IN THE SUPREME COURT OF TEXAS
444444444444
NO. 09-0073
444444444444
MERCK & CO., INC., PETITIONER,
v.
FELICIA GARZA, ET AL., RESPONDENTS
4444444444444444444444444444444444444444444444444444
ON PETITION FOR REVIEW FROM THE
COURT OF APPEALS FOR THE FOURTH DISTRICT OF TEXAS
4444444444444444444444444444444444444444444444444444
Argued January 20, 2010
JUSTICE HECHT delivered the opinion of the Court.
JUSTICE WILLETT and JUSTICE GUZMAN did not participate in the decision.
Respondents contend that Vioxx, a prescription drug, caused their decedent’s death. In
Merrell Dow Pharmaceuticals, Inc. v. Havner,1 we set requirements for determining whether
epidemiological evidence is scientifically reliable to prove causation. The parties here dispute what
those requirements are, whether they apply in this case, and whether they were satisfied. We hold
that Havner’s requirements apply and were not met, and that the evidence was therefore legally
1
953 S.W.2d 706 (Tex. 1997).
insufficient to prove causation. Accordingly, we reverse the judgment of the court of appeals2 and
render judgment that respondents take nothing.
I
A
Leonel Garza had a long history of heart disease. Twenty years before his death at age 71,
he suffered a heart attack and four years later underwent quadruple bypass surgery to alleviate
blockages in four of his coronary arteries. In the years that followed, he had one cardiac
catheterization procedure that revealed additional blockages in three arteries, followed by a second
such procedure that revealed severe recurrent coronary artery disease. He had a stent placed in his
left main artery to increase the blood flow into his heart, but two years later was diagnosed with
atherosclerotic obstructive disease and chronic venous insufficiency in his legs. He was also
diagnosed with an abdominal aortic aneurysm.
Twenty-five days before his death, Garza complained to his cardiologist, Dr. Michael Evans,
of intermittent numbness, pain, and weakness in his left arm. After determining that Garza was not
having a heart attack, Evans ordered an ultrasound of Garza’s neck to check the circulation to his
brain and a stress test to check the circulation to his heart. Evans also gave him a week’s supply of
25 mg Vioxx for pain relief and scheduled a follow-up visit eight days later.
When Garza returned for his appointment, Evans was out of town, and one of his partners,
Dr. Juan Posada, reviewed Garza’s test results with him and his wife. The stress test revealed that
Garza had a stable cardiac status, and Posada noted in Garza’s record that he thought Garza was on
2
277 S.W.3d 430 (Tex. App.–San Antonio 2008).
2
optimal medical management. However, the test did reveal some small areas of apical ischemia,
meaning that a part of the tip of Garza’s heart was not getting enough blood when stressed. Posada
offered the possibility of a cardiac catherization to more fully investigate the cause of the apical
ischemia, but Garza declined, opting to discuss the results with Evans a month later. According to
Mrs. Garza, Posada gave her husband thirty additional 25 mg Vioxx pills. Seventeen days later, on
April 21, 2001, Garza died while alone at his ranch near Rio Grande City, Texas. The autopsy found
that the immediate cause of death was a “probable myocardial infarction” initiated at least in part
by the underlying cause of “severe coronary artery disease”.
Garza’s statutory beneficiaries (“the Garzas”) sued Merck & Co., Inc., the manufacturer of
Vioxx, for products liability, alleging that the drug was defective as designed and as marketed with
inadequate warnings. Merck repeatedly challenged the scientific reliability of the Garzas’ evidence
offered to prove that Vioxx caused Garza’s death. The trial court overruled Merck’s objections.
The jury returned a verdict for the Garzas, awarding $7 million dollars actual damages, plus $25
million dollars in punitive damages, which the trial court reduced to the applicable statutory
maximum of $750,000.3 Merck appealed.
The court of appeals held that the Garzas could not recover on their design-defect claim
because they did not present sufficient evidence of a safer alternative design, but that they could
recover on their inadequate-warning claim.4 The court rejected Merck’s argument that the Garzas
had failed to meet Havner’s requirements for proving causation because they had not produced two
3
See TEX. CIV. PRAC. & REM. CODE § 41.008(b)(1) (as noneconomic damages not exceeding $750,000).
