Sparling et al v. Doyle et al
Filing
331
ORDER GRANTING 184 Motion to Strike ; DENYING 185 Motion to Strike ; GRANTING 186 Motion to Strike ; GRANTING 187 Motion to Strike ; DENIED AS MOOT 258 Motion to exclude. Signed by Judge Anne T. Berton. (mc4)
IN THE UNITED STATES DISTRICT COURT
FOR THE WESTERN DISTRICT OF TEXAS
EL PASO DIVISION
LEANNE SPARLING and MICHAEL J.
SPARLING, on behalf of and as
representatives for MICHAEL L.
SPARLING, deceased,
Plaintiffs,
v.
JONATHAN VINCENT DOYLE,
an individual, JACOB GEISSLER, an
individual, USPLABS JACK3D, LLC,
USPLABS, LLC, USPLABS HOLDING,
LLC, GNC CORPORATION, NATURAL
ALTERNATIVES INTERNATIONAL,
INC., and DOES 1-500, inclusive,
Defendants.
§
§
§
§
§
§
§
§
§
§
§
§
§
§
§
§
§
§
§
No. EP-13-CV-323-DCG
ORDER
On this day, the Court considered “Defendants’ Motion[s] to Strike the Testimony of [Dr.
Louis Cantilena, Dr. Mahmoud ElSohly, Dr. Edward Mills, and Dr. Daniel Rusyniak]”
(“Defendants’ Motions to Strike”) (ECF Nos. 184, 185, 186, 187) filed by Defendants Jonathan
Vincent Doyle, an individual, Jacob Geissler, an individual, USPLABS JACK3D, LLC,
USPLABS, LLC, USPLABS HOLDING, LLC, and GNC Corporation (collectively,
“Defendants”) on January 22, 2015. On January 26, 2015, the matter was referred to this Court
under 28 U.S.C. § 636(b) and Appendix C of the Local Court Rules. (ECF No. 188). Plaintiffs
Leanne Sparling and Michael J. Sparling filed a Response (“Plaintiffs’ Omnibus Response”)
(ECF No. 200) on February 10, 2015. Defendants subsequently filed four Individual Replies1
(ECF Nos. 213, 219, 220, 221) and an Omnibus Reply (ECF No. 218) on March 6, 2015, and
The Court will refer to Defendants’ Individual Motions and Replies by the expert’s name followed by
Mot. or Reply, i.e., (Dr. Cantilena Mot. 1, ECF No. 184).
1
No. EP-13-CV-323-DCG
1
March 10, 2015, respectively. On April 27, 2015, and April 28, 2015, the Court held a hearing
pursuant to Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579 (1993). (See Order 1-3, ECF
No. 235; see also ECF No. 321). On July 24, 2015, the Court received a Joint Notice of Second
Supplemental Reports from the parties containing further Supplemental Rule 26 Expert Reports.2
After considering the testimony of the experts, the pleadings,3 and the applicable law, the
Court orders that Defendants’ Motion to Strike Dr. Cantilena, Dr. Mills, and Dr. Rusyniak
should be GRANTED and Defendants’ Motion to Strike Dr. ElSohly should be DENIED.
I.
BACKGROUND
Plaintiffs allege that Michael L. Sparling (“Decedent”) died as a result of his use of
Jack3d, a dietary supplement containing DMAA.4 Plaintiffs’ First Amended Complaint alleges
causes of action for negligence, strict products liability-defective design, strict products liabilityfailure to warn, breach of express warranty, breach of implied warranty, wrongful death, and
survival action. (See Am. Compl. ¶¶ 34, 90-148).
In support of their allegations, Plaintiffs have designated six experts to testify at trial.
(See ECF No. 106). Defendants now seek to strike the Rule 26 Expert Reports and testimony of
four of those experts: 1) Louis Cantilena, M.D. (“Dr. Cantilena”); 2) Mahmoud ElSohly, Ph.D.
(“Dr. ElSohly”); 3) Edward Mills, Ph.D. (“Dr. Mills”); and 4) Daniel Rusyniak, M.D.
(“Dr. Rusyniak”). (ECF Nos. 184, 185, 186, 187).
2
Per the Court’s request, the parties submitted the Second Supplemental Rule 26 Expert Report and
Declaration of Dr. Cantilena and the Supplemental Rule 26 Expert Report and Declaration of Dr. Mills.
(ECF Nos. 327-1, 327-22).
3
The Court fully considered the parties’ arguments but declines to rehash the extensive briefing, except
when necessary.
4
DMAA is shorthand for the compound 1,3-Dimethylamylamine. (See, e.g., Dr. Cantilena Mot. 9 n.36,
ECF No. 184; Pls.’ Omnibus Resp. 12, ECF No. 200).
No. EP-13-CV-323-DCG
2
II.
LEGAL STANDARD
Federal Rule of Evidence 702, which governs the admissibility of expert testimony,
provides:
A witness who is qualified as an expert by knowledge, skill, experience, training,
or education may testify in the form of an opinion or otherwise if: (a) the expert’s
scientific, technical, or other specialized knowledge will help the trier of fact to
understand the evidence or to determine a fact in issue; (b) the testimony is based
on sufficient facts or data; (c) the testimony is the product of reliable principles
and methods; and (d) the expert has reliably applied the principles and methods to
the facts of the case.
In oft-cited cases, the Supreme Court has articulated the district court's gate-keeping function
under Rule 702. See Daubert, 509 U.S. at 592-98; see also Kumho Tire Co. v. Carmichael,
526 U.S. 137 (1999). In performing this gate-keeping function, the court has broad discretion in
deciding whether or not to admit expert testimony.
See Johnson v. Arkema, Inc.,
685 F.3d 452, 460 (5th Cir. 2012); Moore v. Ashland Chem. Inc., 151 F.3d 269, 276
(5th Cir. 1998) (en banc). The burden of proof on a Daubert issue lies with the proponent of the
expert’s testimony. “The proponent need not prove that the expert's testimony is correct, but [he
or] she must prove by a preponderance of the evidence that the testimony is reliable.”
Moore, 151 F.3d at 276.
In Daubert, the Supreme Court held that Rule 702 imposes an obligation upon the trial
judge to “ensure that any and all scientific testimony admitted is not only relevant, but reliable.”
Daubert, 509 U.S. at 589. Generally, “an expert is permitted wide latitude to offer opinions,
including those that are not based on firsthand knowledge or observation.” Id. at 592. Daubert,
however, sets forth four specific factors that the district court should ordinarily apply when
considering the reliability of scientific evidence: 1) whether the technique can or has been tested;
2) whether it has been subjected to peer review or publication; 3) whether there is a known or
potential rate of error; and 4) whether the relevant scientific community generally accepts the
No. EP-13-CV-323-DCG
3
technique. Id. at 592-94. Daubert also instructs courts that the issue at hand is based “solely on
principles and methodology, not on the conclusions that they generate.” Id. at 595.
In Kumho Tire, the Supreme Court concluded that a district court may consider one or
more of the specific Daubert factors when doing so will help determine the reliability of the
expert’s testimony. Kumho Tire Co., 526 U.S. at 151.
But, as the Court stated in Daubert, the test of reliability is “flexible,” and
Daubert’s list of specific factors neither necessarily nor exclusively apply to all
experts or in every case. Rather, the law grants a district court the same broad
latitude when it decides how to determine reliability as it enjoys in respect to its
ultimate reliability determination.
Id. at 142 (citing General Elec. Co. v. Joiner, 522 U.S. 136, 143 (1997)). Thus, whether
Daubert's suggested indicia of reliability apply to any given testimony depends on the nature of
the issue at hand, the witness's particular expertise, and the subject of the testimony. Id. at 15152; see also Black v. Food Lion, Inc., 171 F.3d 308, 311-12 (5th Cir. 1999) (“In the vast majority
of cases, the district court first should decide whether the factors mentioned in Daubert are
appropriate.”). Therefore, under Kumho Tire, district courts have broad latitude to determine
whether or not the proffered testimony requires an application of the Daubert factors and the
Supreme Court has acknowledged that “[t]oo much depends upon the particular circumstances of
the particular case at issue” to set out rigid requirements to test reliability.” Id. at 150.
In making the reliability determination, the district court should not require certainty but
the testimony must demonstrate that the opinions offered are more than speculation.
In
considering this issue, the district court must consider the validity of the principles applied by the
expert, the accuracy of the data relied upon by the expert, and the precision of the application of
the principles to the relevant data. See Newton v. Roche Labs., Inc., 243 F. Supp. 2d 672, 676
(W.D. Tex. 2002) (citing Marcel v. Placid Oil, 11 F.3d 563, 567 (5th Cir. 1994)). Thus, the
Court’s task is to “determine whether the evidence is genuinely scientific, as distinct from being
No. EP-13-CV-323-DCG
4
unscientific speculation offered by a genuine scientist.” Moore, 151 F.3d at 278 (quoting Rosen
v. Ciba-Geigy Corp., 78 F.3d 316, 318 (7th Cir. 1996)).
The Fifth Circuit has been particularly careful to distinguish evidence that establishes a
causal relationship between the product and the alleged injury, from evidence that merely
“suggests”
an
association
between
the
product
at
issue
Allen v. Pa. Eng'g Corp., 102 F.3d 194, 197 (5th Cir. 1996).
and
the
injury.
See
Although evidence of an
association may indicate the need for further research and be important in the scientific and
regulatory contexts, the Fifth Circuit has cautioned that tort law requires a “higher standard” of
causation than that used in the regulatory context. Id. at 198. Moreover, as Judge Posner has
noted, “[l]aw lags science; it does not lead it.” Rosen, 78 F.3d at 319. Courts “must resolve
cases . . . on the basis of scientific knowledge that is currently available,” and only evidence that
demonstrates a causal relationship between a product and an alleged injury can be admitted as
relevant and reliable. See Moore, 151 F.3d at 274, 276; see also Brumley v. Pfizer, Inc., 200
F.R.D. 596, 602 (S.D. Tex. 2001) (requiring evidence of causation and noting that “the lack of
proof of a drug's safety does not prove that it is dangerous”). However, “[v]igorous crossexamination, presentation of contrary evidence, and careful instruction on the burden of proof
are the traditional and appropriate means of attacking shaky but admissible evidence.” Daubert,
509 U.S. at 596.
“The relevancy requirement ensures that the expert testimony will actually ‘assist the trier
of
fact
to
understand
the
evidence
or
to
determine
a
fact
in
issue.’”
Lofton v. McNeil Consumer & Specialty Pharm. (Lofton I), Civ. A. No. 3:05-CV-1531-L (BH),
2008 WL 4878066, at *2 (N.D. Tex. July 25, 2008) (citing Daubert, 509 U.S. at 589), report and
recommendation adopted, Lofton v. McNeil Consumer & Specialty Pharm. (Lofton II),
682 F. Supp. 2d 662 (N.D. Tex. 2010). Relevant evidence is that which has “any tendency to
No. EP-13-CV-323-DCG
5
make the existence of any fact that is of consequence to the determination of the action more
probable or less probable that it would be without the evidence.” Fed. R. Evid. 401. “Expert
testimony which does not relate to any issue on the case is not relevant and, ergo, non-helpful.”
Lofton I, 2008 WL 4878066, at *2 (citing Daubert, 509 U.S. at 590).
III. ANALYSIS
A.
Defendants’ Challenge to Plaintiffs’ Rule 26 Expert Reports
1. Defendants’ Challenge to Plaintiffs’ Rule 26 Expert Reports Under Rule 37(c)(1)
Defendants argue that the Court should strike the testimony and opinions of Dr.
Cantilena, Dr. Mills, and Dr. Rusyniak under Rule 37(c)(1) of the Federal Rules of Civil
Procedure5 because their Rule 26 Expert Reports do not contain “a complete statement of all
opinions . . . and the basis and reasons for them” and “the facts or data considered by the witness
in forming them.” (See Dr. Cantilena Mot. 6-9, ECF No. 184; Dr. Mills Mot. 6-8, ECF No. 186;
Dr. Rusyniak Mot. 6-7, ECF No. 187).6 Defendants contend that the Rule 26 Expert Reports
“hardly disclose[] anything other than the proposed [experts’] ultimate, generalized conclusion[s]
about causation.” (See Dr. Cantilena Mot. 7, ECF No. 184; Dr. Mills Mot. 7, ECF No. 186;
Dr. Rusyniak Mot. 7, ECF No. 187). Defendants maintain that Dr. Cantilena admitted in his
deposition that he is not qualified to testify on labeling requirements for dietary supplements and
5
Rule 37(c)(1) provides:
If a party fails to provide information . . . as required by Rule 26(a) or (e), the party is not
allowed to use that information or witness to supply evidence on a motion, at a hearing,
or at a trial, unless the failure was substantially justified or is harmless. In addition to or
instead of this sanction, the court, on motion and after giving an opportunity to be heard:
(A) may order payment of the reasonable expenses, including attorney’s fees, caused by
the failure; (B) may inform the jury of the party’s failure; and (C) may impose other
appropriate sanctions, including any of the orders listed in Rule 37(b)(2)(A)(i)-(vi).
6
Where there is a discrepancy between assigned ECF page numbers and internal document page
numbers, the Court adopts ECF pagination. This proviso will not apply to the page numbers of the
experts’ depositions and the hearing transcript, which will be referred to by page and line, where
appropriate.
No. EP-13-CV-323-DCG
6
that he will not be offering opinions as to the labeling or warnings, even though his Rule 26
Expert Report contains an opinion on that issue. (See Dr. Cantilena Mot. 8-9, ECF No. 184).
Defendants also claim that Plaintiffs’ experts’ testimony must be limited to the scope of
their Rule 26 Expert Reports and any other testimony must be stricken.
(See
Defs.’ Omnibus Reply 26, ECF No. 218). Defendants argue that the bases for the experts’
opinions must be included in their Rule 26 Expert Reports rather than as exhibits or references.
(See id. at 24-25). Defendants further contest Plaintiffs’ Rule 26 Expert Reports on the ground
that they do not use the term “mechanism of action.” (See id.)
As to Dr. Cantilena’s Rule 26 Expert Report, Defendants assert that he failed to include
the specific outlier data he relied upon, the source of that data, and the scientific bases for using
that data rather than other data. (See Dr. Cantilena Reply 3-4, ECF No. 219). Defendants further
contend that Dr. Cantilena failed to include scientific evidence or an explanation regarding the
“susceptible population” and how Decedent is part of that population. (See id. at 6-7).
Plaintiffs contend that the challenged Rule 26 Expert Reports are sufficient to meet the
requirements of the Federal Rules. (See Pls.’ Omnibus Resp. 48-53, 55-60, ECF No. 200).
Plaintiffs argue that the Rule 26 Expert Reports contain: 1) opinions on the biological and
pharmacological mechanism of action of DMAA (see id. at 49, 55-56, 58-59); 2) an explanation
as to why no baseline toxic dose exists and information regarding the dose-response relationship
(see id. at 50-51, 58-59); 3) opinions on the use of a differential diagnosis (see id. at 52-53, 5556); and 4) an attached list of references to scientific literature relied upon by the experts.
(See id. at 49, 57-58). Plaintiffs assert that Defendants deposed each of the experts for multiple
hours in which they testified to their methodology and opinions. (See id. at 49, 56). Plaintiffs
further contend that there is no requirement that each premise offered in every paragraph of the
Rule 26 Expert Reports contain a citation and page number. (See id. at 49). Plaintiffs, however,
No. EP-13-CV-323-DCG
7
fail to respond to Defendants’ argument regarding Dr. Cantilena’s opinion as to the labeling and
warnings on the Jack3d label.
Rule 26(a)(2) imposes a “duty to disclose information regarding expert testimony
sufficiently in advance of trial [so] that opposing parties have a reasonable opportunity to prepare
for effective cross examination and perhaps arrange for expert testimony from other witnesses.”
Fed. R. Civ. P. 26(a)(2) advisory committee’s note (1993). “One of the purposes of the Rule 26
disclosure and report is to compel the proponent of the expert to be prepared for the remainder of
the trial of the case by requiring the expert to finalize his opinions at least ninety days prior to
trial.” Bro-Tech Corp. v. Purity Water Co. of San Antonio, Inc., Civ. No. SA-08-CV-0594-XR,
2009 WL 1748539, at *7 (W.D. Tex. June 19, 2009) (citations omitted). Expert reports should
be “detailed and complete” so as “to avoid the disclosure of ‘sketchy and vague’ expert
information.” Sierra Club v. Cedar Point Oil Co. Inc., 73 F.3d 546, 571 (5th Cir. 1996).
Although there is a question of whether Plaintiffs’ Rule 26 Expert Reports satisfy the
plain language of the Rule, the Court finds that any error by Plaintiffs is harmless and that a
sanction of striking the testimony under Rule 37 would be too drastic a remedy. In evaluating
whether a violation of Rule 26 is harmless, the Court examines four factors: 1) the importance of
the evidence; 2) the prejudice to the opposing party of including the evidence; 3) the possibility
of curing such prejudice by granting a continuance; and 4) the explanation for the party's failure
to disclose. See id. at 572.
As for the first factor, it is clear that the evidence contained in the Rule 26 Expert Reports
is of such high importance to Plaintiffs’ case that, without it, Plaintiffs would lack causation
testimony. As for the second factor, Defendants have not clearly explained how they will be
prejudiced in light of the fact they have held multiple hours of depositions and were able to
examine these experts further during the Daubert hearing. As to the third factor, “[w]hile the
No. EP-13-CV-323-DCG
8
Court is sympathetic to Defendants, who first identified the missing information in [the Rule 26
Expert Reports], supplementation may be proper . . . when it is in response to questions or
challenges to the [experts’] opinion[s] raised by the opposing party.” Charles v. Sanchez,
No. EP-13-CV-00193-DCG, 2015 WL 808417, at *9 (W.D. Tex. Feb. 24, 2015)
(Guaderrama, J.) (collecting cases). As for the fourth factor, Plaintiffs make clear that they have
fully disclosed their experts’ opinions in their Rule 26 Expert Reports and that the depositions of
Plaintiffs’ experts allowed Defendants to further explore any questions that arose during
Defendants’ review of Plaintiffs’ Rule 26 Expert Reports.
In considering the four factors
together, the Court finds that the violation of Rule 26(a)(2)(B) was harmless and declines to
strike the testimony of Dr. Cantilena, Dr. Mills, and Dr. Rusyniak under Rule 37. The Court
will, however, strike the portions of Dr. Cantilena’s Rule 26 Expert Report and testimony as it
relates to labeling and warnings on the Jack3d label, because he admitted in his deposition that
he was not offering an opinion on that subject. (See Dr. Cantilena Dep. 211:19-24, 218:7-19,
220:13-17, 350:16-351:11; Pls.’ Ex. HH ¶ 10, ECF No 197-29).
2. Defendants’ Challenge to Dr. Cantilena’s Supplemental Rule 26 Expert Report
Defendants argue that Dr. Cantilena’s Supplemental Rule 26 Expert Report was
submitted untimely and that the Court should, therefore, strike it or prevent Plaintiffs from
relying on the Coyle study.7 (See Dr. Cantilena Mot. 8, ECF No. 184). Defendants contend that
Dr. Cantilena discovered the “Coyle study as much as a month before his deposition” but did not
disclose its existence or his reliance on that study until the middle of his deposition. (See id.)
