# Holt v. Secretary of Health and Human Services

> United States Court of Federal Claims · July 16, 2015

URL: https://www.frixlaw.com/law-library/cases/2817851

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** July 16, 2015
- **Precedential status:** Published
- **Opinion:** Opinion
- **Judges:** Denise Kathryn Vowell
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/2817851

## How later opinions describe it (automated extraction)

- discussing the limited value of case reports
- observing that Congress designed the Vaccine Injury Table to be “overinclusive.”
- rejecting the assertion that lack of any other identified cause can demonstrate vaccine causation, even when the vaccine in question has been associated with the injury claimed and the temporal relationship is appropriate
- emphasizing that a statement of a treating physician is not “sacrosanct” and can be rebutted

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 05-0136V
Filed: June 24, 2015
For Publication

********************************
LAURA HOLT, parent of *
A.H.T., a minor, * Autism; Entitlement;
* Mitochondrial
Petitioner, * Disorder;
* Hepatitis B Vaccine;
v. * Encephalopathy;
* Colic; Gastrointestinal
SECRETARY OF THE DEPARTMENT * Problems; Diagnosis;
OF HEALTH AND HUMAN SERVICES, * Timing; Lack of Logical
* Connection
Respondent. *
*
********************************

Andrew D. Downing, Van Cott & Talamante, PLLC, Phoenix, AZ for petitioner.

Alexis B. Babcock, U.S. Dept. of Justice, Washington, DC, for respondent.

DECISION1

Vowell, Chief Special Master:

On January 21, 2005, Laura Holt [“Ms. Holt” or “petitioner”] filed a “short-form”
petition seeking compensation under the National Vaccine Injury Compensation
Program, 42 U.S.C. §300aa-10, et seq.2 [“Vaccine Act” or “Program”] on behalf of her

1 The E-Government Act of 2002, Pub. L. No. 107-347, 116 Stat. 2899, 2913 (Dec. 17, 2002), requires
that this decision be publicly available. In accordance with Vaccine Rule 18(b), petitioner has 14 days to
identify and move to redact medical or other information, the disclosure of which would constitute an
unwarranted invasion of privacy. If, upon review, I agree that the identified material fits within this
definition, I will redact such material from public access.

2The National Vaccine Injury Compensation Program [“Vaccine Program”] is set forth in Part 2 of the
National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. § 300aa-10 et seq. (2006). All citations in this decision to individual sections of the Vaccine Act
are to 42 U.S.C. § 300aa.
daughter, A.H.T. Such petitions, authorized by Autism General Order #1,3 alleged in a
summarized fashion that the vaccinee has a disorder on the autism spectrum.4

However, petitioner now appears to be repudiating ASD as the claimed injury,
while nevertheless asserting that the neurological symptoms relied on for the ASD

3 By electing to file a Short-Form Autism Petition for Vaccine Compensation, petitioner alleged that:

As a direct result of one or more vaccinations covered under the National Vaccine Injury
Compensation Program, the vaccinee in question has developed a neurodevelopmental
disorder, consisting of an Autism Spectrum Disorder or a similar disorder. This disorder
was caused by a measles-mumps-rubella (MMR) vaccination; by the “thimerosal”
ingredient in certain Diphtheria-Tetanus-Pertussis (DTP), Diphtheria-Tetanus-acellular
Pertussis (DTaP), hepatitis B, and Hemophilus Influenza Type B (Hib) vaccinations; or by
some combination of the two.

Autism General Order #1, 2002 WL 31696785 (Fed. Cl. Spec. Mstr. July 3, 2002), Exhibit A, Master
Autism Petition for Vaccine Compensation at 2. In filing a short-form petition, petitioner joined the
Omnibus Autism Program [“OAP”]. A more detailed discussion of the OAP and the effects of joining it can
be found in the OAP test case decisions. See, e.g., Dwyer v. Sec’y, HHS, No. 03-1202V, 2010 WL
892250, at *3 (Fed. Cl. Spec. Mstr. Mar. 12, 2010).

4I use the abbreviation “ASD” to refer to the broad category of autism spectrum disorders. These
disorders were defined for petitioner by Dr. (Ph.D.) Laurie Grimes, a clinical psychologist who evaluated
A.H.T. in 2004. Her report, which was provided to Ms. Holt (see Petitioner’s Exhibit [“Pet. Ex.”] 17, pp.
154-55), stated:

Autism, also referred to as pervasive developmental disorder (PDD) or autism spectrum
disorder (ASD), is a term for a spectrum of handicaps in which there are impairments in
social communication. The level and nature of impairment varies from child to child so
that no two people with autism have the same blend of communication challenges.
Social communication includes behaviors such as facial expression, emotional gesture,
melody (prosody) of speech, and knowledge of social rules (pragmatics) of
communication that are used in human interaction to convey cognitive and emotional
information. Social communication skills develop early in life and are a primary mode for
learning about the environment through non-verbal means. Autism is sometimes
associated with a lack of language skills, odd and stereotyped behaviors, profound
inability at social interaction, and/or mental retardation. While such children may have
varying degrees of some of these problems, others have normal intelligence and
language and only mild deficits in social interaction skills. What is shared by all people
with autism are handicaps in dealing with other people due to their inability to use and
understand common verbal, gestural, and expressive communication. Current research
uses four domains to evaluate social communication: affective reciprocity (one's ability
to send and receive social signals to others using facial expression, tone of voice, and
social and emotional gestures), emotional joint attention (one's efforts to share
interests with others – show things, talk reciprocally, smile socially, direct others’ attention
to objects of interest, show affection), verbal joint attention (one's ability to be verbal
social[ly], to use give-and-take conversation, to show interest in others), and theory of
mind (in young children seen as social imagination; one's ability to converse
appropriately; one's ability to infer another's intentions).

Id., pp. 144-45 (emphasis original).

2
diagnosis constitute at least part of the compensable injury.5 An amended petition,
which does not use the terms “ASD” or “autism,” was filed on September 22, 2011.6
This petition alleges that, as the result of a hepatitis B vaccination received on April 4,
2002, A.H.T. experienced a variety of symptoms affecting her feeding, sleeping,
temperament, and gastrointestinal function. Petition at 1. However, petitioner does not
appear to be claiming that these particular symptoms are the injury for which she seeks
compensation. Rather, she contends that this vaccination “significantly aggravated an
underlying mitochondrial disorder,”7 presumably with the manifestations being the
symptoms exhibited following the vaccination, and causing “the resulting
encephalopathic event.” Petition, ¶¶ 15-16. The reference to an “encephalopathic
event” is ambiguous, in that it could refer to symptoms after the vaccination or the
behavioral symptoms that resulted in her sensory integration disorder diagnosis many
months after the vaccination, and other diagnoses, including ASD, over the ensuing
years.8

5 Ms. Holt claimed not to understand the term “autism spectrum disorder” during her testimony.
Transcript [“Tr.”] at 73. However, throughout A.H.T.’s medical records, Ms. Holt and A.H.T.’s physicians
used the terms “autism,” “pervasive developmental disorder,” and “PDD-NOS.” See, e.g., Pet. Exs. 47, p.
2052 (intake form for Dr. Andrew Levinson, dated May 23, 2010, with petitioner indicating that A.H.T. had
been diagnosed with autism and pervasive developmental delay-not otherwise specified and that she was
seeking biomedical treatment for that condition); 17, p. 145 (notation in report provided to A.H.T.’s
parents that one test had shown her to be at “moderate risk for autism spectrum disorder”). Moreover,
Ms. Holt frequently reported that her maternal uncle had autism, a disorder on the autism spectrum,
reflecting her understanding of the condition and term. See, e.g., Pet. Exs. 39, p. 1826; 41, p. 1832.
Other health care providers used the term “autism spectrum” in A.H.T.’s medical records. See, e.g., Pet.
Exs. 30, p. 1231 (noting that delayed sleep was seen in “individuals on the autism spectrum”); 44, p. 1878
(letter indicating A.H.T. had an original diagnosis “on the autism spectrum”). The pages of each exhibit
were not individually numbered, resulting in the large page numbers for later-filed exhibits.

6Hereinafter, unless the context clearly indicates otherwise, any references to “petition” are to this
amended petition.

7 A mitochondrial disorder is one affecting the function of the mitochondria—organelles contained in

varying numbers in virtually every cell of the body. Tr. at 424-25. The mitochondria use oxygen and food
to produce adenosine triphosphate [“ATP”], the primary source of energy for all bodily functions, through
a process labeled “the respiratory chain” or “electron transport chain” [“ETC”]. Tr. at 300, 424-25.
Problems with energy production in the ETC can occur as the result of genetic defects in either the
mitochondria’s own DNA [“mtDNA”] or in the DNA found in the nucleus of cells themselves [“nuclear DNA”
or “nDNA”]. Tr. at 430. The sole function of the mtDNA is to make proteins that are components of the
ETC. Tr. at 433. When a DNA defect results in clinical symptoms, a person is said to have a “primary”
mitochondrial disease or defect. Other bodily processes including metabolic disorders, hypoxia, and
some drugs may also affect the ETC, causing diminished ETC function, producing “secondary
mitochondrial dysfunction.” Tr. at 398, 428-29. In the absence of an identified genetic defect or the
presence of clusters of symptoms fitting a known mitochondrial syndrome, diagnosing a mitochondrial
disorder is difficult. See generally, Pet. Ex. 79 (expert report of Dr. Frances Kendall); Respondent’s
Exhibit [“Res. Ex.”] G (expert report of Dr. Shawn McCandless). Doctor Kendall’s report indicated that the
“vast majority of pediatric mitochondrial disease” involves nDNA, with about 10% related to defects in
mtDNA. Pet. Ex. 79 at 2494.

8 The filed medical records do not establish when and how A.H.T. was first diagnosed with an ASD. At
the hearing, petitioner used several pages of an intake form dated August 12, 2005, that she completed
for Dr. Phillip DeMio. See Petitioner’s Trial Exhibit [“Pet. Tr. Ex”] 1. This document contains petitioner’s
assertion that A.H.T. was diagnosed with pervasive developmental delay in September 2004 by Dr.

3
The amended petition in this case and petitioner’s apparent disavowal of an ASD
diagnosis appear to be part of the trend by some former OAP petitioners to re-
characterize their children’s diagnoses as something other than ASD, in an attempt to
render irrelevant the impressive body of evidence produced in the OAP test cases
establishing that vaccines are exceedingly unlikely to be responsible for ASD.9 The
filing (or amendment) of claims for compensation based on the particular theory
advanced in this case—that a vaccine significantly aggravated an underlying
mitochondrial disorder, causing manifestation of ASD or a similar neurological
disorder—stems from another, and widely-publicized, vaccine injury case. In that case,
discussed more extensively in n.76 and in Section IV, Part B(1)(a) below, a child with a
mitochondrial disorder and autistic symptoms received compensation based on her
presentation with severe neurological symptoms within the Table injury10 period for the
vaccines that she received.

Vinjay Puri. Doctor Puri, a pediatric neurologist, evaluated A.H.T. on September 16, 2004. The records
from this visit do not reflect a pervasive developmental disorder or delay diagnosis. Rather, he diagnosed
a sensory integration disorder, night terrors, and a mild language loss or regression. Pet. Ex. 31, p. 1265.
The intake form also reflects that someone in the Jefferson County Public School system diagnosed
A.H.T. with autism in February 2005. Pet. Tr. Ex. 1, p. 1. The records reflecting this diagnosis were not
filed and thus it is unclear what diagnostic testing, if any, led to the school district’s conclusions. I note
that in October 2004, Dr. Grimes, a clinical psychologist, administered standard diagnostic tests for ASD.
She concluded that A.H.T. “has demonstrated behaviors that were suggestive of ASD, though [the test
results] do not support that diagnosis at this time.” Pet. Ex. 17, p. 146. This is the only mention of
diagnostic testing for ASD in the record. However, ASD, autism, and PDD-NOS (pervasive
developmental disorder-not otherwise specified) diagnoses appear throughout A.H.T.’s medical records
after 2005. See, e.g., Pet. Exs. 16, pp. 133, 142; 19, p. 214; 27, pp. 629-30; 31, pp. 1245-46; 38, p.
1689; 51, pp. 2188-89. I also note that in Jan. 2005, just days after filing the short-form petition in this
case and thereby joining the OAP, petitioner and Mr. Tipton revoked permission for Dr. Grimes to disclose
A.H.T.‘s negative test results for autism to the school system. Pet. Ex. 17, pp. 161-62. Three months
later, they wrote Dr. Grimes, requesting that she “correct” her October 2004 evaluation. Id., pp. 157-58.
In doing so, they pointed out the presence of “very abnormal autistic-like behaviors” in A.H.T. Id., p. 158.
Both of respondent’s experts were unwilling to opine that A.H.T. had ASD, in view of the lack of
diagnostic testing, but noted the presence of symptoms commonly seen in children with ASD. Tr. at 537,
545, 560-61.

9 Since January 2007, I have been one of the small group of special masters assigned primarily to the
“autism docket.” I presided over two of the six OAP test case hearings and issued decisions in each.
These lengthy decisions were necessitated by one of the purposes for the omnibus proceeding—to
create a body of evidence that could be relied upon to resolve the remaining OAP cases like this one—as
well as to evaluate the causation theories presented in the context of the individual test cases. After
appellate review of the test case decisions was completed, I oversaw the effort to resolve the remaining
open OAP cases. The majority of these cases were dismissed based on petitioners’ motions. However,
some petitioners elected to proceed with their cases, either on a new theory of causation or based on
injuries other than ASD. Most of the OAP petitioners who have continued to press claims for vaccine
compensation have presented variations on the theory presented here—that vaccines “significantly
aggravated an underlying mitochondrial disorder, resulting in autism-like symptoms.”

10A “Table” injury is an injury listed on the Vaccine Injury Table, 42 C.F.R. § 100.3, corresponding to the
vaccine received within the time frame specified.

