism
may derive from underlying infections -- at least in various autism-spectrum
subgroups. For me, due to a complex coincidence of events in early 1999, this
topic remains uncompleted. However, a miscellany of smaller posts offers
intriguing clues.
EBV and atypical
mosquito bite reactions
Atypical reactions to mosquito bites can reflect an atypical, chronic infection
with Epstein-Barr virus, associated with elevations in the number of Natural
Killer cells. Some parents report that they or their autism- spectrum child has
a hypersensitivity to mosquito bites. These reactions *may* (in some cases)
reflect atypical, chronic EBV infection.
e-mail to: Teresa Binstock
ABBREVIATIONS in the various papers.
BDP = bleeding during pregnancy
CMV = cytomegalovirus
CSF = cerebrospinal fluid
CVID = common variable immune deficiency
EBV = Epstein-Barre virus
HHE = human herpes encephalitis, regardless of viral type
HHV = human herpes virus, from HHV-1 to HHV-8
HSV = herpes simplex virus, HSV-1 or HSV-2
NK = Natural Killer cells of the immune system
PCR = polymerase chain reaction
Tc = my comments
pTHI = prolonged THI
THI = transient hypogammaglobulinemia of infancy
TNFa = Tumor Necrosis Factor alpha
glutathione = an endogenously produced substance
(i) that has anti-oxidant properties, and
(ii) that participates in T-cell and B-cell interactions.
Copyright 1997,1998,1999,2000
This page last updated on August 14, 2000.
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