Based on that ground, Defendants argue that Dr. Cantilena failed to supplement “in a timely
7
The parties refer to Ricardo Mora-Rodriguez et al., Plasma Catecholamines and Hyperglycaemia
Influence Thermoregulation in Man During Prolonged Exercise in the Heat, 491 J. Physiology 529
(1996), as the Coyle study because Dr. Edward F. Coyle is the senior author. (Pls.’ Ex. R-25, ECF No.
197-2).
No. EP-13-CV-323-DCG
9
manner” as required by Rule 26(e) of the Federal Rules of Civil Procedure. (See id.) Defendants
state that Dr. Cantilena’s untimely disclosure prejudiced Defendants by surprising them at Dr.
Cantilena’s deposition. (See id.) Defendants maintain that Dr. Cantilena failed to disclose his
conversions and calculations mentioned in his Supplemental Rule 26 Expert Report or the
scientific bases for the validity of those conversions and calculations.8 (See Dr. Cantilena Reply
3, ECF No. 219).
Plaintiffs argue that Dr. Cantilena’s Supplemental Rule 26 Expert Report was timely
submitted on December 24, 2014.9 (See Pls.’ Omnibus Resp. 54, ECF No. 200). Plaintiffs assert
that Dr. Cantilena’s Supplemental Rule 26 Expert Report was submitted in conjunction with the
Rebuttal Rule 26 Expert Report of Dr. Edward Coyle. (See id.) Plaintiffs contend that it became
necessary to supplement Dr. Cantilena’s Rule 26 Expert Report after Defendants’ expert, Dr.
Laci Alexander, introduced a theory that caused Plaintiffs to hire Dr. Coyle to rebut. (See id.)
At that time, Plaintiffs further contend that Dr. Cantilena reviewed Dr. Coyle’s studies and
determined that one of Dr. Coyle’s studies provided additional data regarding “the effects of
equivalent doses of sympathomimetics on vasoconstriction and increased core temperature
through heat retention.” (See id.) Additionally, Plaintiffs argue that Dr. Cantilena testified about
this research at his deposition on December 15, 2014, and timely submitted his Supplemental
Rule 26 Expert Report in advance of the discovery cutoff and pretrial disclosure deadline. (See
id.) Moreover, Plaintiffs state that they offered Defendants the opportunity to further depose Dr.
8
The Court notes that Dr. Cantilena’s conversions and calculations were first presented to Defendants on
the Monday before the Daubert hearing. (Hr’g Tr. 199:10-18, Apr. 27, 2015 AM, ECF No. 321). A copy
of Dr. Cantilena’s handwritten conversions and calculations were presented at the Daubert hearing. (Pls.’
Ex. 7, Daubert hearing).
9
Although Plaintiffs argue that Dr. Cantilena’s Supplemental Rule 26 Expert Report was submitted on
December 24, 2014, a review of the Supplemental Report indicates that it is dated January 12, 2015. (See
Pls.’ Ex. QQ 3, ECF No. 197-38).
No. EP-13-CV-323-DCG
10
Cantilena on this issue. (See id., citing Dr. Cantilena Dep. 146:5-13).
Supplemental Rule 26 Expert Reports are governed by Rule 26(e). Rule 26(e)(1)(A)
requires that Rule 26 Expert Reports be supplemented “in a timely manner if the party learns that
in some material respect the disclosure or response is incomplete or incorrect, and if the
additional or corrective information has not otherwise been made known to the other parties
during the discovery process or in writing.” An expert’s duty to provide a Supplemental Rule 26
Expert Report “extends both to information included in the report and to information given
during the expert’s deposition.” The supplemental information “must be disclosed by the time
the party’s pretrial disclosures under Rule 26(a)(3) are due.” As Rule 26(a)(3)(B) states that
pretrial disclosures “must be made at least 30 days before trial,” a Supplemental Rule 26 Expert
Report is timely if submitted before that date.
The Court finds that Plaintiffs timely submitted Dr. Cantilena’s Supplemental Rule 26
Expert Report and will consider Dr. Cantilena’s use of the Coyle study in evaluating the
reliability of his opinion.
Plaintiffs designated Dr. Coyle on December 10, 2014.
(See
ECF No. 165). Dr. Cantilena’s deposition took place on December 15, 2014. (See Dr. Cantilena
Dep. 1). During his deposition, Dr. Cantilena testified that he discovered Dr. Coyle’s study
approximately one month to three weeks before his deposition. (See id. at 133:4-16). Dr.
Cantilena’s Supplemental Rule 26 Expert Report is dated January 12, 2015. (See Pls.’ Ex. QQ 3,
ECF No. 197-38). Although this date is after Dr. Cantilena’s deposition, the Court notes that this
date is well before pretrial disclosures were due when the trial was set for June 2015 and is well
before pretrial disclosures are due for the new trial date in February. (See Text Order Sept. 24,
2014; Order 2-3, ECF No. 320). Therefore, the Court finds that Dr. Cantilena’s Supplemental
Rule 26 Expert Report was timely submitted and will not be stricken for that reason.
No. EP-13-CV-323-DCG
11
B.
Applicability of Havner
Throughout
their
briefing,
Defendants
insist
that
the
Court
apply
Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706 (Tex. 1997), as the standard for
relevance under Daubert. (See Dr. Cantilena Mot. 9-11, ECF No. 184; Dr. Mills Mot. 8-10, ECF
No. 186; Dr. Rusyniak Mot. 8-10, ECF No. 187; Defs.’ Omnibus Reply 13-14, ECF No. 218;
Dr. Cantilena
Reply
4-5,
ECF
No.
219;
Dr.
Mills
Reply 3-4,
ECF
No.
220;
Dr. Rusyniak Reply 3-5, ECF No. 221). In applying Havner as the standard for relevance under
Daubert, Defendants argue that Plaintiffs must provide epidemiological studies that demonstrate
more than a doubling of the risk of injury in order to prove general causation.
(See Dr. Cantilena Mot. 9-11, ECF No. 184; Dr. Mills Mot. 8-10, ECF No. 186; Dr. Rusyniak
Mot. 8-10, ECF No. 187; Defs.’ Omnibus Reply 13-14, ECF No. 218; Dr. Cantilena Reply 4-5,
ECF No. 219; Dr. Mills Reply 3-4, ECF No. 220; Dr. Rusyniak Reply 3-5, ECF No. 221). In
Havner, the Texas Supreme Court addressed the issue of whether evidence was legally sufficient
to support the judgment issued by the lower court. See Havner, 953 S.W.2d at 708, 711. The
Havner court held that in order to establish some evidence of general causation, studies must
meet certain requirements, including: 1) demonstrating “more than a doubling of the risk” due to
exposure; 2) a confidence interval that does not include 1.0; and 3) a confidence level of at least
ninety-five percent.10 See id. at 718, 723-24. Additionally, the Havner court stated that the
plaintiff must show that his circumstances are similar to the group analyzed in the study. See id.
10
Confidence levels in epidemiological studies establish the boundaries of the relative risk in a study. See
Merrell Dow Pharm., Inc. v. Havner, 953 S.W.2d 706, 723 (Tex. 1997). The boundaries are called the
confidence interval. See id. (citations omitted). Confidence intervals allow scientists to determine
whether studies are statistically significant at a certain confidence level. See id. (citation omitted). The
confidence interval demonstrates “a range of values within which the results of a study sample would be
likely to fall if the study were repeated numerous times.” See id. (internal quotation marks and citation
omitted). If a confidence interval includes 1.0, a study is not statistically significant because the relative
risk values demonstrate that “the null hypothesis (1.0)” should be both accepted and rejected. See id.
(citations omitted). Therefore, a doubling of the risk refers to a relative risk greater than 2.0. See id. at
721, 724-25.
No. EP-13-CV-323-DCG
12
at 720. Thus, Defendants contend that Plaintiffs’ experts fail to offer studies which meet the
Havner standard and, therefore, are not relevant evidence of causation under Daubert. (See Dr.
Cantilena Mot. 9-11, ECF No. 184; Dr. Mills Mot. 8-10, ECF No. 186; Dr. Rusyniak Mot. 8-10,
ECF No. 187; Defs.’ Omnibus Reply 13-14, ECF No. 218; Dr. Cantilena Reply 4-5, ECF No.
219; Dr. Mills Reply 3-4, ECF No. 220; Dr. Rusyniak Reply 3-5, ECF No. 221).
In support of the argument that Havner applies a standard requiring more than a doubling
of the risk of injury, Defendants state that the Texas Supreme Court reaffirmed the Havner
decision in Bostic v. Georgia-Pacific Corp., 439 S.W.3d 332 (Tex. 2014). (See Dr. Cantilena
Mot. 11, ECF No. 184; Dr. Mills Mot. 10, ECF No. 186; Dr. Rusyniak Mot. 9-10, ECF No. 187;
Defs.’ Omnibus Reply 14, ECF No. 218). Defendants argue that the Bostic court “held that in
toxic tort cases expert testimony of causation must be scientifically reliable in the form of
epidemiological studies showing that the defendant’s product ‘more than doubled the plaintiff’s
risk of injury.’” (See Dr. Cantilena Mot. 11 & n.47, ECF No. 184; Dr. Mills Mot. 10 & n.45,
ECF No. 186; Dr. Rusyniak Mot. 9-10 & n.42, ECF No. 87). In Bostic, the Texas Supreme
Court addressed whether evidence was legally sufficient to support the judgment of the lower
court, but this time in a case involving asbestos and mesothelioma. See Bostic, 439 S.W.3d at
336. The Bostic court acknowledged that “Havner is a foundational part of our jurisprudence[]
[but] [w]e have never held that it applies universally to all tort cases where causation is an
issue.” Id. at 347 (emphasis added). The Bostic court further stated that “[Havner] offers an
alternative method of establishing causation ‘[i]n the absence of direct, scientifically reliable
proof of causation.’” Id. at 347-48. The Bostic court concluded that:
[I]n the absence of direct proof of causation, establishing causation in fact against
a defendant in an asbestos-related disease case requires scientifically reliable
proof that the plaintiff’s exposure to the defendant’s product more than doubled
his risk of contracting the disease. A more than doubling of the risk must be
shown through reliable expert testimony that is based on epidemiological studies
No. EP-13-CV-323-DCG
13
or similarly reliable scientific evidence.
Id. at 350 (emphasis added). Defendants thus argue that the Court must apply a standard of more
than a doubling of the risk of injury to determine whether Plaintiffs’ experts have offered
relevant evidence of causation, as reaffirmed in Bostic. (See Dr. Cantilena Mot. 11, ECF No.
184; Dr. Mills Mot. 10, ECF No. 186; Dr. Rusyniak Mot. 9-10, ECF No. 187; Defs.’ Omnibus
Reply 14, ECF No. 218).
In addition, Defendants cite Cano v. Everest Minerals Corp., 362 F. Supp. 2d 814
(W.D. Tex. 2005) (Rodriguez, J.), as an example of a case from this district where the court
applied Havner to determine that evidence was irrelevant and inadmissible under Daubert. (See
Dr. Cantilena Mot. 10 & n.42, ECF No. 184; Dr. Mills Mot. 9 & n.40, ECF No. 186;
Dr. Rusyniak Mot. 9 & n.37, ECF No. 187; Defs.’ Omnibus Reply 13-14, ECF No. 218). The
Cano court stated:
If evidence is admissible under federal procedural law but fails to constitute
“some evidence” under Texas substantive law, the Plaintiffs’ victory on the
admissibility question would be a hollow one, as the evidence would be deemed
insufficient as a matter of law to survive summary judgment. Moreover, whether
expert testimony will assist the trier of fact is governed in part by whether the
testimony is relevant to the plaintiff’s burden of proof under the substantive law,
and testimony that will not assist the trier of fact by advancing an element of the
plaintiff’s case should be excluded. Thus, the Court concludes that Havner
controls the issue of what evidence is required to establish causation in a toxic tort
case and therefore what evidence is relevant.
362 F. Supp. 2d at 821-22 (internal citations omitted). Defendants thus argue that the Court
should exclude Plaintiffs’ experts because their proffered testimony fails to meet the standards
set forth in Havner and applied in Cano. (See Dr. Cantilena Mot. 10 & n.42, ECF No. 184;
Dr. Mills Mot. 9 & n.40, ECF No. 186; Dr. Rusyniak Mot. 9 & n.37, ECF No. 187;
Defs.’ Omnibus Reply 13-14, ECF No. 218).
Defendants further argue that if the Court declines to apply Havner to the relevance
determination under Daubert, “federal common law” also applies the “doubling of the risk”
No. EP-13-CV-323-DCG
14
standard to satisfy the preponderance of the evidence burden in civil cases. (See Defs.’ Omnibus
Reply 20, ECF No. 218, citing Daubert v. Merrell Dow Pharm., Inc. (Daubert II), 43 F.3d 1311,
1320 (9th Cir. 1995); Pozefsky v. Baxter Healthcare Corp., No. 92CV0314LEKRWS, 2001 WL
967608, at *3 (N.D.N.Y. Aug. 16, 2001)).
Plaintiffs contend that epidemiological studies showing a “doubling of the risk” are not
necessary to determine the admissibility of experts under Rule 702 and Daubert.
(See Pls.’ Omnibus Resp. 38, ECF No. 200). Moreover, Plaintiffs argue that whether an expert’s
opinion is admissible is a matter of federal law rather than state law. (See id.) Although courts
have stated that epidemiologic studies provide useful evidence, Plaintiffs argue that they are not
required under Rule 702 and Daubert.
(See id., citing Allen, 102 F.3d at 195;
Brock v. Merrell Dow Pharm., Inc., 874 F.2d 307, 308 (5th Cir.), modified on reh’g,
884 F.2d 166 (5th Cir. 1989); In re Norplant Contraceptive Prods. Liab.
Litig.,
215 F. Supp. 2d 795, 831 (E.D. Tex. 2002)). Plaintiffs, therefore, conclude that their lack of an
epidemiological study showing a doubling of the risk “is of no consequence under Rule 702.”
(See id. at 40).
The Court relies on Lofton II in holding that the Havner requirements are not applicable
to the question of whether Plaintiffs’ experts’ testimony is relevant under Rule 702 and Daubert.
See Lofton II, 682 F. Supp. 2d at 668-69. In that case, the district court considered Havner and
Cano, other decisions on the issue from the Northern District of Texas, and Fifth Circuit
decisions which considered Havner. See id. The Lofton II court concluded that the Fifth Circuit
has only considered the applicability of Havner in the context of legal sufficiency of the
evidence supporting a jury verdict rather than in the context of Rule 702 and Daubert. See id.
The Court has failed to find any decisions by the Fifth Circuit, subsequent to the Lofton II
decision, in which Havner was applied in the context of Rule 702 and Daubert. Therefore, the
No. EP-13-CV-323-DCG
15
Court rejects Defendants’ argument that Havner sets the standard for relevance in this context.
The Court also rejects Defendants’ argument that Bostic applies to all toxic tort cases as the
Bostic court itself stated that their decision requiring proof of a doubling of the risk standard
specifically applied to asbestos-related disease cases. Bostic, 439 S.W.3d at 350 (emphasis
added). Moreover, the Court rejects Defendants’ argument that the doubling of the risk standard
is the standard under “federal common law” and the default standard under Daubert. (See Defs.’
Omnibus Reply 20, ECF No. 218, citing Daubert II, 43 F.3d at 1320; Pozefsky, 2001 WL
967608, at *3). The precedent cited by Defendants applies the doubling of the risk standard in
cases involving the substantive law on causation and, accordingly, the Court is persuaded by the
Lofton II court’s holding that the doubling of the risk standard does not apply in the context of
Rule 702 and Daubert.
(See id.; see also Daubert II, 43 F.3d at 1320 (birth defect case
considering Rule 702 and motion for summary judgment and applying California substantive law
on causation); Pozefsky, 2001 WL 967608, at *1-7 (breast implant case where, after granting in
part and denying in part a motion for summary judgment, the court excluded the plaintiff’s
experts because the evidence and opinions offered were unreliable as compared to the
defendant’s evidence demonstrating a lack of a causal relationship between breast implants and
systemic injuries)).
The Court further rejects all of Defendants’ arguments as to the reliability and relevance
of Plaintiffs’ experts’ opinions as challenged under state law. “Although state law governs the
substance of the case, whether an individual is qualified to testify as an expert is a question of
federal law.” Charles, 2015 WL 808417, at *2 & n.3 (“The parties’ briefing of admissibility of
expert testimony under Texas law is therefore inapposite.”). Finally, the Court rejects all of
Defendants’ arguments which concern whether Plaintiffs’ experts have provided “sufficient”
evidence to meet the ultimate burden of proof on causation because Daubert does not require this
No. EP-13-CV-323-DCG
16
Court to determine whether causation evidence is sufficient as a matter of law. While the Court
is making this finding as to the current Rule 702 and Daubert challenge, the Court is not making
a determination as to whether Havner applies for purposes of dispositive motions that are not
currently before this Court.
C.
The Relevant Scientific Literature for Dr. Cantilena, Dr. Mills, and Dr. Rusyniak
Dr. Cantilena, Dr. Mills, and Dr. Rusyniak rely on various studies in their attempt to set
forth reliable evidence on whether DMAA can cause hyperthermia in the general population and
whether DMAA caused hyperthermia in Decedent. Therefore, the Court briefly reviews the
relevant scientific literature relied upon by these experts to form their opinions on causation.
1. The Bloomer Studies11
a. Effects of 1,3-Dimethylamylamine and Caffeine Alone or in Combination on Heart
Rate and Blood Pressure in Healthy Men and Women12
In this study, Dr. Bloomer and his group sought to “determine the effect of [DMAA]
intake at [two] different dosages of practical relevance, with and without the addition of caffeine,
on [heart rate] and blood pressure.” (Defs.’ Ex. V 4, ECF No. 223). The study also included a
caffeine-only condition for comparative purposes. (See id.) Each of the ten subjects, five men
and five women, received one serving of each condition and was observed during a two hour
period after ingestion. (See id.) The subjects reported for five test days in a ten hour fasted state
and were instructed not to exercise twenty-four hours prior to the test. (See id.) Heart rate,
systolic blood pressure, and diastolic blood pressure were measured pre-condition and at time
The parties refer to several studies performed by the University of Memphis as the “Bloomer studies.”
(See Dr. Cantilena Mot. 20, ECF No. 184; Pls.’ Omnibus Resp. 40 n.104, ECF No. 200; see also Defs.’
Ex. V, ECF No. 223).
11
12
Richard J. Bloomer et al., Effects of 1,3-Dimethylamylamine and Caffeine Alone or in Combination on
Heart Rate and Blood Pressure in Healthy Men and Women, 39 Physician & Sportsmed. 111 (2011).
(Defs.’ Ex. V 3-12, ECF No. 223).
No. EP-13-CV-323-DCG
17
intervals of thirty, sixty, ninety, and one hundred twenty minutes post-ingestion. (See id. at 5).
The conditions included two hundred fifty milligrams of caffeine, fifty milligrams of DMAA,
seventy-five milligrams of DMAA, fifty milligrams of DMAA plus two hundred fifty milligrams
of caffeine, and seventy-five milligrams of DMAA plus two hundred fifty milligrams of caffeine.
(See id.)
