For more information on our global programs, including the International Decade of Nutrition, and our US based ones, please visit us at www.HealthFreedomUSA.org and www.GlobalHealthFreedom.org and join the free email list for the Health Freedom eAlerts to keep you in the loop, informed and active defending your right to make your own decisions about your health and wellbeing!
Our activities are supported 100% by your tax deductible donations. Please give generously (http://drrimatruthreports.com/index.php?page_id=189) to the Natural Solutions Foundation. Thank you for your support.
Feel free to disseminate this information as widely as possible with full attribution.
Yours in health and freedom,
Dr. Rima

Rima E. Laibow, MD
Medical Director
Natural Solutions Foundation
www.HealthFreedomUSA.org
www.GlobalHealthFreedom.org
www.organics4U.org

Dr. Jon Polling is a Neurologist. he is also the father of the most famous autistic child in America right now, Hannah Poling. In a historic concession, US Assistant Attorney General Peter Keisler and other Justice Department officials conceded on November 9 that Hanna “had a pre-existing mitochondrial disorder that was ‘aggravated’ by her shots, and which ultimately resulted in an ASD diagnosis” or, more specifically, in a diagnosis of “regressive encephalopathy (brain disease) with features consistent with autistic spectrum disorder, following normal development.”

While they did not go as far as saying that vaccination caused the neurological collapse of the previously healthy child, they did admit that for a child with a mitochondrial disorder, the shots could “aggrivate” a tendency toward autism. It is the first time that the US has come even this close to acknowledging the role of vaccines in any chronic neurological injury.

For the approximately 1000 cases behind this one, DR. JON POLING TO DR. STEVEN NOVELLA ON AGE OF AUTISM

PolingsBy Dr. Jon Poling, father of Hannah Poling.

OPEN LETTER TO DR. STEVEN NOVELLA
IN RESPONSE TO “Has the Government Conceded Vaccines Cause Autism?”

Dr. Novella,

Thank you for generating interesting discussion regarding my little girl,
Hannah Poling. I would like to give you additional information in order to
generate further productive discussions on this matter amongst the neurology
community. This information should assist you, Dr. DiMauro, and Dr.
Trevethan, who have also commented publicly, to formulate better theories as
to the significance of Hannah’s mitochondrial dysfunction in relation to her
autism.

1. Mito Dysfunction or Mito Disease? Chicken or Egg?

To begin with, I would like to point out that the spectrum of mitochondrial
dysfunction is probably considered more broad and complex than the spectrum
of neurobehavioral abnormalities seen with autism. Dysfunction of the
mitochondria, specifically dysfunction of the oxidative phosphorylation
pathway, most likely contributes, but may not be the cause of many
diseases—including Parkinson’s disease, Friedreich’s Ataxia, Alzheimer
disease, etc. Thus, it is probably incorrect to refer to mitochondrial
dysfunctional and mitochondrial disease interchangeably. Indeed, the role of
the dysfunctional mitochondrial are yet to be clarified in these diseases.
Thus, I will refer to Hannah’s metabolic condition as a mitochondrial
dysfunction, not a mitochondrial disease.

2. Mito Genetic Finding? Mito mtDNA ‘red herring’ ?

ADDITIONAL GENETIC TESTING NOT AVAILABLE IN THE J CHILD NEUROL CASE REPORT:
Dr. Shoffner performed genetic testing on both Hannah’s muscle and her
mother’s leukocytes subsequent to our case report. Hannah (muscle mtDNA) and
her mother (leukocyte mtDNA) were both found to be HOMOPLASMIC for the mtDNA
T2387C transition mutation.
Our analysis of this genetic finding in the mtDNA was significantly
different than those of other physicians that I’ve seen in scientific blogs
or commentary. I suspect it would have been fatal to both Hannah and her
mother if this homoplasmic mutation was pathogenic since (as I am sure you
are aware) the mutation is on the 16S ribosomal subunit which is highly
conserved. Thus, this mutation probably represents a benign polymorphism
rather than pathogenic mutation. It is unlikely, but possible, that the
mutation is significant to Hannah, but in such a case, it must work in
concert with other nuclear genes to cause her mitochondrial dysfunction. To
our knowledge, this point mutation has not been reported in cases similar to
Hannah’s.

3. Encephalitis? Metabolic Encephalopathy? Or “Regressive Encephalopathy
with Features of Autism Spectrum Disorder”

The other interesting term you used was encephalitis rather than
encephalopathy. We are not sure that she had an “-itis” but we did clearly
document a regressive encephalopathy based on not only our parental
reporting, but also based on the pediatrician’s documents, affidavits from
other family members, and the growth curve measurements (injury pattern).
Early on in the regression we did note back arching (opisthotonus), fever,
and disrupted sleep. Although fever occurred a lumbar puncture was not
performed.

