Analysis of Two Deaths Reportedly Associated with Kratom

Analysis of Two Deaths Reportedly Associated with Kratom Use
Tupper Lake, New York, and Hillsborough County, Florida
Jane Babin, Ph.D., Esq.
University of San Diego School of Law, J.D.
Purdue University, Ph.D., Molecular Biology
Author Note
Independent Analysis authorized by the American Kratom Association

Executive Summary
The purpose of an autopsy is to provide detailed medical information about a death to
obtain information on various factors which may have contributed to the death. The manner of
death, and the actual cause of death, are important considerations from both a legal and public
health perspective.
Even when the cause of death seems clear, the decedent may have had a medical
condition which was not apparent during life. When an unexplained death occurs, it becomes a
matter of public policy for the best efforts to be made by coroners and medical examiners to
conduct a comprehensive assessment of all factors associated with the death, and to provide a
conclusion that considers all of the known and reasonably possible factors contributing to the
In both of these cited cases, the conclusions reported by the coroner and medical
examiner citing “kratom overdose” and “kratom intoxication” appear to add to the long list of
mistaken, inaccurate, and now discredited reports implicating kratom when this botanical
actually was only an ingredient mixed into an adulterated formulation with other toxic
substances in most, if not all of those previously reported cases. These two cases, where it
appears there was a rush to judgment to align with a political narrative promoted by the Drug
Enforcement Administration (DEA) on kratom use, undermine the credibility of the search for
the actual cause of death for the benefit of the decedent’s family and the public.
Sgt. Matthew Dana, Tupper Lake, New York
Sgt. Matthew Dana died from hemorrhagic pulmonary edema with the presence of
mitragynine in his blood. Mitragynine alone has never been found to cause hemorrhagic
pulmonary edema, nor any death, and has only been implicated when other substances or
conditions sufficient to cause death were present. The Coroner and Medical Examiner erred in
not analyzing blood for substances other than opioids and narcotics including cocaine and
anabolic steroids, which could have caused the death, and for presuming kratom caused Sgt.
Dana’s death without considering known causes of sudden death from hemorrhagic pulmonary
edema. In addition, the coroner and medical examiner, based on public statements released to
the media, note that Mr. Dana used kratom as a part of his personal bodybuilding regimen, but
failed to describe whether any investigation was made into reports made in the community that
the decedent had used injectable anabolic steroids as a part of that bodybuilding regimen. If
true, medical literature does provide links between the use of anabolic steroids and
hemorrhagic pulmonary edema. No such literature exists to link kratom to that condition.
Christopher Walden, Hillsborough County, Florida
Christopher Waldron died with mitragynine, a potentially toxic amount of Citalopram,
and Cyclobenzaprine (which is contraindicated in combination with Citalopram) in his blood.
Both of these prescription medicines contain specific warnings required in FDA labeling that, if
used in combination, can cause coma and even death. In addition, the kratom brand and
product Mr. Waldron is believed to have consumed has been known to be counterfeited, and
often adulterated with toxic substances. Mr. Waldron also had left ventricular hypertrophy, an
enlarged liver, and thyroid disease, which may have contributed to his death. The Medical
Examiner rushed to judgment when opining that the active compound in the botanical
supplement, kratom, caused Mr. Waldron’s death, despite numerous findings that point to
sudden death from drug-induced Long QT Syndrome, Torsade de Pointes and/or Serotonin
Syndrome, exacerbated by pre-existing heart disease, thyroid disease and possible liver disease.
The Medical Examiner’s Department in Hillsborough County, FL., has a history of mistakenly
finding sensational causes of death in high profile cases.

The presence of a constituent alkaloid in kratom (“mitragynine”) alone does not explain
the death of either Matthew Dana or Christopher Waldron, and was merely a convenient, if
misunderstood solution to the difficult problem the coroner and medical examiners faced when
the two young men died without clear evidence of the cause of their deaths.