4
277 S.W.3d at 440 .
3
statistically significant epidemiological studies showing that Vioxx at the dose and for the duration
taken by Garza more than doubles the risk of heart attack.5 The court believed that Havner did not
“establish[] such a bright-line test for causation” but mandated that the sufficiency of the evidence
be determined from its totality.6 An expert witness called by the Garzas testified that clinical trials
had “indicated a more than two-fold risk of serious cardiovascular ‘adverse experiences’ suffered
by the people who participated in the studies . . . within twelve weeks or less of taking Vioxx.”7 The
expert had opined that there was “a pretty strong case that the risk of Vioxx for heart attacks can
occur at any time after the initiation of the medicine.”8 The court concluded that this was sufficient
evidence to support general causation.9 However, the court reversed the Garzas’s judgment for juror
misconduct and remanded the case for a new trial.10
We granted Merck’s petition for review complaining that judgment should be rendered
against the Garzas.11
B
Vioxx, or rofecoxib, is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs block
5
Id. at 434-435.
6
Id. at 435.
7
Id.
8
Id.
9
Id. at 435-436
10
Id. at 441-442.
11
53 Tex. Sup. Ct. J. 15 (Oct. 23, 2009).
4
the production of prostaglandins, which are hormone-like chemicals that are released
in the body in response to injury. The prostaglandins cause inflammation, redness,
swelling, pain, and fever. Reducing the amount of protaglandins reduces
inflammation and its symptoms. In order to inhibit production of prostaglandins, the
NSAIDs act by blocking the enzyme cyclooxygenase (COX). After further study
scientists discovered that the COX enzyme has two isoforms, one associated with
inflammation (COX-II) and another thought to protect the lining of the stomach
(COX-1).12
Early NSAIDS were non-selective, meaning that they restricted both forms of the COX enzyme, but
Vioxx and the other selective NSAIDs only restrict COX-2.13 Scientists theorized that, by restricting
only COX-2, a selective NSAID could provide the pain relief afforded by non-selective NSAIDs
while avoiding their gastrointestinal complications, such as perforations, ulcers, and bleeding.14
After following Food and Drug Administration procedure for seeking approval of a new
drug, Merck submitted its application in late 1998. A few months later, the FDA approved Vioxx
as “safe and effective” for the treatment of osteoarthritis, acute pain, and menstrual pain. Merck
then applied to the FDA for approval to use Vioxx to treat rheumatoid arthritis. As part of its
application, Merck commissioned the VIGOR clinical trial, which was “designed to compare the
occurrence of [gastrointestinal] toxicity with twenty-five and fifty milligrams per day of Vioxx or
one thousand milligrams per day of Naproxen,” a non-selective NSAID.15 In addition to finding a
gastrointestinal benefit, VIGOR also revealed a secondary finding that patients taking Vioxx had
12
See Jason M. Weigand, Vioxx: How Strong is the Case Against Merck?, 11 MICH. ST. U. J. MED. & L. 145,
149 (2007).
13
Id.
14
See Richard Epstein, Regulatory Paternalism in the Market for Drugs: Lessons from Vioxx and Celebrex,
5 YALE J. HEALTH POL’Y L. & ETHICS 741, 741-742 (2005).
15
Weigan, supra note 12, at 155.
5
five times the relative risk of adverse cardiovascular events as patients who took Naproxen.16 But
despite the fact that Merck employees had expressed concern since at least 1997 that Vioxx could
present cardiovascular risks, Merck argued that the VIGOR results could be explained by a
combination of chance and the cardio-protective effects of Naproxen.
Eventually, the FDA approved the use of Vioxx to treat rheumatoid arthritis, and after some
negotiation, Merck placed the cardiovascular data from the VIGOR trial on the label for Vioxx,
though not in the warnings section. In 2000, Merck again sought approval from the FDA for
treatment of yet another condition, colon polyps. To test the efficacy of Vioxx in treating colon
polyps Merck commissioned the APPROVe trial. But after APPROVe found that patients taking
Vioxx had a statistically significant increased relative risk of adverse cardiovascular events
compared to placebo after eighteen months of exposure, Merck announced that it would voluntarily
remove Vioxx from the market on September 30, 2004. In 2005, the FDA commissioned an
advisory panel to examine the cardiovascular concerns relating to Vioxx and other selective
NSAIDs. The panel eventually concluded that the drugs did present cardiovascular risks after
prolonged exposure, but it did not find that they presented a risk after only short-term use.
