Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
October 02, 2009
Newly published findings renew concern
for children who had mitochondrial pathology at the time of a
vaccination. The carefully designed study found that some such children
regressed into autism.
Titled "Fever Plus Mitochondrial Disease Could Be Risk Factors for
Autistic Regression", the study reports associations among fever,
mitochondrial profiles, vaccination, and autistic regression (1).
These findings augment insights from Hannah Poling, who had
mitochondria pathology markers and who regressed after a
multiple-vaccinations incident (2-3). Importantly, Hannah and her
mother have a specific mitochondrial genetic marker, even as her mother
remains a high-achieving, well-spoken, non-autistic individual.
Apparently, the mitochondria variant shared by mother and daughter was
insufficient to induce autism in the absence of a sufficient
environmental trigger which, for Hannah, was her being injected with
five vaccines in one day.
The new study by Black et al is oriented towards classically defined mitochondrial disease and
focused upon autistic children with thoroughly evaluated mitochondria
issues. Importantly, the researchers mention that many children are
never evaluated for markers of mitochondria pathology, which can be
difficult to ascertain (1).
In contrast, non-classical mitochondria
dysfunction (MtD) is not necessarily genetic in origin but has
signs and symptoms very similar to those of classic mitochondrial
disease. MtD is elaborated in a free-online, clinician-oriented review
by autism specialists Jeffrey Bradstreet, M.D., and Dan Rossignol, M.D.
(4) These experienced clinicians delineate differences between and
similarities of classic mitochondria disease and mitochondria
dysfunction. Their review offers an important point: "Biomarkers for
mitochondrial dysfunction have been identified, but seem widely
under-utilized despite available therapeutic interventions." (4)
As Black et al discuss their own findings (1), their rhetoric seems to
imply that fever in the context of
mitochondrial disease was crucial for the vaccination-related
regressions. However, as cited below, if an anti-pyrogen such as
acetaminophen (Tylenol) was given somewhat concurrently to the
vaccination that caused regression, then glutathione depletion and/or
fever suppression may have been etiologic co-factors in the children
who regressed. In other words, was the association among fever,
vaccination, and regression into autism dependent upon treatment of the
fever (in the context of mitochondria-related suboptimality)?
Due to the new findings' importance, we repeat: among the autistic
children who regressed into autism, fever and vaccination together were
more significant than was vaccination without fever (1). This finding
and the way it's worded in the study prompt concern for anti-pyrogens
such such as Tylenol, which utilizes and may deplete glutathione (5-8).
Such studies subserve a question: Were the closely watched children
given Tylenol or some other fever-reducing remedy?
Concern regarding treatment of fever is warranted because Tylenol
diminishes glutathione (eg, 9), which is suboptimal in many autistic
children (10-20) and which helps detoxify thimerosal (21-23).
Problematically, thimerosal inhibits a glutathione transferase (24);
and, not surprisingly, thimerosal injections of infants are associated,
among boys, with increased rates of special education services and with
autism (25-26).
But lets return to the important new study by Black et al (1), paying
close attention to the role of fever and possibly the role of
anti-pyrogens such as Tylenol, which has been linked with autism (eg,
27-29). Here are several excerpts:
"In this pilot study, autistic regression was identified in
60.7% (17 of 28) of the study participants representing a statistically
significant increase over the estimated 25% reported in the general
population of autistic spectrum disorders patients (w2, P < .0001;
Table 2). Autistic regression was not identified in 39.3% (11 of 28).
The 17 individuals with autistic regression could be divided into 2
groups, those who regressed with fever (70.6%, 12 of 17) and those who
regressed without identifiable linkage to fever or vaccinations (29.4%,
5 of 17). Autistic regression and fever was not associated with
vaccination in 8 of 12 (66.7%) and was associated with a febrile
response to vaccination in 4 of 12 (33.3%). Information about the
precise vaccine schedule associated with a febrile response was not
available. No individual showed regression with vaccination unless a
febrile response was present." (1)
The Black et al paper (1) ought prompt additional studies with similar
focus, larger numbers - and, we hope, future studies will include data
regarding Tylenol and other anti-pyretics.
In the following excerpts, notice how the description of mitochondrial
disease offered by Black et al is akin to the concept "mitochondrial
dysfunction" offered by Rossignol & Bradstreet:
"The clinical suspicion of mitochondrial disease in autistic
spectrum disorders is increased when patients have additional clinical
features that include hypotonia and motor delay, fatigue with activity,
metabolic abnormalities, poor growth, epilepsy, and affected siblings.