The study indicated that oral DMAA use resulted in an increase in systolic blood
pressure, diastolic blood pressure, and rate pressure product. (See id. at 7). The study further
indicated that fifty milligrams of DMAA plus two hundred fifty milligrams of caffeine did not
have as significant of an increase on systolic blood pressure or diastolic blood pressure as
compared to seventy-five milligrams of DMAA alone. (See id. at 11). The study concluded that
acute oral ingestion of DMAA results in a significant increase in blood pressure without
impacting heart rate. (See id.) It also concluded that the effect seems to be dose dependent, in
particular on systolic blood pressure, with greater blood pressure increases with seventy-five
milligrams of DMAA versus fifty milligrams of DMAA. (See id.) Finally, the study concluded
that the addition of caffeine to fifty milligrams of DMAA caused a percentage change in rate
pressure product but did not increase the other measures in a statistically significant manner.
(See id.)
b. Effect of Caffeine and 1,3-Dimethylamylamine on Exercise Performance and
Blood Markers of Lipolysis and Oxidative Stress in Trained Men and Women13
This study investigated “the effect of caffeine and [DMAA] on exercise performance and
blood markers of lipolysis and oxidative stress in a sample of exercised-trained men and
women.” (Id. at 14). In this study, twelve subjects, six men and six women, reported to the
13
Richard J. Bloomer et al., Effect of Caffeine and 1,3-Dimethylamylamine on Exercise Performance and
Blood Markers of Lipolysis and Oxidative Stress in Trained Men and Women, 1 J. Caffeine Res. 169
(2011). (Defs.’ Ex. V 13-22, ECF No. 223).
No. EP-13-CV-323-DCG
18
laboratory on four test days in a ten hour fasted state and were instructed not to exercise twentyfour hours prior to the test. (See id.) Soon after arriving to the laboratory, heart rate, systolic
blood pressure, and diastolic blood pressure were measured and a blood sample was drawn. (See
id.) Sixty minutes after ingestion of the condition, the study participants underwent a second
round of testing and began a ten kilometer run. (See id.) The same measures were taken five
minutes and thirty minutes after the run ended. (See id.) The tests were performed once per
week for four weeks. (See id.) Running temperatures ranged from 44°F to 68°F. (See id.) The
conditions in this study were a placebo (thirty grams of carbohydrate), caffeine (thirty grams of
carbohydrate plus caffeine at a dose of four mg/kg body mass-1), DMAA (thirty grams of
carbohydrate plus DMAA at a dose of one mg/kg body mass-1), or caffeine and DMAA (thirty
grams of carbohydrate plus caffeine at a dose of four mg/kg body mass-1 and DMAA at a dose of
one mg/kg body mass-1). (See id.)
The study found
that (1) ingestion of caffeine or [DMAA] alone or in combination [did] not
improve exercise performance as measured by run time; (2) ingestion of [DMAA]
results in the greatest increase in postexercise glycerol and [free fatty acids]
concentrations; (3) caffeine or [DMAA] alone or in combination [did] not
differently effect oxidative stress biomarkers pre- or postexercise; (4) caffeine and
[DMAA] alone increase [systolic blood pressure].
(Id. at 16). The study also found that there was no statistically significant effect on run time
when comparing the conditions versus placebo. (See id. at 17). The study demonstrated that
while there was a higher systolic blood pressure with caffeine alone and DMAA alone compared
to placebo, the combination of caffeine and DMAA did not result in a higher systolic blood
pressure compared to placebo. (See id. at 19). This study noted that although the Effects of 1,3Dimethyamylamine study, discussed above, demonstrated there was an additive effect for the
combined condition of caffeine and DMAA, this study did not reach the same findings.
No. EP-13-CV-323-DCG
19
(See id. at 7, 11, 19).
c. Safety Profile of Caffeine and 1,3-Dimethylamylamine Supplementation in Healthy
Men14
The present study tested caffeine and DMAA alone and in combination at dosages that
are used in dietary supplements, for a period of twelve weeks, and performed tests for body mass
and composition, resting respiratory rate, electrocardiography, urinalysis with microscopic
examination, and oxidative stress, inflammatory, and cardiac biomarkers. (See id. at 24). This
study had sixty-six participants but only fifty men completed the study. (See id.) Three testing
days occurred in this study: pre-condition, after six weeks, and after twelve weeks.
(See id. at 25). The participants arrived following an eight hour fast. (See id.) On arrival,
participants turned in a diet log, voided, had an electrocardiography test, had their respiratory
rate, blood pressure, and body mass and composition measured, and had a blood sample drawn.
(See id.) The four conditions in the study were placebo (cellulose), two hundred and fifty
milligrams of caffeine, fifty milligrams of DMAA, and two hundred and fifty milligrams of
caffeine plus fifty milligrams of DMAA. (See id.) The participants were to consume one
capsule per day during the first week and were then to consume two capsules per day for the
remaining weeks; however, no capsules were consumed on the morning of a test day. (See id.)
The investigators found that “[twelve] weeks of supplementation with caffeine and
DMAA, whether alone or in combination, [did] not result in statistically significant changes in
any measured variables.” (Id. at 26). The study concluded that the data is specific to “a sample
of healthy, young men consuming daily dosage of caffeine [two hundred fifty milligrams] and
DMAA [fifty milligrams] that are considered moderate and recommended.” (Id. at 31-33).
14
Richard J. Bloomer et al., Safety Profile of Caffeine and 1,3-Dimethylamylamine Supplementation in
Healthy Men, 32 Hum. & Experimental Toxicology 1126 (2011). (Defs.’ Ex. V 13-22, ECF No. 223).
No. EP-13-CV-323-DCG
20
d. Hemodynamic and Hematologic Profile of Healthy Adults Ingesting Dietary
Supplements Containing 1,3-Dimethylamylamine and Caffeine15
In this study, the investigators “sought to determine the hemodynamic and hematologic
profile of two different dietary supplements containing [DMAA and caffeine] before and after
two weeks of daily intake.” (Id. at 35). The investigators hypothesized that acute intake would
cause an increase in blood pressure but chronic intake would not cause significant changes.
(See id.)
Thirteen people participated in the study and took two servings of OxyElite Pro or
Jack3d. (See id. at 36). Of the thirteen participants, four men and two women took OxyElite Pro
and seven men took Jack3d. (See id.) When subjects arrived for testing, they rested for ten
minutes and then had their heart rate, systolic blood pressure, and diastolic blood pressure
readings taken along with a blood sample. (See id.) Subjects then ingested a condition and had
heart rate and blood pressure measurements taken at thirty, sixty, ninety, and one hundred twenty
minutes post-ingestion. (See id.) The subjects reported to the laboratory between 6:00 am and
9:00 am on two days for testing and were told not to exercise twenty-four hours prior to testing.
(See id. at 35-36).
The investigators stated that their study demonstrated that “acute ingestion of the tested
dietary supplements result[] in an increase in myocardial work (as measured specifically by
[systolic blood pressure]).” (Id. at 42). As to the results of the chronic portion of their study, the
investigators stated that there was “no increase in resting [heart rate] or blood pressure . . . nor
are bloodborne variables negatively impacted with either supplement.” (Id. at 42-43). The study
concluded that use of OxyElite Pro and Jack3d “[did] not elevate resting [heart rate, systolic
15
Tyler M. Farney et al., Hemodynamic and Hematologic Profile of Healthy Adults Ingesting Dietary
Supplements Containing 1,3-Dimethylamylamine and Caffeine, 2012 Nutrition & Metabolic Insights 1
(2012). (Defs.’ Ex. V 34-45, ECF No. 223).
No. EP-13-CV-323-DCG
21
blood pressure, diastolic blood pressure, and rate pressure product] when ingested daily for
[fourteen] days.” (Id. at 44). Additionally, the study concluded that acute ingestion increased
systolic blood pressure but did not have statistically significant increases in diastolic blood
pressure or rate pressure product. (See id.)
e. A Finished Dietary Supplement Stimulates Lipolysis and Metabolic Rate in Young
Men and Women16
This study tested six men and six women in order to determine “the acute effects of
[OxyElite Pro] on blood markers of lipolysis, as well as metabolic rate.” (Id. at 47). In this
study, subjects reported to the laboratory on two occasions, separated by three or four days,
between 6:00 am and 9:00 am. (See id. at 48). Subjects received placebo (cellulose) or OxyElite
Pro. (See id.) Subjects came to the laboratory in a ten hour fasted state and were asked not to
exercise twenty-four hours prior to testing. (See id.) After ten minutes of rest, the participants
had their heart rate, systolic blood pressure, and diastolic blood pressure measured and a blood
sample was drawn. (See id.) After the condition was ingested, subjects were measured again at
thirty, sixty, ninety, and one hundred twenty minutes post-ingestion. (See id.) Blood collections
occurred at the sixty and one hundred twenty minute time points. (See id.)
The investigators concluded that two capsules of OxyElite Pro resulted in an increase in
plasma glycerol and free fatty acids as well as metabolic rate. (See id. at 53). They also noted
that there was an increase in heart rate and blood pressure. (See id.)
16
Cameron G. McCarthy et al., A Finished Dietary Supplement Stimulates Lipolysis and Metabolic Rate
in Young Men and Women, 2012 Nutrition & Metabolic Insights 23 (2012). (Defs.’ Ex. V 46-54, ECF
No. 223).
No. EP-13-CV-323-DCG
22
f. Biochemical and Anthropometric Effects of a Weight Loss Dietary Supplement in
Healthy Men and Women17
The purpose of this study was to determine the effects of OxyElite Pro “on weight loss
and associated markers following an eight week intervention, using a randomized, placebo
controlled, double blind design.” (Id. at 56). The investigators hypothesized “that subjects in the
supplement group would experience more favorable changes in weight loss and associated
parameters compared to subjects in the placebo group.” (Id.) In this study, thirty-two subjects
reported to the laboratory on two occasions between 5:00 am and 11:00 am in a ten hour fasted
state. (See id. at 56-57). After ten minutes of rest, the participants had their heart rate, systolic
blood pressure, and diastolic blood pressure measured and a blood sample was drawn.
(See id. at 57).
Subjects had their height, weight, waist and hip circumference, skinfold
thickness, and body composition measured. (See id.) Subjects were randomly assigned placebo
or OxyElite Pro. (See id.) Sixteen subjects, eight men and eight women, were assigned to the
two conditions. (See id.) They were required to ingest one capsule per day and, starting on day
four, were allowed to ingest a second capsule. (See id.) They were asked not to perform any
exercise two days prior to each test day. (See id. at 58).
The investigators found that OxyElite Pro “may assist in weight and body fat loss, while
improving selected markers of the blood lipid panel.”
(Id. at 59).
They noted that “the
supplement [did] not result in any adverse effects pertaining to bloodborne markers of safety (eg,
liver function).” (Id. at 60). The investigators further stated that “the supplement [did] result in
an increase in resting heart rate of approximately six beats per minute[,] [a]lthough this increase
in heart rate was not accompanied by a significant increase in systolic or diastolic blood pressure
17
Cameron G. McCarthy et al., Biochemical and Anthropometric Effects of a Weight Loss Dietary
Supplement in Healthy Men and Women, 2012 Nutrition & Metabolic Insights 13 (2012). (Defs.’ Ex. V
55-64, ECF No. 223).
No. EP-13-CV-323-DCG
23
. . . .” (Id.)
g. Physiological and Pharmacokinetic Effects of Oral 1,3-Dimethylamylamine
Administration in Men18
The Schilling study sought to “determine the pharmacokinetic profile of a single [twentyfive milligram] oral dosage of DMAA alone through [twenty-four] hours post-ingestion.”
(Id. at 66). The study recruited eight men to participate. (See id.) The subjects reported in the
morning following an eight hour fast, were asked not to use any dietary supplements containing
DMAA for seventy-two hours prior to testing and to refrain from exercise thirty-six hours prior
to testing. (See id.) The subjects had their resting heart rate and blood pressure measured,
cutaneous temperature measured via forehead, and a blood sample drawn. (See id. at 66-67).
Subjects then received a twenty-five milligram dose of DMAA and the same measurements were
taken over a twenty-four hour period at intervals of fifteen minutes, thirty minutes, forty-five
minutes, one hour, one and one half hours, two hours, two and one half hours, three hours, four
hours, five hours, six hours, eight hours, twelve hours, and twenty-four hours. (See id. at 67).
Subjects remained in the laboratory for the first eight hours of testing and were given meals after
the three and six hour mark, between the eight and twelve hour mark, and between the twelve
and sixteen hour mark. (See id.) The subjects were instructed to have minimal physical activity
and return to the laboratory eight hours fasted for the last blood draw. (See id.)
The investigators noted that one subject had extremely high levels of DMAA in his blood
and, therefore, his data was excluded from the results. (See id. at 68-69). The investigators
stated that “[t]he most important finding in this investigation is the relatively low plasma
concentrations of DMAA corresponding to the [twenty-five milligram] oral dose, and the lack of
18
Brian K. Schilling et al., Physiological and Pharmacokinetic Effects of Oral 1,3-Dimethylamylamine
Administration in Men, BMC Pharmacology & Toxicology, Oct. 2013, at 1. (Defs.’ Ex. V 65-74, ECF
No. 223).
No. EP-13-CV-323-DCG
24
meaningful physiologic effects associated with the single dose.”
(Id. at 70).
The study
determined that DMAA has a longer half-life than caffeine. (See id. at 71). The authors
indicated that “[w]hile a significant increase in temperature at [twelve] hours post-ingestion is
noted in our data, the values are still within normal range of 36.1 to 37.8°C, suggesting little
meaningful effect is present.” (Id. (emphasis added)) The authors speculated that the increase in
temperature “is likely attributable to the fact that subjects were out of the laboratory and reported
back for testing, and that activity associated with leaving and returning to the laboratory slightly
[their] elevated temperature.” (Id.) They stated that “[f]urther study of DMAA effects on
temperature in the context of exercise and heat exposure is warranted.” (Id. at 72). On blood
pressure, the study found that blood pressure values were “within normal clinical ranges.” (Id. at
73). The investigators concluded that “it appears that the concern over adverse health-related
effects of DMAA is specific to the dosage ingested by the individual.” (Id.) The investigators
further concluded “our data indicate minimal to no change in heart rate, blood pressure, or body
temperature, and no adverse effects were noted.” (Id.)
h. Impact of a Dietary Supplement Containing 1,3-Dimethylamylamine on Blood
Pressure and Bloodborne Markers of Health: A 10-Week Intervention Study19
In this study, the authors sought to “extend our prior findings related to the use of
[DMAA] in a combined product by using a [ten] week intervention trial to determine the change
in selected markers of health and safety in a sample of healthy men.” (Id. at 76). Here, there
were thirty men who were instructed to maintain their current exercise routine and diet but were
asked to refrain from exercise forty-eight hours prior to coming to the laboratory. (See id.) The
subjects reported to the laboratory in the morning following an eight hour fasted state.
19
Paul N. Whitehead et al., Impact of a Dietary Supplement Containing 1,3-Dimethylamylamine on Blood
Pressure and Bloodborne Markers of Health: A 10-Week Intervention Study, 2012 Nutrition & Metabolic
Insights 33 (2012). (Defs.’ Ex. V 75-81, ECF No. 223).
No. EP-13-CV-323-DCG
25
(See id. at 77). After resting for ten minutes, subjects had their heart rate and blood pressure
measured and a blood sample was drawn. (See id.) Subjects were assigned a placebo powder or
Jack3d and were instructed to consume one to three servings on each workout day, thirty minutes
prior to their exercise. (See id.) Subjects had a mean of four workout days per week and did not
consume the supplement on non-workout days. (See id.) Twenty-five subjects completed the
testing and were included in the results. (See id.)
The investigators found that DMAA “[did] not significantly increase resting heart rate or
blood pressure (although systolic blood pressured increased [approximately six millimeters of
mercury] with the supplement.” (Id. at 79). They further found that “the supplement [did] not
adversely impact bloodborne biomarkers of health.” (Id.) They note, however, that “additional
well-designed experiments of similar scope, inclusive of larger sample sizes, are needed to
extend the findings presented within. It is only through such work that our ability to generalize
these findings to the population at large will be possible.” (Id.) The investigators concluded that
“a dietary supplement contained [DMAA] consumed for a period of [ten] weeks [did] not result
in a statistically significant increase in resting heart rate or blood pressure in a sample of healthy
men, nor [did] the supplement negatively impact bloodborne biomarkers of health.” (Id. at 81).
2. The Marsh Study20
This study was primarily conducted on dogs in order to determine the pharmacology of
various compounds and their effects on blood pressure. (See Pls.’ Ex. R-14 2, ECF No. 196-38).
Sixty-three adult dogs were anesthetized and injected with various compounds tested; five dogs
per compound. (See id.) Seven unanesthetized dogs received one compound every four days.
(See id. at 2-3). Records of pithed dogs were also measured. (See id. at 3). The investigators
20
David F. Marsh, The Comparative Pharmacology of the Isomeric Heptylamines, 94 J. Pharmacology &
Experimental Therapeutics 225 (1948). (Pls.’ Ex. R-14, ECF No. 196-38).
No. EP-13-CV-323-DCG
26
also studied tissue segments from five rabbits. (See id. at 6).
As a result of the Marsh study, an “epinephrine-agent equivalence” table was created.
(Id. at 3-4). This study examined the amount of epinephrine it took in each type of dog to have
the same blood pressure increases. (See id. at 3). The study reported that DMAA was the most
potent of the compounds tested. (See id. at 5).
The study also tested DMAA, one of three of the most active agents, in one human
participant, two and one half hours after a morning meal. (See id. at 6). The investigators
measured blood pressure and heart rate every fifteen minutes for three hours while the subject
remained sitting. (See id.) The dose given was two milligrams per kilogram in an individual
who weighed seventy-nine kilograms. (See id.) For DMAA, “blood pressure slowly rose from a
normal of 112/68 (70) to 134/90 in [ninety] minutes after the ingestion of [DMAA].” (Id.) The
study found that blood pressure and heart rate returned to normal after one hundred fifty to one
hundred eighty minutes. (See id. at 7). The study noted that a three milligram per kilogram dose
was not well tolerated. (See id.) The study found that DMAA had a long duration of action
similar to amphetamine. (See id.) The study concluded that DMAA had pressor action that “is
about 1/200 as active as epinephrine.” (Id. at 8). Additionally, the study stated that “[o]rally, in
man, the [compounds] have but little pressor action.” (Id.)
3. The Coyle Study
The Coyle study was “designed to determine whether manipulation of plasma
catecholamine levels during exercise could alter [cutaneous vascular conductance] and
subsequently core temperature.” (Pls.’ Ex. R-25 3, ECF No. 197-2). The study was also
designed “to determine whether adrenaline or glucose infusion can alter the decline in stroke
volume, cardiac output[,] or blood pressure that we have observed previously during exercise
with concomitant dehydration.” (Id.)
No. EP-13-CV-323-DCG
27
In this study, epinephrine was intravenously infused along with saline in one trial in a
dose of 0.1 micrograms per kilogram per minute. (See id.) In another trial, only saline was
infused. (Id.) In the third trial, glucose was infused. (See id.) The authors hypothesized “that
levels of circulating catecholamines achieved with our treatments (i.e. glucose infusion < saline
infusion < adrenaline infusion) will result in corresponding differences in [cutaneous vascular
conductance] and core temperature.” (Id.)
The study included seven cyclists who were acclimated to the heat in the testing
conditions by cycling at least four times within ten days. (See id.) The environment was set at
approximately 33.1°C.21 (See id.) The subjects were intravenously infused during their exercise
with the conditions, however, when they were administered epinephrine, they exercised for only
one hundred twenty minutes rather than one hundred fifty minutes to prevent heat injury.