Thousands of lawsuits were filed across the country, alleging that Vioxx caused heart attacks
or other adverse cardiovascular events. After a few cases were tried with mixed results, Merck
agreed to pay $4.85 billion into a settlement fund for qualifying claims. The Garzas’ claim did not
qualify.
II
16
Id.
6
To prevail on their inadequate-warnings claim, the Garzas were required to prove that
Garza’s ingestion of Vioxx 25 mg pills over a period of 25 days was the producing cause of his heart
attack. As we explained in Merrell Dow Pharmaceuticals, Inc. v. Havner,17 causation, in this
context, has two components: general and specific. “General causation is whether a substance is
capable of causing a particular injury or condition in the general population, while specific causation
is whether a substance caused a particular individual’s injury.”18 The Garzas relied on testimony
from two cardiologists who based their opinions on data compiled in Merck-sponsored clinical trials
of Vioxx, meta-analyses of those trials, and other observational, epidemiological studies regarding
the possible cardiovascular risks presented by Vioxx. Merck contends that the Garzas’ evidence did
not meet Havner’s requirements for scientific reliability. Specifically, Merck argues that Havner
requires a plaintiff who claims injury from taking a drug to produce two independent
epidemiological studies showing a statistically significant doubling of the relative risk of the injury
for patients taking the drug under conditions substantially similar to the plaintiff’s (dose and
duration, for example) as compared to patients taking a placebo. The Garzas argue that Havner’s
requirements for epidemiological evidence apply only to uncontrolled, observational studies, not to
studies from clinical trials, like the ones on which they rely. Or if the requirements do apply to
clinical trials, then the Garzas argue that Havner does not establish bright-line requirements as
argued by Merck, but charges courts with surveying the totality of the evidence regarding causation.
17
953 S.W.2d 706 (Tex. 1997).
18
Id. at 714.
7
In any event, the Garzas contend that evidence failing Havner’s requirements may nevertheless be
sufficient if accompanied by other reliable evidence of causation.
A
In Havner, the plaintiff claimed that taking Bendectin for morning sickness during her
pregnancy caused birth defects in her baby.19 In analyzing whether there was evidence of causation,
we started with the general proposition that “a determination of scientific reliability is appropriate
in reviewing the legal sufficiency of evidence.”20 We reiterated that courts must look beyond the
bare opinions of qualified experts and independently evaluate the foundational data underlying an
expert’s opinion in order to determine whether the expert’s opinion is reliable.21
If the foundational data underlying opinion testimony are unreliable, an expert will
not be permitted to base an opinion on that data because any opinion drawn from that
data is likewise unreliable. Further, an expert’s testimony is unreliable even when the
underlying data are sound if the expert draws conclusions from that data based on
flawed methodology. A flaw in the expert’s reasoning from the data may render
reliance on a study unreasonable and render the inferences drawn therefrom dubious.
Under that circumstance, the expert’s scientific testimony is unreliable and, legally,
no evidence.22
Causation can sometimes be proved directly.
19
Id. at 708.
20
Id. at 713.
21
Id. at 711-712. See also E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549, 557 (Tex. 1995)
(providing that, in a determination of the admissibility of expert testimony, the court should look to: (1) the extent to
which the theory has been or can be tested; (2) the extent to which the technique relies upon the subjective interpretation
of the expert; (3) whether the theory has been subjected to peer review and publication; (4) the technique's potential rate
of error; (5) whether the underlying theory or technique has been generally accepted as valid by the relevant scientific
community; and (6) the non-judicial uses that have been made of the theory or technique).
22
Havner, 953 S.W.2d at 714.
8
In some cases, controlled scientific experiments can be carried out to determine if a
substance is capable of causing a particular injury or condition, and there will be
objective criteria by which it can be determined with reasonable certainty that a
particular individual's injury was caused by exposure to a given substance.23
Often, however, it can be proved only indirectly, with epidemiological studies.
In the absence of direct, scientifically reliable proof of causation, claimants may
attempt to demonstrate that exposure to the substance at issue increases the risk of
their particular injury. The finder of fact is asked to infer that because the risk is
demonstrably greater in the general population due to exposure to the substance, the
claimant's injury was more likely than not caused by that substance.24
Allowing such proof
concedes that science cannot tell us what caused a particular plaintiff's injury. It is
based on a policy determination that when the incidence of a disease or injury is
sufficiently elevated due to exposure to a substance, someone who was exposed to
that substance and exhibits the disease or injury can raise a fact question on
causation.25
The epidemiological evidence on which the experts in Havner relied consisted largely of
unpublished, retroactive, observational studies. The Garzas argue that their evidence of clinical
trials involving Vioxx is more reliable. The difference between the two types of epidemiological
evidence is this:
Epidemiological studies may be characterized as experimental or observational.