Tupper Lake, New York, and Hillsborough County, Florida
Sgt. Matthew Dana died from hemorrhagic pulmonary edema (HPE), with a high level of
mitragynine (the active compound in kratom) in his blood. Media reports indicate that Sgt.
Dana had 3,500 ng/ml in his blood, from which the coroner concluded that death by HPE was
caused by mitragynine overdose.1 Based on the disclosed facts, there is insufficient
information to make the leap from correlative findings to the cause of Sgt. Dana’s death.
While the available information does not exclude the possibility that mitragynine, like
virtually any drug or other substance, may be toxic at very high doses, there is no scientific
evidence that the dose Sgt. Dana consumed was toxic or was responsible for Sgt. Dana’s HPE.
At most, the information reported in the press describes a tragic death from HPE with
coincident mitragynine in blood, and raises more questions than it answers.
Franklin County Coroner Shawn Stuart said, “the cause of death was a hemorrhagic
pulmonary edema — blood in the lungs — as a result of an overdose of mitragynine, the active
chemical in kratom.”2 The coroner also stated “I think we always assumed that kratom played
a role. That was the only substance found at the scene.”3 This raises the question of whether
other possible causes of HPE were thoroughly investigated or were thought unnecessary due to
the coroner’s presumptive conclusion of mitragynine overdose. Without a thorough
investigation of other possible causes of HPE and an understanding of how mitragynine
contributed to HPE, if at all, it is likely that detection of mitragynine in Sgt. Dana was
coincidental rather than causative of his death.
Stuart stated that the toxicology screen performed on Sgt. Dana only analyzed the
presence of narcotics and opioids.4 Failure to screen for other classes of drugs, particularly
benzodiazepines, antidepressants and steroids, may have omitted key pieces of information

Cerbone “Coroner: Police sergeant died from high concentration of kratom” Adirondack Daily Enterprise,
Sept. 12, 2017 (viewed at

necessary to fully understand the cause of this unfortunate death. Other cases where
mitragynine or kratom has been found in the body of a decedent involved at least one other
drug, ranging from some over-the-counter medications such as antihistamines and cough
suppressants, to antidepressants, anxiolytics, analgesics and alcohol. While each individual
drug or substance may have been within non-toxic, therapeutic levels, combinations of drugs
with known or unknown metabolism, interactions, and side effects can produce lethal
Stuart, along with local medical examiner Dr. C. Francis Varga reportedly used
information from the Journal of Analytical Toxicology and the Journal of Forensic Sciences
during their investigation. A “possible kratom toxicity” case (a former heroin addict who was
also found with large amounts of cold medicine and benzodiazepines in his system) factored in
as a reason kratom was implicated.
It seems unlikely that Stuart and Varga closely analyzed the previous reports of
mitragynine-associated deaths, including those cited by the DEA and analyzed by Dr. Jack
Henningfield in his 2016 8-factor analysis of Kratom. If they had, they would have recognized
that multi-drug interactions, polypharmacy and other factors contributed to all deaths in which
kratom has been implicated. For example:

• A report in the Journal of Analytical Toxicology, a variety of substances were in
the decedent’s body including: venlafaxine and O-desmethylvenlafaxine (both
SNRI class antidepressants); mirtazapine (a SSRI class antidepressant with a
variety of off-label uses); diphenhydramine (an antihistamine); alcohol and

Cerbone “Coroner reveals details behind Kratom overdose report” Adirondack Daily Enterprise, Sept. 14,
2017 (viewed at
 Schedules of Controlled Substances: Temporary Placement of Mitragynine and 7-Hydroxymitragynine
into Schedule I; 3-Factor Analysis, DEA Docket No. DEA-2016-0015-0001.
 Henningfield, “Assessment of Kratom under the CSA Eight Factors and Scheduling Recommendation”,
November 28, 2016, pp. 1-128, submitted on, Docket No. DEA-442W, on behalf of the American
Kratom Association; see
shows-no-basis-for-dea-to-restrict-herb-Kratom-300371521.html (“Henningfield”).
 McIntyre et al., “Mitragynine Kratom’ Related Fatality; A Case Report with Postmortem Concentrations.”
J. Anal. Toxicol 39:152-55 (2015).

