1 of 1 DOCUMENT

Military Medicine

December 2012

Case Reports: Death of Active Duty Soldiers Following Ingestion of Dietary Supplements Containing 1,3-Dimethylamylamine (DMAA)

BYLINE: Eichner, Amy; Cancio, Anthony; Bestervelt, Lori; Adams, Bruce D; Deuster, Patricia A; Eliason, Michael J. 
ENS Michael J. Eliason, MC USN*; Amy Eichner, PhD[dagger]; 2LT Anthony Cancio, MC USA*;
Lori Bestervelt, PhD[double dagger]; COL Bruce D. Adams, MC USA§; Patricia A. Deuster, PhD, MPH*
*Uniformed Services University, 4301 Jones Bridge Road, Bethesda, MD 20814.
[dagger]U.S. Anti-Doping Agency, 5555 Tech Center Drive, Suite 200, Colorado Springs, CO 80919.
[double dagger]NSF International, 789 North Dixboro Road, Ann Arbor, MI 48113.
§William Beaumont Army Medical Center, 5005 North Piedras Street, El Paso, TX 79920.
d. oi: 10.7205/MILMED-D-12-00265

SECTION: Pg. 1455 Vol. 177 No. 12 ISSN: 0026-4075

LENGTH: 2582 words

ABSTRACT Dietary supplements and their associated adverse events are not uncommon in the U.S. military, and selected dietary supplements have been associated with a number of nontraumatic deaths in service members. Specific ingredients and dietary supplement products in the civilian community are often associated with multiple adverse events and some have subsequently been removed from the marketplace; the most notable in the last decade is ephedra. We present case reports for two soldiers who were taking commercially available dietary supplements containing multiple ingredients to include the sympathomimetic, 1,3-dimethylamylamine (DMAA); both collapsed during physical exertion from cardiac arrest and ultimately died. A presentation of their clinical courses and a discussion of the history and pharmacology of dietary supplement ingredients, including DMAA, are provided. Our cases highlight concerns that DMAA in combination with other ingredients may be associated with significant consequences, reminiscent of previous adverse events from other sympathomimetic drugs previously removed from the market.
INTRODUCTION
Most nontraumatic deaths of military service members occur during exertion, with the two primary causes being cardiovascular events followed by heat injury.1-3 Sudden death in this population has been reported several times in association with various dietary supplements, most notably in the last decade from ephedra.4-7 The multiple adverse events associated with ephedra ultimately led to its removal from the U.S. market,8-11 although it is still readily available. Ephedra and other dietary stimulants, alone and in combination with caffeine, can induce a sympathomimetic toxidrome10 as well as increase metabolic rate.12-16 When taken in combination with strenuous exercise, the results can be very serious5,6,17 and even fatal.
One ingredient of concern in dietary supplements is 1,3- dimethylamylamine (also known as methylhexanamine) or DMAA.18,19 This sympathomimetic ingredient was first used commercially in 194820 as a nasal decongestant, but was removed from the market in 1983 at the request of its manufacturer. 21 It has since reappeared in over-the-counter dietary supplements, first as "Geranamine" (a "constituent of flower oil" according to the trademark application), then simply as geranium oil or extract, and now more recently as 1,3- dimethylamylamine or by various other synonyms. DMAA continues to be available in dietary supplements despite the lack of evidence that it qualifies as a dietary ingredient.
An early study on methylhexanamine (DMAA) noted that "The systemic toxicity of DMAA in animals is greater than that of ephedrine and less than that of amphetamine, its vasopressor action is more prolonged than that of epinephrine."22 Also, an early animal study showed DMAA exerted a pressor effect 3.5 times that of epinephrine.23 We present here two case reports of military personnel who were taking a commercially available dietary supplement containing DMAA combined with other ingredients, and subsequently collapsed during exercise from cardiac arrest and ultimately died.
CASE REPORTS
Case 1
A 22-year-old male infantry soldier, who was in excellent physical condition (last physical fitness test placed him above the 85th percentile), experienced leg cramps followed by loss of consciousness while running in formation with his battalion for about 10 minutes. The soldier was found to be pulseless; bystanders initiated CPR and he was transported via ambulance to the emergency department. Upon arrival at the hospital, physical examination was remarkable for hyperthermia (40.8°C/105.5°F) and dry hot skin. Initial laboratory values were remarkable for renal insufficiency (potassium 7.4 mEq/L, sodium 149 mEq/L, carbon dioxide 9 mEq/L, creatinine 2.3 mg/dL, glucose 188 mg/dL), anion gap metabolic acidosis (pH 6.91, PCO2 112.5 mm Hg, PO2 205 mm Hg, lactate 38.2 mg/dL), and elevated cardiac and muscle enzymes (creatine kinase MB 7.3 U/L, myoglobin 6227.2 mg/L, troponin I cardiac 0.069 ng/mL). Aggressive resuscitation efforts were applied including active core cooling via an endovascular device, endotracheal intubation, and fluid restoration. Return of spontaneous circulation was achieved several times, but the patient eventually devolved into refractory asystole and resuscitative efforts were terminated after a 4-hour course. Autopsy results were consistent with the clinical evidence of shock and heat stroke, but otherwise unrevealing. As the ambient temperature at the time of collapse was approximately 23.9°C/75°F and the humidity was less than 40%, and the average wet bulb globe temperatures (composite temperature used to estimate the effect of temperature, humidity, wind speed/wind chill and solar radiation on humans) 3 days before death were below 70°F, environmental temperature alone is an unlikely explanation for cause of death. Toxicology analyses of antemortem blood were remarkable for the presence of DMAA = 0.22 mg/L and caffeine = 2.9 mg/L, with no findings of drugs of abuse or ethanol. He was taking only one dietary supplement and according to persons in his immediate community, he was taking the supplement according to the recommendations on the product label; he had been taking it for about 4 weeks.