4
Prior to the hearing, petitioner filed a joint submission of the parties, listing the
jurisdictional and factual issues upon which they agreed. The parties indicated that
“[t]he issue to be decided is whether the vaccinations [A.H.T. received] (either alone or
in combination) caused-in-fact her subsequently diagnosed developmental,
neurological, or mitochondrial issues.” Joint Submissions at ¶ 7. This joint submission
clarifies the injuries for which compensation is sought.

Regardless of how A.H.T.’s condition is characterized, petitioner has the burden
to demonstrate by preponderant evidence that a vaccine actually caused or significantly
aggravated A.H.T.’s condition.11 For the reasons set forth below, I find that petitioner
has failed to do so and thus is not entitled to compensation.

I. Procedural History.

After the short-form petition was filed, A.H.T.’s case, like most other OAP cases,
remained on hold until litigation in the test cases was completed.12 After the resolution
of the test cases in 2010, the special masters began the process of determining how the

11 Because the Vaccine Injury Table, 42 C.F.R. § 100.3, lists no injuries for the hepatitis B vaccine (the
only vaccine A.H.T. ever received), petitioner cannot avail herself of any presumption in favor of
causation. Her burden of proof is the traditional tort burden: she must produce preponderant evidence
that a vaccine caused or significantly aggravated A.H.T.’s condition. 42 U.S.C. § 300aa-13(a)(1)(A);
Moberly v. Sec’y, HHS, 592 F.3d 1315, 1322 (Fed. Cir. 2010) (citing de Bazan, 539 F.3d 1347, 1351
(Fed. Cir. 2008); Pafford v. Sec’y, HHS, 451 F.3d 1352, 1355 (Fed. Cir. 2006); Capizzano v. Sec’y, HHS,
440 F.3d 1317, 1320 (Fed. Cir. 2006); Althen v. Sec’y, HHS, 418 F.3d 1274, 1278 (Fed. Cir. 2005)).
Loving v. Sec’y, HHS, 86 Fed. Cl. 135, 144 (2009), established a methodology for evaluating a significant
aggravation claim. The first three steps require the fact-finder to: (1) determine the vaccinee’s condition
prior to administration of the vaccine; (2) determine the vaccinee’s current condition or condition following
the vaccine; and (3) decide whether the vaccinee’s condition was significantly worsened after the
vaccination. The remaining three steps involve the application of Althen in a significant aggravation
context, and require the petitioner to produce preponderant evidence of (4) a medical theory causally
connecting the significantly worsened condition to the vaccine; (5) a logical sequence of cause and effect
demonstrating that the vaccine was the reason for the significant aggravation; and (6) a proximate
temporal relationship between the vaccine and the significant aggravation. This methodology has been
cited with approval by the Federal Circuit. W.C. v. Sec’y, HHS, 704 F.3d 1352, 1357 (Fed. Cir. 2013).

12The Petitioners’ Steering Committee [“PSC”], an organization formed by attorneys representing
petitioners in the OAP, litigated six test cases presenting two different theories on the causation of ASD.
Decisions in each of the three test cases pertaining to the PSC’s first theory rejected the petitioners’
causation theories. Cedillo v. Sec’y, HHS, No. 98-916V, 2009 WL 331968 (Fed. Cl. Spec. Mstr. Feb. 12,
2009), aff’d, 89 Fed. Cl. 158 (2009), aff’d, 617 F.3d 1328 (Fed. Cir. 2010); Hazlehurst v. Sec’y, HHS, No.
03-654V, 2009 WL 332306 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff’d, 88 Fed. Cl. 473 (2009), aff’d, 604
F.3d 1343 (Fed. Cir. 2010); Snyder v. Sec’y, HHS, No. 01-162V, 2009 WL 332044 (Fed. Cl. Spec. Mstr.
Feb. 12, 2009), aff’d, 88 Fed. Cl. 706 (2009). Petitioners in Snyder did not appeal the decision of the U.S.
Court of Federal Claims. Decisions in each of the three “test cases” pertaining to the PSC’s second
theory also rejected the petitioners’ causation theories, and petitioners in each of the three cases chose
not to appeal. Dwyer, 2010 WL 892250; King v. Sec’y, HHS, No. 03-584V, 2010 WL 892296 (Fed. Cl.
Spec. Mstr. Mar. 12, 2010); Mead v. Sec’y, HHS, No. 03-215V, 2010 WL 892248 (Fed. Cl. Spec. Mstr.
Mar. 12, 2010). The petitioners in each of the three Theory 2 cases did not seek review of the special
masters’ decisions.

5
approximately 4,800 remaining OAP claims would be resolved by ordering each
claimant to indicate if he or she wished to proceed or exit the Vaccine Program.

On March 15, 2011, petitioner filed a motion to substitute Mr. Downing as her
attorney of record. I granted the motion and, interpreting it as evincing petitioner’s intent
to proceed with her claim, I ordered her to file an amended petition that asserted the
specific basis for her causation claim. Order, issued Apr. 4, 2011. Petitioner complied
on September 22, 2011, filing several statements or declarations and some medical
records and other evidence along with the petition. See Pet. Exs. 1-6. Over the next
six months, petitioner filed additional medical records, statements and affidavits, 13 and
some medical literature.14 Petitioner filed a statement containing an opinion on
causation and the curriculum vitae [“CV”] of Dr. Levinson on February 29, 2012 and a
similar opinion and CV from Dr. Phillip C. DeMio on March 12, 2012.15 See Pet. Exs.
59-60; 62-63. She filed the expert report and CV of Dr. Fran D. Kendall on May 15,
2012. See Pet. Exs. 79-80.

In July 2012, respondent filed her Rule 4(c) report; and the expert reports and
accompanying medical literature from Drs. Max Wiznitzer and Shawn McCandless. See
Respondent’s Rule 4(c) report; Respondent’s Exhibits [“Res. Exs.”] A-Q. After
consultation with the parties, I scheduled an entitlement hearing in Washington, D.C.
from February 13-15, 2013. Order, issued Aug. 16, 2012; Pre-Hearing Order, issued
Aug. 31, 2012.

Four physicians, Drs. DeMio, Kendall, McCandless, and Wiznitzer, testified in
person. Petitioner, Garrick Tipton (A.H.T’s father), and Mrs. Christy Holt [“Christy Holt”]
(A.H.T.’s aunt) also testified in person. I heard telephonic testimony from Mrs. Mary Jo
Holt Dunn (A.H.T.’s maternal grandmother), and Ms. Amy Hunter, the doula who
assisted with A.H.T.’s birth.16

Based on testimony at the hearing about the availability of video evidence
supporting petitioner’s case (see Tr. at 116, 121), I ordered petitioner to file video
records of A.H.T. from birth to three years of age. Three DVDs were filed on April 4,
2013 as Pet. Tr. Ex. 3.17 Post hearing briefs were received from petitioner on May 9,
2013, and from respondent on June 17, 2013. On September 3, 2013, I also filed a
medical journal article, N. Wolf & J. Smeitink, Mitochondrial disorders: a proposal for
13 See Pet. Exs. 73-78.

14 See Pet. Exs. 67-71.

15The filed documents are titled “statements” rather than expert reports, although they do contain
opinions on vaccine causation.

16Petitioner intended to call Dr. Levinson to testify telephonically, but efforts to reach him were not
successful. See Tr. at 284, 290.

17Subsequent references to the videos will identify them as Video 1, Video 2, and Video 3. Pertinent
provisions will be identified by the date of the recording and elapsed time from the start of the video.

6
consensus diagnostic criteria in infants and children, Neurol. 59(9): 1402-05 (2002)
[cited hereinafter as “Wolf & Smeitink, Court Exhibit [“Court Ex.”] I, and provided the
parties and their experts an opportunity to comment on the exhibit. See ECF # 90; Pet.
Resp. to Court’s Order and Ex., filed on September 30, 2013; Res. Ex. S. This article
sets forth the diagnostic criteria ostensibly used by the physician who diagnosed A.H.T.
with a mitochondrial disorder.

II. Summarized Medical History.

A.H.T. was born in 2002, following a normal pregnancy. Tr. at 11-12; Joint
Submissions at ¶ 2, filed on January 22, 2013. She was delivered at home, with the
assistance of a midwife, Juliet Dietsch, and doula, Amy Edwards Hunter. See
Petitioner’s Exhibits [“Pet. Exs”] 77, 82 (statements of Amy Edwards Hunter18 and Juliet
Dietsch). A.H.T. had Apgar scores of 7 and 9.19 Id. Both Ms. Dietsch and Ms. Hunter
said that A.H.T. was healthy, alert, and nursing well shortly after birth. Id.

At her initial visit to her pediatrician, Dr. Rhonda Buttleman, A.H.T. was alert and
her physical examination was normal. Pet. Ex. 58, p. 2330.20 A.H.T.’s parents
indicated that she was nursing every few hours and was voiding and stooling frequently.
Id.; Tr. at 109-10 (testimony of Mr. Tipton). Ms. Holt testified that A.H.T. was sleeping
18-20 hours per day and that she had gained 10 ounces since birth. Tr. at 16-17; see
also Pet. Ex. 58, pp. 2313 (birth weight), 2330 (weight at five days of age).

The only two vaccinations A.H.T. ever received (two hepatitis B vaccinations)
were administered before she was six weeks old. She received the first at this initial
pediatric visit. Pet. Ex. 58, pp. 2313, 2326, 2330. The documentary evidence and
testimony establish that, within days after the first vaccination, A.H.T. developed
problems with constipation and that she cried more often and more robustly than many
infants. Tr. at 22-23, 56 (Ms. Holt); 129-30 (Mr. Tipton); Pet. Exs. 52, p. 2234; 34, p.
1287. Her sleeping patterns changed and Ms. Holt testified about problems with
breastfeeding. See, e.g., Tr. at 20-22, 24, 29, 32, 56, 91-92. These issues are
discussed in more detail in Section V, Part B(4), below.

Mr. Tipton did not remember any specific reactions to the second vaccination.
He testified that A.H.T. “continued to worsen as time went on,” but stopped short of
18 Petitioner filed two statements from Ms. Hunter. The first statement was labeled “Statement of Amy
Edwards” and filed on September 22, 2011 as Pet. Ex. 3. The second statement was labeled “Statement
of Amy Edwards Hunter” and filed on April 16, 2012 as Pet. Ex. 77. The substance of the two statements
is the same.

19 The Apgar score is a numerical assessment of a newborn’s condition (with lower numbers indicating
problems), usually taken at one minute and five minutes after birth. The score is derived from the infant’s
heart rate, respiration, muscle tone, reflex irritability, and color, with from zero to two points awarded in
each of the five categories. See DORLAND’S ILLUSTRATED MEDICAL DICTIONARY (32d ed. 2012)
[“DORLAND’S’”] AT 1682; NELSON TEXTBOOK OF PEDIATRICS (19th ed. 2011) [“NELSON’S ”] at 536-37.

20 Doctor Buttleman’s records were also filed as Pet. Ex. 4.

7
saying that she regressed or lost skills. Tr. at 131, 133. Ms. Holt also testified that
A.H.T. got worse, but more as a progression of the symptoms she was already
experiencing.21 Tr. at 37, 63. However, prior to their testimony, A.H.T.’s parents told
Dr. John D. Shoffner, the physician who diagnosed her with a probable mitochondrial
disorder, that there were no adverse reactions to the second hepatitis B vaccination.22
Pet. Ex. 61, p. 2343.

Over time, some of the problems that first manifested in the days and weeks after
A.H.T’s initial vaccination varied in intensity. The medical records and the testimony of
her parents and other family members about the persistence and intensity of these
problems were often in conflict with other evidence. What seems clear from the record
as a whole is that A.H.T. was a difficult infant and toddler. Behavioral problems
continued as she grew older, and by the time she was six years old, they accounted for
most of the health care visits and support services rendered. See generally, Pet. Exs.
16 (2008 therapy records of Dr. (Ph.D.) Julie Murray, a treating psychologist); 51 (2009
neuropsychological evaluation by Dr. (Ph.D.) Andrew Jones, clinical psychologist); 38
and 54 (2009-12 records from an agency providing behavior analysis and support
services); 7, p. 51 (2010 letter from psychiatrist Dr. Arehanna Barry).23

Notwithstanding any temperament, sleep, feeding, and gastrointestinal issues,
A.H.T. appeared to be developing normally for her first 15-17 months of life. See
generally, Pet. Exs. 52, 58. She gained weight appropriately. See Pet. Ex. 58, p. 2314
(growth chart). She interacted with parents at home and caregivers at her pediatric

21 When pressed for a specific symptom that worsened after the second vaccination, Ms. Holt testified
that A.H.T.’s bowel movements became either rock hard, or loose and foul-smelling, and that nursing got
worse. Tr. at 37. Although she did not attach a specific time frame to onset of loose stools, there is no
corroborating, and much contradictory, evidence for any assertion that A.H.T. experienced loose stools in
close temporal proximity to the second vaccination. Both the contemporaneous medical records and
histories Ms. Holt provided later reflect that A.H.T. suffered from constipation throughout much of her first
year of life. See, e.g., Pet. Exs. 34, p. 1287; 28, p. 1088. The first complaint of loose stools or diarrhea
does not appear until January 10, 2003, when A.H.T., then nine months old, experienced a bout of
enteritis. Pet. Ex. 52, 2233. Thereafter, reports of both diarrhea and constipation were common,
although the diarrhea was generally noted in conjunction with an illness or in response to one of the many
medical interventions she received. See, e.g., Pet. Exs. 52, p. 2230, 23, p. 239 (reporting diarrhea after
treatment with a chelating agent), p. 259 (diarrhea in conjunction with illness (the abbreviation “N/V/D”
representing nausea, vomiting, and diarrhea)); 46, p. 2037 (reporting chronic problems with alternating
constipation and diarrhea at a January 2005 evaluation); 38, p. 1690 (indicating a drug A.H.T. took
caused diarrhea); 19, p. 214 (reporting that dairy products caused diarrhea).

22Petitioner’s Tr. Ex. 1, the intake form for Dr. DeMio (dated August 12, 2005), reflects the two
vaccinations, followed by a comment that she had such severe reactions to these two vaccinations that
no other vaccines had been administered. Id., p. 3.