• Nine cases of fatal intoxication from adulterated kratom in Sweden, in which a
substance sold as kratom (“Krypton”) was contaminated with Odesmethyltramadol,
a metabolite of the opioid, Tramadol. This cluster of
deaths was later confirmed to result from the opioid adulterant, not
mitragynine, and in each case, additional drugs (up to eight) and/or alcohol were
detected. Autopsy findings were described as “non-specific” and most cases
“included brain and lung edema and congestion of internal organs.” Non-specific
edema (swelling) differs significantly from hemorrhagic pulmonary edema, or
bleeding from the lungs.
• A death caused by polyhexidrine (a stimulant related to methamphetamine), but
reported as kratom-associated because mitragynine was also detected in
combination with morphine, acetaminophen, and promethazine.
• A fatality in which mitragynine, dextromethorphan, diphenhydramine,
temazepam (a benzodiazepine), and 7-amino-clonazepam (a benzodiazepine
metabolite), were detected in the body of a teenager with a history of heroin
These and other reports were reviewed by Dr. Henningfield in the 8-factor analysis
submitted to the DEA in opposition to placing mitragynine and 7-hydroxymitragynine in
Schedule I of the Controlled Substances Act. Henningfield concluded from these reports that
“[w]e do not rule out the possibility that there have been overdose deaths involving extremely
high doses of kratom; however, to date, we have been unable to document a single death in
which kratom overdose can reasonably be concluded to have been “causal” in the death.” It
should also be noted that while non-specific pulmonary edema was observed in many if not all

( Kronstand et al., “Unintentional Fatal Intoxications with Mitragynine and O-Desmethyltramadol from the
Herbal Blend Krypton.” J. Anal. Toxicol 35:242-47 (2013).
 Holler et al., “A Drug Toxicity Death Involving Propylhexedrine and Mitragynine.” J. Anal. Toxicol 35:54-
59 (2011).
 Neerman et al., “A Drug Fatality Involving Kratom.” J. Forensic Sci. 58:S278-S279.
 Henningfield, supra.

the cases that may have led Stuart and Varga to implicate kratom, no previous report involving
kratom described autopsy findings of HPE.
Because kratom has not been studied extensively in placebo-controlled clinical trials in
humans, the basis for interactions between mitragynine and other drugs is unknown. Rather
than suspecting mitragynine as a primary cause of death, the literature suggests that
combinations of other drugs with mitragynine is unpredictable. Neither mitragynine alone nor
a combination of mitragynine and any other drug(s) has been reported to cause HPE. Thus, it is
critical to determining the cause of death, to establish whether Sgt. Dana had undiagnosed
condition or other drugs or substances in his body, which may have caused his death by such an
unusual cause. It is perplexing that Stuart and Varga limited their toxicology study to opioids
and narcotics when deaths or adverse effects in which mitragynine has been implicated
involved combinations of non-opioid, non-narcotic drugs including benzodiazepines, antidepressants,
alcohol and even the wakefulness-promoting drug, Modafinil.14 In the latter case,
an individual used kratom for 3.5 years without incident, but suffered a seizure when Modafinil
was also consumed.
Death from hemorrhagic pulmonary edema (HPE) is rare and has never been reported in
conjunction with kratom use in humans or animals. Sudden death from HPE is rarer still. Most
patients with HPE display pulmonary symptoms (shortness of breath, gasping, coughing, foamy
lung secretions, dizziness, stridor, hypoxia) hours or days before seeking medical attention and
often the condition can be treated with respiratory supportive care. Sgt. Dana, was reportedly
healthy, and asymptomatic, but suddenly dropped dead.

Causes of HPE include acute lung injury following intubation or trauma; inhalation of
noxious substances (e.g. mustard gas, chlorine gas, insecticides); infection (e.g., enterovirus,
SARS); inflammatory disorders (e.g., SLE); and aspiration. HPE can also result from systemic
poisoning with selenium, or certain drugs, notably cancer chemotherapy drugs

(e.g., Boyer et al., “Self-treatment of opioid withdrawal using Kratom (Mitragynia speciosa korth).” Addiction
103:1048-50 (2008)Raymo “Tupper Lake mourns death of Police Sgt. Matt Dana at 27” Press Republic August 9, 2017
(viewed at

bleomycin); cocaine; and anabolic steroids.

