Fairbanks City Transit bus 142 in July 1993, on the Stampede Trail in Alaska. Photo © Jon Krakauer

How Chris McCandless Died

An update to ‘Into the Wild’

The debate over what killed Chris McCandless, and the related question of whether he is worthy of admiration, has been smoldering and occasionally flaring for more than two decades now. Shortly after the first edition of Into the Wild was published in January 1996, University of Alaska chemists Edward Treadwell and Thomas Clausen shot down my theory that the cause of McCandless’s death was a toxic alkaloid contained in the seeds of the Eskimo potato plant, Hedysarum alpine, also known as wild potato. When Treadwell and Clausen completed chemical analyses of the Eskimo potato seeds I’d sent them, they found no trace of any poisonous compounds. “I tore that plant apart,” Dr. Clausen explained to Men’s Journal in 2007. “There were no toxins. No alkaloids. I’d eat it myself.”

My theory about the seeds was based on the alarming entry McCandless wrote in his journal on July 30, 1992:

EXTREMELY WEAK. FAULT OF POT[ATO] SEED. MUCH TROUBLE JUST TO STAND UP. STARVING. GREAT JEOPARDY.

Assuming that McCandless must have had a good reason to believe the seeds were to blame for his failing health, when Treadwell and Clausen proclaimed that H. alpinum seeds are completely benign, I proposed a new hypothesis to explain his demise, which I included in an updated edition of Into the Wild printed in 2007: It wasn’t the seeds that killed McCandless, but rather a mold growing on the seeds, which produced a toxic alkaloid called swainsonine.

Eskimo potato seeds (Hedysarum alpinum) harvested by McCandless for food on July 18, 1992, in a 0ne-gallon Ziploc bag. Estimated dry weight 600 grams. Photo courtesy of the Chris McCandless Memorial Foundation

I had no hard evidence to support this hypothesis, however, so I continued searching for information that would allow me to reconcile McCandless’s unambiguous journal entry — stating he had become physically incapacitated because he ate Eskimo potato seeds — with the equally unambiguous results of the chemical analyses performed by Treadwell and Clausen. These results were reinforced in 2008, moreover, when they published a peer-reviewed paper titled, “Is Hedysarum mackenziei (Wild Sweet Pea) Actually Toxic?” in the journal Ethnobotany Research & Applications. Upon completing “an exhaustive comparison of the secondary chemistry between the two plants [H. mackenzii and H. alpinum are closely related] as well as a search for nitrogen containing metabolites (alkaloids) in both species,” Treadwell and Clausen wrote, “no chemical basis for toxicity could be found.”

In August 2013, I happened upon a paper titled “The Silent Fire: ODAP and the Death of Christopher McCandless,” by Ronald Hamilton, which appeared to solve the conundrum. Hamilton’s essay, posted online, presented hitherto unknown evidence that the Eskimo potato plant was in fact highly toxic, contrary to the assurances of Treadwell, Clausen, and apparently every other expert who had ever weighed in on the subject. According to Hamilton, the toxic agent in H. alpinum was not an alkaloid, as I had speculated, but rather an amino acid, and it was the ultimate cause of McCandless’s death.

“I now walk into the wild.” Postcard that Chris McCandless sent to his friend Wayne Westerberg the day before he headed down the Stampede trail on his fatal journey. Photo © Jon Krakauer

Hamilton is neither a botanist nor a chemist; he’s a writer who until recently worked as a bookbinder at the Indiana University of Pennsylvania library. As Hamilton explains it, he became acquainted with the McCandless story in 2002, when he happened upon a copy of Into the Wild, flipped through its pages, and suddenly thought to himself, “I know why this guy died.” His hunch derived from his knowledge of Vapniarca, a little-known World War II concentration camp in what was then German-occupied Ukraine.

“I first learned about Vapniarca through a book whose title I’ve long forgotten,” Hamilton told me. “Only the barest account of Vapniarca appeared in one of its chapters…. But after reading Into the Wild I was able to track down a manuscript about Vapniarca, which has been published online.” Later, in Romania, he located the son of a man who served as an administrative official of the camp, and who sent Hamilton a trove of documents.