23 This letter merely reflects A.H.T.’s diagnoses; therapy records from Dr. Barry were not provided,
although there is evidence that she ordered laboratory testing and an electrocardiogram. See Pet. Ex.
37, pp. 1324-26. Medical records contain conflicting references regarding whether A.H.T. was receiving
ongoing psychiatric treatment. See, e.g., Pet. Ex. 7, pp. 54, 67 (Medicaid form from 2010 (dated on p.
67), reflecting continuing treatment by Dr. Berry); 30, p. 1230 (initial note from sleep clinic during same
period in 2010 reflecting that A.H.T. had seen a psychiatrist but that she was no longer doing so).

8
visits. Videos of her taken at one to nine months of age show an alert and interactive
infant engaged with toys, household items, and her parents. See generally Videos 1
and 2.24 At her regular pediatric visits, she was observed to be developing at a pace
appropriate for her age and meeting developmental milestones,25 although she may not
have begun walking until 14-15 months of age, a little later than average. See, e.g., Pet
Exs. 31, p. 1262 (reporting she began walking at 15 months); 46, p. 2037 (reporting that
she began walking at 14 months); but see Pet Ex. 52, p. 2229 (15 month well-child visit
with notation that A.H.T. had been walking for 2 months).

Neither her first pediatrician, Dr. Rhonda Buttleman, who saw her from five days
to about nine months of age, nor the family practice physician, Dr. Richard Hefner,26
who was her primary care provider thereafter, recorded any concerns about her
development during this period. See generally Pet. Exs. 52, 58. Doctor Hefner, who
saw A.H.T. for the first time when she was about five months old for a second opinion
on her gastrointestinal problems, observed her while she was crying. He diagnosed her
with colic. Pet. Ex. 52, p. 2234. Nevertheless, he referred her to a pediatric
gastroenterologist, Dr. Stephen, who diagnosed mild constipation and mild
gastroesophageal reflux when A.H.T. was six months old. Pet. Ex. 34, p. 1287.

24Video 1, from 46:51 (recorded May 18, 2002) through 3:23:22 (recorded October 31, 2002); Video 2,
Set 1, from 00:01 (recorded November 23, 2002) through 15:46 (recorded January 3, 2003).

25 The medical records contain notes and marks on developmental checklists reflecting A.H.T.’s
development. At about five weeks of age, A.H.T. was “alert” and her general appearance was “AFA,” an
acronym for “appropriate for age.” Pet. Ex. 58, p. 2326. She was holding her head up, startling with loud
sounds, grasping fingers, and making noises. Id., p. 2327. At her two month checkup, A.H.T. was
smiling, cooing, holding her head up, focusing on people, and holding a rattle. Pet. Ex. 58, p. 2325. At
her four month well-child visit, she was described as alert, and she was rolling over, holding her head up,
reaching for toys, playing with her hands, looking at a mobile, vocalizing with her parents, and laughing
and smiling. Pet. Ex. 58, p. 2323. Doctor Thomas Stephen, a pediatric gastroenterologist, described her
as a “well developed, well-appearing young infant, happy, in no distress” when she was six months old.
Pet. Ex. 34, p. 1287. At her six month well-child visit, she was sitting with help with no head lag, rolling
over, moving toys from hand to hand, reaching for toys, bearing some weight, laughing and babbling,
turning to sounds, and making sounds. Pet. Ex. 58, p. 2320. At nine months of age, A.H.T. was pulling
up on furniture, sitting by herself, crawling, banging toys, playing patty-cake and peek-a-boo,
understanding words such as “no, no” and “bye-bye,” starting to feed herself, and having stranger anxiety.
Id., p. 2316. She did not yet utter one or two meaningful syllables, and did not respond to her name. Id.
However, according to Dr. Hefner’s assessment, she met all developmental milestones at one year of
age, including the use of some words. Pet. Ex. 52, p. 2232. He also found that she met all
developmental milestones at 15 months of age: she could stand alone, imitate scribbling, play patty cake,
say “mama” or “dada”, and take lids off containers. Id., p. 2229. Doctor Wiznitzer testified that A.H.T.’s
development was normal through 15 months of age. Tr. at 639-42; see also Res. Ex. A at 7.

26Doctor Hefner’s specialty does not appear in his records, but is referred to in the records of clinical
psychologist Dr. Laurie Grimes, who noted that Dr. Hefner was a family practice specialist. Pet. Ex. 17,
pp. 166, 168.

9
Aside from a one-page document from Dr. James O’Dell, a naturopath who saw
A.H.T. in July 2002,27 there were no records from other health care providers covering
A.H.T.’s first 17 months of life.28

Developmental problems were first noted in September 2003 at A.H.T.’s 18
month well-child visit, when Dr. Hefner observed that A.H.T. was not using two-word
phrases, indicating a possible language delay. Pet. Ex. 52, p. 2226. In a history taken
in May 2004, Ms. Holt reported that her concern about A.H.T.’s speech arose at about
18 months of age as well.29 Pet. Ex. 55, p. 2255. Doctor Hefner elected to take a “wait
and see” approach, but by A.H.T.’s next well-child visit six months later when A.H.T.
was about two years of age,30 the delay was still evident. Although the records of this
visit do not reflect it (see Pet. Ex. 52, p. 2226), Dr. Hefner apparently referred A.H.T. for
an evaluation by the state’s early intervention program (see id., p. 2225 (records from
next visit to Dr. Hefner in August 2004, with the chief complaint listed as “here to
discuss therapy recommended [at] 2 yr well baby”)).

The remaining medical treatment and therapy records are extensive, and except
when relevant to one of the issues in controversy, are not set forth in detail in this
decision. In summary, A.H.T. was seen by many different health care providers, in
addition to her primary care provider, Dr. Hefner. These caregivers fall into four

27See Pet. Ex. 73; see also http://drjamesodell.com/index.php/about for information regarding Dr. O’Dell’s
qualifications and practice. Ms. Holt’s journal entries (Pet. Ex. 6, pp. 44-45) also reflect this visit. A
naturopathic doctor is one who subscribes to “a drugless system of health care, making use of a wide
variety of therapies, including hydrotherapy, heat, massage, and herbal medicine.” DORLAND’S at 1233.

28 According to a March 14, 2012 statement, Dr. Sean Brady (a chiropractor who had previously treated
Ms. Holt) began treating A.H.T. on June 13, 2002. Pet. Ex. 66 at 2366. Inexplicably, there are no records
for such treatment before June 9, 2004, and although Dr. Brady indicated that he had billing and medical
coding records establishing the dates of initial and subsequent treatment, the billing and coding records
were not filed. His records of A.H.T.’s treatment from June 2004 onward were filed as Pet. Ex. 48.
Doctor Brady did not opine on causation in this March 2012 statement; he merely stated that he recalled
clearly Ms. Holt’s statements that A.H.T.’s problems began shortly after the vaccination that she received
at five days of age. Pet. Ex. 66 at 2366-67. Given the lack of contemporaneous records of treatment, I
attach little weight to a statement made nearly 10 years after the events in question, particularly as the
statement was made after Dr. Brady read Ms. Holt’s own affidavit. See id. at 2367. There is a journal
entry reflecting a consultation with a Dr. Zieve (Pet. Ex. 6, pp. 40-41) from mid-May 2002, but Ms. Holt
testified that this was a telephonic consultation. Tr. at 62.

29 In a developmental chronology prepared for A.H.T.’s first appointment with Dr. Kartzinel in June 2007,
Ms. Holt reported that she first noticed developmental problems at about 18 months of age. Pet. Ex. 24,
p. 464. In a much later history (provided in May 2010), Ms. Holt reported that her concerns about delayed
development first arose at around 12 months of age. Pet. Ex. 47, p. 2052 (email intake form completed
for Dr. Levinson). She also reported that speech problems were first noted at 18 months of age to Dr.
Cecil in December 2011. Pet. Ex. 56, p. 2287. However, she testified that the report from May 2004
about her concerns first arising at 18 months of age was not correct. Tr. at 70.

30 The filed medical records show no health care provider visits between 18-24 months of age. This six-
month gap appears to be the longest period A.H.T. went without seeing a health care provider, although it
is possible that she saw Dr. Brady during this period. See n.28, supra.

10
categories: therapists addressing specific areas of developmental delay or behavior
concerns; several different types of mental health specialists; at least five alternative or
complementary medicine providers; and specialists who assessed or treated her for
gastrointestinal, urinary, and sleep disorders. Other than Dr. Hefner and Dr. Puri and
his associates, none of the health care providers treated A.H.T. over a long period of
time.

Aside from the primary care records, the records from the early intervention
program provide the evidence prepared closest in time to the events after A.H.T.’s initial
hepatitis B vaccination. Through the early intervention program, A.H.T. received
Applied Behavioral Analysis [“ABA”] therapy31 (which appears to have been termed
developmental intervention [“DI”] services),32 speech and language therapy [“ST”],33 and
occupational therapy [“OT”].34 Each of these records supplies some insights into the
nature and severity of A.H.T.’s developmental delays and behavioral symptoms at
around the time delays became apparent.

31ABA therapy consists of the “application of learning theory based on operant conditioning” and “is the
only intervention recommended by the Surgeon General” for ASD. Dwyer, 2010 WL 892250, at 272,
n.650.

32 No therapy records specifically identified as ABA therapy were filed as a part of the early intervention
records, but there are references indicating that A.H.T. received ABA therapy. See, e.g., Pet. Exs. 31, p.
1257 (July 2005 note by Dr. Puri that A.H.T. was “making good progress on ABA therapy”); 24, p. 466
(June 2007 note that she was receiving four to five hours of ABA therapy). The developmental
intervention services she received through Carriage House were likely the ABA therapy referred to in
these records. See, e.g., Pet. Ex. 39, p. 1818 (progress summary in December 2004 for developmental
intervention services rendered since June 2004). Pet. Ex. 25 contains some ABA-type worksheets, but
no actual therapy records.

33See generally Pet. Ex. 18. The initial assessment and testing for speech and language services took
place on May 19, 2004. Pet. Ex. 39, pp. 1822-23. A.H.T., then 26 months old, had the language
comprehension skills of a 9-12 month old, and the expressive language skills of a 6-9 month old, with
scattered skills in both categories up to the 15 month level. Id., p. 1823. However, the developmental
assessment performed two weeks earlier had placed her receptive and expressive language skills in the
12-14 month range. Id., p. 1827.

34 See generally Pets. Ex. 28 and 55. A thorough but concise summary of A.H.T.’s medical history and
level of functioning appears in the September 2004 OT assessment. Pet. Ex. 28, pp. 1088-91. The
evaluator assessed A.H.T.’s fine and gross motor skills at the 17-18 month level. Id., p. 1090. She was
28 months old at that point. In addition to OT, A.H.T. attended a two-week sensory learning center
program at the Therapy Learning Center in Ohio in November 2005, for which no records are available.
Pet. Ex. 49, p. 2178 (letter dated Jan 11, 2012, explaining the lack of records and providing the writer’s
recollection of A.H.T.’s issues). This treatment did not appear to be helpful, as Ms. Holt cancelled a
December 2004 OT appointment explaining that A.H.T. had “regressed” since returning from the sensory
learning program. Pet. Ex. 28, pp. 1083, 1094. Subsequent occupational therapy records do not appear
to be complete, and many of those filed are handwritten and difficult to read, but it appears she received
some OT services from Cardinal Hill in 2005-07 and through the school system in 2007-08. See, e.g.,
Pet. Exs. 27, pp. 630, 705; 16, p. 142. Intensive OT began again in March 2010 and continued into 2011.
See generally Pet. Ex. 27. According to testimony at the hearing, A.H.T. was discharged from OT in 2011
at around the time she began treatment for a mitochondrial disorder. Tr. at 117.

11
She received ST with the early intervention program until she was discharged in
March 2005, because early intervention services terminated at three years of age. Pet.
Ex. 18, p. 184. She continued to receive ST services, according to her primary care
records (see Pet. Ex. 52, p. 2219 (well-child visit at four years of age reflecting
improvements with speech therapy)). There are some speech therapy records from
Cardinal Hill in 2011. See, e.g., Pet. Ex. 27, pp. 606-23. According to testimony at the
hearing, A.H.T. was still receiving ST services. Tr. at 117; See also Pet. Ex. 27, p. 614
(last ST record filed).

A.H.T. began receiving physical therapy [“PT”] services in March 2007, at the
recommendation of Dr. Puri. Pet. Ex. 37, p. 1495. She was discharged from PT in
February 2008, based on her improved functioning. Pet. Ex. 33, pp. 1285-86. She was
re-evaluated in 2009 and received services again until February 2010.35 Pet. Ex. 37,
pp. 1356, 1362-63.

Beginning in late 2010, the primary therapy for addressing A.H.T.’s continuing
behavior problems was behavioral analysis and ancillary support services from
Community Ties and Homeplace Support Services. These problems included defiance,
temper tantrums or meltdowns, verbal aggression, and physical aggression towards
property, pets, and people. Services continued at least into early 2012. See generally
Pet. Exs. 38, 57.36 These very detailed records of A.H.T.’s behavior overlap with the
diagnosis and initiation of treatment for a probable mitochondrial disorder and, thus,
provide insights into the efficacy of such treatment. She also saw her pediatric
neurologist occasionally in 2011 (after more than a year’s break in treatment). See Pet.
Ex. 31, pp. 1234-41 (2011 records), pp.1243-45 (prior visit in August 2009). The
records from Dr. Puri and his associates also overlap with the period when she was
diagnosed and treated for a mitochondrial dysfunction or disorder.

A.H.T.’s treatment by alternative or complementary medical providers began as
early as July 2004 when she saw Anne Linden Steele.37 Another treatment facility, the

35For a brief period beginning in early March 2011, A.H.T. again received PT, but this was due to injuries
sustained in an automobile accident. Services were discontinued in April 2011 because she no longer
seemed to be in pain. See Pet. Ex. 43, pp. 1869-74 (noting inconsistent reports of pain and not enough
objective findings to “legitimate” neck and back pain).