The major difference between the two is that in an experimental setting, the
epidemiologist controls the conditions under which the study is to be conducted; in
an observational setting, the epidemiologist is not able to control these conditions.
In experiments, the epidemiologist controls the method of assigning subjects to either
the treatment or the comparison groups. A commonly used means of assignment is
23
Id. at 714-715.
24
Id.
25
Id. (internal citation omitted).
9
to randomly allocate similar persons to the treatment or the comparison group; such
an experiment is called a randomized clinical trial . . . .26
But while the controlled, experimental, and prospective nature of clinical trials undoubtedly make
them more reliable than retroactive, observational studies, both must show a statistically significant
doubling of the risk in order to be some evidence that a drug more likely than not caused a particular
injury. The superior way in which a study is conducted does not justify taking its conclusion to be
anything other than what it is. The purpose of the structure of epidemiological studies and the
statistical evaluation of their results is to provide “objective criteria by which it can be determined
with reasonable certainty that a particular individual’s injury was caused by exposure to a given
substance.”27 Havner’s requirements necessarily apply to all epidemiological evidence, including
the causation evidence the Garzas presented at trial.
B
In Havner, we surveyed the opinions of other courts and scholarly commentary and
concluded:
Although we recognize that there is not a precise fit between science and legal
burdens of proof, we are persuaded that properly designed and executed
epidemiological studies may be part of the evidence supporting causation in a toxic
tort case and that there is a rational basis for relating the requirement that there be
more than a "doubling of the risk" to our no evidence standard of review and to the
more likely than not burden of proof.28
26
DAVID E. LILIENFELD & PAUL D, STOLLEY, FOUNDATIONS OF EPIDEMIOLOGY 151 (3rd ed. 1994) (internal
citation omitted).
27
Havner, 953 S.W.2d at 715.
28
Id. at 717.
10
To demonstrate the thinking behind the doubling of the risk requirement we then used the following
admittedly oversimplified example:
Assume that a condition naturally occurs in six out of 1,000 people even when they
are not exposed to a certain drug. If studies of people who did take the drug show
that nine out of 1,000 contracted the disease, it is still more likely than not that
causes other than the drug were responsible for any given occurrence of the disease
since it occurs in six out of 1,000 individuals anyway. Six of the nine incidences
would be statistically attributable to causes other than the drug, and therefore, it is
not more probable that the drug caused any one incidence of disease. This would
only amount to evidence that the drug could have caused the disease. However, if
more than twelve out of 1,000 who take the drug contract the disease, then it may be
statistically more likely than not that a given individual's disease was caused by the
drug.29
In essence, we acknowledged that “frequency data, such as the incidence of adverse effects in the
general population when exposed, cannot indicate the actual cause of a given individual’s disease
or condition.”30 However, we found that “[t]he use of scientifically reliable epidemiological studies
and the requirement of more than a doubling of the risk strikes a balance between the needs of our
legal system and the limits of science.”31
The Garzas argue that Havner did not ultimately hold that a study had to show a doubling
of the risk in order to be found reliable evidence of causation. They point out that Havner states:
We do not hold, however, that a relative risk of more than 2.0 is a litmus test or that
a single epidemiological test is legally sufficient evidence of causation. Other factors
must be considered. As already noted, epidemiological studies only show an
association. There may in fact be no causal relationship even if the relative risk is
high. . . . Likewise, even if a particular study reports a low relative risk, there may
in fact be a causal relationship. The strong consensus among epidemiologists is that
29
Id. (emphasis omitted).
30
Id. at 718.
31
Id.