Increases in metabolites such as lactate, pyruvate, and alanine in
blood, urine, or cerebrospinal fluid can be important findings that
support a diagnosis of mitochondrial disease. However, metabolic
testing is often normal in mitochondrial disease, even in patients with
severe disorders.... Although hypotonia, motor developmental delay, and
fatigue are observed, the muscle histology shows only nonspecific
changes. This finding is consistent with routine histopathologic
assessments of most patients with mitochondrial disease who rarely have
diagnostic features such as cytochrome c oxidase-deficient fibers and
ragged-red fibers." (1)
"The biochemical heterogeneity observed in the autistic
spectrum disorder group is similar to the biochemical heterogeneity
observed in other groups of patients with mitochondrial disease.
Diagnosis of mitochondrial disease is complex, requiring a multifaceted
and well-coordinated clinical and laboratory approach. In most
individuals, no single test is sufficient for the diagnosis of
mitochondrial disease." (1)
"Classical mitochondrial diseases occur in a subset of
individuals with autism and are usually caused by genetic anomalies or
mitochondrial respiratory pathway deficits. However, in many cases of
autism, there is evidence of mitochondrial dysfunction (MtD) without
the classic features associated with mitochondrial disease. MtD appears
to be more common in autism and presents with less severe signs and
symptoms. It is not associated with discernable mitochondrial pathology
in muscle biopsy specimens despite objective evidence of lowered
mitochondrial functioning." (4)
Important insights with clinical significance can occur if
mitochonddrial evaluations occur:
"In all patients with mitochondrial disease, identification of
treatable metabolic changes such as deficiencies in coenzyme Q10 and
defects in cerebral folate metabolism is important. Patients with
mitochondrial disease are at increased risk of developing a defect in
cerebral folate metabolism... Cerebral folate deficiencies are also
reported in autistic spectrum disorders..." (1, p4)
"Unfortunately, many children with abnormal development caused by
mitochondrial diseases are not diagnosed..." (1; p4), yet most children
are virtually forced to abide by one-size-fits-all vaccination
policies.
Conclusion: The researchers who participated in Black et al are to be
congratulated. Their findings add importantly to peer-reviewed
literature about vaccinations and autistic regression in the presence
of signs and symptoms of classical mitochondrial disorder and, we add,
possibly MtD. Furthermore, the study calls attention to an important
issue: Had the anti-pyretic Tylenol been given to the children who
regressed in response to vaccination while having fever and signs
and/or symptoms of mitochondrial pathology?
More generally, as explained by William Egan, M.D., of the FDA's Center
for Biologics Evaluation & Research, policy regarding vaccinations
had long been to avoid the vaccinating of sick or recently sick
children. However, so as to increase vaccination rates (ie, coverage),
that policy had been changed to one of recommended that sick and
recently sick children be vaccinated (30).
Unfortunately, that policy change and the vaccinating of sick or
recently sick children -- particularly when multiple vaccines are
injected during the same incident -- may have been etiologically
significant in many cases wherein the child regressed into autism. And
why this policy change may be been significant can be found (i) in
peer-reviewed studies about glutathione (GSH), weak alleles of
GSH-related genes, and Tylenol (eg, 9-24, 27-29), and (ii) amid
specific children's clinical lab data consistent with MtD (4).
Furthermore, as informed by the tragedy of Hannah Poling's
vaccination-induced regression, these various risk factors may be all
the more important among infants and toddlers who have at least some
signs and symptoms of MtD but have not been properly evaluated prior to
being vaccinated.
Science - even clinical lab science - is running far ahead of
vaccination policies determined and enforced by zealotistic
practitioners of vaccinology.
Perhaps infants and toddlers ought be screened for weak alleles
and for indications of mitochondrial dysfunction.
References:
1. Fever Plus Mitochondrial Disease Could
Be Risk Factors for Autistic Regression
John Shoffner, MD, Lauren Hyams, PhD... and Keith Hyland, PhD1
Journal of Child Neurology 000(00) 1-6 2009.
http://www.ncbi.nlm.nih.gov/pubmed/19773461
Autistic spectrum disorders encompass etiologically heterogeneous
persons, with many genetic causes. A subgroup of these individuals has
mitochondrial disease. Because a variety of metabolic disorders,
including mitochondrial disease show regression with fever, a
retrospective chart review was performed and identified 28 patients who
met diagnostic criteria for autistic spectrum disorders and
mitochondrial disease. Autistic regression occurred in 60.7% (17 of
28), a statistically significant increase over the general autistic
spectrum disorder population (P < .0001). Of the 17 individuals with
autistic regression, 70.6% (12 of 17) regressed with fever and 29.4% (5
of 17) regressed without identifiable linkage to fever or vaccinations.