In one report, two young body builders
independently presented to an Emergency Department with worsening symptoms of dyspnea,
cough and hemoptysis following abuse of anabolic steroids. Both denied using any other
drugs, were given supportive care, and recovered from HPE after discontinuing steroids.
In the case of Sgt. Dana, it is unclear whether the coroner or medical examiner
considered any of the known causes of HPE or analyzed post-mortem specimens (e.g., lung
tissue) by microscopic and histological analysis for findings consistent with any cause of HPE
other than suspected mitragynine overdose.
Further questions revolve around the specific kratom product that Sgt. Dana used and
how he consumed it. The coroner reportedly told the Associated Press that Dana had been
mixing powdered Red Vein Maeng Da kratom into a paste and then eating it. It is unlikely
that Dana could have eaten sufficient unadulterated kratom paste to obtain the level of
mitragynine found in his blood.
A rare study of mitragynine concentrations in plasma from human volunteers showed
linear pharmacokinetics for mitragynine over the oral dosage range of kratom tea ingested, and
followed a two-compartment distribution model. A dose of kratom (10 mg mitragynine) gave
a peak plasma concentration of about 35 ng/ml within less than an hour, and thereafter plasma
concentrations declined rapidly. Dana’s blood level of mitragynine was about 100 times greater
than the range tested, and may not reflect the linear kinetics reported. However, extrapolation
of the data in this paper would indicate that a dose of up to 1 gram of mitragynine was required
to obtain a blood level equal to Dana’s. To achieve this level of mitragynine in the blood, Dana
Lee, “Drug-Induced Pulmonary Disease.” Merck Manual, viewed at

disease#v919657 on October 1, 2017.
 Hvid-Jensen et al. “Pulmonary hemorrhage following anabolic agent abuse: Two cases.” Pulmonary
Medicine Case Reports 18:45-47 (2016).
 Hvid-Jensen et al. “Pulmonary hemorrhage following anabolic agent abuse: Two cases.” Pulmonary
Medicine Case Reports 18:45-47 (2016).
 Esch, “Officer’s death intensifies scrutiny of herbal supplement,” ABC News, Oct 1, 2017 (viewed at
 Trakulsrichai, et al., “Pharmacokinetics of mitragynine in man.” Drug Design, Dev. Ther. 9:2421-29
(2015) (“Trakulsrichai”).

would have needed to consume 50-100g of whole leaf kratom powder (at 1-2% mitragynine) in
less than one hour. Regular leaf kratom consumers doubt that would have been possible
without vomiting, suggesting that more concentrated extracts of mitragynine may have been
consumed by Dana, and/or he administered the mitragynine in a manner other than eating a
paste. If only whole leaf kratom products were found at the scene, this may suggest someone
disposed of other products (e.g., kratom extracts) or substances prior to arrival of investigators.
Extracts, concentrates and purified mitragynine products are sold in liquid and powder
forms, and adulteration of such products has been implicated in previous fatalities attributed to
kratom. Indeed, the manufacturer of one concentrated mitragynine product advises
consumers to look for signs of counterfeiting when purchasing their products and even suggests
that some counterfeiters “have been known to add dangerous ingredients into their mix.”
Alternatively, vomiting followed by aspiration could factor into the cause of death itself
because aspiration is a known cause of HPE. Intentional or unintentional inhalation/aspiration
of dry powdered kratom (an occasional complaint of kratom users who use a “Toss and Swish”
consumption method), aspiration of kratom paste, smoking, vaping or snorting kratom or
mitragynine may also have played a role in HPE. The full autopsy may shed light on these
questions if samples of stomach, trachea, nasal and lung tissue and contents, as well as samples
of the actual kratom product(s) Dana used were collected and analyzed.
Because so many questions surrounding Sgt. Dana’s death remain unanswered, any
reasonable person should refrain from drawing conclusions on the role of kratom or
mitragynine in his death until full autopsy and toxicology reports are made available to the
public. In the meantime, the AKA continues its efforts to advocate for the right of all Americans
to use the natural botanical kratom for improved health and well-being, while working tirelessly
toward standards that will ensure availability of safe, unadulterated kratom.
Christopher Waldron died with a “high” level of mitragynine in his blood. The
Associate Medical Examiner, Leszak Chrostowski, who conducted the autopsy, concluded that