An interesting developing story in autism research is the
immune/inflammatory connection. In her senior resident thesis, Dr. Anne
Comi, a former JHU colleague, along with Dr. Andy Zimmerman, reported, the
increased prevalence of autoimmune disease in families of autistic
offspring. Interesting, Hannah also has a maternal family history of
autoimmune disease. Dr. Carlos Pardo, another one of my former chief
residents, along with Andy and Dr. Vargas, published a beautiful study in
the Archives of Neurology, demonstrating neuroinflammation on autopsy of
brain samples and inflammation cytokine markers in the CSF of individuals
with Autism. The interesting thing was that inflammation was demonstrated in
autopsy specimens from adults as old as 44 years of age. The conclusion was
that further research would be required to determine if inflammation was a
primary disorder in autism or; alternatively, if inflammation and microglial
activation was secondary to neurodegeneration. Dr. Sudhir Gupta at UC Irvine
has a nice model of how the two pathways of neuroinflammation and mito
dysfunction may not be mutually exclusive. This remains to be seen; however,
study of mitochondrial dysfunction and neuroinflammation hold the promise of
treatment development. The two avenues of research deserve funding at the
highest levels.

4. How many Hannah Polings are out there?

The short answer is that nobody knows. However, there is emerging data to
suggest that she is not alone.

Dr. Shoffner will be presenting his experience with 37 patients with
combined autism and mitochondrial dysfunction at the AAN meeting in Chicago
this April. 65% of his referrals are positive for mitochondrial dysfunction.
Of course, his yield is subject to referral bias as a mito expert, so the
prevalence of mitochondrial dysfunction in Autism is surely less than 65%.

The best estimate to date of the prevalence of mitochondrial dysfunction in
autistic patients comes from Oliviera et al. in a population of 120, 5 of 69
(or 7.2%) showed mitochondrial dysfunction. If this is generalized to the US
estimate of 1 million patients with ASDs, then the number of kids like
Hannah could be 72,000! Isn’t this worth further study?

Dr. Shoffner furthermore advocates, along with us, that vaccination is
important even for kids with mitochondrial dysfunction. I would argue that
you should not give nine at one time and that none of them should contain
Thimerosal (mercury).

5. Thimerosal—On or Off the Table?

I don’t want to dwell on mercury, as this theory is not why HHS conceded
Hannah’s case (imo). Dr. DiContanzo just wrote an interesting blog about how
his opinion of mercury in vaccines has changed
(http://drugs.about.com/b/2008/03/08/mercury-in-vaccines-and-autism-the-burd
en-of-proof-may-shift.htm).

My opinion is that mercury is a potent neurotoxin. Therefore, don’t inject
it into kids! Interestingly, basic research studies have shown that
Thimerosal toxicity occurs through mitochondrial pathways. Officials point
to the large epidemiology studies as proof that there is no link between
thimerosal and autism. However, these studies are not powered to disprove
the null hypothesis when considering that the mitochondrial autistic
population may be just a small percent of the case totals. Remember that
while the CDC sponsored Verstraten study is hyped as a negative study, it
DID find a statistically significant increase in childhood tics in those
exposed to higher doses of thimerosal.

6. Hannah was destined to regress? Or was she?

Some experts have already stated that ‘mitochondrial disease’ is
degenerative so the vaccine reaction was just the start of an inevitable
decline. This was neither the opinion of Dr. Richard Kelley at KKI nor Dr.
John Shoffner. In fact, the markers that led us down the mitochondrial trail
(inc AST but not ALT, low serum bicarbonate, and slight increased CK,
increase in the alanine to lysine ratio on PAA) are no longer present.
Furthermore, in our pilot study (unpublished but mentioned in the J child
neurol paper), Dr. Frye (the statistician for our study and also a child
neurologist) found a non-significant trend that AST decreased toward normal
with increasing age. With further studies we hoped to examine the hypothesis
that this abnormality may be representative of a developing/immature
biochemical pathway present in some children.

7. Triple Hit Hypothesis—#1Underlying genetic susceptibility #2Insult must
occur during specific developmental period #3 A certain vaccination or
combination thereof is the environmental trigger (?vaccine component like
thimerosal ?direct immune stim/fever reaction ?live virus reaction?)

The implication is that Hannah’s type of autism requires a genetic
susceptibility and properly timed insult to manifest disease. We have not
subjected Hannah to another muscle biopsy or re-examined ox phos functional
assays that were published in the paper. I can inform your readers though
that the serum biochemical markers have resolved, growth resumed and
continues along a normal trajectory, and there have been no other episodes
of regression since 2000. We are however left with autism and later in 2006,
epilepsy.
It is recommended that studies be initiated immediately to screen siblings
of cases to identify biochemical markers so as to identify potential
screening tests.

I agree with the mainstream that my daughter’s case has raised many
intelligent discussions and questions. I’m very proud of her for starting
this discussion. Our hope is that further research into this case and others
like it, we will be also to find screening tests to prevent what happened to
my daughter from happening to anybody else.

(Dr. Poling acknowledges the editorial comments and insightful suggestions
of Dr. Richard E. Frye. He also would like to declare his conflicts of
interest. First of all, he is the father of Hannah Poling. Dr. Poling has
also accepted consultancy or speakers honoraria from Pfizer, Eisai,
Ortho-McNeil, Biogen, Teva, Immunex (now Amgen), and Allergan.)

PS While I thought it useful to clarify some of the neurological issues
raised by the government’s concession of my daughter’s case, please
understand that I will not be able to respond to individual comments posted.
Thank-you. Jon