In 1942, as a macabre experiment, an officer at Vapniarca started feeding the Jewish inmates bread and soup made from seeds of the “grasspea,” Lathyrus sativus, a common legume that has been known since the time of Hippocrates to be toxic. “Very quickly,” Hamilton writes in “The Silent Fire,”

a Jewish doctor and inmate at the camp, Dr. Arthur Kessler, understood what this implied, particularly when within months, hundreds of the young male inmates of the camp began limping, and had begun to use sticks as crutches to propel themselves about. In some cases inmates had been rapidly reduced to crawling on their backsides to make their ways through the compound…. [O]nce the inmates had ingested enough of the culprit plant, it was as if a silent fire had been lit within their bodies. There was no turning back from this fire — once kindled, it would burn until the person who had eaten the grasspea would ultimately be crippled…. The more they’d eaten, the worse the consequences — but in any case, once the effects had begun, there was simply no way to reverse them….
Even today, at this moment, Lathyrus sativus is maiming [and] crippling…. It is currently estimated that [throughout the twentieth century] more than 100,000 people worldwide [suffered] from irreversible paralysis due to the consumption of the plant. The disease is called, simply, neurolathyrism, or more commonly, “lathyrism.”
Dr. Arthur Kessler, who… initially recognized the sinister experiment that had been undertaken at Vapniarca, was one of those who escaped death during those terrible times. He retired to Israel once the war had ended and there established a clinic to care for, study, and attempt to treat the numerous victims of lathyrism from Vapniarca, many of whom had also relocated in Israel.

The injurious substance found in grasspea plants turned out to be a neurotoxin, beta-N-oxalyl-L-alpha-beta diaminoproprionic acid, a compound commonly referred to as beta-ODAP or, more often, just ODAP. According to Hamilton, ODAP

affects different people, different sexes, and even different age groups in different ways. It even affects people within those age groups differently…. The one constant about ODAP poisoning however, very simply put, is this: those who will be hit the hardest are always young men between the ages of 15 and 25 and who are essentially starving or ingesting very limited calories, who have been engaged in heavy physical activity, and who suffer trace-element shortages from meager, unvaried diets.

ODAP was identified in 1964. It brings about paralysis by overstimulating nerve receptors, causing them to die. As Hamilton explains,

It isn’t clear why, but the most vulnerable neurons to this catastrophic breakdown are the ones that regulate leg movement.… And when sufficient neurons die, paralysis sets in.… [The condition] never gets better; it always gets worse. The signals get weaker and weaker until they simply cease altogether. The victim experiences “much trouble just to stand up.” Many become rapidly too weak to walk. The only thing left for them to do at that point is to crawl.

After Hamilton read Into the Wild and became convinced that ODAP was responsible for McCandless’s sad end, he approached Dr. Jonathan Southard, the assistant chair of the biochemistry department at Indiana University of Pennsylvania, and persuaded Southard to have one of his students, Wendy Gruber, test the seeds of both H. alpinum and H. mackenzii for ODAP. Because the two species are very similar and hard to distinguish from one another, there had been speculation that McCandless confused the plants, and actually ingested H. mackenzii rather than H. alpinum.

Upon completion of her tests in 2004, Gruber determined that ODAP appeared to be present in both species of Hedysarum, but her results were less than conclusive. “To be able say that ODAP is definitely present in the seeds,” she reported, “we would need to use another dimension of analysis, probably by HPLC-MS” — high-pressure liquid chromatography. But Gruber possessed neither the expertise nor the resources to analyze the seeds with HPLC, so Hamilton’s hypothesis remained unproven.

Hedysarum alpinum seeds. Photo © Jon Krakauer

Hoping to learn whether Hamilton should be believed, in August 2013 I sent 150 grams of freshly collected Eskimo potato seeds to Avomeen Analytical Services in Ann Arbor, Michigan, for HPLC analysis, which determined that the seeds contained .394 percent ODAP by weight, a concentration well within the levels known to cause lathyrism in humans. On September 12, 2013, I reported Avomeen’s results in “How Chris McCandless Died,” an article published on The New Yorker website.

Five days later, Dermot Cole, a journalist in Fairbanks, posted an article titled “Krakauer’s Wild Theory on McCandless Gives Short Shrift to Science” on the website Alaska Dispatch. Cole wrote,

Krakauer should take the advice of Tom Clausen, the retired organic chemist from UAF who has spent much of his career studying plants in Alaska and their properties.
Clausen said that absent peer-reviewed scientific research he would not make any conclusions about what amounts to a highly technical and complicated scientific question.
The difference between a popular account for a general audience and a peer-reviewed journal is that an editor or two may check the former, while the latter will be subject to critical examination aimed at uncovering sloppy work.
Clausen said he has nothing to refute the conclusion, reached by both [Ron Hamilton] and Krakauer, that ODAP was present.
“With that said, let me follow with the comment that I am very skeptical about the entire story,” Clausen wrote in an e-mail…. “I would be much more convinced if I was reading the report from a credible peer-reviewed professional.”