None showed regression with vaccination unless a febrile response was
present. Although the study is small, a subgroup of patients with
mitochondrial disease may be at risk of autistic regression with fever.
Although recommended vaccinations schedules are appropriate in
mitochondrial disease, fever management appears important for
decreasing regression risk.
2. Developmental regression and
mitochondrial dysfunction in a child with autism
Poling JS, Frye RE, Shoffner J, Zimmerman AW.
Department of Neurology and Neurosurgery, Johns Hopkins Hospital
J Child Neurol. 2006 Feb;21(2):170-2.
{free online}
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2536523&blobtype=pdf
Autistic spectrum disorders can be associated with mitochondrial
dysfunction. We present a singleton case of developmental regression
and oxidative phosphorylation disorder in a 19-month-old girl. Subtle
abnormalities in the serum creatine kinase level, aspartate
aminotransferase, and serum bicarbonate led us to perform a muscle
biopsy, which showed type I myofiber atrophy, increased lipid content,
and reduced cytochrome c oxidase activity. There were marked reductions
in enzymatic activities for complex I and III. Complex IV (cytochrome c
oxidase) activity was near the 5% confidence level. To determine the
frequency of routine laboratory abnormalities in similar patients, we
performed a retrospective study including 159 patients with autism
(Diagnostic and Statistical Manual of Mental Disorders-IV and Childhood
Autism Rating Scale) not previously diagnosed with metabolic disorders
and 94 age-matched controls with other neurologic disorders. Aspartate
aminotransferase was elevated in 38% of patients with autism compared
with 15% of controls (P <.0001). The serum creatine kinase level
also was abnormally elevated in 22 (47%) of 47 patients with autism.
These data suggest that further metabolic evaluation is indicated in
autistic patients and that defects of oxidative phosphorylation might
be prevalent.
3. Hannah Poling, her medical issues, and her post-vaccinal regression
into autism have been widely discussed. Her father and mother have
participated in some of these discussions. Noteworthy is the fact that
the U.S. Department of Health & Human Services conceded a suit
regarding Hannah's vaccination-induce autism. Here are three examples
regarding the significance of the HHS concession regarding Hannah
Poling, mitochondria disorders, vaccinations, and autism:
3a. Vaccine Injury Case Offers a Clue to
the Causes of Autism
Could a group of disorders involving the "power plants of the cell"
explain why some vaccinated children develop autism but the vast
majority don't?
By Nikhil Swaminathan, April 22, 2008
http://www.scientificamerican.com/article.cfm?id=vaccine-injury-case-offer
3b. Father: Child's case shifts autism
debate
By Jon S. Poling
Atlanta Journal-Constitution, 04/11/08
http://www.ajc.com/services/content/opinion/stories/2008/04/11/polinged0411.html
3c. Hanna Poling v. Secretary of HHS:
Landmark First Concession of Vaccine-Induced Autism by U.S. Dept. of
Health & Human Services
http://www.drhusbands.com/articles/March%2008%20Newsltr%20Article.pdf
4. Evidence of Mitochondrial Dysfunction in
Autism and Implications for Treatment
Daniel A. Rossignol, J. Jeffrey Bradstreet
American Journal of Biochemistry and Biotechnology 4 (2): 208-217,
2008
{free online}
http://www.scipub.org/fulltext/ajbb/ajbb42208-217.pdf
Classical mitochondrial diseases occur in a subset of individuals with
autism and are usually caused by genetic anomalies or mitochondrial
respiratory pathway deficits. However, in many cases of autism, there
is evidence of mitochondrial dysfunction (MtD) without the classic
features associated with mitochondrial disease. MtD appears to be more
common in autism and presents with less severe signs and symptoms. It
is not associated with discernable mitochondrial pathology in muscle
biopsy specimens despite objective evidence of lowered mitochondrial
functioning. Exposure to environmental toxins is the likely etiology
for MtD in autism. This dysfunction then contributes to a number of
diagnostic symptoms and comorbidities observed in autism including:
cognitive impairment, language deficits, abnormal energy metabolism,
chronic gastrointestinal problems, abnormalities in fatty acid
oxidation, and increased oxidative stress. MtD and oxidative stress may
also explain the high male to female ratio found in autism due to
increased male vulnerability to these dysfunctions. Biomarkers for
mitochondrial dysfunction have been identified, but seem widely
under-utilized despite available therapeutic interventions. Nutritional
supplementation to decrease oxidative stress along with factors to
improve reduced glutathione, as well as hyperbaric oxygen therapy
(HBOT) represent supported and rationale approaches. The underlying
pathophysiology and autistic symptoms of affected individuals would be
expected to either improve or cease worsening once effective treatment
for MtD is implemented.