 See “O.P.M.S.® Kratom Authenticity Guide” viewed at on
October 1, 2017.
 Chrostowsky, “Report of Diagnosis and Autopsy of Christopher Waldron.” Hillsborough County, FL
Medical Examiner Dept., August 22, 2017.

he died from Intoxication by Mitragynine.24 Based on available information, this conclusion is
highly speculative given that mitragynine/kratom has never been causally linked to a death.
The only deaths in which kratom has been detected have been determined to be caused by
other substances or conditions. A particularly frequent occurrence is polypharmacy, in which
multiple legal and/or illicit substances were used. The death of Mr. Waldron appears not only a
case of polypharmacy, but a toxic combination of contraindicated pharmaceuticals.
The circumstances and conditions surrounding Mr. Waldron’s death have not been
described in detail, and may shed light on the death. This discussion focuses on autopsy and
toxicology reports that are a matter of public record along with news reports. Mr. Waldron
struggled with addiction to prescription opioids for a decade, and used kratom to help him
withdraw and to maintain his abstinence from opioids. His mother, Laura Lamon, gave
conflicting accounts of what she believed to be the cause of his death. In a memorial posted on she stated “[H]e was young, though, and felt invincible so gave in one last
time. He didn’t want to die, but his luck ran out.”25 These statements suggest his mother may
have been aware that Mr. Waldron used before his death. In another report, she stated that
she was thankful that the medical examiner had not found opioids in Christopher’s system, and
“was glad that he was being truthful and at the end he really was clean.”26
Ms. Lamon reported that she found empty packages of O.P.M.S. Gold in her son’s
room27, which likely prompted the Medical Examiner to test for mitragynine, in addition to the
over 100 substances routinely tested by the Hillsborough County Medical Examiner
Department. The label on the O.P.M.S. package indicated the contents were capsules
containing Mitragyna Speciosa Leaf Extract with 60 mg mitragynine per capsule.
Toxicology analysis revealed the presence of three substances in Mr. Waldron’s
peripheral blood: 0.22 mg/L Citalopram; < 0.10 mg/L Cyclobenzaprine; and 1.8 mg/L


Lamon, “Christopher Waldron Memorial Statement” viewed at
 Paluska, “Hillsborough Co. medical examiner confirms 1st death by herbal supplement Kratom.” ABC
Action News, September 28, 2017 (viewed at

Mitragynine. The contribution of each of these substances, as well as any unknown
interactions, must be considered before a cause of death can be definitively determined.
Extrapolation of the dose-response curve from the study discussed above28, 8-9 capsules
(480-520 mg mitragynine) may have been sufficient to give a peak plasma concentration of 1.8
mg/L within 1 hour after swallowing the capsules.
There are no reports of the mitragynine toxicity in humans. Studies in animals suggest
that the dose Mr. Waldron consumed was only a small fraction of the toxic dose of mitragynine
(if there is a toxic dose in humans). In mice, LD50 values (the amount of a substance lethal to
50% of subjects) determined for various extract preparations were reported as 173.2 mg/kg29,
591 mg/kg30, and 4.9 g/kg31, corresponding to doses of 16.09 g, 54.95 g, and 455.63 g,
respectively for a man of 205 lbs. (Mr. Waldron’s reported weight). In rats, the LD50 was
determined to be 200 mg/kg for both mitragynine and an alkaloid extract32 33, corresponding
to a dose of 18.6 g for Mr. Waldron. The dose he likely consumed (around 0.5 g or less) was
well below the lowest toxic dose of 173.2 mg/kg in animals (16.09 g for Mr. Waldron). These
results combined with the absence of any report of death due solely to kratom or mitragynine
suggest that kratom or mitragynine alone did not kill Mr. Waldron.