11
conclusions about causation should not be drawn, if at all, until a number of criteria
have been considered.32
The opinion further noted that epidemiological studies “are subject to many biases and therefore
present formidable problems in design and execution and even greater problems in interpretation.”33
Accordingly, we stated that
there are a number of reasons why reliance on a relative risk of 2.0 as a bright-line
boundary would not be in accordance with sound scientific methodology in some
cases. Careful exploration and explication of what is reliable scientific methodology
in a given context is necessary.34
But these statements must be read in context. Our concern was that statistically reliable
studies showing a doubling of the risk might nevertheless be insufficient to prove causation, not that
they would ever be unnecessary. We noted that “[a] few courts that have embraced the
more-than-double-the-risk standard have indicated in dicta that in some instances, epidemiological
studies with relative risks of less than 2.0 might suffice if there were other evidence of causation.”35
We declined to join those courts, leaving undecided “whether epidemiological evidence with a
relative risk less than 2.0, coupled with other credible and reliable evidence, may be legally
sufficient to support causation.”36
32
Id.
33
Id. at 719 (quoting Marcia Angell, The Interpretation of Epidemiologic Studies, 323 NEW ENG. L. REV. 823,
824 (1996)).
34
Id.
35
Id.
36
Id.
12
We concluded that the studies in Havner were unreliable when they did not show a doubling
of the risk that was statistically significant at the 95% confidence level. After analyzing and
adopting the “methodology that is at present generally accepted among epidemiologists”37 —
namely, that studies finding a doubling of the risk are statistically significant at the 95% confidence
level — we considered each of the studies that served as the foundation for the opinions of the
Havners’ experts. We concluded that any study that did not find a doubling of the risk that was
statistically significant at the 95% confidence level was unreliable.38 Also, we indicated that an
expert’s opinion that relied on a combined analysis of several studies was unreliable because the
studies did not show a doubling of the risk.39
Havner holds, and we reiterate, that when parties attempt to prove general causation using
epidemiological evidence, a threshold requirement of reliability is that the evidence demonstrate a
statistically significant doubling of the risk. In addition, Havner requires that a plaintiff show “that
he or she is similar to [the subjects] in the studies” and that “other plausible causes of the injury or
condition that could be negated [are excluded] with reasonable certainty.”40 Havner also requires
that even if studies meet the threshold requirements of reliability, sound methodology still
necessitates that courts examine the design and execution of epidemiological studies using factors
37
Id. at 712.
38
Id. at 724-726.
39
Id. at 725 (“[The expert] also said that these studies were consistent with a relative risk that was between 0.7
and 1.8. That is not a doubling of the risk. It may support her opinion that it is more probable than not that there is an
association between Bendectin and limb reduction defects, but the magnitude of the association she gleaned from these
studies is not more than 2.0, based on her own testimony.”).
40
Id. at 720.
13
like the Bradford Hill criteria41 to reveal any biases that might have skewed the results of a study,42
and to ensure that the standards of reliability are met in at least two properly designed studies.43
Thus, a plaintiff must first pass the primary reliability inquiry by meeting Havner’s threshold
requirements of general causation. Then, courts must conduct the secondary reliability inquiry that
examines the soundness of a study’s findings using the totality of the evidence test. As we
concluded in Havner:
In sum, we emphasize that courts must make a determination of reliability from all
the evidence. Courts should allow a party, plaintiff or defendant, to present the best
available evidence, assuming it passes muster under Robinson, and only then should
a court determine from a totality of the evidence, considering all factors affecting the
reliability of particular studies, whether there is legally sufficient evidence to support
a judgment.44
C
The Garzas contend that they presented more than two studies showing a statistically
significant doubling of the risk of heart attack from taking Vioxx, thereby satisfying Havner’s
requirements. First, they point to the VIGOR study. Although the results of VIGOR indicate
statistically significant results showing five times as many heart attacks for the patients on Vioxx
compared to the patients on Naproxyn, that study involved a dosage of 50 mg and a median duration
of 9 months—double the dosage Mr. Garza took (25 mg) and a much longer duration than Mr.
41
Havner, 953 S.W.2d 706, 718 n.2. Those criteria, published by Sir Austin Bradford Hill in 1965 and widely
used by epidemiologists, are more fully described in Havner. The criteria are grouped in nine categories: strength of
association, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy.
42
Id. at 718-719.
43
Id. at 727.
44
Id. at 720.