5. Tylenol ® acetaminophen
pharmacology
http://www.tylenolprofessional.com/pharmacology.html
6. Comparative efficacy of aspirin and
acetaminophen in the reduction of fever in children
Yaffe SJ.
Arch Intern Med. 1981 Feb 23;141(3 Spec No):286-92.
Antipyretics should be employed in the pediatric population whenever it
is the clinical judgment of the attending physician that fever should
be lowered. Aspirin and acetaminophen are equally effective as
antipyretics. The efficacy and safety of these two most common
antipyretic agents are examined, and various studies with these agents
are critically reviewed. Since acetaminophen has a greater margin of
safety at antipyretic dosages, it is preferred to aspirin when an
anti-inflammatory effect is not required. The efficacy and safety of
combination therapy with acetaminophen and aspirin in pediatric
patients--or an alternative treatment regimen with both these
drugs--warrant investigation.
7. The antipyretic effect of ibuprofen and
acetaminophen in children
Wahba H.
Pharmacotherapy. 2004 Feb;24(2):280-4.
OBJECTIVE: To determine whether evidence in the medical literature
supports ibuprofen or acetaminophen for reducing fever in children.
METHODS: Both MEDLINE and the Science Citation Index were searched
using various medical subject headings for all articles published
worldwide from 1966-2000. The language of publication was not
restricted. RESULTS: Initially, 4132 articles were found that dealt
with either ibuprofen or acetaminophen. Limiting these articles to
humans and children, and cross-referencing with the Science Citation
Index resulted in 68 articles; 22 satisfied the inclusion criteria and
were further assessed for validity, design, and methods of reporting
data. CONCLUSION: Acetaminophen and ibuprofen have equal tolerability.
Acetaminophen produced a greater body temperature reduction at 0.5 hour
after intervention compared with ibuprofen. However, ibuprofen provides
a longer duration of antipyretic effect than acetaminophen 4 hours
after intervention, and the initial temperature decrement lasts
longer.
8. Antipyretic efficacy and safety of
ibuprofen and acetaminophen in children
Goldman RD et al.
Ann Pharmacother. 2004 Jan;38(1):146-50.
OBJECTIVE: To evaluate the antipyretic effects and safety of ibuprofen
compared with acetaminophen in febrile children. DATA SOURCES: Searches
of MEDLINE (1966-November 2003) and EMBASE (1988-November 2003) were
conducted using the terms ibuprofen and acetaminophen. Bibliographies
of selected articles were reviewed. DATA SYNTHESIS: Ibuprofen was
significantly more effective than acetaminophen in reducing fever after
a single dose. Ibuprofen was found to be more effective after 6 hours,
but not after a longer period of time. Studies with multiple doses have
also failed to show that one drug is better than the other.
CONCLUSIONS: The efficacy and effectiveness of acetaminophen and
ibuprofen in their recommended dosages are similar, with slightly more
beneficial effects shown with ibuprofen.
9. Glutathione, glutathione-dependent
enzymes and antioxidant status in erythrocytes from children treated
with high-dose paracetamol
Kozer E et al.
Br J Clin Pharmacol. 2003 Mar;55(3):234-40.
{free online}
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1884208&blobtype=pdf
AIM: To investigate glutathione and antioxidant status changes in
erythrocytes from febrile children receiving repeated supratherapeutic
paracetamol doses. METHODS: Fifty-one children aged 2 months to 10
years participated in the study. Three groups were studied: group 1 (n
= 24) included afebrile children who did not receive paracetamol; and
groups 2 (n = 13) and 3 (n = 14) included children who had fever above
38.5 degrees C for more than 72 h. Patients in group 2 received
paracetamol at a dose of 50 +/- 15 (30-75) mg kg(-1) day(-1) and those
in group 3 received paracetamol above the recommended therapeutic dose,
ie 107 28 (80-180) mg kg(-1) day(-1). A blood sample was taken for the
measurement of liver transaminases, gammaglutamil transferase (GGT),
reduced glutathione (GSH), glutathione reductase (GR), glutathione
peroxidase (GPX), glutathione S-transferase (GST), superoxide dismutase
(SOD) and antioxidant status. RESULTS: Aspartate aminotransferase
activity in group 3 was higher than in the other groups (P = 0.027).