Case 2
A 32-year-old female, African American female soldier with a history of mild obesity and sickle cell trait (SCT) had recently started dietary supplements for the purpose of losing weight. She was nearing completion of a 2-mile physical fitness test when she experienced dyspnea and leg cramps, went to lie down, and subsequently became unresponsive. She was found to be in asystole; CPR was initiated and she was emergently transported to the local military hospital. The patient responded to standard advanced cardiac life support measures with a return of spontaneous circulation. Initial physical examination demonstrated that the patient was in shock and hypotensive (77/36 mm Hg), tachycardic (109 beats per minute), hyperthermic (core temperature 105° F), unresponsive to noxious stimuli, and with dry mucous membranes. Initial laboratory values were remarkable for anion gap metabolic acidosis (pH 6.67, PCO2 46.1 mm Hg, PO2 292 mm Hg, HCO3 5.0 mmol/L, lactate 21.5 mmol/dL), renal insufficiency (potassium 5.2 mEq/L, sodium 133 mEq/L, creatinine 1.8 mg/dL, glucose 261 mg/dL), liver dysfunction (GGT 56 IU/L, AST/ALT 5 IU/L, albumin 3.3mg/dL), and suggestion of disseminated intravascular coagulation (PT 20.2 seconds, INR 1.72, PTT 52.2 seconds). The ambient temperature at time of collapse was approximately 23°C/73°F and thus an unlikely explanation for cardiac arrest. Toxicology analysis performed 4 days after admission revealed a DMAA level of 0.04 mg/L and caffeine level of 1.9 mg/L, but was negative for acetaminophen, ethanol, salicylates, or drugs of abuse. Two different supplements were found in her car and it is assumed she was taking both, which contained DMAA. The quantities of the various supplements she was taking and the time period over which she was taking themare unknown.
Upon transfer to the intensive care unit, the patient remained in a comatose state and developed progressive multiple organ failure to include rhabdomyolysis (creatine kinase peaked at 161,000 U/L), renal failure, liver failure, pancreatitis, disseminated intravascular coagulopathy, and pulmonary edema. One week following initial presentation, her liver failure significantly worsened so she was transferred to a regional transplant center. During the ensuing weeks, the patient's condition briefly improved as she regained consciousness and was at one point extubated and communicating with her family. However, she developed ultimately refractory sepsis and died 5 weeks after the initial collapse.
DISCUSSION
In the case studies presented, both patients had ingested the same product marketed as a dietary supplement containing (among other ingredients) DMAA, b-alanine, arginine a-ketoglutarate, caffeine, creatine monohydrate, and Schizandrol A. Whereas the toxicological profiles of creatine, arginine, b-alanine, Schizandrol A, and caffeine have been relatively well established, little is known about DMAA. As with any case report, no causal relationship between the supplement ingredients and deaths can be confirmed. However, based on the structure and biochemistry of DMAA as a drug, the symptoms and toxidrome that developed in these two cases are in line with what could be expected of DMAA alone or in combination with the other ingredients.23-25
DMAA was originally developed in 194424,26 for topical use for nasal decongestion. In early efficacy studies, local application of DMAA via nasal route of administration produced little or no effect upon the pulse rate or blood pressure in adult humans although potential side effects were known including headache, nervousness, mental stimulation, and tremors. The Council of Pharmacy and Chemistry of the American Medical Association recommended the occurrence of such side effects warrant discontinuing use of the drug.22 The systemic toxicity of DMAA lies on a spectrum between ephedrine and amphetamines.20 Over time, the actions of DMAA on the body were established to be similar to amphetamine and ephedrine, and in vitro studies demonstrated it was ~200 times less potent than epinephrine as a vasopressor, but had a longer duration of action.27,28 DMAA eventually fell out of favor and was removed from the market in 1983 at the request of the manufacturer.21 DMAA reappeared in dietary supplements as early as 2005.29 Since then the number of products containing DMAA as a supplement has increased and have become best sellers in mainstream nutrition stores. It appears DMAA gained acceptance as a dietary ingredient on the (now discredited) premise that it was extracted from Pelargonium graveolens, a plant in the Geranium family.30 Numerous groups publicly dispute the methodology and conclusions of the article,31,32 and no other published evidence exists to establish DMAA as a dietary ingredient. However, DMAA continues to be available in dietary supplements so it is important for clinicians to query service members who have experienced adverse events such as those described here for the use of dietary supplements.