Id. See Trakulsrichai, supra.
 Reanmonekol et al., “Effects of the extracts from Mitragyna speciosa Korth. leaves on analgesic and
behavioral activities in experimental animals.” Songklanakarin J. Sd. Technol. 29Supp:39-48 (2007).
 Sabetghadam et al, “Dose-Response Relationship, Acute Toxicity, and Therapeutic Index between the
Alkaloid Extract of Mitragyna speciosa and Its Main Active Compound Mitragynine in Mice.” Drug Dev. Res. 74:23-
 Janchawee et al., “A high-performance liquid chromatographic method for determination of
mitragynine in serum and its application to a pharmacokinetic study in rats.” Biomed. Chromatog. 21:176-83
 Aziz et al., “In vitro and in vivo effects of three different Mitragyna speciosa Korth leaf extracts on phase
II drug metabolizing enzymes – glutathione transferases (GSTs).” Molecules 15:432-41 (2010).

Citalopram (Celexa), is a selective serotonin reuptake inhibitor (SSRI) class antidepressant.
The therapeutic range for Citalopram is 50 to 100 ng/mL in plasma; levels greater
than 220 ng/mL are considered toxic and require an alert to the prescribing physician.
Waldron’s level of 0.22 mg/L (220 ng/mL) is thus borderline toxic and should have raised a red
The FDA has issued several warnings regarding the use of Citalopram due to the risk of
QT prolongation, a potentially fatal cardiac arrhythmia that is associated with to sudden
death. Prescribing information includes the following warning40:
Citalopram causes dose-dependent QT prolongation which, in some cases, has
been associated with torsade de pointes (TdP), ventricular tachycardia, and
sudden death. Citalopram is not recommended for use in patients with
congenital long QT syndrome, bradycardia, hypokalemia, hypomagnesemia,
recent acute myocardial infarction, uncompensated heart failure, or in patients
receiving medications associated with QT prolongation.
The prescribing information also states:
Torsade de Pointes has been reported postmarketing. Celexa should not be used
in patients with congenital long QT syndrome. Hypokalemia and
hypomagnesemia should be corrected prior to initiation of treatment and

 Celexa Label, Forrest Pharmaceuticals, St. Louis, MO.
 Heimke et al., “AGNP consensus guideline for therapeutic monitoring in psychiatry: update 2011.”
Pharmacopsychiatry 44:195-235 (2011).
 Mayo Medical Laboratories, “Citalopram, Serum Reference Values” (viewed at
 FDA Drug Safety Communication: Revised recommendations for Celexa (Citalopram hydrobromide)
related to a potential risk of abnormal heart rhythms with high doses, March 28, 2012 (viewed at
 Selective serotonin reuptake inhibitor (SSRI) antidepressants FDA Drug Safety Communication,
December 14, 2011 (viewed at
 Celexa (Citalopram hydrobromide) FDA Drug Safety Communication, August 24, 2011 (viewed at
 Celexa Label, supra.

periodically monitored. ECG monitoring is recommended in patients with
congestive heart failure, bradyarrhythmias, or patients on concomitant
medications that prolong the QT interval. Dose escalations over 20 mg/day in
CYP2C19 poor metabolizers or patients taking concomitant cimetidine or
another CYP2C19 inhibitor are not recommended.
Regarding drug interaction, prescribing information for Citalopram describes the
potentially “Major” interaction with Cyclobenzaprine, the other drug found in Waldron’s
concurrent use of Citalopram with other drugs that prolong the QT interval is not
recommended. If concurrent therapy is considered essential, ECG monitoring is
recommended. Citalopram causes dose-dependent QT interval prolongation.
Cyclobenzaprine is structurally similar to tricyclic antidepressants. Tricyclic
antidepressants have been reported to prolong the QT interval, especially when
given in excessive doses (or in overdosage settings). Cyclobenzaprine is
associated with a possible risk of QT prolongation and torsades de pointes (TdP),
particularly in the event of acute overdose.
Furthermore, the Citalopram label warns of potentially fatal Serotonin Syndrome:
Based on the mechanism of action of SNRIs and SSRIs including Celexa, and the
potential for serotonin syndrome, caution is advised when Celexa is
coadministered with other drugs that may affect the serotonergic
neurotransmitter systems, such as triptans, linezolid (an antibiotic which is a
reversible non-selective MAOI), lithium, tramadol, or St. John’s Wort (see
WARNINGS-Serotonin Syndrome). The concomitant use of Celexa with other
SSRIs, SNRIs or tryptophan is not recommended.
Mr. Waldron had a very high, potentially lethal level of Citalopram in his blood.
Therefore, the Medical Examiner should have suspected Long QT syndrome, Torsade de Pointes
or Serotonin Syndrome as possible causes of death.