(See id.) The subjects reported in a euhydrated and twelve hour fasted state and were given the
same diet forty-eight hours prior to testing. (See id.) The subjects were fitted with a heart
monitor and had catheters inserted into their arms for blood sampling and infusion. (See id.)
The subjects entered the environmental chamber and instruments were attached to measure blood
flow. (See id.) After fifteen minutes of rest, temperatures were recorded and a blood sample was
drawn before exercise began.
(See id.)
While the subjects were exercising, heart rate,
temperature, oxygen uptake, cardiac output, blood pressure, and blood flow were measured.
(See id.)
The study found that epinephrine caused “a rapid and maintained decrease” in cutaneous
blood flow and cutaneous vascular conductance, a 0.3-0.4°C increase in oesophageal
21
Dr. Coyle agreed that this was between approximately 90.1°F and 92.8°F. (See Dr. Coyle Dep. 104:49).
No. EP-13-CV-323-DCG
28
temperature,22 and an increase in heart rate. (Id. at 10). The authors concluded that “these
observations indicate that large increases in plasma catecholamine levels cause hyperthermia
during exercise by vasoconstricting the skin.
This suggests a possible role of adrenergic
vasoconstriction of skin in causing hyperthermia during prolonged exercise in the heat.”
(Id. at 12).
4. The Department of Defense Study23
The Department of Defense conducted a study on DMAA after removing all DMAAcontaining products from military bases. (See Pls.’ Ex. R-16 4, ECF No. 196-40). The study
contains three phases: 1) a literature review and survey of adverse events; 2) patient interviews
and a review of FDA reported adverse events; and 3) a case control study on the association
between DMAA and adverse health effects. (See id. at 7). In Phase I, the investigators reviewed
forty adverse medical event reports and “reviewed the likelihood of DMAA being casually
linked with the events using a Naranjo Scale methodology.”24 (Id.) The investigators also
reviewed available case reports in the scientific literature, the Bloomer Studies, FDA warning
letters, and literature on whether DMAA is naturally-occurring in geranium plants and oils.
(See id. at 8-9). In Phase II, the Armed Forces Medical Examiner System reviewed autopsy data
and fluid samples from service members who died from exercise and heat-related injuries.
(See id. at 9). In Phase III, the authors reviewed responses of 1,789 soldiers to determine if
DMAA-containing supplements caused various adverse injuries. (See id.) The study determined
22
Dr. Coyle agreed that this was approximately a 0.6°F to a 1°F increase in temperature. (Dr. Coyle Dep.
163:22-168:6).
23
Col. John Lammie et al., Report of the Department of Defense 1,3 Dimethylamylamine (DMAA) Safety
Review Panel (2013). (Pls.’ Ex. R-16, ECF No. 196-40).
24
The study admits that there can be flaws with the use of this methodology because if any alternative
potential causes exist, that cause becomes the accepted explanation. (See Pls.’ Ex. R-16 22, ECF No.
196-40).
No. EP-13-CV-323-DCG
29
that the soldiers were no more likely to have used DMAA than controls with an adjusted odds
ratio of 0.85. (See id.) There was a ninety-five percent confidence interval including 1.0, which
means that the results were not statistically significant. (See id. at 9-10). The study stated that
“[t]he existing evidence does not conclusively establish that DMAA-containing substances are
causally-associated with adverse events.” (Id. at 11). The study also stated that “a consistent
theme among the studies is that DMAA use potentially affects cardiovascular function, just as
other sympathomimetic stimulants.” (Id.)
D.
Defendants’ Rule 702 and Daubert Challenges to Dr. Cantilena, Dr. Mills, and Dr.
Rusyniak
Dr. Cantilena, Dr. Mills, and Dr. Rusyniak are Plaintiffs’ experts on causation.25
(See Pls.’ Omnibus Resp. 19-20, ECF No. 200; Hr’g Tr. 103:5-13, Apr. 28, 2015, ECF No. 324).
Although the Court is not tasked with determining whether the evidence offered through
Plaintiffs’ experts is sufficient to meet their ultimate burden of proof, Plaintiffs’ experts must
establish reliable methodology for their opinions on general and specific causation. “General
causation is whether a substance is capable of causing a particular injury or condition in the
general population.”
Johnson, 685 F.3d at 468 (quoting Knight, 482 F.3d 347, 351
(5th Cir. 2007)). “[S]pecific causation is whether a substance caused a particular individual’s
injury.” Id. (quoting Knight, 482 F.3d at 351).
In this case, Dr. Cantilena and Dr. Mills offer opinions on general causation: that DMAA
can cause hyperthermia in susceptible individuals. (See Pls.’ Ex. HH ¶ 20, ECF No. 197-29;
25
Plaintiffs use a large portion of their brief arguing the collective opinions of Dr. Cantilena, Dr. Mills,
and Dr. Rusyniak. (See Pls.’ Omnibus Resp. 19-31, ECF No. 200). The Court must, however, evaluate
each expert individually to determine if their opinions are relevant and reliable.
No. EP-13-CV-323-DCG
30
Pls.’ Ex. JJ ¶ 14, ECF No. 197-31). Dr. Cantilena and Dr. Rusyniak26 offer opinions on specific
causation: that DMAA was a substantial contributing factor in Decedent’s hyperthermia and
death.27 (See Pls.’ Ex. HH ¶ 21, ECF No. 197-29; Pls.’ Ex. II ¶ 9, ECF No. 197-30).
1. Dr. Cantilena
Dr. Cantilena opined that DMAA is a sympathomimetic compound of the aliphatic amine
class. (See Pls.’ Ex. HH ¶ 8, ECF No. 197-29). He further opined that sympathomimetic
compounds cause vasoconstriction and increased blood pressure, and that increased blood
pressure is a surrogate marker for increased heat production. (See id. at ¶ 15; Dr. Cantilena Dep.
154:6-8; Hr’g Tr. 107:4-109:16, Apr. 27, 2015 PM, ECF No. 323). Dr. Cantilena connected
DMAA to other sympathomimetics by stating that scientific literature showed DMAA
demonstrates a biologically plausible mechanism of action that DMAA “can” cause adverse
events or harm in susceptible individuals. (See Pls.’ Ex. HH ¶¶ 15, 20, ECF No. 197-29;
Pls.’ Ex. QQ, ECF No. 197-38; Dr. Cantilena Dep. 46:2-6, 46:20-25, 99:3-21, 132:15-19;
Hr’g Tr. 202:14-206:13, Apr. 27, 2015 AM, ECF No. 321; Hr’g Tr. 31:12-21, 35:6-23,
Apr. 27, 2015 PM, ECF No. 323). He explained that the notion that certain individuals are
susceptible to DMAA is based on outliers in the Bloomer studies,28 which are individuals who
Plaintiffs stated in their Omnibus Response and at the Daubert hearing that the “thrust” of Dr.
Rusyniak’s opinion relates to specific causation but he is qualified to testify about general causation. (See
Pls.’ Omnibus Response 55, ECF No. 200; Hr’g Tr. 103:8-14, Apr. 28, 2015, ECF No. 324). As to Dr.
Rusyniak’s differential diagnosis in his specific causation opinion, the Court will only consider the
parties’ arguments and Dr. Rusyniak’s opinion on general causation as they pertain to Dr. Rusyniak’s
ability to rule in DMAA as a cause.
26
27
Defendants argue that Decedent died of heat stroke rather than hyperthermia and that Plaintiffs have to
show that the amount of DMAA that Decedent took more likely than not caused his core body
temperature to go above 104°F. (See Defs.’ Omnibus Reply 45, ECF No. 218). Although the Court is not
considering the sufficiency of the evidence offered by Plaintiffs’ experts, the Court notes that the cause of
death listed in Decedent’s autopsy is “hyperthermia.” (See Defs.’ Ex. W 3, 8-9, ECF No. 215-5).
28
Dr. Cantilena identified two individuals out of ten in the Effects of 1,3 Dimethylamylamine study by
Bloomer and three individuals out of twelve in the A Finished Dietary Supplement study by McCarthy.
(See Dr. Cantilena Dep. 78:18-98:12; Hr’g Tr. 225:4-7, Apr. 27, 2015 AM, ECF No. 321;
see also Defs.’ Ex. V 3-12, 46-54, ECF No. 223).
No. EP-13-CV-323-DCG
31
had
a
more
dramatic
increase
in
systolic
blood
pressure
than
the
mean.
(See Dr. Cantilena Dep. 59:18-60:1, 78:18-98:12; Hr’g Tr. 209:4-212:24, 213:8-215:6, 217:8219:13, 222:10-234:2, Apr. 27, 2015 AM, ECF No. 321; Hr’g Tr. 4:7-7:9, Apr. 27, 2015 PM,
ECF No. 323). He also relied on the Schilling study to state that DMAA significantly increases
cutaneous temperature as measured at the forehead, although forehead temperature likely
underestimated core temperature by approximately 2°C. (See Pls.’ Ex. HH ¶ 15, ECF No. 19729; Hr’g Tr. 205:22-206:6, Apr. 27, 2015 AM, ECF No. 321).
To further confirm his theory of a biologically plausible mechanism of action, Dr.
Cantilena relied on the Coyle study, measuring core temperature and cutaneous vasoconstriction
from an infusion of epinephrine in seven humans, and the Marsh study, measuring the blood
pressure effects of epinephrine and DMAA, among other compounds, injected into dogs.
(See Pls.’ Ex. QQ, ECF No. 197-38; Dr. Cantilena Dep. 99:3-21, 101:1-7, 262:15-263:9, 265:17; Hr’g Tr. 12:14-43:5, 107:7-108:23, 120:1-135:23, 143:21-154:22, Apr. 27, 2015 PM,
ECF No. 323). Using these two studies, Dr. Cantilena converted the level of DMAA found in
Decedent’s antemortem blood to an epinephrine equivalent and determined that the converted
level was close enough to the plasma levels of epinephrine found in the Coyle study.
(See Hr’g Tr. 12:14-43:5, Apr. 27, 2015 PM, ECF No. 323).
Although there was an
approximately thirty percent difference between the values,29 Dr. Cantilena opined that DMAA
can increase core temperature, just as epinephrine did in the Coyle study, and he ultimately
concluded that “DMAA can cause adverse events in susceptible individuals.” (See id. at 35;
29
After making the conversions and calculations based on the Coyle and Marsh studies, Dr. Cantilena
found that the DMAA found in Decedent’s antemortem blood was equivalent to 0.97 micrograms of
epinephrine per liter. (Pls.’ Ex. 7, Daubert hearing). Dr. Cantilena then compared 0.97 to 1.30
micrograms of epinephrine per liter, the converted and calculated plasma concentrations of epinephrine
found in the subjects of the Coyle study. (Pls.’ Ex. 7, Daubert hearing). His conversions and calculations
concluded that 0.97 micrograms of epinephrine per liter is approximately equivalent to 1.30 micrograms
of epinephrine per liter. (Pls.’ Ex. 7, Daubert hearing).
No. EP-13-CV-323-DCG
32
Pls.’ Ex. HH ¶ 15, ECF No. 197-29).
The Court recognizes that “[t]rained experts commonly extrapolate from existing data”
and that “an expert may extrapolate data from studies of similar chemicals.”
Johnson,
685 F.3d at 460 (quoting Joiner, 522 U.S. at 146). However, “[s]everal post-Daubert cases have
cautioned [against] leaping from an accepted scientific premise to an unsupported one.” Moore,
151 F.3d at 279 (emphasis added) (collecting cases). “To support a conclusion based on such
reasoning, the extrapolation or leap from one chemical to another must be reasonably and
scientifically valid.” Id. (collecting cases). That is because “nothing in either Daubert or the
Federal Rules of Evidence requires a district court to admit opinion evidence which is connected
to existing data only by the ipse dixit of the expert. A court may conclude that there is simply
too great of an analytical gap between the data and the opinion proffered.”
Id. at 277
(quoting Joiner, 522 U.S. at 146).
A close examination of Dr. Cantilena’s opinion demonstrates that “there is simply too
great an analytical gap between the data and the opinion proffered.” Id. (quoting Joiner, 522
U.S. at 146). Plaintiffs state that a class effects theory would be “merely asserting that because
DMAA is a sympathomimetic and because other sympathomimetics have been demonstrated to
increase core body temperature leading to heat stroke, DMAA can also increase core body
temperature leading to heat stroke.”
(Pls.’ Omnibus Resp. 31, ECF No. 200).
Plaintiffs,
however, argue that their theory is that
DMAA causes heat stroke because other sympathomimetics . . . have been proven
to cause heat stroke through a mechanism of action that involves the exact same
effects DMAA has been demonstrated to have (vasoconstriction and metabolic
heat) in peer-reviewed, randomized clinical trials in humans. Further, that
mechanism is not theoretical but has been clinically proven at comparable levels
(accounting for potency and pharmacokinetics) to that found in [Decedent’s]
antemortem blood. It is not the class alone that connects DMAA to these other
drugs but the shared mechanism of action while accounting for differences in
potency and pharmacokinetics.
No. EP-13-CV-323-DCG
33
(Id.) While Plaintiffs argue that Dr. Cantilena’s opinion offers more than a class effects theory,
it is clear to the Court from Dr. Cantilena’s Rule 26 Expert Report, his Supplemental Rule 26
Expert Report, his deposition testimony, and his Daubert hearing testimony that all he is
asserting is a class effects theory.
Furthermore, because the Court finds below that Dr.
Cantilena’s conversions and calculations are unreliable, Plaintiffs’ argument that Dr. Cantilena
accounted for differences in potency and pharmacokinetics to support his mechanism of action
theory is ultimately tainted.
a. Class Effects
Dr. Cantilena’s methodology demonstrates that he is extrapolating from the class effects
of other sympathomimetics to form his opinion on DMAA without accounting for any of the
differences in sympathomimetics. See, e.g., Wells v. SmithKline Beecham Corp., 601 F.3d 375,
377-80 (5th Cir. 2010) (rejecting expert testimony analogizing between drugs in the class of
dopamine agonists and their ability to cause impulsive behaviors); Huss v. Gayden, 571 F.3d
442, 458-59 (5th Cir. 2009) (rejecting expert’s class of chemical theory as to sympathomimetic
drugs); see also McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1244-46 (11th Cir. 2005)
(rejecting expert’s analogy between ephedrine and PPA for failing to show the reliability of each
step of expert’s analysis). Dr. Cantilena testified in his deposition that “it is very impossible for
me to divorce DMAA from the known class effect of sympathomimetics” and later opined that
“[i]f it is established that DMAA is sympathomimetic, there is more than adequate evidence to
say that sympathomimetics are a known risk factor for drug-induced hyperthermia.”
(Dr. Cantilena Dep. 210:18-21, 211:15-18 (emphasis added)).
Dr. Cantilena’s opinion that
DMAA, like other sympathomimetics, increases blood pressure, heart rate, rate pressure product,
causes vasoconstriction, and increases cutaneous temperature, is similar to the expert’s opinion
excluded in Huss, which stated that sympathomimetics as a class tend to “rev the individual up.”
No. EP-13-CV-323-DCG
34
Huss, 571 F.3d at 458-59. Dr. Cantilena even used the same phrase by stating that “[t]he Jack3d
product has been shown to increase energy consumption by studies that were . . . conducted with
this specific product, and so that sort of increased energy use, if you will, revving up the body’s
metabolism, result[s] in an increased heat generation.” (Hr’g Tr. 204:15-20, Apr. 27, 2015 AM,
ECF No. 321 (emphasis added)).
Dr. Cantilena explained that his use of studies of other sympathomimetics to make
conclusions that DMAA causes hyperthermia was based on “a class effect, a known
pharmacologic situation.” (Dr. Cantilena Dep. 210:25-211:8 (emphasis added)). He explained
that “human data from Schilling and from McCarthy . . . supports what the molecule is expected
to do by virtue of its pharmacologic category . . . an alpha agonist.” (Hr’g Tr. 204:15-20, Apr.
27, 2015 AM, ECF No. 321).
However, Dr. Cantilena also acknowledged that
sympathomimetics can have dissimilar effects. (See id. at 136:13-15; 138:5-140:12). Given that
Dr. Cantilena’s opinion merely compares sympathomimetics as a class, without accounting for
any differences, the Court concludes that his opinion is unreliably extrapolating from the class
effects of sympathomimetics to reach his conclusion that DMAA can cause hyperthermia in
susceptible individuals.
b. The Bloomer Studies
Dr. Cantilena relies on the Bloomer studies to provide a biologically plausible
mechanism of action demonstrating that DMAA can cause hyperthermia in the general
population. Although the Bloomer studies represent the majority, if not the totality, of clinical
studies where participants took DMAA and had various health parameters measured, the studies
lack a significant sample size which may affect the statistical significance of their outcomes.
See, e.g., Orthoflex, Inc. v. ThermoTek, Inc., 986 F. Supp. 2d 776, 801-02 (N.D. Tex. 2013)
(citing Overton v. City of Austin, 871 F.2d 529, 544 (5th Cir. 1989) (Jones, J., concurring)
No. EP-13-CV-323-DCG
35
(“Whether a given [test result] should be regarded as statistically significant must be determined
on a case by case basis since the value signifying statistical significance is dependent upon
sample size.”). In fact, in the Whitehead study, Impact of a Dietary Supplement Containing 1,3Dimethylamylamine on Blood Pressure and Bloodborne Markers of Health: A 10-Week
Intervention Study, the authors stated
Due to the fact that our sample size is small, additional well-designed experiments
of similar scope, inclusive of larger sample sizes, are needed to extend the
findings presented within. It is only through such work that our ability to
generalize these findings to the population at large will be possible.
(Def.’s Ex. V. 79, ECF No. 223). Moreover, all of the Bloomer studies indicate that further
studies need to be performed in order to better understand the effects of DMAA on humans. (See
id. at 9-10, 19, 33, 44, 53, 63, 73, 81).
It is clear from Dr. O’Brien, Plaintiffs’ expert biostatistician, that the scientific literature
on DMAA presents insufficient data to conclude that DMAA is safe or that DMAA causes harm
because the sample sizes are too small. (See Pls.’ Ex. TT ¶¶ 5-9, ECF No. 197-41; Dr. O’Brien
Dep. 32:25-33:3, 72:18-77-6, 78:19-81:25, 128:21-129:12). In line with Dr. O’Brien’s testimony
and the Court’s concern with relating small study populations to the general population, Dr.
Cantilena’s Rule 26 Expert Report opined that “no adequately powered study has ever been
performed on DMAA to accurately assess the occurrence of uncommon or relatively rare
adverse health outcomes in the general population.” (Pls.’ Ex. HH ¶ 8, ECF No. 197-29
(emphasis added)). Dr. Cantilena admitted that the Bloomer studies do not conclude that DMAA
causes harm in individuals. (See Dr. Cantilena Dep. 59:5-9, 60:20-23). In reference to the
Schilling study, Dr. Cantilena testified that “it would be really unrealistic to expect that seven
subjects in one trial would truly characterize the entire population.” (Hr’g Tr. 219:4-10, Apr.
27, 2015 AM, ECF No. 321 (emphasis added)). Thus, the Court finds that Dr. Cantilena fails to
No. EP-13-CV-323-DCG
36
reliably use scientific methods to reach his conclusions on a biologically plausible mechanism.