14
Garza’s 25 days. The Garzas argue, and we agree, that this finding of an increased risk does not
necessarily mean that there is no increased risk at a lower dose and smaller duration. But the point
is not that the VIGOR study suggests that a lesser exposure to Vioxx is less risky, but that the study
suggests nothing at all about significantly lesser exposure. The usage involved in a study need not
match the claimant’s usage exactly, but the conditions of the the study should be substantially
similar to the claimant’s circumstances. The Garzas simply cannot argue that the VIGOR study
showed a statistically significant doubling of the relative risk for a person like Garza, who took a
much smaller dosage of Vioxx for much less time.45
Another study presented, the Shapiro meta-analysis, also falls short. The Shapiro meta-
analysis, performed in 2000 by Merck employee Deborah Shapiro, combined and analyzed much
of the cardiovascular data that the company had gathered up to that point. In one arm of the
analysis, Shapiro compared the relative risks of heart attack of people who had taken Vioxx to the
risks of people who had taken other NSAIDs. This analysis found that patients who had taken
Vioxx had a relative risk of 2.02 compared to the users of other NSAIDs. The results were
significant at the 95% confidence level with a confidence interval from 1.14 to 3.55. However, as
meta-analysis, it combines the results of a number of different studies, with differing dosages,
durations, and comparison drugs. This is especially problematic given the influence of the VIGOR
results on the analysis. VIGOR, as we have said, used double Garza’s dose of Vioxx with patients
for a median period of nine months. When the VIGOR results were removed from the meta-
45
The Graham study is similarly unreliable because the statistically significant finding applied only to 50 mg
dosages.
15
analysis, Shapiro found the relative risk of heart attack of Vioxx patients to other NSAID recipients
dropped to 1.19 at the 95% level with an interval from 0.60 to 2.35. And even those remaining
results are skewed by differences in dose and duration compared to Garza’s exposure.
The Garzas also rely on the APPROVe study. That study found an overall relative risk
greater than 2 for APTC (Antiplatelet Trialists' Collaboration criteria) events, a category of events
which includes “the combined incidence of death from cardiovascular, hemorrhagic, and unknown
causes; of nonfatal myocardial infarction; and of nonfatal ischemic and hemorrhagic stroke.”
However, the other category studied, Cardiovascular Thrombotic Events, a narrower category still
containing Mr. Garza’s injury, found an overall risk of 1.92. Moreover, the study took place over
a three-year period and did not show statistically significant differences until after eighteen months,
a much longer duration than Mr. Garza’s use.
Finally,46 the Garzas presented the VICTOR study, a clinical trial designed to measure the
efficacy of Vioxx in treating patients with colorectal cancer. At trial, the only evidence of VICTOR
was an e-mail containing two charts of preliminary results and cursory testimony regarding
VICTOR’s protocol and findings. However, although the VICTOR study was discontinued after
two years, it does appear that these preliminary findings achieve statistically significant results for
confirmed “thrombotic events” with a relative risk of over 3.0. But even if VICTOR qualifies under
Havner’s test, it cannot do so alone. Another study is still necessary, but lacking here.
46
The Garzas presented a total of six other studies throughout the course of litigation. Two of the studies
(ADVANTAGE and Protocol 090) contain a relative risk factor greater than 2.0, but neither of these studies contain
sufficient data to achieve statistical significance. The Garzas do not contend that any one of the remaining four studies
(the Juni paper, the Solomon study, the Ingenix study, and the Protocol 010 study) sufficiently indicate a statistically
significant doubling of the risk of heart attack.
16
Thus, the two cited by the Garzas do not meet Havner’s standards of reliability.
D
While we have held that epidemiological evidence used to prove general causation must meet
Havner’s requirements for scientific reliability, we return briefly to the Garzas’ argument that the
totality of the evidence in this case shows general causation. They point to evidence that Merck
largely excluded patients with a history of cardiovascular disease from its studies. They argue that
the trials suffer from selection bias in that they excluded a subset of people who were at an elevated
risk of suffering a Vioxx-induced heart attack. But several of the studies did include patients who
had some history of cardiovascular disease, and in any event, the absence of evidence cannot
substitute for evidence. The Garzas argue that the risk doubling for Garza required by Havner can
be extrapolated from studies finding a doubling of the risk at much higher doses and longer
durations. But the Garzas cannot point to any scientific basis for such an extrapolation.
The totality of the evidence cannot prove general causation if it does not meet the standards
for scientific reliability established by Havner. A plaintiff cannot prove causation by presenting
different types of unreliable evidence. Thus, we are constrained to hold that the Garzas did not
present reliable evidence of general causation and are therefore not entitled to recover against
Merck.
17
* * *
Accordingly, the judgment of the court of appeals is reversed and judgment rendered that the
Garzas take nothing.
Nathan L. Hecht
Justice
Opinion delivered: August 26, 2011
18