Celexa Label, supra.

Cyclobenzaprine (Flexeril), is a tricyclic skeletal muscle relaxer. The therapeutic range
for Cyclobenzaprine is 10 to 30 ng/mL in plasma. Few reports of Cyclobenzaprine overdose with
postmortem blood concentrations have been published. One report, based on two cases,
concluded that blood concentrations of > 0.8 mg/L Cyclobenzaprine may be associated with
fatal outcomes. Waldron’s level of < 0.10 mg/L was likely non-toxic on its own. However, the
warnings of potentially fatal interaction of Cyclobenzaprine and Citalopram are repeated in the
Flexeril label.
Additional warnings for both Cyclobenzaprine and Citalopram are included regarding
patients with hepatic impairment (due to the metabolism of both drugs via hepatic P450
isoenzymes) and thyroid disease. Mr. Waldron displayed signs of both an enlarged liver,
possibly signaling hepatic impairment, and Hashimoto thyroiditis, a thyroid disease.
It is unclear if both Cyclobenzaprine and Citalopram were prescribed to Waldron and if
so, whether they were prescribed by the same physician, or whether any physician carefully
monitored his heart or screened for congenital long QT syndrome during use of these drugs.
An estimated 5-10% of sudden cardiac deaths may remain unexplained by autopsy
findings, particularly those due to arrhythmias such as long QT syndrome and Torsade de
Pointes. In this case, toxicology on Mr. Waldron showed a dangerous combination of drugs
(one of which was present at toxic levels) that increase the risk of long QT Syndrome, Torsade
de Pointes and Serotonin Syndrome. Furthermore, autopsy findings present evidence of left
ventricular hypertrophy, further increasing the likelihood that the prescription drug
combination caused this death. Given evidence of a toxic level of Citalopram, in a

 Celexa Label, Forrest Pharmaceuticals, St. Louis, MO.
 Spiller, et al., “Fatal cyclobenzaprine overdose with postmortem values.” J. Forensic Sci. 48:883-84
 Soliman et al., “Inter-relationship between electrocardiographic left ventricular hypertrophy and QT
prolongation as predictors of increased risk of mortality in the general population.” Circ Arrhythm
Electrophysiol.7:400-6. (2014).
 Haugaa et al., “Impact of left ventricular hypertrophy on QT prolongation and associated mortality.”
Heart Rhythm.11:1957-65(2014).

potentially fatal combination with Cyclobenzaprine, as well as other risk factors and findings
consistent with a sudden cardiac death from long QT syndrome/Torsade de Pointes, and at the
same time pointing to a second possible cause of sudden death (Serotonin Syndrome), it is
puzzling that the Medical Examiner chose to opine that mitragynine intoxication was the cause
of Christopher Waldron’s death. Based on the available information, AKA justifiably has
concluded that the only basis for this opinion is an attempt to match inconclusive physical
findings with an unknown, controversial botanical for the sensationalist impact it might have.
Any contribution of mitragynine or kratom in this death can only be attributed to
polypharmacy involving at least two other substances, and is merely speculation. Moreover,
based on statements from the kratom extract manufacturer and users that counterfeit,
adulterated O.P.M.S. Kratom extract capsules have been sold by unscrupulous vendors, the
possibility that another, as yet unidentified drug(s) may have been present in the capsules Mr.
Waldron consumed cannot be excluded.
Of course, there is precedent for the Hillsborough County Medical Examiner getting it
wrong in high profile cases. It singled out a more controversial substance (cocaine) as the cause
of the heart disease that killed OxiClean pitchman, Bill Mays, despite finding painkillers, antianxiety
drugs and alcohol in his system at the time of his death. A second autopsy,
commissioned by the family, demonstrated that “the autopsy specimens and findings were not
consistent with the cardiac conditions normally observed in a person chronically using cocaine”
and concluded that cocaine was not the cause of Mr. Mays’ death.
Based on the totality of circumstances, any reasonable person could be confident that
kratom did not kill Christopher Waldron any more than cocaine killed Billy Mays.