See Knight, 482 F.3d at 354 (“Where an expert otherwise reliably utilizes scientific methods to
reach a conclusion, the lack of textual support may go to the weight, not the admissibility of the
expert’s testimony.” (emphasis added) (internal quotation marks and citations omitted)).
Moreover, the Court finds that it is improper for Dr. Cantilena to extrapolate from the
Bloomer studies that DMAA causes hyperthermia in the general population because DMAA
demonstrated an acute increase in systolic blood pressure in a small number of individuals. See
Anderson v. Bristol Myers Squibb Co., No. Civ. A. H-95-0003, 1998 WL 35178199, at *1
(S.D. Tex. Apr. 20, 1998) (holding that an expert may not use studies purporting to prove one
issue in order to infer that the same study proves a different issue because the inferential process
is subject to Daubert); see also McClain, 401 F.3d at 1246 (“As the court stated, ‘[e]vidence
suggest[ing] that [a chemical] may cause ischemic stroke does not apply to situations involving
hemorrhagic stroke. This is a ‘leap of faith’ supported by little more than the fact that both
conditions are commonly called strokes.’” (quoting Rider v. Sandoz Pharm. Corp.,
295 F.3d 1194, 1202 (11th Cir. 2002)). The Bloomer studies simply do not make conclusions
about DMAA causing hyperthermia. See Huss, 571 F.3d at 459 (“It is axiomatic that causation
testimony is inadmissible if an expert relies upon studies or publications, the authors of which
were themselves unwilling to conclude that causation had been proven.” (collecting cases)). Dr.
Cantilena admitted that he had not relied on any studies indicating that an increase in blood
pressure related to an increase in cutaneous vasoconstriction in humans. (See Hr’g Tr. 108:2023, Apr. 27, 2015 PM, ECF No. 323). Thus, Dr. Cantilena’s attempt to go from vasoconstriction
and increased blood pressure to increased heat production, thereby causing harm to susceptible
individuals, ultimately has too many analytical gaps in the causal chain. Therefore, the Court
finds that Dr. Cantilena is not exhibiting the rigors of science that he would use in the laboratory
No. EP-13-CV-323-DCG
37
but rather, he is attempting to use unscientific speculation to support his opinion.
c. Outliers
Dr. Cantilena’s used outliers in the raw data from the Effects of 1,3-Dimethyamlamine
study by Bloomer and the A Finished Dietary Supplement study by McCarthy to support his
causation opinion.
Dr. Cantilena admitted that these studies did not measure cutaneous
vasoconstriction or core temperature in the subject participants. (See Hr’g Tr. 106:18-107:3,
Apr. 27, 2015 PM, ECF No. 323).
He also readily acknowledged that the outliers only
demonstrate safety signals rather than a causal relationship between DMAA and hyperthermia in
the general population. (See Dr. Cantilena Dep. 58:16:21, 74:10-19; Hr’g Tr. 58:3-11, 70:21-23,
75:19-77:7, Apr. 27, 2015 PM, ECF No. 323). Dr. Cantilena further testified that “I never make
the statement that this is proof of a definitive causal safety issue.” (Hr’g Tr. 90:6-7 (emphasis
added)). He opined that outliers are “not proof that it is a true safety finding, but it’s suggestive
of a signal.” (Id. at 89:113-14 (emphasis added)). Dr. Cantilena conceded that “[a]ssociation is
the initial step in the attempt for causation.” (Dr. Cantilena Dep. 47:18-19).
Despite his reliance on outliers, Dr. Cantilena was unable to explain how the outlier data
related to the general population.
He testified that the outliers demonstrated adverse
hemodynamic outcomes “for those individuals” and that “to see if those individuals would be
represented in [twenty] percent or [twenty-five] percent of a population taking the product . . .
would be an area of concern.” (Dr. Cantilena Dep. 150:19-151:3 (emphasis added)). He
explained that he was not relying on statistical analysis to identify outliers and that he did “not
believe a statistical definition [was] required in [this] setting as we don’t require that in the
context of drug review for safety signals.” (Hr’g Tr. 62:6-17, Apr. 27, 2015 PM, ECF No. 323).
While the outliers Dr. Cantilena relies on may represent safety signals that could be important in
the regulatory context, the courtroom is not the place to develop the research necessary to create
No. EP-13-CV-323-DCG
38
a causal connection in the tort context. See Allen, 102 F.3d at 198 (a regulatory agency’s
“threshold of proof is reasonably lower than that appropriate in tort law, which ‘traditionally
makes more particularized inquiries into cause and effect’”).
As Dr. Cantilena’s outlier
testimony demonstrates, a relationship merely suggestive of association is not scientifically
reliable evidence of causation. See id. at 197.
When the Court asked Dr. Cantilena to explain what literature supports the use of outliers
for his causation opinion, he discussed the difference between statistical definitions and
clinically meaningful differences. (See Hr’g Tr. 67:9-69:25, Apr. 27, 2015 PM, ECF No. 323).
He further explained that with small clinical trials, “[y]ou don’t know the generalized ability
through the whole world. It’s probably not [twenty] percent, but because you had such a small
sample size, it just happened to be [twenty] percent.” (Id. at 69:16-19). When the Court again
asked Dr. Cantilena to state what literature supported his opinion, he stated “there are guidances
at FDA that sort of talk about, you know, safety.” (Id. at 70:1-13). He also opined that “the
FDA would never accept such . . . a small sample to characterize the population. But this is all
we had.” (Hr’g Tr. 218:24-219:3, Apr. 27, 2015 AM, ECF No. 321 (emphasis added)). Despite
this testimony, Plaintiffs ask the Court to find Dr. Cantilena’s opinion reliable but the Court
simply cannot oblige.
Furthermore, Dr. Cantilena failed to explain how Decedent is similar to the outliers and
dissimilar to the remaining study population but admits that Decedent “has characteristics that
are similar to both groups.” (Dr. Cantilena Dep. 162:17-22). He testified that he could not use
the raw data in isolation to reach the conclusion that Decedent was similar to the outliers rather
than the other study participants. (See id. at 163:22-164:5). Of the five outliers that Dr.
Cantilena recognized, three were female. (See Hr’g Tr. 228:25-232:6, Apr. 27, 2015 AM,
ECF No. 321; Hr’g Tr. 6:15-7:9, Apr. 27, 2015 PM, ECF No. 323). Furthermore, the outliers
No. EP-13-CV-323-DCG
39
from the A Finished Dietary Supplement study by McCarthy used OxyElite Pro rather than
Jack3d, the difference of which Dr. Cantilena found to be irrelevant because both substances
contain DMAA. (See Hr’g Tr. 233:21-234:2, Apr. 27, 2015 AM, ECF No. 321; Hr’g Tr. 77:1378:18, Apr. 27, 2015 PM, ECF No. 323). Additionally, the outliers from the Effects of 1,3Dimethylamylamine study by Bloomer ingested seventy-five milligrams of DMAA plus two
hundred fifty milligrams of caffeine, almost double the amount of DMAA ingested by Decedent,
which is assumed to be forty milligrams. (See Hr’g Tr. 4:7-7:9, 81:17-82:6, Apr. 27, 2015 PM).
The Court finds that these unexplained gaps further demonstrate the unreliability of Dr.
Cantilena’s opinion.
d. Conversions and Calculations
Even given Plaintiffs’ argument that Dr. Cantilena asserts more than a class effects theory
and assuming without deciding that Dr. Cantilena’s conversions and calculations were timely
submitted,30 the Court finds that they are unreliable. It is clear that Dr. Cantilena’s conversions
and calculations do not stem from research conducted independent of this litigation but rather,
they have been developed for the purpose of his testimony in this case.31
See Newton,
243 F. Supp. 2d at 678 (citing Daubert II, 43 F.3d at 1317 (“One very significant fact to be
considered is whether the experts are proposing to testify about matters growing naturally and
directly out of research they have conducted independent of the litigation, or whether they have
On the Friday before the Daubert hearing, Defendants filed a “Pre-Hearing Motion to Exclude
Untimely Disclosures by Plaintiffs’ Expert Louis Cantilena” (ECF No. 258), to challenge the timeliness
of Dr. Cantilena’s conversions and calculations that were produced on the Monday before the Daubert
hearing. At the hearing, the Court made clear that it would hear testimony from Dr. Cantilena on his
conversions and calculations, which were a subject set forth in the Court’s Order, and would reserve
ruling on Defendants Motion until a later time. (See Hr’g Tr. 199:7-200:13, Apr. 27, 2015 AM, ECF No.
321; Order 2, ECF No. 235). As the Court ultimately finds Dr. Cantilena’s conversions and calculations
to be unreliable, the Court will deny Defendants’ Pre-Hearing Motion as moot.
30
31
Although it is unclear when exactly Dr. Cantilena created his conversions and calculations, it appears
to the Court that they may have been prepared sometime in December 2014 after he received the Coyle
study. (Hr’g Tr. 12:22-17:7, Apr. 27, 2015 PM, ECF No. 323).
No. EP-13-CV-323-DCG
40
developed their opinions expressly for purposes of testifying.”)). Moreover, this methodology
has not been tested or subject to peer review. See Daubert II, 43 F.3d at 1318 (“Peer review and
publication do not, of course, guarantee that the conclusions reached are correct . . . . But the test
under Daubert is not the correctness of the expert’s conclusions but the soundness of his
methodology.” (citation omitted)). Dr. Cantilena provides no indication that other experts in his
field use similar methodologies to extrapolate between sympathomimetics and he pointed to no
literature making these comparisons to validate his approach.
See id. at 1317 (“That the
testimony proffered by an expert is based directly on legitimate, preexisting research unrelated to
the litigation provides the most persuasive basis for concluding that the opinions he expresses
were ‘derived by the scientific method.’”). Compounding the concern the Court has with Dr.
Cantilena’s development of his conversions and calculations solely for the purpose of this
litigation, the conversions and calculations are supported merely by his assurances amounting to
too large of an analytical gap to allow the trier of fact to hear this testimony.
In support of his conversions and calculations in translating from one sympathomimetic
to another, Dr. Cantilena testified that
[t]he pharmacologic principles and methodology are standard when you look at
receptors specific actions for which there is known potency. Any drug reference
will give you, for example, morphine equivalence, to allow you to transfer from
one opiate analgesic to another based on relative potency, so that you don’t
change pain medicine and inadvertently overdose a patient, because the different
molecule has a different potency. This is a [well-established] pharmacologic
method that is actually used in clinical practice.
(Dr. Cantilena Dep. 134:24-135:10). He further explained that he had support from
clinical teaching material from my lectures. It’s also in handbooks of pharmacy,
handbooks of pharmacotherapeutics. And the example was the translation to
equal potent analgesics, based on morphine equivalence. That is, being able to
compare different chemical molecules that have the same receptor effect,
analogous to sympathomimetics, to be able to translate their differential potency.
(Id. at 190:17:191:14). Other than the morphine equivalence technique used in clinical situations
No. EP-13-CV-323-DCG
41
and Dr. Cantilena’s assurances that unidentified literature exists on the topic, Dr. Cantilena
provided no other literature to support his conversions and calculations from epinephrine to
DMAA. Therefore, the Court finds that Dr. Cantilena’s blanket assurances are an insufficient
basis for the Court to accept regarding the reliability of his conversions and calculations.
See Moore, 151 F.3d at 276 (“The expert’s assurances that he has utilized generally accepted
scientific methodology is insufficient.” (citation omitted)).
Dr. Cantilena began his conversions and calculations with the Marsh study which
measured blood pressure effects in barbitalized, unanesthetized, and pithed dogs following the
injection of various compounds, including DMAA.
(See Hr’g Tr. 15:15-16:4, 20:6-23:25,
119:12-123:18, Apr. 27, 2015 PM, ECF No. 323). Although animal studies are not per se
inadmissible, the Fifth Circuit has “previously recognized the ‘very limited usefulness of animal
studies when confronted with questions of toxicity.’”
Johnson, 685 F.3d at 463
(quoting Allen, 102 F.3d at 197). Moreover, “studies of the effects of chemicals on animals must
be carefully qualified in order to have explanatory potential for human beings.”
Id.
(quoting Allen, 102 F.3d at 197). Dr. Cantilena explained that he was being “very conservative”
in choosing the epinephrine equivalence calculated in the Marsh study for barbitalized dogs.
(See Hr’g Tr. 21:4-23:23, Apr. 27, 2015 PM, ECF No. 323). Given that he did not choose
unanesthetized dogs because they have confounding factors that can have an effect on the results
and that he declined to use pithed dogs because they are an unrealistic model, the Court finds that
Dr. Cantilena was essentially left with barbitalized dogs by default. (See id. at 22:4-23:21,
123:2-18). While Dr. Cantilena stated that dog models are “the most used” by the FDA and that
the dog model is still “valid,” he provided no support for his extrapolation from the dog data to
human data other than his assurances that literature existed on the subject. (See id. at 20:16-21:1,
126:25-127:18, 133:2-137:22). Moreover, even if it did exist, Dr. Cantilena freely admitted that
No. EP-13-CV-323-DCG
42
he did not rely on that material to form his opinion. (See id. at 135:5-136:11).
Dr. Cantilena then used the Coyle study, which injected epinephrine into seven cyclists
exercising in a temperature-controlled chamber at 92°F, to find the blood levels of epinephrine
that resulted in a change in body temperature. (See id. at 12:22-13:14, 144:3-8, Apr. 27, 2015
PM, ECF No. 323). Dr. Cantilena stated that “it really would have been ideal to have an infusion
of DMAA and [perform] the same type of experiment, but for a lot of, you know, reasons, that
was not feasible.” (Id. at 13:22-24). Thus, Dr. Cantilena compared plasma concentrations found
in the subjects in the Coyle study and blood levels of DMAA in Decedent, which Dr. Cantilena
stated “removes all the bioavailability variables” from his analysis. (See Dr. Cantilena Dep.
139:14-22, 140:24-141:8). The Court finds that Dr. Cantilena ignored the fact that the Coyle
study subjects were injected with epinephrine and that the dogs in Marsh were injected with
epinephrine and DMAA, as compared to Decedent who took DMAA orally. The Court finds
that Dr. Cantilena’s extrapolation from the Coyle study to prove a causal relationship between
DMAA and hyperthermia in the general population is based on nothing more than his ipse dixit,
which is an insufficient basis for the Court to find that his opinion is reliable.
Moreover, the Court finds that Dr. Cantilena failed to explain how a thirty percent
difference in the epinephrine equivalence of Decedent’s DMAA blood levels impacted his
conversions and calculations.32 (See Hr’g Tr. 35:6-23, Apr. 27, 2015 PM, ECF No. 323). Dr.
Cantilena does not explain why he chose 7.1 pmol ml-1 rather than 7.9 pmol ml-1, which is the
higher value in the range that caused the same temperature increase. Dr. Cantilena also failed to
explain how the same temperature increase shown in the Coyle study, of approximately 1°F,
would be the same as Decedent’s temperature increase with a thirty percent lower level of
32
As mentioned above, the values were 0.97 micrograms of epinephrine per liter and 1.30 micrograms of
epinephrine per liter. (Pls.’ Ex. 7, Daubert hearing).
No. EP-13-CV-323-DCG
43
epinephrine. Thus, the Court finds that Dr. Cantilena’s conversions and calculations are “not an
exercise in scientific logic but in the fallacy of post-hoc propter-hoc reasoning, which is as
unacceptable in science as in law.” Black, 171 F.3d at 308.
e. Case Reports
Finally, insofar as Dr. Cantilena used case reports to support his opinion, the Court finds
this methodology to be unreliable. Dr. Cantilena’s Rule 26 Expert Report cites to a variety of
case reports including FDA MedWatch reports and a case study by Gee et al. to demonstrate
evidence of causation.
(See Pls.’ Ex. HH 17, ECF No. 197-29; Pls.’ Ex. R-1-R-9, R-26,
ECF Nos. 196-26-196-33, 197-3). A review of the case reports indicate that some of them deal
with products other than Jack3d, involve much higher doses of DMAA, and have injuries which
are different than those that Decedent suffered. (See, e.g., Pls.’ Ex. R-3, ECF No. 196-27
(injured male took Jack3d, “Pro Performance AMP, and Mega Men Sport” and was diagnosed
with hepatitis); Pls.’ Ex. R-5, ECF No. 196-29 (injured party “[a]woke one morning with intense
muscle aches” and was diagnosed with “hypokalemic myopathy”); Pls.’ Ex. R-8, ECF No. 19632 (injured male took seven scoops of Jack3d and had palpitations and weakness); Pls.’ Ex. R26, ECF No. 197-3 (explaining that three individuals who took pills or a powder containing
various doses of DMAA and also drank alcohol experienced cerebral hemorrhaging)).
Moreover, courts have rejected the use of case reports to form opinions on causation.
See Newton, 243 F. Supp. 2d at 680 & n.11 (“The Fifth Circuit and many other courts have
soundly rejected case reports as an acceptable basis for causation.” (footnote omitted));
Castellow v. Chevron USA, 97 F. Supp. 2d 780, 787 (S.D. Tex. 2000). Even Dr. Cantilena stated
that “individual case reports would not be able to establish causation and would be hypothesisgenerating signals requiring further confirmation.”
(Dr. Cantilena Dep. 56:1-9 (emphasis
added)). Therefore, the Court rejects Dr. Cantilena’s opinion based on the cited case reports.
No. EP-13-CV-323-DCG
44
f. Dr. Cantilena’s Second Supplemental Rule 26 Expert Report and Declaration
Despite the unreliability of Dr. Cantilena’s opinion established above, he sets forth a
theory discussing the quantity and properties of the ingredients that form OxyElite Pro and
Jack3d in order to demonstrate that “without DMAA [Decedent’s] mild dehydration would not
have caused his hyperthermia or death.”33 (Dr. Cantilena Second Supplemental Report & Decl.
¶¶ 5-15, ECF No. 327-1). Assuming arguendo that his Second Supplemental Rule 26 Expert
Report and Declaration is timely,34 the Court finds that Dr. Cantilena’s opinion is unreliable.
After reviewing the ingredients and their quantities found in OxyElite Pro, Dr. Cantilena opines
that “DMAA and caffeine account[] for a substantial part of the increase metabolic activity found
in the McCarthy study, A Finished Dietary Supplement.”
(Id. at ¶ 9 (emphasis added)).
Likewise, for Jack3d, Dr. Cantilena states that the other ingredients and their quantities are “not
capable of causing vasoconstrictive reduction of heat dissipation and/or the heat generation
caused by DMAA.” (Id. at ¶ 11). However, the Court finds that Dr. Cantilena assumes, without
providing any further scientific bases, that DMAA can cause “increased heat generation” and
“cutaneous vasoconstriction causing hyperthermia and death,” which the Court has already
deemed unreliable. (Id. at ¶¶ 9, 11). Therefore, Dr. Cantilena’s Second Supplemental Rule 26
Expert Report and Declaration should also be excluded.
g. Conclusion on General Causation
In conclusion, the Court finds that Dr. Cantilena’s entire general causation opinion is
unreliable. Dr. Cantilena failed to account for any of the differences in extrapolating between
33
As mentioned above, Dr. Cantilena’s Second Supplemental Rule 26 Expert Report and Declaration was
filed on July 24, 2015. (ECF No. 327-1).
34
Dr. Cantilena’s Second Supplemental Rule 26 Expert Report and Declaration is dated May 1, 2015.