Caffeine is an analeptic or central nervous system stimulant. 33 Similar to the serious adverse events occurring with combination ephedra-caffeine products,25,34 caffeine combined with DMAA may be synergistic, producing a more powerful stimulant effect and a lower dosage threshold for adverse events. In addition to the caffeine that is included in supplements, consumers may ingest caffeine from other sources further increasing the risk of adverse events.
The dietary supplement product in these case studies also contains two amino acid substances (b-alanine and arginine aketoglutarate) as well as creatine, all of which could contribute to adverse effects in both kidney and liver.35,36 Although creatine is generally believed to be safe at low doses, supplementation can increase urinary excretion of creatinine 10% to 30% and creatine up to 100 times greater than normal.37 The longterm effects of this combination of ingredients have not been investigated, but the possibility for a variety of nephrotoxic effects exists, particularly in those with compromised kidney function.36 Interestingly, Bailes et al38 presented evidence that amphetamine derivatives and creatine together may contribute to dehydration and heatstroke by shifting water out of the extracellular space into muscle cells. Such an effect may also occur in response to DMAA/creatine combinations.
Since the only known source of DMAA in the United States is from products marketed as dietary supplements, it is likely that the DMAA discovered in the patients' blood and urine samples was from the dietary supplement they were using at the time. Caffeine was also found in the blood of both, although there are many potential sources of caffeine other than the supplements. Levels of caffeine found in the soldiers' blood were not within the range associated with caffeine fatalities (79-344 mg/L),39 although as stated earlier, the presence of DMAA and caffeine together might produce a toxic effect at a lower dose, given the known interactions between caffeine and ephedra.15,16 Although toxic levels of DMAA are unknown, Gee et al40 have published three cases of cerebral hemorrhage following DMAA ingestion with plasma DMAA values of 0.75, 1.09, and 2.31 mg/L as compared to our values of 0.22 and 0.02 mg/L. The critical cutofffor toxicity is unknown.
One of the case study patients had SCT, which has previously been associated with fatal exertional heat stroke and rhabdomyolysis.5,41-48 DMAA and caffeine could have contributed to catecholamine neurotransmitter persistence and adenosine receptor antagonism33 in this patient, and mutual potentiation of the stimulant effects might have resulted in excessive metabolic heat production, and possibly hypokalemia. 49 Previous studies have demonstrated increases in metabolic rate when caffeine and sympathomimetics, such as ephedra, synephrine, and/or yohimbine, are combined.13,15,16 Unfortunately, data on stimulant effects in persons with SCT are limited, but such ingredients may exacerbate any intrinsic complications of SCT.49
At least nine other case reports published or reported have shown a possible association between an adverse event and DMAA.18,40,50,51 All of the case reports list one or more of the following symptoms: hypertension, agitation, headache, vomiting, bradycardia, and/or stroke following the use of DMAA and bear hallmark similarity to those observed for ephedrine.5,6,17
Some government agencies around the world are taking regulatory action to curb the availability of DMAA. The New Zealand Health Ministry in 2008 issued a request for the voluntary suspension of the sale of pure DMAA powder by retailers following adverse reactions to this substance, and all products containing DMAA will effectively be banned, removed from shelves, and no longer sold over the Internet in New Zealand from April 9, 2012 forward.51-53 In August 2011, Health Canada classified DMAA as a drug and it is now subject to their Food and Drug Regulations.54 Authorities in France and Italy are in the midst of investigations with regards to banning products with this ingredient entirely, and the UK division of the Council for Responsible Nutrition has pointed out that DMAA is not authorized for use in food supplements in the European Union.55
The fact that at least two previously healthy soldiers died after ingesting a product marketed as a dietary supplement that contained DMAA raises questions, especially since only a few studies funded by industry have been conducted on this stimulant.56-61 Thus, the safety of DMAA remains an open question. Importantly, the types of adverse findings in these cases are consistent with known effects of sympathomimetic drugs and this entire scenario is reminiscent of ephedra, which ultimately was banned by the FDA.62 Otherwise, healthy individuals who present for medical treatment with exertional rhabdomyolysis, exercise-related syncope, heat injury, hypertension, cardiac arrhythmias, and the like should be queried about their use of dietary supplements.
ACKNOWLEDGMENTS
The funding for this work was provided by the Defense Health Program, Center Alliance for Dietary Supplement Research.

LOAD-DATE: February 5, 2013

LANGUAGE: ENGLISH

ACC-NO: 38133

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