36The records from these two agencies are in the same format, likely reflecting a name change in the
agency rather than two different service providers.

37Ms. Steele’s records do not reflect her specialty, but her website (http://www.annelindensteele.com/)
does (last visited Oct. 23, 2014). Ms. Holt’s journal contains recommendations for treatment by a cranial-
sacral therapist (Pet. Ex. 6, p. 45), and a reference to having tried this therapy appears in the treatment
history provided at the Carriage House (early intervention) intake interview. See Pet. Ex. 39, p. 1826.
There was no evidence discussing what this therapy involved or what specific problems it was intended to
address.

12
Biohealth Centers, was consulted in late 2004 to obtain orders for testing by Great
Plains Laboratory.38 Pet. Ex. 76.

The unidentified health care provider who saw A.H.T. at Integrative Health
Specialists from March-June 2005 assessed her with “candida” (yeast overgrowth),
vitamin and mineral deficiency, and “metal toxicity.”39 A.H.T. was prescribed nystatin
(an antifungal agent) and probiotics. She was also chelated with DMSA during this
period,40 but she developed increased behavior problems during chelation. Pet. Ex. 19,
pp. 213-15. Diagnoses included sensory integration disorder, PDD, central nervous
system dysfunction, delays in fine motor skills, and expressive and receptive language
disorder. Id. at 214.

A.H.T. saw three Defeat Autism Now! [“DAN!”]41 physicians: Dr. DeMio (from
September 2005-November 2008),42 Dr. Kartzinel (from June-October 2007),43 and Dr.
Levinson (beginning in May 2010).44 These physicians, along with the provider from
38Testing by Great Plains laboratory is common in OAP cases. Great Plains laboratories test blood, urine,
and stool for many different minerals, parasites, and nutritional markers. See Pet. Ex. 76, pp. 2462-84
(A.H.T.’s test results).

39 It is unclear from these records which “toxic” metals were of concern.

40 See Snyder, 2009 WL 332044, at *67 n.192. Chelation is the use of chemicals to break the bond
formed between some heavy metals and body tissue. Chelation therapy has been approved to reduce
lead levels in children and for cases of mercury poisoning. Its use in treating children with ASD remains
highly controversial, as there are no controlled studies testing its efficacy and there are significant risks
associated with the treatment. DMSA (dimercaptosuccinic acid) is a water-soluble and relatively non-
toxic chelating agent. Dwyer, 2010 WL 892250, at 103, n.428. DMPS (2, 3–dimercaptopropane–1–
sulfonate).is another chelating agent that A.H.T. received. See Snyder, 2009 WL 332044, at *177, n.506
(internal citations omitted); see, e.g., Pet. Ex. 23, p. 236 (A.H.T.’s treatment with DMPS by Dr. DeMio).

41 DAN! physicians subscribe to “biomedical” treatment protocols developed by the Autism Research
Institute. These treatments may include chelation and other therapies not vetted as efficacious by
controlled clinical studies. Dwyer, 2010 WL 892250, at *20, *178. See also Pet. Ex. 60 at 2340 (Dr.
Levinson’s CV, listing several lectures on “biomedical” approaches to autism treatment he delivered at
Autism Research Institute meetings). Both Drs. Wiznitzer and McCandless characterized Dr. DeMio, Dr.
Kartzinel, and Dr. Levinson as “alternative” or “complementary” health care providers. See Res. Exs. A at
4; G at 1. In his testimony, Dr. DeMio discussed DAN!, the Autism Research Institute, its annual
conferences, and biomedical treatment and training. Tr. at 265-67, 269. According to Dr. DeMio, the
biomedical view of autism considers ASD to be a metabolic, gastrointestinal, immune, and nutritional
disorder often caused by environmental toxins, including vaccines and mercury. Tr. at 233.

42Although the last record from Dr. DeMio in Pet. Ex. 23 is dated November 18, 2008 (id., p. 290; Tr. at
247-48 ),Dr. DeMio began treating her again in August 2012 (see Pet. Ex. 87; Tr. at 247-48).

43Ms. Holt identified Dr. Kartzinel as a “DAN” doctor when providing an updated client history to Easter
Seals in 2007. Pet. Ex. 27, pp. 629-30. According to Dr. Kartzinel’s records, he renewed a prescription
for Singulair for A.H.T. in February 2008, but the last treatment record is dated October 29, 2007. Pet.
Ex. 24, p. 452.

44
According to Ms. Holt, she consulted Dr. Levinson because she wanted to return to the DAN! treatment
methods. Pet. Ex. 47, p. 2055.

13
Integrative Health Specialists, recommended or administered a variety of alternative
treatments including chelation, hyperbaric oxygen therapy [“HBOT”], secretin
infusions,45 intravenous immunoglobulin [“IVIG”],46 vitamin and mineral supplements,
antifungal and antiviral medications, folinate or folinic acid, methyl B-12, and Actos,47
among many others. See generally Pet. Exs. 19, 23, 24, 47. In addition to occasional
in-person consultations, most consultations with Drs. DeMio, Kartzinel, and Levinson
were by telephone or email. Id.; see also Tr. at 242-44 (testimony by Dr. DeMio
acknowledging that many of the medical consultations regarding A.H.T. were
telephonic). A DNA test ordered by Dr. Levinson revealed a single MTHFR mutation
(A1298C).48 A.H.T. stopped seeing Dr. Levinson in 2011 (see Pet. Ex. 47, p. 2058
(most recent treatment)), as Ms. Holt was “uncomfortable with his office policies.” Tr. at
77-78.

45In controlled studies, secretin was found less effective than a placebo in treating ASD and
gastrointestinal symptoms in those with ASD. See Snyder, 2009 WL 332044, at *175.

46IVIG infusions are used to treat individuals with immune system deficiencies or dysfunction. “IVIG”
stands for intravenous immunoglobulin. Neil M. Davis, MEDICAL ABBREVIATIONS, 15th Edition, at 178
(2011). There is no objective evidence that A.H.T. has an immune system problem. Immunoglobulin
testing performed by Great Plains laboratory in 2004 showed her IgA level to be mildly elevated and her
IgM to be slightly low, but Dr. Puri, who reviewed and commented on these results, did not indicate that
the results were of any concern. Pet. Ex. 31, p. 1259. Immunoglobulin testing by Baptist Hospital in 2007
showed results within the reference ranges. Pet. Ex. 15, p. 126. Nevertheless, in 2012 Dr.DeMio began
IVIG therapy. Tr. at 220; Pet. Ex. 87, pp. 2558-59.

47Actos (Pioglitazone Hydrochloride) is used in the treatment of type 2 diabetes, acting to decrease
insulin resistance. See PHYSICIANS’ DESK REFERENCE [“PDR”] (66th ed. 2012), at 2805. There are
no tests or diagnostic records showing that A.H.T. had type 2 (or any other type of) diabetes.

48 MTHFR stands for methylenetetrahydrofolate reductase, which is a protein involved in getting rid of
homocysteine. According to Dr. McCandless, A.H.T.’s MTHFR test result is unimportant. A couple of
common polymorphisms had been identified in this MTHFR gene that were once thought to increase the
risk of having elevated homocysteine, a risk factor for blood clots. When testing based on this hypothesis
began, a lot of people with the altered genes were found, but no increased risk for blood clots or other
problems. It has nothing to do with the folate deficiency later found in A.H.T.’s cerebrospinal fluid. Tr. at
602. A polymorphism is a DNA change, but not one that is disease causing or with functional
implications. A common polymorphism is one found in more than 1% of the population. Tr. at 600-02.

14
In addition to treatment by the DAN! physicians, A.H.T. saw a developmental
pediatrician, several pediatric neurologists,49 several child psychologists,50 and a
psychiatrist.
A comprehensive neurodevelopmental evaluation was performed in early 2005 at
the Weisskopf Child Evaluation Center [“Weisskopf Center”], a part of the University of
Louisville School of Medicine Department of Pediatrics. Pet. Ex. 46. Doctor Gail
Williams, a developmental pediatrician, diagnosed A.H.T. with a regulatory disorder51
and with central nervous system dysfunction, as “manifested by toe walking and
decreased muscle tone.” Pet. Ex. 46, pp. 2038, 2041, 2045. Like Dr. Grimes, she
concluded that A.H.T. did not meet the diagnostic criteria for autism, based on her
“better developed social skills” and “clear evidence of joint attention.” Id., pp. 2038,
2041.

49She saw the first pediatric neurologist, Dr. James McKiernan, in August 2004 to determine if she had
been experiencing seizures. He concluded that it was “unlikely” she was having seizures. Pet. Ex. 40, p.
1831. She initially saw Dr. Puri, the pediatric neurologist who treated her for the longest period of time, in
September 2004, also for possible seizures. He ordered several diagnostic tests for seizures and
metabolic disorders. Pet. Ex. 31, p. 1265 (tests ordered). A.H.T. continued to see Dr. Puri, at least into
2011. Testing, including an EEG and MRI, failed to find any evidence of a seizure disorder. See Pet. Ex.
31, pp. 1273, 1275. Much later, some of the “seizure-like” spells were identified as self-stimulatory
behavior. See Pet. Ex. 16, pp. 136-37. One of Dr. Puri’s associates, Dr. A.C. Anikumar, saw A.H.T. in
July 2007 regarding possible seizures or a movement disorder, but concluded that the movements were
most probably behaviorally related and non-epileptic in nature. Pet. Ex. 31, p. 1249. However, Dr.
DeMio’s records contain several references to A.H.T. experiencing “extrapyramidal” signs or effects which
could possibly be related to seizures (involuntary movements) (abbreviated “EX SXS” on several
records), based on viewing videos of A.H.T. in 2006. See, e.g., Pet. Ex. 23, pp. 245, 247-48, 250.
A.H.T.’s neurologist apparently viewed the same video records and told A.H.T.’s parents that the videos
showed normal child behavior. See id., p. 245.

50These included Dr. (Ph.D.) Grimes, the clinical psychologist who concluded in 2004 that A.H.T. did not
meet the criteria for an ASD diagnosis (Pet. Ex. 17, p. 146); Dr. (Ph.D.) Julie Murray, who saw A.H.T. or
her parents for nine sessions between July and October 2008 for symptoms of anxiety, obsessiveness,
impulsivity, and poor concentration, and for assistance in managing temper tantrums and symptoms of
anxiety. Pet. Ex. 16, pp. 133 (initial assessment) and 134-41; Dr. (Ph.D.) Andrew Jones, a clinical and
forensic psychologist who administered a battery of tests and, in spite of some concerns about their
validity (see Pet. Ex. 51, p. 2195 (expressing concern about “multiple elevated T scores… which were
greater than anticipated”), diagnosed her with a bipolar disorder with depressed mood (id., p. 2210)). She
also saw Dr. Michael Cecil, a clinical neuropsychologist, in late 2011. He conducted many tests and
made recommendations as to educational accommodations and the need for ongoing OT and ST. Pet.
Ex. 56, pp. 2286-89.

51I was unable to find a clear definition for regulatory disorder, as the diagnosis does not appear in
standard medical references such as DORLAND’S or NELSON’S or in either the 4th or 5th editions of the
DIAGNOSTIC AND STATISTICAL MANUAL OF MENTAL DISORDERS. According to an article posted on the
National Institutes of Health website (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2765395/),
“Regulatory Disorders of Sensory Processing (RDSP) constitute a specific diagnostic category in the
Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood
(DC: 0-3R). . . .Children with regulation disorders exhibit specific symptom constellations in sensory,
motor and behavioral domains.” Tr. at 686-87. Doctor Wiznitzer testified that the regulatory disorder
diagnosed by Dr. Williams explained A.H.T.’s behavior problems. Tr. at 687-88.

15
By 2007, Dr. Puri’s practice seemed to have accepted a pervasive
developmental disorder diagnosis, although it is unclear whether this was based on the
history of the diagnosis provided by Ms. Holt or on an independent assessment of
A.H.T.’s functioning. See Pet. Ex. 31, pp. 1246 (noting a previous diagnosis of “sensory
integration disorder/PDD” in the history section of the office notes in 2007), 1249
(recording diagnoses of pervasive developmental disorder, sensory integration disorder,
autistic disorder, and behavioral disorder later in 2007).

In February 2009, when A.H.T. was almost seven years old, Dr. Jones diagnosed
her with a bipolar disorder and depression and, according to Dr. Puri, he referred A.H.T.
to Dr. Barry. Pet. Exs. 31, p. 1243; 51, p. 2207. In August 2009, Dr. Puri recorded
diagnoses of PDD-NOS, bipolar affective disorder, learning disability, central auditory
processing disorder, and insomnia. Doctor Puri seemed particularly concerned about
A.H.T.’s sleeping difficulty, since lack of sleep “can be a problem in some
temperamental children like her.” Pet. Ex. 31, p. 1245.

A.H.T. also received care and treatment for several medical issues not directly
related to her behavior problems. She had an endoscopy and colonoscopy in the spring
of 2007. Pet. Ex. 12, p. 102. She also saw a pediatric urologist in 2008 for frequent
urinary tract infections [“UTI”]. Pet. Ex. 14, p. 116.52 She saw a pediatric cardiologist,
Dr. Roddy McDowell, in 2009, based on a reportedly abnormal electrocardiogram. After
additional testing, he concluded that A.H.T.’s heart was structurally normal, in spite of
an “innocent heart murmur.” Pet. Ex. 13, pp. 105-06. She saw Dr. McDowell one more
time in July 2010 when he made a similar assessment. Id., p. 103.