GSH, SOD and antioxidant status were significantly lower in group 3
compared with groups 1 and 2 (mean differences: for GSH 3.41 micromol
gHb(-1), 95% confidence interval (CI) 2.10-4.72, and 2.15 micromol
gHb(-1), 95% CI 0.65-3.65, respectively; for SOD 856 U min(-1) gHb(-1),
95% CI 397-1316, and 556 U min(-1) gHb(-1), 95% CI 30-1082,
respectively; and for antioxidant status 0.83 mmol l(-1) plasma, 95% CI
0.30-1.36, and 0.63 mmol l(-1) plasma, 95% CI 0.02-1.24, respectively).
GR activity was significantly lower in groups 3 and 2 in comparison
with group 1 (mean differences 3.44 U min(-1) gHb(-1), 95% CI
0.63-6.25, and 5.64 U min(-1) gHb(-1), 95% CI 2.90-8.38, respectively).
Using multiple regression analysis, paracetamol dose was found to be
the only independent variable affecting GR, GST and SOD activities (P =
0.007, 0.003 and 0.008, respectively). CONCLUSIONS: In febrile
children, treatment with repeated supratherapeutic doses of paracetamol
is associated with reduced antioxidant status and erythrocyte
glutathione concentrations. These significant changes may indicate an
increased risk for hepatotoxicity and liver damage.
10. Analysis of case-parent trios at a
locus with a deletion allele: association of GSTM1 with
autism
Buyske S et al. BMC Genet. 2006 Feb 10;7:8.
{free online}
http://www.biomedcentral.com/1471-2156/7/8
11. A clinical and laboratory evaluation of
methionine cycle-transsulfuration and androgen pathway markers in
children with autistic disorders
Geier DA, Geier MR. Horm Res. 2006;66(4):182-8.
12. Metabolic endophenotype and related
genotypes are associated with oxidative stress in children with
autism
James SJ et al. Am J Med Genet B Neuropsychiatr Genet. 2006 Dec
5;141B(8):947-56.
{free online}
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2610366/pdf/nihms68264.pdf
13. Risk of autistic disorder in affected
offspring of mothers with a glutathione S-transferase P1
haplotype
Williams TA et al. Arch Pediatr Adolesc Med. 2007 Apr;161(4):356-61.
{free online}
http://archpedi.ama-assn.org/cgi/content/full/161/4/356
14. Abnormal
transmethylation/transsulfuration metabolism and DNA hypomethylation
among parents of children with autism
James SJ et al. J Autism Dev Disord. 2008 Nov;38(10):1966-75.
15. Biomarkers of environmental toxicity
and susceptibility in autism
Geier DA et al. J Neurol Sci. 2009 May 15;280(1-2):101-8.
16. Low natural killer cell cytotoxic
activity in autism: the role of glutathione, IL-2 and
IL-15
Vojdani A et al. J Neuroimmunol. 2008 Dec 15;205(1-2):148-54.
17. Efficacy of methylcobalamin and folinic
acid treatment on glutathione redox status in children with
autism
James SJ et al. Am J Clin Nutr. 2009 Jan;89(1):425-30.
18. Genetic variant of glutathione
peroxidase 1 in autism.
Ming X et al. Brain Dev. 2009 Feb 3. [Epub ahead of print]
19. Metabolic biomarkers related to
oxidative stress and antioxidant status in Saudi autistic
children
Al-Gadani Y et al. Clin Biochem. 2009 Jul;42(10-11):1032-40.
20. Cellular and mitochondrial glutathione
redox imbalance in lymphoblastoid cells derived from children with
autism
James SJ et al. FASEB J. 2009 Aug;23(8):2374-83.
21. Homozygous gene deletions of the
glutathione S-transferases M1 and T1 are associated with thimerosal
sensitization
Westphal GA et al. Int Arch Occup Environ Health. 2000
Aug;73(6):384-8.
22. Biochemical and molecular basis of
thimerosal-induced apoptosis in T cells: a major role of mitochondrial
pathway
Makani S et al. Genes Immun. 2002 Aug;3(5):270-8.
{free online}
http://www.nature.com/gene/journal/v3/n5/abs/6363854a.html
23. Thimerosal neurotoxicity is associated
with glutathione depletion: protection with glutathione
precursors
James SJ et al. Neurotoxicology. 2005 Jan;26(1):1-8.