(Dr. Cantilena Second Supplemental Report & Decl. 4, ECF No. 327-1). As the Court ultimately finds
Dr. Cantilena’s Second Supplemental Rule 26 Expert Report and Declaration unreliable, the Court will
deny Defendants’ Pre-Hearing Motion as moot. (See Def.’s Reply 3, 10-11, ECF No. 303).
No. EP-13-CV-323-DCG
45
the class effects of other sympathomimetics and DMAA. Moreover, he provides no reliable
grounds to support his conclusion of a biologically plausible mechanism of action because the
Bloomer studies’ small sample sizes do not allow Dr. Cantilena to translate their results to the
general population and the studies do not reach the same conclusions drawn by Dr. Cantilena. In
addition, Dr. Cantilena’s use of outliers is not reliable as he admitted that these outliers did not
provide evidence of causation and would not translate to the general population. Furthermore,
the biggest gap in Dr. Cantilena’s testimony comes from his conversions and calculations,
prepared for the purposes of litigation, which are ultimately only supported by his blanket
assurances that literature exists on similar methodology. Turning to the Daubert factors, the
Court finds that Dr. Cantilena’s conversions and calculations were not tested or subject to peer
review. Moreover, Dr. Cantilena failed to provide a rate of error or evidence that his conversions
and calculations are generally accepted in the scientific community and, therefore, the Court
finds that his conversions and calculations are entirely speculative. Additionally, Dr. Cantilena
relies on animal studies without qualifying how they apply differently to humans. As admitted
by Dr. Cantilena, his use of case reports cannot establish causation. Finally, Dr. Cantilena’s
Second Supplemental Rule 26 Expert Report and Declaration fail to provide reliable evidence
that DMAA can cause “increased heat generation” and “cutaneous vasoconstriction causing
hyperthermia and death.” Dr. Cantilena’s opinion must provide more than studies “showing
correlation, accompanied by unrelated anecdotes and quasi-scientific musings about how a class
of drugs affects the human body.” Huss, 571 F.3d at 459. Based on the foregoing, the Court
finds that Dr. Cantilena’s entire general causation opinion is excluded.
h. Differential Diagnosis
Given the Court’s finding that Dr. Cantilena’s general causation opinion is excluded and,
as discussed below, the Court’s decision to exclude Dr. Mills’ opinion and Dr. Rusyniak’s
No. EP-13-CV-323-DCG
46
opinion on general causation, the Court further concludes that Dr. Cantilena cannot rule in
DMAA as a potential cause in his differential diagnosis.35 See Johnson, 685 F.3d at 468-69
(holding that the district court did not abuse its discretion in excluding an expert’s differential
diagnosis because the expert failed to satisfy general causation requirements). Without being
able to rule in DMAA as a potential cause, Dr. Cantilena’s differential diagnosis is unreliable.
The Johnson court explained that “Moore illustrates that an expert may not rely on a differential
diagnosis to circumvent the requirement of general causation.” Id. at 468 (citing Moore, 151
F.3d at 278). Therefore, the Court rejects Dr. Cantilena’s specific causation testimony.
2. Dr. Mills
Dr. Mills opined that DMAA is a sympathomimetic in the aliphatic amine class.
(See Pls.’ Ex. JJ ¶ 4, ECF No. 197-31; Dr. Mills Dep. 18:25-19:6; Hr’g Tr. 5:15-6:4,
Apr. 28, 2015, ECF No. 324).
He further opined that generally sympathomimetics cause
vasoconstriction, increased heart rate and blood pressure, decreased gut motility, increased body
temperature, and increased lipolysis, plasma glycerol, and free fatty acids. (See Pls.’ Ex. JJ ¶ 4,
ECF No. 197-31; Dr. Mills Dep. 28:24-29:12, 62:22-63:7, 155:2-256:8; Hr’g Tr. 5:15-6:4,
Apr. 28, 2015, ECF No. 324). Dr. Mills maintained that DMAA can cause the same effects as
other sympathomimetics based on its development as a nasal decongestant and various animal
and human studies demonstrating a biologically plausible mechanism of action. (See Pls.’ Ex. JJ
¶ 4, ECF No. 197-31; Dr. Mills Dep. 35:18-22, 135:6-22, 148:5-149:24; Hr’g Tr. 5:15-6:4, 23:4A differential diagnosis is defined as “the determination of which one of two or more diseases or
conditions a patient is suffering from, by systematically comparing and contrasting their clinical
findings.” Dorland’s Illustrated Medical Dictionary 507 (32d ed. 2012). One court within this district
has defined differential diagnosis as “the distinguishing of a disease or condition from others presenting
similar symptoms.” Johnson v. United States, No. EP-02-CA-580-PRM, 2005 WL 1605822, at *3 n.21
(W.D. Tex June 30, 2005) (citation omitted). Additionally, another court observed that a differential
diagnosis is “accomplished by determining the possible causes for the patient’s symptoms and then
eliminating each of these potential causes until reaching one that cannot be ruled out or determining
which of those that cannot be excluded is the most likely.” Johnson v. Arkema, Inc., 685 F.3d 452, 468
(5th Cir. 2012) (quoting Westberry v. Gislaved Gummi AB, 178 F.3d 257, 262 (4th Cir. 1999)).
35
No. EP-13-CV-323-DCG
47
18, Apr. 28, 2015, ECF No. 324).
Dr. Mills explained that sympathomimetics cause hyperthermia through a number of
processes that include the stimulation of the sympathetic nervous system, the uncoupling of
proteins, heat production, and heat dissipation through vasoconstriction. (See Pls.’ Ex. JJ ¶¶ 610, ECF No. 197-31; Dr. Mills Dep. 121:21-122:1; Hr’g Tr. 5:15-7:23, 62:18-63:9, Apr. 28,
2015, ECF No. 324). He relied on the Schilling study to support his opinion that DMAA has
hyperthermic properties based on those subjects’ increase in forehead temperature, which was
within normal limits, but he noted that no other study supported this position. (See Pls.’ Ex. JJ ¶
4, ECF No. 197-31; Dr. Mills Dep. 44:2-54:8, 55:6-14; 58:15:64:12, 79:22-80:7; Hr’g Tr. 6:137:23, 38:1-6, Apr. 28, 2015, ECF No. 324). He also relied on his education, training, and
experience and his “knowledge of pharmacology that suggests that [DMAA] is . . . likely, very
likely [a] sympathomimetic agent.” (Dr. Mills Dep. 107:23-108:8).
Dr. Mills opined that “Jack3d and OxyElite are preparations containing DMAA, a drug
that possesses the structural, functional, and pharmacologic properties that define the classical
sympathetic neurotransmitters and their sympathomimetic acting agents. Like ingestion of other
sympathomimetics DMAA can be a substantial contributing cause of hyperthermia.”
(Pls.’ Ex. JJ ¶ 13, ECF No. 197-31).
He explained “that based upon [DMAA’s]
sympathomimetic properties and the fact that in a peer-reviewed paper . . . [which] showed that a
rise in body temperature can occur by DMAA, . . . I think DMAA poses a significant risk to the
development of hyperthermia in susceptible individuals.” (Dr. Mills Dep. 121:21-122:1). Dr.
Mills concluded that “[c]onfirmed use of DMAA in mild to moderate temperature conditions
with low humidity, moderate exercise and absence of use of anesthetics is a setting where
DMAA can be a substantial contributing factor causing hyperthermia, related complications and
death.” (Pls.’ Ex. JJ ¶ 4, ECF No. 197-31).
No. EP-13-CV-323-DCG
48
a. The Schilling Study
It is clear that the only clinical study specific to DMAA and body temperature that Dr.
Mills relies on is the Schilling study. In assessing that study, Dr. Mills testified that the results
showed a statistically significant increase in body temperature over the baseline temperature after
twelve hours. (See Dr. Mills Dep. 47:18-48:2; Hr’g Tr. 6:13-7:23, 38:1-19, Apr. 28, 2015,
ECF No. 324). While that increase was within normal body temperature limits and Dr. Mills
indicated that the results do “[n]ot necessarily” represent an adverse medical event, he opined
that “anything that increases body temperature to any degree can be a substantial risk factor for
causing hyperthermia under certain conditions.” (Dr. Mills Dep. 81:3-13). Furthermore, Dr.
Mills opined that the core temperature of the subjects was likely higher than their forehead
temperature. (See Hr’g Tr. 44:7-23, Apr. 28, 2015, ECF No. 324). Although the subjects were
allowed to leave the laboratory for several hours before the final blood draw, Dr. Mills found it
“remarkable” that there was still a rise in body temperature. (See Dr. Mills Dep. 49:15-21, 50:753:21, 59:16-64:12, 84:22-25, 86:1-18; Hr’g Tr. 39:14-41:22, 42:23-43:5, Apr. 28, 2015,
ECF No. 324). Thus, Dr. Mills opined that the Schilling study supported his opinion on general
causation. (See Dr. Mills Dep. 49:10:14, 51:3-53:21, 59:16-64:12, 84:13-21, 86:1-18; Hr’g Tr.
41:14-42:3, 46:14-17, 47:11-22, Apr. 28, 2015, ECF No. 324).
Dr. Mills disagreed with the authors’ conclusions in the Schilling study that the change in
body temperature was not “meaningful.” (See Dr. Mills Dep. 45:7-54:8, 59:11-15, 76:19-79:6;
Hr’g Tr. 33:21-35:7, 47:17-22, Apr. 28, 2015, ECF No. 324).
He admitted that he was
interpreting the data from the Schilling study in a way that differed from what the authors
concluded. (See Hr’g Tr. 47:11-48:9, Apr. 28, 2015, ECF No. 324). Dr. Mills explained that he
“thinks it’s likely that DMAA would substantially raise the risk of exercise induced
hyperthermia.”
(Dr. Mills Dep. 145:13-15).
No. EP-13-CV-323-DCG
49
He further testified that the Schilling study
demonstrates that “taking DMAA gives rise to a substantial risk that in certain susceptible
individuals, their body temperatures can increase.” (Id. at 87:19-22). However the authors of
the Schilling study stated that “[f]urther study of DMAA effects on temperature in the context of
exercise and heat exposure is warranted.” (Defs.’ Ex. V 72, ECF No. 223).
Like Dr. Cantilena’s use of several of the other Bloomer studies to make conclusions
about the general population, Dr. Mills’ use of the Schilling study also lacks a significant sample
size to make causal conclusions about DMAA’s ability to increase body temperature in the
general population. Dr. Mills acknowledged Dr. O’Brien’s testimony that the Schilling study
does not provide a large enough sample size to make a conclusion as to whether DMAA elevates
body temperature. (See Hr’g Tr. 58:20-23, Apr. 28, 2015, ECF No.; see also Dr. O’Brien Dep.
72:18-74:20). Dr. Mills further acknowledged that the Department of Defense study concluded
that there was no relationship between DMAA and heat injuries.
(See Hr’g Tr. 59:1-18,
Apr. 28, 2015, ECF No. 324). Dr. Mills’ only real attempt to justify his reliance on the Schilling
study, despite the lack of a significant sample size, was his explanation that with “positive”
scientific results “one can feel fairly confident . . . that [a] statistically significant event may have
actually occurred” but when there are “negative” scientific results, the “small number of people”
could create error. (Dr. Mills Dep. 56:3-19). He testified that more studies were needed to make
conclusions about DMAA. (See id. at 55:2-5, 64:21-22, 68:23-69:20, 128:20-129:4, 138:11-23;
Hr’g Tr. 56:2-5, 94:12-22, Apr. 28, 2015, ECF No. 324). When asked if the opinion he had
formed about DMAA and body temperature was “more of a correlation than causation,” he
responded “I don’t think in this case that matters.” (Dr. Mills Dep. 65:4-6). In determining
whether DMAA was the cause of hyperthermia, Dr. Mills opined that “would require a properly
controlled, randomized, case controlled study, and that’s difficult to do in humans with a
suspected toxi[n].” (Id. at 144:20-145:3).
No. EP-13-CV-323-DCG
50
Only evidence demonstrating a causal relationship between a product and an alleged
injury is admissible as relevant and reliable.
See Moore, 151 F.3d at 274, 276;
see also Brumley, 200 F.R.D. at 602. However, Dr. Mills does not opine that the Schilling study,
or any other evidence, establishes a causal relationship which can be demonstrated in the general
population. Instead, he relies on the Schilling study to opine that susceptible individuals can
have increased body temperature. When the Court asked Dr. Mills how to determine who is
susceptible to DMAA, he indicated that scientists do not know what causes people to have
idiosyncratic responses. (See Hr’g Tr. 63:20-64:10, Apr. 28, 2015, ECF No. 324). He defined
idiosyncratic as a “response [that] occurs rarely in individuals . . . with an underlying
susceptibility factor that may or may not be understood yet.” (Dr. Mills Dep. 157:11-18). Dr.
Mills fails to explain how susceptible individuals relate to the general population. His failure to
do so ultimately makes his use of the Schilling study and his opinion on DMAA’s ability to
increase body temperature unreliable.
Assuming arguendo that Dr. Mills’ Supplemental Rule 26 Expert Report and Declaration
is timely,36 the Court addresses the reliability of his “statistical regression analysis” using the
individual subject data from the Schilling study.37 (Dr. Mills Supplemental Report & Decl. ¶ 6,
ECF No. 327-22).
While it appears to the Court that Dr. Mills’ analysis of the data is
“supportive” of his opinion “that changes measured at the forehead were caused by the ingestion
of 25 mg of DMAA,” this presumes the reliability of the Schilling study, which the Court has
already found unreliable above. (Id.) Moreover, like Dr. Cantilena, Dr. Mills’ “statistical
36
Dr. Mills’ Supplemental Rule 26 Expert Report and Declaration is dated April 30, 2015. (Dr. Mills
Supplemental Report & Decl. 3 ECF No. 327-22). As the Court ultimately finds Dr. Mills’ “statistical
regression analysis” to be unreliable, the Court will deny Defendants’ Pre-Hearing Motion as moot. (See
Def.’s Reply 3, 10-11, ECF No. 303).
37
As mentioned above, Dr. Mills’ Supplemental Rule 26 Expert and Declaration was filed on July 24,
2015. (ECF No. 327-22).
No. EP-13-CV-323-DCG
51
regression analysis” has been developed solely for the purposes of his testimony in this case,
further undercutting its reliability. See Newton, 243 F. Supp. 2d at 678 (citing Daubert II, 43
F.3d at 1317). Accordingly, the Court finds that Dr. Mills’ Supplemental Rule 26 Expert Report
and Declaration should be excluded.
b. Class Effects
Dr. Mills not only fails to bridge the gap in his extrapolation from the class effects of
sympathomimetics to DMAA, he relies on animals studies using other sympathomimetics to
form his opinion on DMAA. In discussing the Schilling study, it appears to the Court that Dr.
Mills relied on the class effects of sympathomimetics. He testified that “I would suspect that
they would have seen a rise in body temperature, as we do in animals with sympathomimetics . . .
like DMAA[,] that we all agree . . . induce[s] vasoconstriction.” (Hr’g Tr. 44:11-19, Apr. 28,
2015, ECF No. (emphasis added)). In further discussing the Schilling study, Dr. Mills stated that
“it is likely that DMAA caused a metabolic heat production, which is the effect of a class of
sympathomimetics, all of which induce metabolic rate and heat production, and also decrease
heat dissipation and release from the body, because they induce vasoconstriction.” (Id. at 7:4-10
(emphasis added)).
Dr. Mills further maintained that “MDMA is the prototypical sympathomimetic resulting
in increased heat production, [which] . . . is an effect that is shared by all drugs in its class.”
(Pls.’ Ex. JJ ¶ 9, ECF No. 197-31 (emphasis added)).
He stated that “[t]he strongest
demonstration of a molecular mechanism of sympathomimetic-induced hyperthermia was
revealed by our work published . . . in 2003 showing that mice lacking the gene encoding
[Uncoupling Protein 3] were profoundly resistant to hyperthermia and completely protected from
death induced by MDMA.” (Id.) Dr. Mills testified that “most” sympathomimetics pose safety
risks for heat stroke and that “[t]hese are class effects.” (Dr. Mills Dep. 146:23-148:4 (emphasis
No. EP-13-CV-323-DCG
52
added)). However, he further testified that not all sympathomimetics cause increased core body
temperature, vasoconstriction, or hyperthermia. (See id. at 27:19-24, 71:15-22). Thus, it is clear
that despite Dr. Mills’ generalizations, there are many differences in sympathomimetics and their
potential effects which Dr. Mills fails to account for in his opinion.
Dr. Mills defined sympathomimetics broadly, stating that sympathomimetics include
“any agent that bears structural and functional / pharmacologic similarity with [norepinephrine
and epinephrine].” (Pls.’ Ex. JJ ¶ 4, ECF No. 197-31 (emphasis added)). He acknowledged that
DMAA lacked an aromatic or benzene ring in its chemical structure. (See Dr. Mills Dep. 18:2519:23; Hr’g Tr. 27:1-28:4, Apr. 28, 2015, ECF No. 324). He also opined that “[a]ny chemical
structure difference can cause a variation either up or down in the efficacy potency of any agent
on its receptor systems including sympathomimetics.” (Dr. Mills Dep. 24:23-25:1 (emphasis
added)).
Furthermore, Dr. Mills recognized that sympathomimetics have “class effects” as well as
“distinctive properties.” (See id. at 103:19-104:1). He testified that sympathomimetics have
different chemical structures, dose-response relationships, and potency. (See id. at 15:22-16:6;
Hr’g Tr. 21:6-24, 25:23-28:21, Apr. 28, 2015, ECF No. 324). When asked if he would want to
take into account the distinctive properties of sympathomimetics in performing an analysis, Dr.
Mills responded “[w]ell, that you could, you would want to do everything possible to understand,
giving your findings’ levels and opportunities to do so.” (Hr’g Tr. 32:9-14, Apr. 28, 2015,
ECF No. 324). Dr. Mills also opined that in order to compare sympathomimetics, “[y]ou have to
do a variety of studies . . . to fully characterize the sympathomimetic effects.” (Dr. Mills Dep.
28:5-12 (emphasis added)).
Dr. Mills also relied on class comparisons to support his opinion on dose-response and
potency. He explained that there is data “on all sympathomimetics as a class” that “suggest[s]
No. EP-13-CV-323-DCG
53
that the [dose-response] relationships . . . are weak.” (Id. at 156:25-157:9).
Analogizing to
ecstasy and MDMA, Dr. Mills stated that sympathomimetics do not have a clear dose-response.
(See Hr’g Tr. 65:4-15, Apr. 28, 2015, ECF No. 324). He noted that no literature demonstrates a
dose-response curve for DMAA and cutaneous vasoconstriction. (See id. at 21:18-22:23). He
also explained that “[w]ith respect to DMAA especially and heat . . . that is also a class effect
that is misunderstood by most of the sympathomimetics.” (Dr. Mills Dep. 158:7-11 (emphasis
added); Hr’g Tr. 63:13-65:15, Apr. 28, 2015, ECF No. 324).
Dr. Mills further opined that while case-controlled studies on DMAA would be helpful,
“there’s information out there to suggest that [DMAA] can be a substantial causing risk factor
for hyperthermia.” (Hr’g Tr. 65:24-66:2, Apr. 28, 2015, ECF No. (emphasis added)). He stated
that “my opinion would be that it’s a risk factor because of its alpha-agonist activities that are
undisputed.
It’s a sympathomimetic.