Beginning in June 2010, A.H.T. was evaluated and treated at the Behavioral
Sleep Medicine Clinic, a part of the University of Louisville’s Pediatric Sleep Medicine
Center, where she saw Dr. (Ph.D.) Sarah Honaker, a clinical psychologist, and Dr.
Vincent McCarthy. The records from this clinic reflect a significant behavioral
component to A.H.T.’s widely varying sleep hours, and a great degree of difficulty in
getting A.H.T.’s parents to document sleeping patterns and to implement the
recommended changes.53 Ms. Holt sought physiological explanations for A.H.T.’s sleep
difficulties, but laboratory testing did not find any physiological problems, according to

52She had previously been seen by or consulted with Dr. Kartzinel and Dr. Hefner, her primary care
provider, for such infections. See Pet. Exs. 24, p. 452 (telephonic consultation in October 2007 with Dr.
Kartzinel referencing five or six prior UTIs); 52, p. 2216 (sick child visit in February 2008 with Dr. Hefner
for a UTI, mentioning one prior UTI in 2005).

53See Pet. Ex. 30, pp. 1231 (reporting A.H.T. was awake for 26 hours, slept for 6 hours and then awake
for another 22 hours; parents unable to keep sleep log); 1228-29 (parents resistant to melatonin use in
spite of assurances that it was unrelated to prior nightmares); 1225 (parents inconsistent in sitting with
her until she falls asleep and are not sure of times of sleep onset); 1223 (therapist reporting that there
were two major barriers to success of therapy, in that parents had great difficulty in waking A.H.T. at the
scheduled time and A.H.T. resisted going to bed, and therapist was unsure how well parents enforced
bedtime).

16
the therapist.54 Id., p. 1224. A.H.T.’s sleep improved markedly during the therapy. Id.,
p. 1217.

The sleep center observations by Dr. (Ph.D.) Honaker regarding parental
inconsistency in setting and enforcing bedtimes and in seeking physiological
explanations for A.H.T.’s sleeping difficulties were mirrored by the behavior analysis
specialists who saw her from October 2010 through at least January 2012. After
several months of observation of A.H.T. and her caregivers, these analysts developed a
plan to change targeted behaviors, which scripted certain daily activities and
implemented a “token economy” reward system in which completion of tasks was
rewarded by tokens which A.H.T. could redeem weekly for preferred activities or
objects. See Pet. Ex. 38, pp. 1690-98. The records reflect numerous concerns by the
analysts about A.H.T.’s parents’ poor compliance with the behavior modification
program.55 Over time, both parental compliance and A.H.T.’s behavior improved,
although there were peaks and valleys. See Pet. Exs 38, pp. 1750-58; 57, pp. 2309-10.

The medical and therapy records relevant to the factual conflicts and other issues
in this case are discussed in more detail below.

III. Expert Qualifications.

Five physicians offered opinions on vaccine causation and other matters in
dispute. Three of the experts (Drs. Kendall, McCandless, and Wiznitzer) were well-
qualified to offer expert opinions; the other two (Drs. Levinson and DeMio) had
experience in treating children with autism and children with mitochondrial disorders, but
are best characterized as alternative or complementary medical providers who lacked
the academic background, research qualifications, or specialized training important in
my assessments of the bases for and reliability of the opinions they offered.56 They
treated A.H.T. for periods of time far removed from the manifestation of the symptoms
after her initial vaccination or the onset of her autistic-like behaviors. I have carefully
considered their records as treating physicians and their opinions on causation in light
54 Toward the end of the sleep therapy treatment, Dr. Vincent observed that A.H.T had “not been
optimally medicated for those diagnoses [referring to issues other than sleep-related] that are medical.”
Pet. Ex. 30, p. 1221. He also stated: “It is difficult for me to tell whether some of her activities are just
totally behavioral in nature or whether there is actually an underlying medical/psychiatric diagnosis.” Id.,
p. 1222.

55 See, e.g., Pet Ex. 38, pp. 1773 (parents have not yet implemented task analysis and token economy,
resulting in minimal progress in behavioral changes), 1774 (parents have not yet used reinforcement for
motivation), 1784 (parents had not taken data requested by behavior analyst and claimed that A.H.T.’s
sleep disorder prevented them from implementing most procedures outlined in the behavior plan), 1778
(mom’s report that playtime was contingent upon completing home school was contrary to observations of
behavioral analyst and parents were inconsistent with keeping data); 1781 (parents not providing tokens
at the time of task performance and reinforcing A.H.T.’s escape from and avoidance of tasks), 1793
(parents not recording data).

56According to Dr. McCandless, most of what Dr. Levinson said about mitochondrial function was simply
wrong (see Res. Ex. G at 3; Tr. at 588-89) and Dr. Kendall did not appear to place any reliance on Dr.
Levinson’s opinion, as it was not mentioned at all in her testimony.

17
of Federal Circuit precedent on the value of treating physicians’ opinions. See
Capizzano, 440 F.3d at 1326 (commenting that treating physicians are likely to be in the
best position to determine whether ‘a logical sequence of cause and effect show[s] that
the vaccination was the reason for the injury.’”) (internal citations omitted). See also
Moberly, 592 F.3d at 1325 (“Weighing the persuasiveness of particular evidence often
requires a finder of fact to assess the reliability of testimony, including expert testimony,
and we have made clear that the special masters have that responsibility in Vaccine Act
cases.”) (citing Terran v. Sec’y, HHS, 195 F.3d 1302, 1316 (Fed. Cir. 1999)); Cedillo,
617 F.3d at 1339 (“[a] court may conclude that there is simply too great an analytical
gap between the data and the opinion proffered”) (quoting Gen. Elec. Co. v. Joiner, 522
U.S. 136, 146 (1997) (additional internal citations omitted); Lalonde v. Sec’y, HHS, 746
F.3d 1334, 1337-38 (Fed. Cir. 2014) (“In Vaccine Act cases, petitioners must proffer
trustworthy testimony from experts who can find support for their theories in medical
literature in order to show causation under the preponderance of the evidence
standard.”); Snyder v. Sec’y, HHS, 88 Fed. Cl. 706, 745 n.67 (2009) (emphasizing that
a statement of a treating physician is not “sacrosanct” and can be rebutted).

The Federal Circuit has upheld the special masters’ use of Daubert and
summarized the four Daubert factors as “(1) general acceptance in the scientific
community, (2) whether the theory has been subjected to peer review and publication,
(3) whether the theory can and has been tested, and (4) whether the known potential
rate of error is acceptable.” Cedillo, 617 F.3d at 1339 (citing Daubert v. Merrell Dow
Pharms., Inc., 509 U.S. 579, 593–94 (1993)); see also Andreu v. Sec’y, HHS, 569 F.3d
1367, 1379 (Fed. Cir. 2009). The Federal Circuit also approved the use of the Daubert
factors in evaluating an expert’s “reliability” as well as their “methodology.” Cedillo, 617
F.3d at 1339.

In this case, Drs. Levinson and DeMio’s status as treating physicians adds little
to the reliability of their causation opinions, which largely consisted of conclusory
statements. With regard to the logical connection between vaccination and injury, these
particular treating physicians are no more percipient as witnesses about what actually
transpired after the vaccinations than any other physician who testified in this case.
Moreover, nothing in Capizzano requires special masters to give weight to the opinions
of treating doctors who espouse “junk science,” and who treat children based on
unproven hypotheses, with drugs with no known efficacy against the medical conditions
presented,57 and without test results to warrant the speculative diagnoses proffered.58

57In ordering tests, Dr. DeMio recorded a number of diagnoses, including static encephalopathy,
metabolic derangement, metabolic error, glycemic disorder, autoimmune disease, and hypothyroidism.
See, e.g., Pet. Ex. 37, pp. 1533-35, 1577, 1591, 1665. Other than static encephalopathy, these were all
new diagnoses unsupported by the medical testing ordered.

58Doctor DeMio ordered many standard laboratory tests on a monthly basis between February 2006 and
June 2007, in spite of repeated results within reference ranges. See generally Pet. Exs. 23; pp. 293-370;
37, pp. 1534-1665; 42, pp.1836-67. He also ordered tests that were less routine. He had a standing
order for a comprehensive metabolic panel and complete blood count [“CBC”] with differential and
platelets, on a monthly basis. Pet. Ex. 37, p. 1533. Other tests ordered included plasma amino acids,
red blood cell elements, urine toxic metals, various virus antibodies, stool parasites and bacteria, thyroid,

18
See Capizzano, 440 F.3d at 1325-27. See also Dwyer, 2010 WL 892250, at *116, 141
(criticizing the practitioners and researchers who convinced parents of the efficacy of
various specious treatment methods for their children with ASD). Both Drs. DeMio and
Levinson prescribed treatments of dubious efficacy, ordered tests with results that
conflicted with their hypotheses, and made diagnoses unsupported by the evidence. I
have not entirely rejected their observations about A.H.T., but I cannot credit their
statements about the connection between A.H.T.’s vaccination and her subsequent
medical and behavioral problems.

However, I have fully credited the records of the treating physicians, Drs.
Buttleman and Hefner, who saw A.H.T. during her first year of life and who treated her
for irritability and constipation, and diagnosed colic.

The four physicians who testified at the hearing offered opinions regarding
symptoms A.H.T. allegedly displayed after the vaccinations and whether these were
symptoms that suggested a mitochondrial regression had occurred. Although they were
not percipient witnesses, their testimony about the likelihood of the events described is
a factor in the factual findings set forth in Section V, Part C, below. The primary
contributions of the experts were in explaining mitochondrial disorders, the distinction
between primary mitochondrial disorders and secondary mitochondrial dysfunction, and
explaining the evidence and conflicting opinions surrounding A.H.T.’s diagnosis and
vaccine causation.

The witnesses’ training and experience that bear on their qualifications to testify
as experts and on the weight I accorded their testimony are set forth below, along with
some observations and impressions regarding their testimony.

A. Petitioner’s Experts.

All three of petitioner’s experts opined that the hepatitis B vaccination was
responsible for the symptoms A.H.T. displayed after vaccination. All three stated that

myelin antibodies, and fecal metals, among many others. Most results were entirely within reference
ranges, but occasionally, a few individual results would be slightly high or low. See, e.g., Pet. Ex. 23, pp.
364 (all red blood cell elements within reference range, except selenium), 356 (urine toxic metals all
within reference range), 345 (CBC and metabolic panel with nearly all results within reference ranges),
320 (comprehensive metabolic panel with results all within reference ranges); 24, pp. 378-79 (viral panel,
stool culture, and thyroid testing all within reference ranges). Most of these laboratory reports were from
Doctors’ Data, a laboratory seen with some frequency in records from OAP cases, and one with some
difficulties with licensing agencies. See Dwyer, 2010 WL 892250, at *182 n.687. Although Dr. DeMio
testified that he saw a lot of immune and metabolic issues in A.H.T. on testing (Tr. at 211-12), he did not
point to specific tests that demonstrated those problems. He testified that she had “issues eventually with
organisms like yeast and viruses.” and had “accumulated a lot of metal toxins.” Id. Like Dr. DeMio, Dr.
Levinson ordered many laboratory tests (see Pet. Ex. 47, pp. 2059-2107, 2129-43). With the exception of
some elevated white blood cell counts and a positive streptococcus antibody test, all the results on the
traditional laboratory tests were within the reference ranges, including the comprehensive metabolic
panel. Id., pp. 2140-43. Testing by Geneva Diagnostics encompassed a toxic element clearance profile,
completed on June 17, 2010 (Pet. Ex. 47, pp. 2134-39), and a nutritional evaluation completed on June
28, 2010, assessing oxidative stress, organic acids, amino acids, essential fatty acids, and toxic and
nutrient elements (Pet. Ex. 47, pp. 2059-86).

19
A.H.T. had a mitochondrial disorder or dysfunction which was aggravated by her
hepatitis B vaccination, but their theories about how the vaccination did so varied
considerably. Their backgrounds and qualifications were likewise quite divergent as
well.

1. Doctor Levinson.

Doctor Levinson graduated from the University of Miami School of Medicine, and
completed a residency in psychiatry. Pet. Ex. 60 at 2339. He did not list any
publications on his CV, although the CV included a reference to his dissertation on the
use of valerian root as a sleep aid. According to his CV, he has lectured on the
“biomedical” treatment of autism and gastrointestinal issues in autistic patients, as well
as on “detoxification” and dietary interventions. He has also appeared in several
television programs on subjects as diverse as reversing aging, autism, and heavy metal
poisoning. Id. at 2340-41. According to his February 2012 statement, he regularly
treated patients “with mitochondrial disease, metabolic disorders, and immune-system
related conditions” and “frequently lecture[d] on mitochondrial disorder[s]and the
potential for environmental and biological triggers of this condition.”59 Pet. Ex. 59 at
2336.

From the filed records, it is difficult to determine what diagnoses informed his
treatment of A.H.T., as his records from 2010 and 2011 do not reflect a diagnosis. He
referred A.H.T. to Dr. Shoffner for mitochondrial disorder testing about a year after Ms.
Holt completed his intake form. In his February 2012 statement, Dr. Levinson
mentioned his treatment of A.H.T. for a mitochondrial disorder and her improvement on
such treatment, but he did not indicate the nature of the treatment, when it began, or
what constituted improvement or how it differed from the treatment he provided prior to
her diagnosis. See Pet. Ex. 59 at 2336-37.

His February 2012 statement was conclusory in nature. He did not explain his
reasoning or point to anything that supported the opinions he expressed regarding
diagnosis and causation. These were serious deficiencies, given his lack of any training
in immunology, oxidative stress, or mitochondrial disorders, matters about which he
opined.

2. Doctor DeMio.

59Doctor McCandless expressed skepticism about Dr. Levinson’s qualifications to lecture about
mitochondrial disorders, pointing out three specific statements in Dr. Levinson’s causation opinion “that
demonstrate a lack of understanding of mitochondrial biology and physiology.” Res. Ex. G at 3. He
added in testimony that these three statements were not supported by solid, underlying research. Tr. at
588. He explained that most people who treat children with mitochondrial diseases “often see some
deterioration associated with viral illnesses and fever,” but to opine why this happens or to attribute it
happening to a vaccination in a five-day old was simply speculation. Tr. at 589.

