New: Several documents about vaccinal ethylmercury and autism are now available.

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.

  
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  

  
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.

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.