Like all sympathomimetics, they could lead to
hyperthermia. Exercise increases that risk. I think this is a risk factor for hyperthermia and
death.” (Id. at 66:13-21 (emphasis added)). When asked if DMAA was only a potential risk, Dr.
Mills agreed and stated it was “[t]he same with MDMA.” (Id. at 66:25-67:3 (emphasis added)).
Despite all the differences that Dr. Mills acknowledged in his Rule 26 Expert Report, his
deposition testimony, and his Daubert hearing testimony about sympathomimetics, Dr. Mills still
attempted to compare sympathomimetics to DMAA to demonstrate that the same effects would
occur in the general population. The Court cannot accept this leap in logic as support for his
expert opinion. Dr. Mills lacks scientific literature as a basis for each step in his analysis as it
relates to extrapolating from sympathomimetics as a class to the effects that DMAA has on the
general population.
c. Animal Studies
The only information Dr. Mills relies on to show dose-response for DMAA is a dog study
No. EP-13-CV-323-DCG
54
which used a dose of six to ten milligrams per kilogram in a dog, as opposed to a human dose of
approximately one half milligram per kilogram. (See Dr. Mills Dep. 39:20-40:15). Although he
testified that “[t]he dog is the undisputed, gold standard model in thousands and thousands of
papers and laboratories for human cardiovascular biology, and especially in terms of drug
development and the predictive effects of toxicity in humans related to cardiovascular function
and blood pressure,” he presents no clear evidence other than his assurances. (Hr’g Tr. 10:17-21,
Apr. 28, 2015, ECF No. 324).
Dr. Mills conceded that data from animal studies does not always extrapolate accurately
to effects in humans.
(See Dr. Mills Dep. 99:22-100:4, 101:11-102:2).
Dr. Mills’ mere
assurances that dogs are a good model to predict human effects are insufficient to establish
reliability and even so, his opinion on dose-response fails to account for the different doses used
in animals and humans. See, e.g., Joiner, 522 U.S. at 144-45 (holding that it was not an abuse of
discretion to reject experts’ reliance on animal studies where infant mice were injected with large
doses of chemicals because the study was distinguishable from the facts presented in the
litigation); Gulf S. Insulation v. U.S. Consumer Prod. Safety Comm’n, 701 F.2d 1137, 1146 (5th
Cir. 1983) (rejecting rat study based on the small sample size, the large dose given to the rats,
and the difficulty extrapolating the study results to humans).
d. Biologically Plausible Mechanism of Action
Insofar as Dr. Mills relies on a biologically plausible mechanism of action to form his
opinion, the Court rejects that theory as well. Dr. Mills testified that dosage, time, route of
administration, species, sex, and environmental conditions are important factors for toxicologists
to review in determining the adverse effects of chemicals on living organisms.
(See Dr. Mills Dep. 7:25-10:25, 112:21-113:18; Hr’g Tr. 12:7-11, 15:3-18:24, 28:17-21, Apr. 28,
2015, ECF No. 324). He further testified that while “those [factors] aren’t required to conclude .
No. EP-13-CV-323-DCG
55
. . that a drug can cause hyperthermia, those [factors] are required to understand how it is
happening.” (Dr. Mills Dep. 71:23-72:7 (emphasis added)). He further opined that it was
unnecessary to know the pharmacodynamics or pharmacokinetics of a drug to reach a causal
conclusion but they are only necessary “to understand how the drug caused the effect.” (Id. at
108:24-111:19 (emphasis added)). Moreover, when Dr. Mills was given the chance to discuss
DMAA’s biologically plausible mechanism of action to cause heat-related injuries, he instead
chose to discuss how DMAA is a sympathomimetic and “has clear undisputed alpha-1-agonistic
activity.” (See Hr’g Tr. 5:9-6:4, Apr. 28, 2015, ECF No. 324).
The Court finds that there is a glaringly large gap in Dr. Mills’ theory of a biologically
plausible mechanism of action. Dr. Mills is extrapolating from other sympathomimetics, such as
amphetamine, methamphetamine, ecstasy, and MDMA, and how they cause heat-related injury,
to form his opinion that DMAA also causes heat-related injury. (Pls.’ Ex. JJ ¶ 8, ECF No. 19731). In making this comparison, Dr. Mills fails to examine the factors listed above which would
allow him to form an opinion on how DMAA causes heat-related injury. Instead, Dr. Mills
compares DMAA to other sympathomimetics and speculates that DMAA has the same
biologically plausible mechanism of action. Dr. Mills fails to rely on scientific literature to
explain the various factors mentioned above which would allow him to opine as to how DMAA
acts on the human body or, in essence, DMAA’s biologically plausible mechanism of action. Dr.
Mills testified that there has been no study performed on DMAA demonstrating cutaneous
vasoconstriction in humans and he agreed that he did not find any studies that indicated that
DMAA caused hyperthermia. (See id. at 25:4-19, 32:24-33:2). Dr. Mills also agreed that no
peer reviewed scientific study involved the measurement of core temperature after acute
ingestion of Jack3d. (See id. at 69:12-17, 94:24-95:7). He further agreed that there were no
studies on absorption rates of DMAA. (See id. at 64:11-13). Therefore, the Court finds that Dr.
No. EP-13-CV-323-DCG
56
Mills’ theory of a biologically plausible mechanism of action is nothing more than pure
speculation which the Court cannot allow to reach the trier of fact.
e. Conclusion on General Causation
The Court finds that Dr. Mills’ opinion suffers from many of the same flaws as Dr.
Cantilena’s opinion and, therefore, should be excluded.
Dr. Mills’ opinion is full of
contradictions and equivocations that ultimately weaken the value of his opinion and make his
methodology unreliable. The Schilling study’s small sample size, which Dr. Mills
acknowledged, does not allow Dr. Mills to translate the results to the general population. He
further admitted that whether the Schilling study demonstrated causation rather than correlation
does not matter, yet, at the same time, he contradicts himself by requiring case controlled studies
to show a causal relationship between DMAA and hyperthermia.
Moreover, in using the
Schilling study, Dr. Mills simply opined that DMAA could affect susceptible people without
explaining who is susceptible and how that translates to the general population. Dr. Mills’
“statistical regression analysis,” which was created for his Supplemental Rule 26 Expert Report
and Declaration, presumes the reliability of the Schilling study and is ultimately improper for
that reason. Dr. Mills also acknowledged that the Department of Defense study found that there
was no relationship between DMAA and heat injuries. Like Dr. Cantilena, Dr. Mills failed to
account for any of the differences in extrapolating between the class effects of other
sympathomimetics and DMAA. He further relies on animal studies for his opinion without
qualifying how they apply differently to humans or accounting for the differences in dose
between dogs and humans. Finally, Dr. Mills admittedly failed to rely on several important
factors used to determine the adverse effects of chemicals on living organisms, which would
have allowed him to determine a biologically plausible mechanism of action. Accordingly, the
Court finds that Dr. Mills’ assurances as to the reliability of his opinion are not enough to satisfy
No. EP-13-CV-323-DCG
57
the standard under Daubert and, therefore, his entire general causation opinion is excluded.
3. Dr. Rusyniak
In order to rule in DMAA as a potential cause, Dr. Rusyniak relied on his research,
training, and experience, the scientific literature on DMAA, the opinion of Dr. Cantilena on the
pharmacologic properties of DMAA, and the opinion of Dr. Mills on the hyperthermic properties
of DMAA. (See Pls.’ Ex. II ¶¶ 4-5, ECF No. 197-30; Dr. Rusyniak Dep. 12:2-4, 32:23-36:9,
38:2-39:4, 64:25-67:10; 86:23-87:17, 100:11-25, 102:15-103:8).
In order to rule out other
potential causes, Dr. Rusyniak reviewed Decedent’s medical records, statements made by
Benjamin Tuthill, Decedent’s toxicology report, Decedent’s autopsy, temperature, humidity, and
wet bulb data for Fort Bliss on the day of Decedent’s death, statements regarding the time and
nature of physical training, and statements made by those rendering care on the scene.
(See Pls.’ Ex. II ¶ 6, ECF No. 197-30; Dr. Rusyniak Dep. 32:20-23, 135:5-12, 220:1-223:9;
Hr’g Tr. 58:16-60:1, Apr. 27, 2015 AM, ECF No. 321). He opined that Decedent was wellconditioned, acclimated to the environment, and not dehydrated. (See Pls.’ Ex. II ¶¶ 7-8,
ECF No. 197-30; Dr. Rusyniak Dep. 32:10-14, 132:18-134:16, 135:13-21; Hr’g Tr. 57:10-58:15,
63:21-65:3, 106:19-107:23, 108:24-109:1, 148:19-149:4, 164:23-165:10, Apr. 27, 2015 AM,
ECF No. 321).
He found that Decedent did not have other medications, stimulants, or
sympathomimetics in his system, sickle cell trait, an infection, or a family history of malignant
hyperthermia.
(See Dr. Rusyniak Dep. 21:4-25, 32:15-19; Hr’g Tr. 56:24-57:9, 63:1-20,
Apr. 27, 2015 AM, ECF No. 321).
Dr. Rusyniak further opined that DMAA, combined with
exertion and other contributing factors, such as temperature, humidity, acclimation, and physical
fitness, led to Decedent’s hyperthermia and death. (See Dr. Rusyniak Dep. 53:7-55:18; Hr’g Tr.
60:18-22, Apr. 27, 2015 AM, ECF No. 321). Dr. Rusyniak considered the temporal association
No. EP-13-CV-323-DCG
58
between Decedent’s DMAA use and his hyperthermia,38 whether it was biologically plausible
that DMAA could cause hyperthermia, and whether other factors could have increased
Decedent’s risk of hyperthermia. (See Hr’g Tr. 54:22-58:15, Apr. 27, 2015 AM, ECF No. 321).
After taking these various factors into consideration, Dr. Rusyniak concluded that DMAA was a
substantial factor in causing Decedent’s hyperthermia and ultimate death. (See Pls.’ Ex. II ¶¶ 4,
9, ECF No. 197-30).
a. Class Effects
1) Sympathomimetics Generally
The Court first reviews whether Dr. Rusyniak is merely relying on the class effects of
sympathomimetics in order to come to conclusions about DMAA. Dr. Rusyniak testified that the
literature he reviewed demonstrated that DMAA “caused similar physiologic and clinical
responses that we see with drugs that are in the sympathomimetic class.” (Dr. Rusyniak Dep.
87:18-25 (emphasis added)). When questioned about literature relating to sympathomimetics
and their ability to increase temperature during exertion in warm environments, Dr. Rusyniak
explained that he was referring to “MDMA, amphetamine or dextroamphetamine,
methamphetamine.
A variety of, and I’ll say variety because I can’t name them all, of
substituted phenylethylamines, synthetic cathinones.” (Id. at 67:13-18). He explained that
“drugs that are sympathomimetics all increase body temperature when given to animals in a
warm environment while they’re exerting themselves.”
(Id. at 68:5-14 (emphasis added)).
However, Dr. Rusyniak admitted that methamphetamine, ecstasy, and DMAA “are structurally
38
“[T]he Fifth Circuit has rejected expert testimony that relies ‘substantially on the temporal proximity
between exposure and symptoms.’” Newton v. Roche Labs., Inc., 243 F. Supp. 2d 672, 683 (W.D. Tex.
2002) (citing Moore v. Ashland Chem. Inc., 151 F.3d 269, 278 (5th Cir. 1998) (en banc); Black v. Food
Lion, Inc., 171 F.3d 308, 313 (5th Cir. 1999) (rejecting reliance on temporal proximity as ‘not an exercise
in scientific logic but in the fallacy of post-hoc propter-hoc reasoning, which is as unacceptable in science
as in law’); Lassiegne v. Taco Bell Corp., 202 F. Supp. 2d 512, 517 (E.D. La. 2002) (rejecting opinion
based on ‘temporal proximity alone’ as ‘present[ing] no scientific basis for [the] ultimate conclusion”)).
No. EP-13-CV-323-DCG
59
different compounds.” (Id. at 68:22-69:4). He also admitted that not all sympathomimetics have
the same dose-response curve, effects on blood pressure, vasoconstriction, and body temperature,
and that they are not absorbed at the same rate in the body. (See Hr’g Tr. 88:13-20, 90:10-93:7,
Apr. 27, 2015 AM, ECF No. 321). Contrary to Dr. Cantilena, Dr. Rusyniak explained that route
of entry and rate of absorption would have an effect on blood concentrations of various
sympathomimetic substances. (See id. at 92:13-93:7).
Although Dr. Rusyniak testified that the sympathomimetics that he was familiar with are
capable of causing vasoconstriction, he admitted that he had not studied the relative effects of
DMAA and other sympathomimetics. (See Dr. Rusyniak Dep. 105:13-25, 110:18-25). He
opined that, based on animal studies with MDMA, methamphetamine, and amphetamine, and
human studies with cocaine, “[d]rugs that cause vasoconstriction . . . impair your ability to
dissipate heat because you would not be able to dilate.” (Id. at 118:20-119:5). He explained that
“[d]rugs that are vasoconstrictors, like DMAA, are going to interfere with the cutaneous blood
vessels, and as such, you are going to decrease your ability to dissipate heat.” (Hr’g Tr. 52:9-12,
Apr. 27, 2015 AM, ECF No. 321). Dr. Rusyniak based this explanation on an Eli Lilly study that
demonstrated that DMAA was a “potent vasoconstrictor.” (See Dr. Rusyniak Dep. 119:20-24;
see also Hr’g Tr. 53:20-22, Apr. 27, 2015 AM, ECF No. 321). He opined that DMAA impairs
the dissipation of heat at the cutaneous blood vessels “[b]ecause it shares similar
sympathomimetic properties to . . . other drugs that do that.” (Dr. Rusyniak Dep. 119:25-120:6
(emphasis added)).
He added that he would expect “all drugs that share those common
pharmacologic and physiologic properties . . . to impair the dissipation of heat.” (Id. at 122:8-17
(emphasis added)).
Dr. Rusyniak testified that if an increase in blood pressure is due to an alpha agonist
working on alpha receptors, the substance will result in an increase in cutaneous
No. EP-13-CV-323-DCG
60
vasoconstriction, however, he admitted that no studies demonstrated this specifically about
DMAA. (See Hr’g Tr. 135:1-18, Apr. 27, 2015 AM, ECF No. 321). While Dr. Rusyniak
pointed to no literature on DMAA, he explained that his opinion was “based on properties that
drugs that work like sympathomimetics and alpha receptors share.” (Id. at 135:17-18 (emphasis
added)). He opined that “[i]n terms of dissipation, cutaneous blood flow would be probably the
biggest single factor that a drug like DMAA[,] . . . a vasoconstrictor[,] is going to hit.” (Id. at
52:21-23). Dr. Rusyniak admitted that increased blood pressure does not necessarily correspond
with an increase in body temperature. (See Dr. Rusyniak Dep. 105:3-12). He further stated that
“based on its pharmacologic properties, I would infer that . . . DMAA contributed to [heat
stroke] in part through increased heat production by uncoupling.” (Id. at 116:16-21 (emphasis
added)).
Dr. Rusyniak opined that “if you give somebody a drug that works like a
sympathomimetic, very often that will mask the delay or onset of fatigue and allow people to
exert themselves longer, and that usually comes at the expense of body temperature.”
(Hr’g Tr. 53:13-19, Apr. 27, 2015 AM, ECF No. 321 (emphasis added)). In response to a
question from the Court, Dr. Rusyniak stated that no study investigated whether DMAA causes a
delay or masks the onset of fatigue. (See id. at 132:9-17). This testimony demonstrates to the
Court that Dr. Rusyniak is simply relying on the class effects of sympathomimetic drugs to
extrapolate to his opinion on DMAA in order to rule it in as a potential cause.
2) Lack of Relevant Scientific Experience
While Dr. Rusyniak has experience studying various sympathomimetics, including
amphetamine, methamphetamine, and MDMA in animals, he lacks scientific experience with
DMAA, which is a factor that weighs against the reliability of his opinion. (See Dr. Rusyniak
Dep. 67:19-25). Dr. Rusyniak stated that he has not conducted research on DMAA in humans or
No. EP-13-CV-323-DCG
61
animals and has no personal experience, which he is aware of, in treating someone who used
DMAA. (See id. at 43:3-19, 68:20-21). He further explained that he has not performed a direct
comparison between methamphetamine, amphetamine, and MDMA in any experiments in order
to determine heat production or temperature changes and agreed that these types of studies had
not been performed with respect to DMAA. (See id. at 70:4-71:10). In forming the opinion that
Decedent’s dose of DMAA was sufficient to cause his exertional heat stroke, Dr. Rusyniak
testified that he had not performed a scientific comparison between Decedent’s dose of DMAA,
in milligrams per kilogram, to the doses used in animal studies on DMAA. (See id. at 151:16153:7). He explained that while no studies indicate the dosage at which DMAA can cause a
hyperthermic response or increase in core temperature, there are studies indicating that DMAA is
a vasoconstrictor “suggest[ing] it would contribute to hyperthermia.” (Hr’g Tr. 69:13-17, 93:814, Apr. 27, 2015 AM, ECF No. 321 (emphasis added)). Despite Dr. Rusyniak’s experience
studying animals, the Court finds that he fails to demonstrate how he can extrapolate from
animals to humans in any of the steps of his analysis.
3) Lack of Reliable Scientific Literature
Moreover, Dr. Rusyniak testified that he knew of no peer reviewed epidemiological
studies or any studies, outside of case reports, that demonstrate causal links between DMAA and
death, heat stroke, hyperthermia, and increased core temperature. (See Dr. Rusyniak Dep. 39:540:8, 41:7-21, 42:5-12, 47:15-48:11). While Dr. Rusyniak explained that “the case reports . . .
ultimately determine whether something caused harm,” he stated that even a single case report
would make it hard to determine a cause. (Id. at 49:22-50:22). Dr. Rusyniak also opined that
while some of the case reports reported an association between DMAA and various injuries,
“[f]rom a pure scientific standpoint, you’d need to do a randomized placebo-controlled trial to
properly determine causation.” (Id. at 88:1-91:5 (emphasis added)). He further stated that in
No. EP-13-CV-323-DCG
62
order to quantify the percentage or likelihood that DMAA caused Decedent’s death, it “would
take a large controlled trial to determine what the incident rate is for [DMAA].”
(Hr’g Tr. 104:19-21, Apr. 27, 2015 AM, ECF No. 321).
Additionally, Dr. Rusyniak testified that the increase in temperature demonstrated in the
Schilling study did not meet the definition of hyperthermia and that the study was not accurate
because the sample size was too small. (See Dr. Rusyniak Dep. 40:17-41:6, 141:3-145:7). He
testified that “none of the human studies . . . were set up or designed to properly detect whether
[DMAA] would cause hyperthermia.” (Hr’g Tr. 69:7-9, Apr. 27, 2015 AM, ECF No. 321
(emphasis added)). He further stated that the Bloomer studies had no “significant bearing” on
his opinion. (See Dr. Rusyniak Dep. 161:22-162:6). However, he agreed that the literature on
DMAA demonstrates a “trend that . . . acutely . . . DMAA and caffeine increase . . . systolic
blood pressure in individuals.” (Hr’g Tr. 155:23-156:4, Apr. 27, 2015 AM, ECF No. 321
(emphasis added)). He clearly admits that the scientific evidence on DMAA is lacking and that
the only studies he is familiar with on DMAA had no “significant bearing” on his opinion, yet he
agrees that the literature demonstrates a trend that would be helpful for his opinion. It appears to
the Court that Dr. Rusyniak is not using the same scientific rigor in the courtroom as he would in
the laboratory. Thus, the Court finds that Dr. Rusyniak’s testimony fails to bridge the analytical
gap between the generalized nature of the class of sympathomimetics and the specific
characteristics of DMAA.