20
Doctor DeMio testified as both treating physician and expert, although precisely
what qualified him as an expert in either mitochondrial disorders or the causes of autism
spectrum disorders remains elusive. He graduated from medical school at Case
Western Reserve University. Pet. Ex. 63, p. 2358. He is board certified in emergency
medicine. Tr. at 226. He has no formal specialized training in metabolic diseases or in
any of the several areas (pediatrics, immunology, neurology, or gastroenterology), in
which he proffered opinions. Tr. at 227-28. His only publications involved chapters on
arthritis, gout, inflammation, and nutrition in an integrative medicine textbook. Pet. Ex.
63, p. 2360.

He did partial residencies in pathology and internal medicine, followed by a three-
year residency in emergency medicine, all in the Cleveland, OH area. Tr. at 183-84. As
a part of his emergency medicine residency, he received some pediatric training. Tr. at
226-27; Pet. Ex. 63, p. 2359. After completing his residency in 1989, he worked briefly
in Massachusetts, before returning to Cleveland’s Mount Sinai hospital as a part-time
faculty member. He also worked at emergency medicine departments in two other
hospitals and in their residency training programs. Tr. at 185-86. None of his
appointments during this period were full-time faculty or clinical positions at any one
institution. Tr. at 186-87. He also maintained a private medical practice in which he
offered nutritional treatments as an alternative to drugs. Tr. at 188.

At the time of his testimony, he held no faculty appointments, although he had
privileges at several hospitals. Tr. at 228. He currently treats patients with immune
dysfunction, metabolic disorders, mitochondrial disorders, developmental problems,
behavior and mood issues, and cognitive dysfunction diagnosed “by other people who
basically aren’t doing much, if any, medical treatment for them.” Tr. at 188-89, 230.
The majority of his patients are children with developmental disabilities, including ASD,
obsessive compulsive disorder [“OCD”], attention deficit hyperactivity disorder,
dyspraxia, apraxia, mitochondrial dysfunction, and mitochondrial disease. Mitochondrial
dysfunction patients comprised from a quarter to a third of his patients over the last nine
years. Tr. at 194-95. His clinical practice is a “cash office,” which does not directly bill
medical insurers for the care rendered. Tr. at 229-30.

He serves as the Chief Medical Officer of the U.S. Autism and Asperger’s
Association (Tr. at 190) and has assisted the Autism Research Institute with their “think
tanks” and meetings (Tr. at 191). He is the founder and executive director of the
American Medical Autism Board, which he described as “the board certified by medical
doctors who do the kind of treatment that several of us out there are doing” (Tr. at 192),
presumably referring to biomedical approaches to the treatment of autism. He
acknowledged that this board is not recognized by the American Board of Medical
Specialties. Tr. at 231.

Much of Dr. DeMio’s testimony involved broad, general statements, even when
he was discussing his own treatment of A.H.T. In describing that treatment, he used
medical terminology vaguely and indiscriminately. For example, he testified regarding

21
his treatment of A.H.T. that: “then there’s methylation[60] and some other metabolic
support that we did. Methylation’s one of the metabolic things that we do, and so we
added in a lot of those treatments.” Tr. at 213. He “found [A.H.T.] to have accumulated
a lot of metal toxins,” but did not indicate which metals were toxic or how he knew that
they were at toxic levels.61 Id. The tests initially performed for various metals were all
within the reference ranges. See, e.g., Pet. Ex. 23, pp. 328, 350, 356. One later urine
test, which was performed after chelation began, showed one slightly elevated result for
tin, but no results were significantly above the reference ranges.62 Id., p. 348. Although
he testified that he found many immune and metabolic issues as the result of the testing
he ordered for A.H.T. (Tr. at 211-12), he did not point to any specific tests that
demonstrated these issues. He found her gastrointestinal system was not “to the
balance that we want and we also found issues eventually with organisms like yeast
and viruses” either based on tests or “clinically,” but once again, he did not point to
specific tests. Tr. at 213.

He was equally vague about how A.H.T. responded to his “biomedical”
treatments. He testified that:

She definitively had responses, and a lot of them were very good, and
then she ended up getting some upheavals I call them. Many people call
them side effects, things that showed she was able to respond to those. . .
.Some of them for a few months would really help her a lot to kind of
impress the speech therapist that she was able to learn better. . . a lot of
[her symptoms of OCD, cognitive function, and focus] got better, and
some of them either got worse or she shifted over to some other things, so
she had had hallucinations or some very intense preoccupations.

Tr. at 214.

To summarize, I did not find his testimony reliable in general or useful in
resolving either the factual disputes or causation questions. Although Dr. DeMio had

60 “Methylation” is defined chemically as the addition of methyl groups to a substance. DORLAND’S at
1152. I doubt that this was what Dr. DeMio meant. It is likely that he was referring to the methyl B 12
(methylcobalamin) treatments he ordered during his early treatment of A.H.T. Testing by Geneva
Diagnostics encompassed a toxic element clearance profile, completed on June 17, 2010 (Pet. Ex. 47,
pp. 2134-39), and a nutritional evaluation completed on June 28, 2010, assessing oxidative stress,
organic acids, amino acids, essential fatty acids, and toxic and nutrient elements (Pet. Ex. 47, pp. 2059-
86). I note that problems in methylation of DNA and methylcobalamin treatments were discussed in the
Theory 2 test case decisions (see. e.g., Dwyer, 2010 WL 892250, at *140-42) as a part of the oxidative
stress aspects of the mercury causation theory, a theory rejected in each of the Theory 2 OAP test cases.

61On cross-examination, Dr. DeMio acknowledged that a section of his website discussed his belief that
one of the major causes of the “autism epidemic” is mercury and aluminum in vaccines. Tr. at 232-33.

62As chelation is performed to remove metals such as lead and mercury from the body, increases in
urinary levels of metals susceptible to chelation is expected. This does not mean that toxic levels were
present in the body prior to chelation. Snyder, 2009 WL 332044, at *176-78; Pet. Ex. 23, p. 348.

22
treated A.H.T.,63 I gave little weight to his testimony about the events after the
vaccination as the testimony was based primarily on what was reported to him by
A.H.T.’s parents, years after the events in question. As for his opinions regarding their
credibility and ability as historians (see Tr. at 203), I had the opportunity to assess these
matters for myself. Unlike Dr. DeMio, I carefully reviewed every medical record filed
and noted that Ms. Holt’s recitations of A.H.T.’s medical history varied over time, and
some of the matters she reported were inexplicably absent from the contemporaneous
records.64 See, e.g., n.30, supra. On at least one occasion, Mr. Tipton’s reports
seemed calculated to mislead health care providers about A.H.T.’s medical history. See
Pet. Ex. 43, p. 1876 (screening form signed by Mr. Tipton in which he falsely reported
that A.H.T. had received the chickenpox vaccine and was up to date on immunizations).

63 Doctor DeMio began treating A.H.T. about three years after the events in question.

64For example, after reviewing the early pediatric records during cross-examination, Dr. Kendall
acknowledged that the normal growth and development described in the primary care records through
nine months of age were inconsistent with the testimony of A.H.T.’s family members. Tr. at 388-89.

23
3. Doctor Kendall.

Doctor Kendall, a biochemical geneticist and mitochondrial disease specialist,
obtained her medical degree from the New Jersey Medical School. Tr. at 291; Pet. Ex.
80 at 2504.65 She completed a residency in pediatrics, followed by a fellowship in
genetics and metabolism at Boston Children’s Hospital and Harvard Medical School,
and then a research fellowship in genetics and metabolism at Tufts. Tr. at 291-92; Pet.
Ex. 80 at 2504. Both fellowships involved an active clinical practice in patients with
suspected or known genetic and metabolic disorders. The research fellowship involved
work in a mitochondrial research laboratory as well. Tr. at 292. After her fellowship,
she began a mitochondrial disorders program at Boston’s Children’s Hospital which
focused on the diagnosis, care, and management of mitochondrial disease patients. Tr.
at 295. She has been treating patients with mitochondrial disorders for 22 years and is
board certified in biochemical genetics. Tr. at 293, 298. Although Dr. Kendall trained as
a pediatrician and had been board certified in pediatrics at one time, her certification
was not current, and she did not see pediatric patients for treatment other than that
related to mitochondrial disease. Tr. at 298-300, 332-33.

She has held academic appointments at both Harvard Medical School and
Emory Medical School as a geneticist in the pediatrics department. Tr. at 293-94.
She currently teaches and lectures at symposiums, at Emory University Nursing School,
and annually at the United Mitochondrial Disease Foundation’s symposium. She has a
hospital appointment at Children’s Healthcare of Atlanta as a clinical geneticist. Tr. at
295. However, her primary work is in an outpatient setting, in her role as President,
Virtual Medical Practice, where she manages patients with a known diagnosis,
evaluates patients for mitochondrial disease, and provides second opinion consultations
throughout the world as the “virtual” part of the practice. Pet. Ex. 80 at 2505; Tr. at 295,
298-99. She also evaluates patients being considered for enrollment in clinical trials.
Tr. at 299.

Doctor Kendall’s CV listed three research interests: inborn errors of metabolism;
the pathophysiology of multisystem problems in disorders of mitochondrial energy
production; and the efficacy of clinical treatment in disorders of mitochondrial energy
production. Pet. Ex. 80 at 2505. There were eight journal articles listed as “Original
Reports” on her CV, Pet. Ex. 80, but only one of them explicitly involved mitochondrial
disorders. Id., p. 2509. However, she testified that her most recent publication (which
did not appear on Pet. Ex. 80, her CV) was a review article on mitochondrial disease
and diagnostics. Tr. at 296-97. The CV also listed “Reviews,” which appeared to
include book chapters and journal articles, including one on testing in mitochondrial
disorders and one entitled “Bridging the Gap between ASD and Mitochondrial Disease.”

65Doctor Kendall testified that this CV was out of date and indicated that she would provide a copy of the
new one. Tr. at 297. An updated CV was never filed.

24
Pet. Ex. 80, at 2509.66 She did not indicate that she was a peer reviewer or editor for
any professional publications.

Unlike Dr. DeMio, Dr. Kendall possessed the requisite qualifications to opine
about mitochondrial disorders. The reliability and credibility problems posed by Dr.
Kendall’s testimony did not concern her qualifications to opine about mitochondrial
disorders, but rather her lack of familiarity with the medical records regarding A.H.T.’s
growth, development, and treatment during the relevant periods, and her evasiveness in
answering my questions as well as those from opposing counsel.

Her lack of familiarity about the medical records was somewhat unusual for an
expert witness testifying in the Vaccine Program. She was unsure what diagnostic
criteria Dr. Shoffner used (Tr. at 324-25), although it was clearly identified in the
diagnostic report. Pet. Ex. 61, pp. 2349-50. She was unable to recall when A.H.T.
manifested some of the symptoms upon which the diagnosis was based. See Tr. at
310. When asked if she had reviewed A.H.T.’s medical records from her first year of
life, Doctor Kendall replied that she was “assuming” that she did. Tr. at 339. She could
not recall if fever was mentioned in the medical records as a symptom occurring after
A.H.T.’s vaccination. Tr. at 341-42. She could not recall when A.H.T. was diagnosed
with hypotonia. Tr. at 344. She could not recall when A.H.T. started having autistic-like
behaviors. Tr. at 345. She could not recall when A.H.T. began displaying symptoms of
dysautonomia (temperature instability),67 nor did she recall how often this symptom
occurred. Tr. at 345-46. She believed that the medical records reflected A.H.T.
suffered from fatigue, but could not identify a particular time frame when fatigue was
reported as a problem. Tr. at 348. She testified that the medical records described
A.H.T. as lethargic after her vaccination (Tr. at 339-40), but that description does not
appear in any contemporaneous record. After reviewing the early pediatric records
during cross-examination, Dr. Kendall acknowledged that the normal growth and
development described in the primary care records through nine months of age were
inconsistent with the testimony of A.H.T.’s family members. Tr. at 388-89. Her lack of
preparation for testimony was disappointing.

Additionally, Dr. Kendall avoided giving straight answers to straightforward
questions. When asked whether a neonate with primary mitochondrial disease would
likely have normal growth and weight gain, she replied, “[t]hey can.” When pressed to
indicate if such growth and weight gain would be expected, she responded “it depends
on the patient.” She was similarly evasive in answering questions regarding motor and
intellectual development in a neonate with a primary mitochondrial disease, responding
again, “it depends on what their clinical presentations are.” Tr. at 348. These
tautological answers were not informative about what is generally or typically seen in

66The CV listed “abstracts” separately. Pet. Ex. 80 at 2510. In general, they appeared to be the
abstracts of the journal publications listed earlier.

67Doctor Kendall‘s report indicated that dysautonomia, including temperature instability, was a possible
symptom of mitochondrial disease. Pet. Ex. 79 at 2500; see also Tr. at 308-09.

25
such patients. This evasiveness, coupled with the lack of support for some aspects of
her opinion, caused me to question whether her testimony was entirely reliable.

Her testimony provided details on her theory of vaccine causation that her expert
report lacked. The portion of her report addressing causation (Pet. Ex. 79 at 2496-97)
was very short, only about two paragraphs long, and was based on two cited journal
articles, one of which was largely a case report, discussing autistic regression in
children with diagnosed mitochondrial disorders. As Dr. Kendall admitted on cross
examination, A.H.T. did not experience autistic regression in the classic sense of losing
“speech and those type of things,” and she agreed that there were many differences
between the children described in the studies and A.H.T.’s presentation. Tr. at 356;
357-58.

When asked about support for specific aspects of her theory of causation, she
avoided a direct answer, as exemplified by the following exchange:

Q: What other literature are you relying on for your theory?
A: As I indicated, some of the other articles that talk about temperature.
Q: Can you be more specific?
A. They are noted in some of the other articles.
Q: Nothing was filed with your report, so I’m just - -
A: No, I understand. I’m just mentioning it based on the questions that you’re
posing, and it’s coming up, so that’s what I’m saying.
Q: But you did not submit anything to support your theory, is that correct?
A. I did not submit those articles, no.