24. Inhibition of the human erythrocytic
glutathione-S-transferase T1 (GST T1) by thimerosal
Muller M et al. Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81.
25. Hepatitis B triple series vaccine and
developmental disability in US children aged 1-9
years
Gallagher C, Goodman M. Toxicol Environ Chem 2008 90(5):997-1008.
{free online}
http://fourteenstudies.org/pdf/hep_b.pdf
26. Hepatitis B vaccination of male
neonates and autism
[conference abstract as published]
CM Gallagher, MS Goodman, Graduate Program in Public
Health, Stony Brook University Medical Center, Stony Brook, NY
Annals of Epidemiology, p659
Vol. 19, No. 9 Abstracts (ACE) September 2009: 651–680
27. Is fever suppression involved in the
etiology of autism and neurodevelopmental disorders?
Torres AR.
BMC Pediatr. 2003 Sep 2;3:9. Epub 2003 Sep 2.
{free online}
http://www.biomedcentral.com/1471-2431/3/9
BACKGROUND: There appears to be a significant increase in the
prevalence rate of autism. Reasons for the increase are unknown,
however, there is a substantial body of evidence that suggests the
etiology involves infections of the pregnant mother or of a young
child. Most infections result in fever that is routinely controlled
with antipyretics such as acetaminophen. The blocking of fever inhibits
processes that evolved over millions of years to protect against
microbial attack. Immune mechanisms in the central nervous system are
part of this protective process. HYPOTHESIS: The blockage of fever with
antipyretics interferes with normal immunological development in the
brain leading to neurodevelopmental disorders such as autism in certain
genetically and immunologically disposed individuals. TESTING THE
HYPOTHESIS: Epidemiological studies to determine associations between
the use of antipyretics and neurodevelopmental disorders should be
undertaken. Biochemical tests will involve the examination of
fluids/serum by mass spectrometry and the determination of
cytokine/chemokine levels in serum and cell culture fluids after
stimulation with fever-inducing molecules from bacteria, viruses and
yeast. Postmortem brain can be examined by immunohistochemistry or
other methods such as fluorescent in situ hybridization (FISH) to
determine altered expression levels of chemokines/cytokines and other
molecules. IMPLICATIONS OF THE HYPOTHESIS: 1) The use of antipyretics
during pregnancy or in young children may be reserved for more severe
fevers. 2) The perplexing genetic findings in autism may be better
understood by categorizing genes along functional pathways. 3) New
treatments based on immune, cell, pharmacological or even heat
therapies may be developed.
28. Acetaminophen (paracetamol) use,
measles-mumps-rubella vaccination, and autistic disorder: the results
of a parent survey
Schultz ST et al.
Autism. 2008 May;12(3):293-307.
The present study was performed to determine whether acetaminophen
(paracetamol) use after the measles-mumps-rubella vaccination could be
associated with autistic disorder. This case-control study used the
results of an online parental survey conducted from 16 July 2005 to 30
January 2006, consisting of 83 children with autistic disorder and 80
control children. Acetaminophen use after measles-mumps-rubella
vaccination was significantly associated with autistic disorder when
considering children 5 years of age or less (OR 6.11, 95% CI
1.42-26.3), after limiting cases to children with regression in
development (OR 3.97, 95% CI 1.11-14.3), and when considering only
children who had post-vaccination sequelae (OR 8.23, 95% CI 1.56-43.3),
adjusting for age, gender, mother's ethnicity, and the presence of
illness concurrent with measles-mumps-rubella vaccination. Ibuprofen
use after measles-mumps-rubella vaccination was not associated with
autistic disorder. This preliminary study found that acetaminophen use
after measles-mumps-rubella vaccination was associated with autistic
disorder.
29. Similarities in features of autism and
asthma and a possible link to acetaminophen use.
Becker KG, Schultz ST.
Med Hypotheses. 2009 Sep 10. [Epub ahead of print]
Autism and autism spectrum disorders are enigmatic conditions that have
their origins in the interaction of genes and environmental factors. In
this hypothesis, genes statistically associated with autism are
emphasized to be important in inflammation and in innate immune
pathways, including pathways for susceptibility to asthma. The role of
acetaminophen (paracetamol) in an increased risk for asthma is
described and a possible similar link to an increased risk for autism
is suggested.
30. Personnel communication.
William Egan, M.D., 2000, then acting director of the FDA's Center for
Biologics Evaluation & Research (CBER), in their offices in
Rockville, Maryland.
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Binstock by email
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