Even in Dr. Rusyniak’s attempt to explain that a susceptible population has an increased
risk to DMAA use, he testified that “I’m not sure we, from a scientific standpoint, know all the
features that might increase somebody’s susceptibility.”
(Dr. Rusyniak Dep. 125:2-8;
see also Hr’g Tr. 146:12-147:15, Apr. 27, 2015 AM, ECF No. 321). He also testified that “I
think everyone can develop exertional heat stroke, yes, absolutely.” (Dr. Rusyniak Dep. 129:15No. EP-13-CV-323-DCG
63
20 (emphasis added)). He explained that he meant that everyone is susceptible “[u]nder the right
conditions.” (Id. at 129:21-130:6). He further testified that “it is my belief that if you took
people and randomized them to DMAA or not and had them run in a warm environment, you
would have significant[ly] more cases of exertional heat stroke in those getting DMAA.” (Id. at
130:23-131:2). Dr. Rusyniak admitted that he was not aware of any peer reviewed literature that
identified a susceptible population with regard to DMAA and heat stroke and hyperthermia.
(See Hr’g Tr. 128:13-16, Apr. 27, 2015 AM, ECF No. 321). Although a scientist can have
doubts in the scientific literature available, it is hard for the Court to find Dr. Rusyniak’s opinion
on DMAA reliable when he admits that science has not found explanations for a portion of his
theory. As “[l]aw lags science,” the Court finds that this portion of Dr. Rusyniak’s opinion is
entirely speculative.
b. Reliance on Other Experts
As to Dr. Rusyniak’s reliance on Dr. Cantilena and Dr. Mills, the Court finds that, insofar
as Dr. Rusyniak blindly adopts those experts’ opinions, Dr. Rusyniak’s opinion is unreliable.
See Lightfoot v. Hartford Fire Ins. Co., Civ. A. No. 07-4833, 2011 WL 39010, at *4
(E.D. La. Jan. 4, 2011) (“Rule 703 does not allow ‘the wholesale adoption of another expert’s
opinions without attempting to assess the validity of the opinions relied on.” (citation omitted)).
Dr. Rusyniak attempted to explain that the phrasing used in his Rule 26 Expert Report that he
was “relying” on Dr. Cantilena and Dr. Mills meant that he found them reliable.
(See Hr’g Tr. 161:1-12, Apr. 27, 2015 AM, ECF No. 321). Although Dr. Rusyniak stated that he
agreed with Dr. Mills’ conclusions on the hyperthermic and sympathomimetic properties of
DMAA and that they confirmed his own conclusions, he testified that “it would have been
important to know from pharmacologists that this drug or compound, chemical, was a
sympathomimetic or at least had sympathomimetic properties.” (Dr. Rusyniak Dep. 86:23-87:10
No. EP-13-CV-323-DCG
64
(emphasis added)). Dr. Rusyniak specifically stated that he relied on Dr. Mills’ explanation of
the expected pharmacologic properties of DMAA and the role of uncoupling proteins, fatty free
acids, and plasma glycerol. (See id. at 100:11-25, 102:15-103:8). In relying on Dr. Mills’
opinion, Dr. Rusyniak testified he did so because Dr. Mills continues to perform research in
areas relating to sympathomimetics that Dr. Rusyniak no longer focuses on. (See Hr’g Tr. 61:1316, Apr. 27, 2015 AM, ECF No. 321). As to Dr. Cantilena, Dr. Rusyniak explained that he does
not “routinely” work with outliers and he relied on Dr. Cantilena for that opinion. (See id. at
62:10-15).
Dr. Rusyniak stated that he “deferred in terms of having [Dr. Mills and Dr.
Cantilena] discuss the pharmacology [of DMAA].” (Id. at 141:11-15).
c. Conclusion on Ruling in DMAA as a Potential Cause
The Court finds that Dr. Rusyniak’s opinion is unreliable as it suffers from many of the
same pitfalls as the opinions of Dr. Cantilena and Dr. Mills. Dr. Rusyniak failed to account for
any of the differences in extrapolating between the class effects of other sympathomimetics and
DMAA. Furthermore, Dr. Rusyniak relies on animal studies without qualifying how they apply
differently to humans. He lacks experience studying DMAA and does not account for the
differences in dose in his extrapolations. Moreover, Dr. Rusyniak relied almost exclusively on
animal studies and case reports, as he found that the Bloomer studies had no significant bearing
on his opinion. He also could not explain how he could translate any of the studies to the general
population. Finally, the reliability of Dr. Rusyniak’s entire opinion is significantly undermined
by his reliance upon the already excluded opinions of Dr. Cantilena and Dr. Mills, thus, the
Court finds that Dr. Rusyniak’s entire opinion purporting to rule in DMAA as a potential cause is
excluded.
d. Differential Diagnosis
In light of the Court’s findings as to Dr. Cantilena and Dr. Mills on general causation and
No. EP-13-CV-323-DCG
65
Dr. Rusyniak’s opinion on ruling in DMAA as a potential cause, the Court finds Dr. Rusyniak’s
differential diagnosis to be unreliable. Without being able to rule in DMAA as a potential cause,
Dr. Rusyniak cannot find that DMAA was a substantial factor in Decedent’s hyperthermia and
ultimate death. See Johnson, 685 F.3d at 468-69. Accordingly, the Court rejects the entirety of
Dr. Rusyniak’s specific causation testimony.
E.
Defendants’ Rule 702 and Daubert Challenges to Dr. ElSohly
Defendants challenge the reliability and relevance of Dr. ElSohly’s opinion. (See Dr.
ElSohly Mot. 8, 10, ECF No. 185; Dr. ElSohly Reply 3, ECF No. 213; Hr’g Tr. 42:1-45:1, 47:849:1, Apr. 27, 2015 AM, ECF No. 321). Dr. ElSohly offers an opinion on whether DMAA is
naturally-occurring in geranium plants and oils. He explained that he has studied geranium
plants and oils and published a peer-reviewed study on that subject, which found that the
geranium plants and oils he studied did not have detectable amounts of DMAA despite using
methods with various detection levels. (See Pls.’ Ex. VV ¶ 3, ECF No. 197-43). Dr. ElSohly has
since published a second peer-reviewed study which was performed in conjunction with three
other laboratories, again failing to detect the presence of DMAA in geranium plants and oils. 39
(See id. at ¶ 9; Dr. ElSohly Dep. 25:19-28:4). He noted that he reviewed four other published,
peer-reviewed studies that performed a similar analysis and did not find the presence of DMAA
in geranium. (See Pls.’ Ex. VV ¶ 4, ECF No. 197-43). He criticized the Ping, Li, and Fleming
Neither party produced Dr. ElSohly’s 2012 study, or a finalized version of his 2014 study. A prepublication version of Dr. ElSohly’s 2014 study is attached to his Rule 26 Expert Report. (See Pls.’ Ex.
VV 24-53, ECF No. 197-44).
39
No. EP-13-CV-323-DCG
66
studies, which purported to find DMAA in geranium plants, as unreliable scientific literature.40
(See id. at ¶¶ 5-6, 12). He also opined that “[e]ven if the studies reportedly finding the presence
of DMAA naturally occurring in geranium were valid at the levels they found DMAA it would
be impossible to naturally extract DMAA from the natural source to be used at levels commonly
found in products like Jack3d and OxyElite Pro.” (Id. ¶ 12). Therefore, Dr. ElSohly concluded
that “it is my opinion to a reasonably degree of scientific probability that DMAA is not a natural
constituent of Pelargonium graveolens, Pelargonium graveolens oil, geranium or geranium
oil.”41 (Id. at ¶ 13).
1. Reliability
Defendants challenge to Dr. ElSohly’s testimony is based on Dr. ElSohly’s failure to use
the same methodology (detection level and samples) as used in the Ping, Li, and Fleming studies
and his criticisms of those studies. (Dr. ElSohly Mot. 8-10, ECF No. 185; Dr. ElSohly Reply 35, ECF No. 213). It is clear to the Court that Defendants are not attacking the reliability of Dr.
ElSohly’s use of ten parts-per-billion as a detection level in his studies in the sense that in
analytic and forensic chemistry, scientists use a different standard detection level. Dr. ElSohly
testified that “we don’t select the limits of detection. . . . You start doing the analytical process,
you start doing all the work, and as a result of that work, you come up with the limit of
detection.” (Hr’g Tr. 14:9-18, 35:23-36:19, Apr. 27, 2015 AM, ECF No. 321). According to Dr.
Dr. ElSohly’s Rule 26 Expert Report lists all three studies among those he reviewed and provided with
his Report. (See Pls.’ Ex VV ¶ 11, ECF No. 197-43). The Ping study is Zang Ping et al., A Study on the
Chemical Constituents of Geranium Oil, 25 J. Guizhou Inst. Tech. 83 (1996). (Defs.’ Ex. 2, Daubert
hearing). The Li study is J.S. Li. Et al., Identification and Quantification of Dimethylamylamine in
Geranium by Liquid Chromatography Tandem Mass Spectrometry, 2012 Analytical Chemistry Insights
47 (2012). (Defs.’ Ex. 1, Daubert hearing). The Fleming study is Heather L. Fleming et al., Analysis and
Confirmation of 1,3-DMAA and 1,4-DMAA in Geranium Plants Using High Performance Liquid
Chromatography with Tandem Mass Spectrometry at ng/g Concentrations, 2012 Analytical Chemistry
Insights 59 (2012). (Defs.’ Ex. F., ECF No. 178-9).
40
Dr. ElSohly testified that pelargonium and geranium are used synonymously. (See Hr’g Tr. 35:16-22,
Apr. 27, 2015 AM, ECF No. 321).
41
No. EP-13-CV-323-DCG
67
ElSohly a standard detection level is “not set by any organization.” (Id. at 36:16). Furthermore,
it is also clear that Defendants are not attacking the reliability of Dr. ElSohly’s collection and
authentication of geranium plants and oils in the sense that he did not provide collection
information about the plants and oils in his studies.
Insofar as Defendants’ argument is an argument about the reliability of Dr. ElSohly’s
testimony, the Court rejects it because Dr. ElSohly’s failure to use the same methodology as the
authors of other studies who have detected the presence of DMAA in geranium plants does not
show that Dr. ElSohly’s methodology is inherently flawed. Defendants’ challenge equates to an
attack on the conclusions of Dr. ElSohly’s studies, i.e., that DMAA does not occur naturally in
geranium plants and oils, which is not the type of challenge considered in the context of Rule
702 and Daubert. The Court recognizes that it is possible for multiple scientists to conduct tests
on the same or similar plants and oils and reach different conclusions. Indeed, that much is clear
from the literature referenced in the Fleming study. (See Defs.’ Ex. F 3-4, ECF No. 178-9).
Thus, Defendants’ challenge fails to attack the methodology used by Dr. ElSohly as required in
the context of Rule 702 and Daubert.
Dr. ElSohly testified that in his conducting his studies, he had no “preconceived idea
whether [DMAA] was there or not [in geranium plants and oils].” (Hr’g Tr. 10:8-9, Apr. 27,
2015 AM, ECF No. 321). In fact, while Dr. ElSohly would not agree that it is “impossible that
DMAA will be present in geranium plants,” he testified that the scientific literature that he was
relying on did not find the presence of DMAA in geranium plants. (Dr. ElSohly Dep. 28:5-21).
Furthermore, Dr. ElSohly acknowledged that there are factors that would affect whether DMAA
is present in geranium plants, including: the environment, the time of collection, the age of the
plant, the altitude, the soil composition, the exposure to light, the ambient temperature, the time
that the plant sample was picked, the storage conditions after it was picked, whether the sample
No. EP-13-CV-323-DCG
68
was dry or fresh, and the water moisture level. (See id. at 29:2-30:14; Hr’g Tr. 16:23-18:18,
27:19-28:6, Apr. 27, 2015 AM, ECF No. 321). Dr. ElSohly testified that while these conditions
may affect the amount of DMAA in geranium plants, it could not have an effect on whether or
not DMAA existed at all. (See Dr. ElSohly Dep. 31:6-14; Hr’g Tr. 16:23-18:18, 27:19-28:6,
Apr. 27, 2015 AM, ECF No. 321). He expanded upon that answer as well:
Q. Is it possible, then, for a plant from one part of a country or the world could have a
different chemical composition as a plant from another part?
...
A. If it’s the same species, the differences would be [a] quantitative difference, not [a]
qualitative [difference].
Q, So, you are saying . . . you couldn’t find the presence of certain trace oils or minerals
or compounds in a plant of the same species that was grown in China versus Africa?
A. I’m saying the amount would be different.
Q. But you’re saying there couldn’t be different ones at all?
A. It might be because of the level of detection, or you know . . . some of the
components that are not, you know, photosynthesized. For example, if you are
looking for the presence of rare metal cadmium or some kind of element that will
have something to do with the soil of that plant, where that plant is growing. You
might find it in one area but not in another area. But as far as compounds that are
photosensitized by the plant, by the enzyme machine of the plant - Q. Sure.
A. - - will be there, though it might be a different quantity, so you have - - you know,
I’ve done some work, like I say again, with cannabis to determine the country of
origin based on the chemical composition.
Q. Because there’s a signature - A. Based on the chemical composition. Based on the signature. Based on that chemical
composition . . . it’s not that you’re going to find, you know, a whole set of different
compounds here but not here. All of them are there, it’s just the ratio of those
different compounds in there change from one location to the other.
(Dr. ElSohly Dep. 31:21-33:10). Dr. ElSohly admitted that he had not studied all of the same
samples as the Ping, Li, and Fleming studies, in which those authors discovered the presence of
DMAA in geranium plants.
No. EP-13-CV-323-DCG
(See id. at 35:5-38:14, 63:3-24, 73:17-77:3, 78:16-79:22;
69
Hr’g Tr. 20:9-18, 26:9-15, Apr. 27, 2015 AM, ECF No. 321). Moreover, when he did, in fact,
test one sample from the same province that Dr. Li tested and purportedly found DMAA at a
different detection level, Dr. ElSohly failed to detect DMAA at ten parts-per-billion. (See Hr’g
Tr. 16:4-22, 18:10-18, 26:11-12, Apr. 27, 2015 AM, ECF No. 321). Dr. ElSohly testified that
though he thought the analytics of the Li and Fleming studies were sound, he felt that their
findings, that DMAA was present in geranium plants, were based on the samples being
contaminated. (See id. at 28:22-24).
Furthermore, Dr. ElSohly testified that “it would take so much [geranium] to get [enough
DMAA] to put in one bottle . . . [that the DMAA used in Jack3d could not] be . . . under any
circumstances . . . from the natural source.” (See id. at 31:12-21). Specifically, he explained that
even taking the “highest level” of DMAA that Dr. Li purported to find in geranium plants,
“180,000 kilos of plant material [would be needed] to produce one bottle of [Jack3d].”
(Id. at 31:12-18). Given the amount of DMAA used in Jack3d, Dr. ElSohly stated that the
DMAA used in Jack3d could not be from a natural source and had to be synthetic.42
(See id. at 31:19-32:24).
Furthermore, Dr. ElSohly added that the Li and Fleming studies
demonstrated that the DMAA they purported to find in geranium matched the composition of
synthetic DMAA. (See id. at 32:7-13). Dr. ElSohly clarified that natural products do not exist in
nature in the same composition as synthetic products. (See id. at 32:14-24).
Although Dr. ElSohly did not test the same samples using the same detection levels as
those used in the Ping, Li, and Fleming studies, the Court finds that the work Dr. ElSohly
performed and his opinion based on that work is reliable because, in applying the Daubert
factors, the Court finds that Dr. ElSohly’s technique has been tested, subject to peer-review and
42
Dr. ElSohly testified that he tested a bottle of Jack3d to determine the amount of DMAA in the product.
(See Hr’g Tr. 33:18-35:8, Apr. 27, 2015 AM, ECF No. 321).
No. EP-13-CV-323-DCG
70
publication, with a potential rate of error, and his technique is generally accepted in the scientific
community. (See Dr. ElSohly Dep. 25:6-28:4, 38:25-39:8, 49:8-53:1, 59:23-62:8, 63:17-24,
73:17-77:3, 96:10-99:25; Hr’g Tr. 9:16-18:18, Apr. 27, 2015 AM, ECF No. 321; see also
Daubert, 509 U.S. at 592-94). The Court further finds that because Dr. ElSohly’s first study was
published before this litigation commenced, it adds to the reliability of Dr. ElSohly’s opinion. In
the context of Rule 702 and Daubert, the Court also finds that Defendants cannot merely attack
Dr. ElSohly’s conclusion that DMAA is not naturally-occurring in geranium plants and oils
instead they must challenge whether or not the methodology that he used in forming that opinion
is reliable.
The Court concludes that whether DMAA is naturally-occurring substance in
geranium plants and oils is a proper subject for cross-examination and, therefore, Dr. ElSohly’s
expert opinion should not be excluded.
2. Relevance
The Court finds that Dr. ElSohly’s opinion is relevant to assist the trier of fact in
determining Plaintiffs’ causes of action. While it may be that none of Plaintiffs’ claims “turn
on” whether DMAA occurs naturally in geranium plants and oils, the Court believes that Dr.
ElSohly’s opinion may assist the trier of fact in making determinations about causes of action,
such as products liability and misrepresentation. Plaintiffs First Amended Complaint alleges that
Defendants advertised and marketed Jack3d as a natural supplement, when they knew it was not.
(See Am. Compl. ¶ 80, ECF No. 98). Plaintiffs further allege that misrepresentations about
whether Jack3d was a natural product “falsely reassure[d] consumers that Jack3d is a safe
product.” (Id.) Plaintiffs also contend that the FDA warned companies that syntheticallyproduced DMAA is not a “dietary ingredient” and could not be used in a dietary supplement.
(See id. at ¶ 81). Moreover, Plaintiffs allege that Dr. ElSohly’s study refutes claims that
synthetic DMAA is identical to naturally-occurring ingredients because geranium plants and oils
No. EP-13-CV-323-DCG
71
do not have DMAA at detectable levels. (See id. at ¶ 84). Accordingly, the Court finds that Dr.
ElSohly’s opinion is relevant and, therefore, denies Defendants’ Motion to Strike his opinion.
IV.
CONCLUSION
For the reasons stated above, it is HEREBY ORDERED that Defendants’ Motions to
Strike Dr. Cantilena (ECF No. 184), Dr. Mills, (ECF No. 186), and Dr. Rusyniak (ECF No. 187)
are GRANTED and Defendants’ Motion to Strike Dr. ElSohly (ECF No. 185) is DENIED.
Accordingly, Defendants’ Motion to Exclude Untimely Disclosures (ECF No. 258) is
DENIED AS MOOT.
SIGNED and ENTERED this 27th day of July, 2015.
ANNE T. BERTON
U.S. MAGISTRATE JUDGE
No. EP-13-CV-323-DCG
72
Disclaimer: Justia Dockets & Filings provides public litigation records from the federal appellate and district courts. These filings and docket sheets should not be considered findings of fact or liability, nor do they necessarily reflect the view of Justia.
Why Is My Information Online?