Tr. at 358. She clarified that not all the articles she cited in her report were actually filed
as evidence. Tr. at 360. The failure of petitioner to file supportive evidence for her
opinions, particularly after Dr. McCandless challenged her reliance on other literature
she claimed was supportive of her opinions (see Res. Ex. G at 4), was troubling.

B. Respondent’s Experts.

With regard to A.H.T.’s symptoms after vaccination and the likelihood that they
occurred as described by the witnesses, I accorded greater weight to the testimony of
respondent’s two experts. Both were currently board certified in pediatrics, displayed
familiarity with the contemporaneous records, gave careful attention to the testimony of
A.H.T.’s parents and fact witnesses, and provided reasons for their conclusions. Both
Drs. Wiznitzer68 and McCandless were far better prepared to discuss A.H.T.’s medical

68 During his testimony, Dr. Wiznitzer indicated that he did not have Dr. Hefner’s records at the time he
wrote his expert report (Res. Ex. A), thus explaining why his comments in that report about A.H.T.’s
development ended at nine months of age, when she stopped seeing Dr. Buttleman. Res. Ex. A at 7; Tr.
at 670. Also, on cross-examination, petitioner’s counsel noted that Dr. Wiznitzer’s report referred to
A.H.T.’s birth as occurring in a hospital. See Tr. at 691-92. I note that the filed medical records do not
include any records regarding A.H.T.’s home birth; Dr. Buttleman’s records do not mention where A.H.T.
was born; and Dr. Puri, A.H.T.’s pediatric neurologist, referred obliquely to a hospital birth. See generally
Pet. Exs. 58 (Dr. Buttleman’s records); 31, p. 1262 (recording “vaginal delivery and was home with the

26
records than Dr. Kendall. With regard to neurological issues, including
encephalopathies in general, I found Dr. Wiznitzer to be the most qualified and reliable
witness. Although he displayed the unfortunate tendency of sparring with opposing
counsel, particularly with respect to hypothetical questions, his responsiveness to my
questions distinguished him from Dr. Kendall. Of the two mitochondrial disease experts,
Dr. McCandless was the better witness, and his opinions were better supported than
hers. His explanations were clear and he genuinely tried to answer questions, rather
than to dodge them.

1. Doctor McCandless.

Doctor McCandless holds three board certifications: pediatrics, clinical genetics,
and clinical biochemical genetics. After completing medical school and a residency in
pediatrics, he practiced pediatric medicine for five years. He then completed a clinical
genetics residency at Case Western Reserve University in Cleveland, Ohio. Tr. at 414.
This was followed by a faculty position in clinical genetics at the University of North
Carolina. He later returned to Cleveland for a fellowship in clinical biochemical
genetics. Tr. at 413-14.

In his current positions at Rainbow Babies and Children’s Hospital and Case
Medical Center, he evaluates and cares for patients who have, or are suspected to
have, biochemical genetic disorders. Tr. at 414. He is also involved in outpatient care
for the same disorders. He is the medical director of a Prader-Willi syndrome clinic and
of the Center for Human Genetics. He diagnoses and treats children and adults with
mitochondrial disorders. He has been caring for such patients for the last 17 years. Tr.
at 414-16.

Doctor McCandless holds a faculty appointment at the Case Western Reserve
School of Medicine, where he teaches genetics to medical students and graduate
students, and serves as the director of the residency training program in medical
genetics. Since 1996, his teaching has focused primarily on inborn errors of
metabolism, some general genetics, and mitochondrial diseases as a part of the
biochemical genetics program. He is a member of several professional societies,
including the American Academy of Pediatrics, is a fellow of the American College of
Medical Genetics, and a member of the board of directors for the Society for Inherited
Metabolic Disorders. Tr. at 416-17. He lectures about mitochondrial disorders at the
medical school, and developed the program on mitochondrial disorders for a national
meeting of the American College of Medical Genetics and the Society for Inherited
Metabolic Disorders joint session.

His research has focused primarily on fatty acid oxidation disorders, with fewer
publications in the area of respiratory chain disorders. Tr. at 418. He is the principal
site investigator for a multicenter clinical trial of coenzyme Q-10 therapy for children with

mother in a few days). I thus do not consider this incorrect statement regarding A.H.T.’s birth location as
a dereliction on Dr. Wiznitzer’s part.

27
mitochondrial disorders. His research laboratory uses mouse models to try to
understand how mitochondrial dysfunction leads to symptoms and how to better treat
those symptoms. He is involved in several clinical trials related to the treatment of urea
cycle disorders and drug trials to treat phenylketonuria and other lysomal storage
diseases. Tr. at 419.

Doctor McCandless has testified as an expert witness twice for plaintiffs and
once for a defendant in courts other than the Vaccine Program. This was his first
appearance as a witness in a Vaccine Act case. Tr. at 421-22.

Although not lengthy, his opinion (Res. Ex. G) was well-written and well-
reasoned. The primary discrepancy in his opinion—stating that Dr. Shoffner diagnosed
a possible, rather than a probable, mitochondrial disorder—is not inaccurate, just
incomplete. Because Dr. Shoffner’s records regarding A.H.T. were filed as a part of
three different exhibits (Pet. Exs. 26, 47, and 61) and Dr. Shoffner apparently changed
his diagnosis between August 1 and August 10, 2011, without any reference to the
earlier diagnosis, much less an explanation for the change, Dr. McCandless apparently
missed the later diagnosis of a probable mitochondrial disorder. I find this oversight
understandable, particularly as there was no additional testing conducted by Dr.
Shoffner between the two visits that would account for the change in diagnostic
category.

2. Doctor Wiznitzer.

After graduating from medical school, Dr. Wiznitzer completed a three year
residency in pediatrics at what is now Cincinnati Children’s Hospital, followed by a year-
long fellowship in developmental pediatrics at the Cincinnati Center for Developmental
Disorders. Tr. at 619. He then completed a three year fellowship in child neurology at
the University of Pennsylvania and an additional two year fellowship at the National
Institutes of Health on disorders of higher cortical function in children. Tr. at 619-20. He
is board certified in pediatrics, neurology (with special qualifications in child neurology),
and neurodevelopmental disabilities. Tr. at 620.

At the time of the hearing, he was an associate professor of pediatrics,
neurology, and international health at Case Western Reserve University School of
Medicine, and teaches at the nursing and medical schools. Tr. at 620-21. His primary
clinical appointment is as a child neurologist at Rainbow Babies and Children’s hospital.
His clinical responsibilities there include services at the inpatient unit, outpatient clinical
practice, the epilepsy service and teaching residents. His responsibilities also include
administration of research grants, including one involving autism treatments. Tr. at 621.

He is a member of and holds positions in several relevant professional
organizations, including teaching and course development as a fellow of the American
Academy of Neurology [“AAN”], where he has presented courses or lectures on ADHD,
autism, and pediatric behavioral neurology. He is part of an AAN task force charged
with developing a position paper on interventions in autism. Tr. at 621-22. He is a

28
member of the executive committee of the American Academy of Pediatrics [“AAP”] and
serves as that organization’s liaison to the executive committee of the Council on
Children with Disabilities. He is a member of the autism subcommittee of the AAP and
a member of various AAP working groups, including one on neuromotor examinations in
children. Tr. at 622. He chairs a task force dealing with dyspraxia, a developmental
coordination disorder. Tr. at 646. He is also a member of the Child Neurology Society
and the International Society for Autism Research. Tr. at 622-23.

Doctor Wiznitzer is a member of the editorial boards of two professional journals.
He is a peer reviewer on a regular basis for medical journals dealing with pediatrics,
neurology, and other specialties. Tr. at 623. As a member of the Brighton
Collaboration, an international organization dealing with vaccine safety, he has helped
to develop definitions for various conditions to help in standardizing studies into adverse
events after vaccination. Tr. at 623. He also develops questions for various medical
certification examinations. Tr. at 624.

He has diagnosed and treated children with ASD and other developmental
disabilities for about 25 years. He has conducted research into and has numerous peer
reviewed publications, including journal articles, book chapters, and abstracts, on the
topics of autism (including co-morbid conditions such as tuberous sclerosis), ADHD,
and other developmental disabilities. Tr. at 624-25. He treats children with
mitochondrial dysfunction and disorders in his clinical practice. He refers children with
suspected mitochondrial disorders to the genetics department and the mitochondrial
team for testing and diagnosis. Tr. at 625.

In addition to his clinical, teaching, writing, and research responsibilities, Dr.
Wiznitzer devotes about four to five hours per week to litigative consultations. Although
he primarily reviews cases for respondent in the Vaccine Program, he has
recommended compensation in some of those cases, and has supported claims of his
own patients for compensation. Tr. at 625-26. He has testified frequently on behalf of
respondent in the Vaccine Program. Doctor Wiznitzer was offered as an expert in
pediatric neurology and developmental disabilities, without objection. Tr. at 626-27.

IV. The Causation Theories Presented.

A. Mitochondrial Disorder, Disease, and Dysfunction.

Neither party filed much background information about mitochondrial disorders in
general. The comprehensive literature review filed by petitioner, D. Rossignol & R.
Frye, Mitochondrial dysfunction in autism spectrum disorders: a systematic review and
meta-analysis, MOLEC. PSYCHIATRY, 17: 290-314 (2010), Pet. Ex. 71 [hereinafter
“Rossignol & Frye, Pet. Ex. 71”], did not discuss the wide variety of mitochondrial
disorders, focusing more on the co-morbidities in mitochondrial dysfunction,
mitochondrial disease, and ASD, and the relative rates of various clinical findings.
Some of the various clinical phenotypes, such as Alper and Leigh syndromes, were
mentioned in C. Verity, et al., The clinical presentation of mitochondrial diseases in

29
children with progressive intellectual and neurological deterioration: a national,
prospective, population-based study, DEV. MED. & CHILD NEUROL., 52: 434-40 (2010).69
As this study focused on patients with progressive disease, it did not provide information
on the wide variety of other mitochondrial disorders.

Mitochondrial disease can present in a wide variety of ways, according to Dr.
McCandless. Tr. at 435. He added that “it has been said that mitochondrial dysfunction
can cause almost any symptom in any part of the body at almost any time, which to a
certain extent is true.” Id. However, “mitochondrial diseases tend to present in some
very characteristic ways [which are] usually related to the tissue that’s most involved,
and those are the tissues that use the most energy.” Id. Doctor Kendall explained that
“there are subtypes of mitochondrial disease that are clearly defined [that] are
descriptive of a group of clinical features that are seen over and over again and often in
constellation with a specific gene defect or a specific biochemical feature,” but that most
patients do not fall into a “well-categorized subtype.” Tr. at 349. She testified that
A.H.T. does not fit into one of these subtypes. Tr. at 349-50.

Initially, petitioner claimed that A.H.T. has a mitochondrial disorder, one which
was “significantly aggravated” by A.H.T.’s initial hepatitis B vaccination. Petition, ¶¶15-
16. This claim appears to have been modified by petitioner’s post-hearing brief.
Drawing from the headings in the brief, petitioner claims that A.H.T. has mitochondrial
dysfunction (Petitioner’s Post-Hearing Brief [“Pet. Br.”] at 1-3), which was vaccine
induced (id. at 3-10), entitling her to compensation (id. at 10-13). Likewise, Dr.
Kendall’s expert report claimed that A.H.T. has a mitochondrial disorder, but in
questioning Dr. Kendall, petitioner’s counsel primarily asked about “mitochondrial
dysfunction.” For example, Dr. Kendall testified that A.H.T. had probable mitochondrial
dysfunction (Tr. at 328-29), but her report referred to “clinical features and biochemical
and enzymatic data in support of a mitochondrial disorder.” (Pet. Ex. 79 at 2497)
(emphasis added).

The terms used to characterize A.H.T.’s condition varied throughout the post
hearing brief, suggesting that petitioner thinks the terms mitochondrial disorder and
dysfunction are interchangeable.70 They are not. The distinction is significant, in that
while respondent conceded that A.H.T. has laboratory evidence of some moderate
mitochondrial dysfunction, respondent contends that such dysfunction is not responsible
for A.H.T.’s clinical symptoms, and that it is unlikely A.H.T. has a mitochondrial disorder

69Hereinafter cited as “Verity, Res. Ex. K” or as the “PIND study” (Progressive Intellectual and
Neurological Deterioration). Witnesses referred to this study either as “Verity” or “PIND.”

70 Petitioner’s post hearing brief uses the terms mitochondrial “dysfunction” and “disorder”
interchangeably throughout. See, e.g., header using “Mitochondrial Dysfunction” at 1; “mitochondrial
disorder” at 1; citations to testimony about “mitochondrial dysfunction” at 2-3; citations to articles
discussing mitochondrial disease at 3. I note that even Dr. DeMio agreed that the terms “mitochondrial
disease” and “mitochondrial dysfunction” have different meanings. Tr. at 262-63.

30
or disease.71 Tr. at 471-501, 565-66; Respondent’s Post-Hearing Brief [“Res. Br.”] at
18-19. Id.

The most helpful information concerning the distinction between mitochondrial
disorders and mitochondrial dysfunction came from Dr. McCandless. He defined
primary mitochondrial disease as “a set of clinical abnormalities that directly result from
mitochondrial dysfunction.” Res. Ex. G at 2. In primary mitochondrial disease, there is
evidence that the mitochondria do not function normally and there is a measurable
clinical effect of the dysfunction. Tr. at 423, 564-66.

In testimony, Dr. Kendall defined a primary mitochondrial disorder as one “in
which there is an alteration in a gene that alters a protein that is directly involved in
energy production.” Tr. at 396-97. In essence, she asserted that a defect in either
mtDNA or nDNA is necessary to have a primary mitochondrial disorder or disease. Tr.
at 397-98. Doctor McCandless agreed that the defect had to be one that “leads to a
protein in the mitochondria that’s not doing its job properly and that leads to the
dysfunction,” but he did not require that the defect be genetic. Tr. at 428. In a primary
mitochondrial disorder, “the basic underlying problem is the mitochondrial structure or
function is wrong from the beginning,” leading to symptoms of mitochondrial disease.
Tr. at 429.

According to Dr. McCandless, secondary mitochondrial defects exist when some
other process causes dysfunction of the mitochondria, leading to symptoms. Tr. at 429.
When dysfunction of the mitochondria is observed in a laboratory setting, there must be
some evidence that the dysfunction also causes an identifiable clinical finding or
symptom before the patient can be characterized as having a mitochondrial disease or
disorder. Res. Ex. G at 2; Tr. at 428. In testimony, he clarified that one can infer from
in vitro (laboratory) testing of tissue to what may happen in vivo, but there still must be
some evidence of dysfunction in the body. This evidence may be test results or some
clinical symptomology. He pointed to hypoxia or rotenone (a fish poison) as examples
of an outside agent that could produce mitochondrial dysfunction. Tr. at 428-29.

Most of the few studies filed in this case focused on individuals with diagnosed
mitochondrial disorders, rather than individuals with some evidence of mitochondrial
dysfunction. Thus, the applicability of these studies to someone with mitochondrial
dysfunction, rather than a mitochondrial disorder, is questionable. Additionally, although
A.H.T. has been diagnosed with a probable mitochondrial disorder, the evidence
supporting that diagnosis rests on the presence of certain symptoms, about which there
are significant factual disputes. This may explain petitioner’s shift in focus from
mitochondrial disorder to mitochondrial dysfunction in petitioner’s post hearing brief.
And, as it is more difficult to establish how a vaccine can trigger a genetic condition

71 The parties’ witnesses agreed that the terms “mitochondrial disorder” and “mitochondrial disease” were
interchangeable. Tr. 264 (DeMio); 428 (McCandless). Doctor McCandless also testified that it is very
important to clarify what people mean when they use the terms “disease,” “disorder,” and “dysfunction” in
discussing mitochondrial problems. Tr. at 426-27.

31
present since birth, the focus on dysfunction rather than disorder eases, to some extent,
petitioner’s burden to prove that a vaccination can, more likely than not, be responsible
for A.H.T.’s symptomology.

B. The Theories.

The causation theory identified in the amended petition—that mitochondrial
disease can be aggravated by an outside event—builds on an observed characteristic
of mitochondrial disorders that is not particularly controversial, even if it has not been
well studied or documented. That is, the condition of individuals with mitochondrial
disorders often worsens over time. This may occur gradually, or there may be abrupt
regressions or decompensations that result in illness and/or the inability to perform
motor or cognitive tasks once mastered. Pet. Ex. 79 at 2494; Res. Ex. A at 8; Res. Ex.
G at 2; Tr. at 444-46, 588.

These regressions may occur without any apparent cause or may be temporally
related to events such as viral or febrile illness, anesthesia, dehydration, surgery, and
the use of some drugs, such as HIV medications and statins. Pet. Ex. 79 at 2494; Res.
Ex. G at 4; Tr. at 392-93, 398, 572, 588-89, 608-09. Some of those who experience
decompensation or regression return to baseline, some plateau, and in many, the loss
of skills signals a downward spiral in the progression of mitochondrial disease.
Unfortunately, many mitochondrial diseases are relentlessly progressive and ultimately
fatal. Res. Ex. G at 2-3; see also Verity, Res. Ex. K at 435, 439 (noting that mortality
rates of children with mitochondrial disease enrolled in this study were high, with 40 of
the 112 children enrolled in the study beginning in1997 having died by 2008).

In certain types of mitochondrial or metabolic disorders, there is a measurable
physiological response that causes the decompensation. In individuals with urea cycle
disorders, an illness (or dehydration due to an illness) may produce an excess of
ammonia in the body, termed “hyperammonemia,” resulting in a metabolic
decompensation. See J. Kingsley, et al., Immunizations for Patients with Metabolic
Disorders, PEDIATRICS, 118(2): e460-70 (2006), filed as Pet. Ex. 70, at e464
(hyperammonemiac states are produced by breakdown of muscle tissue during periods
of anorexia, such as may be seen in ill children) [hereinafter “Kingsley, Pet. Ex. 70]; T.
Morgan, et al., Vaccines are not Associated with Metabolic Events in Children with Urea
Cycle Disorders, PEDIATRICS 127: e1147-53 (2011) [hereinafter “Morgan, Res. Ex. I” or
the “Morgan study”] at e1148 (“children with [urea cycle disorders] are at high risk of
devastating metabolic decompensation in the setting of acute childhood illnesses”).
See also Tr. at 502-03 (Dr. McCandless discussing vaccinations in children with urea
cycle disorders and the Morgan study).

Decompensation or regression occurs in other types of mitochondrial or
metabolic disorders as well as in urea cycle disorders. A correlation has been drawn
between metabolic stressors, such as illnesses and surgery, and periods of regression
in these patients, based on a temporal relationship between such stressors and a
regression or decline in health. This relationship has not been well documented, but it

32
appears to be generally accepted as a causal one. Res. Ex. G at 4; Tr. at 502-03.
Fever, in particular, has been recognized as a stressor that can possibly aggravate a
mitochondrial disorder, although fever in the absence of an illness has not been
systematically studied. Tr. at 352, 392, 572; Pet. Ex. 61, pp. 2347-48. Several of the
filed medical journal articles discussed the connection between fever, febrile illness, and
decompensation. However, Dr. McCandless testified that it was the underlying illness,
and not merely the febrile response to it, that was responsible for the deterioration. Tr.
at 512-13, 572-73.

The lack of both specificity and strength in the association between illness and
decompensation or regression has contributed to the uncertainty about the causal
mechanism—that is, what is it about a fever or illness that causes the loss of skills? Not
all individuals with mitochondrial disorders experience periods of decompensation with
such stresses, and many experience such periods of decompensation even in the
absence of metabolic stress.72 The same patient may experience an illness and lose
skills, but handle the next several illnesses without any apparent regression. Tr. at 445-
46, 590-91. The nature of the underlying mitochondrial disorder, the specific
manifestation in a particular individual, the type of illness, and the nature of the
regression are all factors affecting the response of a patient with a mitochondrial
disorder to an illness. Whether the regression persists is also quite variable among and
within the various types of mitochondrial disorders.73

Both Drs. Kendall and McCandless testified about some of the theories regarding
the causal mechanism for decompensation or loss of skills. Tr. at 352-53, 444-45.
Petitioner’s theory that a vaccine can cause onset of a dormant or underlying
mitochondrial disease or cause long-lasting mitochondrial dysfunction was presented
primarily by Dr. Kendall. This theory extends what is generally accepted about
mitochondrial disorders in three specific ways. First, petitioner contends that an
external event can trigger onset of a mitochondrial disorder that would otherwise have
remained dormant, not simply cause regressions or loss of skills in individuals with a
diagnosed or, at least suspected, mitochondrial disorder. Second, petitioner claims that
a vaccine, not just an illness, can exacerbate, aggravate, or trigger this onset or cause
mitochondrial dysfunction. Third, petitioner claims that this aggravation can cause the
manifestation of symptoms, not only shortly after vaccination, but new symptoms

72 To illustrate the frequency of illness or regression, Dr. McCandless testified that observations over a
period of several years of 100 hypothetical children with confirmed mitochondrial disease would show that
somewhere between 40-60% of them would get sicker and stay sick longer than their siblings without
mitochondrial disease when confronted with a cold or influenza, and that they would return to baseline
more slowly than their siblings. Of those who got sicker, less than ten would have a severe or significant
deterioration. Some of these might not return to baseline. However, not all illnesses would produce this
effect of being sicker for longer, even in the small percentage of children who experienced a severe
deterioration with illness. Tr. at 590-93. The response to illness may be cyclic, occurring several times in
one year, and then not occurring at all in subsequent years. Tr. at 593-94.

73For example, Dr. Kendall testified that, in individuals who present with a mitochondrial encephalopathy,
some improve, 20-30% experience severe progressive deterioration, and the remainder are stable with
periodic ups and downs. Tr. at 338.

33
manifesting many months later. Petitioner attributed A.H.T.’s post vaccination irritability
and constipation to aggravation of her mitochondrial disorder or causation of
mitochondrial dysfunction, signaling some form of brain injury, and also contended that
the behavioral symptoms and developmental delays that manifested more than 15
months later were likewise the result of this injury.

The medical witnesses petitioner presented did not agree on the specific nature
and mechanism of the damage. During the hearing and in her post hearing brief,
petitioner advanced Dr. DeMio’s theory that ongoing “brain inflammation” was
responsible for A.H.T.’s symptoms. The “brain inflammation” theory ostensibly
incorporated most of Dr. Kendall’s theory that a vaccination can trigger an underlying
mitochondrial disorder, producing a loss of skills. However, Dr. DeMio also claimed that
the initial insult of the hepatitis B vaccine produced inflammation in A.H.T.’s brain and
this inflammation was responsible for A.H.T.’s early and later symptoms. Yet a third
theory was proposed by Dr. Levinson—that A.H.T.’s symptoms were the result of
oxidative stress as the result of the interaction of her underlying mitochondrial disorder
and the immunological stress of the hepatitis B vaccine. This theory was not explicitly
argued in the post hearing brief, but petitioner quoted a portion of Dr. Levinson’s
statement regarding this position in her post hearing brief. Pet. Br. at 10. Each of these
theories, along with some of the evidence provided by respondent, is discussed in more
detail below.

1. Doctor Kendall’s Theory.

Doctor Kendall’s expert report provided few details on her theory of causation.
The portion of Pet. Ex. 79 that addressed causation was very short, only two
paragraphs long. Id. at 2497. She referenced two medical journal articles as the
support for her assertions.74 When examined carefully, neither article provided
substantial support and one contradicted her assertion that vaccines alone could cause
or trigger a decompensation in a patient with a mitochondrial disorder.

Her testimony provided some of the details that her expert report lacked. She
testified that A.H.T. had an underlying mitochondrial disorder, that the hepatitis B
vaccination was “an immunological trigger” for her fever (Tr. at 352), which stressed her
system, “outstrip[ped] the body’s ability to develop energy for functionality” and primarily
led to damage to her central nervous system. (Tr. at 353).

In terms of timing, she pointed to symptoms that developed between hours to
days after the vaccination. Tr. at 353-54. Her theory accounting for the observed

74Petitioner’s Ex. 69, which was also filed as Res. Ex. P, is primarily a case report. J. Poling, et al.,
Developmental Regression and Mitochondrial Dysfunction in a Child with Autism, J. CHILD NEUROL., 21(2):
170-72 (2008) [hereinafter “Poling, Pet. Ex. 69”]. Doctor Shoffner, the physician who diagnosed A.H.T.
with a probable mitochondrial disorder, was one of the co-authors of this case report. The second journal
article was filed as Pet. Ex. 68 and Res. Ex. Q: J. Shoffner, et al., Fever Plus Mitochondrial Disease
Could be Risk Factors for Autistic Regression, J. CHILD NEUROL., 25 (4): 429:34 (2010) [hereinafter
“Shoffner, Pet. Ex. 68”].

34
temporal link between illnesses and deterioration or regression in mitochondrial disease
was based on the increased energy demands that such illnesses or stressors place on
the body and the inability of impaired or defective mitochondria to meet those increased
energy demands. Brain and muscle tissue require high levels of energy, and when
illness increases the demands, the supply available to brain and muscle is reduced,
resulting in lost motor and cognitive skills, among other symptoms. Tr. at 301, 303-04,
352.

This theory could account for the observation in Wolf and Smeitink, Court Ex. I,
at 1402, that the presenting symptom in children with mitochondrial disorders is often
neuromuscular in nature. However, it does not account for deterioration observed
without an identifiable triggering event.

The specific mechanism of an energy deficit to account for clinical deterioration is
less well accepted than the fact that regressions do occur. See Res. Ex. G at 4 (Dr.
McCandless stating that the “strength and mechanism of any such association are not
at all clear”); Tr. at 556-57 (discussing Dr. Kendall’s theory, another theory, and his
opinion that both might contribute to diminished energy production in the mitochondria,
along with other factors as yet unknown). Nevertheless, in this decision, I will assume,
arguendo, that Dr. Kendall’s increased energy demand mechanism is correct. The
difficulty comes in finding evidence, other than her very cursory opinion and testimony
(Dr. Kendall’s direct examination, including establishing her qualifications to opine,
encompassed only about 40 pages of testimony), to support the other contested
aspects of her opinion.

a. Can a Dormant Mitochondrial Disorder Be Triggered by an External
Event?

Doctor Kendall was unequivocal in stating that a vaccination does not cause
alteration in a “genetic blueprint” or alter “the functionality of . . . protein structure.” Tr.
at 334. She testified that an individual can “harbor either DNA changes or the
propensity for these diseases and not exhibit them from the time of birth, for example.”
Tr. at 303. Although she did not explicitly testify that an external trigger is required for
an underlying mitochondrial disorder to manifest, she appeared reasonably certain that
A.H.T.’s disorder was so triggered. Tr. at 352-54.

Other than Dr. Kendall’s opinion, there is little evidence in this record to suggest
that a metabolic stressor can trigger a dormant or unrecognized mitochondrial disorder.
The anecdotal evidence linking stress to a regression is based on what mitochondrial
disease specialists have seen in their own patients (see, e.g., Tr. at 557), necessarily
implying that the mitochondrial disorder was already diagnosed or strongly suspected
(see also Verity, Res. Ex. K, at 436 (reporting that 33 of the 112 participants diagnosed
with mitochondrial disease had experienced an exacerbation of their condition “in
association with fever or minor illness”)). Doctor McCandless testified that he could not
recall any patient who was normal and then experienced a sudden decompensation
(“crash and burn”) due to illness. Tr. at 608-09.

35
Relying on the anecdotal experience of one of her patients and Pet. Exs. 68-69,
Dr. Kendall claimed that an event such as an illness could trigger a previously
unrecognized mitochondrial disorder. She described an asymptomatic teenager who
developed symptoms of a mitochondrial disorder (progressive muscular manifestations)
after a severe case of influenza. Later, genetic testing disclosed a previousl

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/2817851. Public record. Not legal advice.