Clausen, I realized, was right: I couldn’t be absolutely certain the seeds were toxic until I did additional, more sophisticated analysis, and then published the results in a reputable peer-reviewed journal. So I embarked on another round of testing.

I began by asking Avomeen to analyze the seeds with liquid chromatography-mass spectrometry (LC-MS). This test detected a prominent seed component with a molecular mass of 176, the molecular mass of ODAP, which appeared to corroborate the earlier HPLC results.

Next, Avomeen suggested that we take the analysis to an even higher resolution by using liquid chromatography-tandem mass spectrometry (LC-MS/MS). These results confirmed that the mass of the compound in question was 176, but the fragmentation-ion pattern, or “fingerprint,” for the compound didn’t match the fragmentation-ion fingerprint of a sample of pure ODAP that was also analyzed. The results were unequivocal: ODAP was not present in H. alpinum seeds. LC-MS/MS conclusively disproved Hamilton’s hypothesis.

The LC-MS/MS analysis nevertheless suggested the possibility that a significant concentration of a compound structurally similar to ODAP might be present in the seeds. So I combed the scientific literature yet again, even more exhaustively this time, reading every paper I could find about toxic nonprotein amino acids with a molecular mass of 176. Eventually, to my surprise, I discovered an article by a scientist named B. A. Birdsong, published in the 1960 edition of the Canadian Journal of Botany, which reported that H. alpinum seeds contained a toxic amino acid called L-canavanine. And the mass of L-canavanine, it so happens, is 176.17.

Compounds presumed or known to be present in Hedysarum alpinum. The alkaloid swainsonine and the amino acid beta-Noxalyl-L-alpha-beta diaminoproprionic acid (ODAP) had been suggested as possible toxic constituents but their presence has not been demonstrated. L-Canavanine, shown to be present in seeds, is an antimetabolite that can replace L-arginine during protein synthesis.

My earlier searches had missed this article because I had been looking for a toxic alkaloid instead of a toxic amino acid. Clausen and Treadwell had overlooked the article, as well.

Birdsong and his coauthors had determined the presence of L-canavanine in the seeds using a technique called paper chromatography-trisodium pentacyanoammonioferrate colorimetric analysis, or PCAF. Given all the controversy, and because methods for analysis of plant constituents have advanced significantly during the fifty-four years since Birdsong’s investigation, I asked Avomeen to evaluate the presence of L-canavanine in the seeds using LC-MS/MS, the same technique that had disproved the presence of ODAP. When the Avomeen scientists completed their work, they determined that H. alpinum seeds do indeed contain a significant concentration of L-canavanine — 1.2 percent by weight.

Liquid chromatography–tandem mass spectrometry (LC-MS/MS) analyses. (A) MS spectrum of L-canavanine reference standard [M.H]. 177. (B) MS/MS spectrum of L-canavanine reference standard [M.H]. 177. (C) MS spectrum of the peak of [M.H]. 177 at retention time 2.40 minutes from water extract of Hedysarum alpinum seeds. (D) MS/MS spectrum of the peak of [M.H]. 177 at retention time 2.40 minutes from water extract of H alpinum seeds. (E) MS spectrum of the peak of [M.H]. 177 at retention time 2.42 minutes from 50/50 mixture of L-canavanine and water extract of H alpinum seeds. (F) MS/MS spectrum of the peak of [M.H]. 177 at retention time 2.42 minutes from 50/50 mixture of L-canavanine and water extract of H alpinum seeds.

L-canavanine, it turns out, is an antimetabolite stored in the seeds of many leguminous species to ward off predators, and its toxicity in animals is well documented in the scientific literature. Numerous cases have been observed of cattle poisoned after foraging on jack beans, Canavalia ensiformis, the seeds of which contain about 2.5 percent L-canavanine by dry weight; symptoms included stiffness of the hindquarters, progressive weakness, emphysema, and hemorrhages of the lymph glands. Although there have been few clinical or epidemiological studies on canavanine-induced illness in humans, there have been anecdotal reports of toxic effects in people who ingested jack-bean seeds. An article published in the prestigious German journal, Die Pharmazie, observed that “the scattered reports about poisoning by this plant probably stand in no relation to actual number of incidences that are caused by it in agricultural practice, because the cause is so difficult to recognize.”

Dr. Jonathan Southard, Dr. Ying Long, Dr. Andrew Kolbert, Dr. Shri Thanedar, and I co-authored a paper titled, “Presence of L-canavanine in Hedysarum alpinum seeds and its potential role in the death of Chris McCandless,” which was published in the peer-reviewed journal Wilderness and Environmental Medicine in October 2014. In the conclusion of our paper, we wrote,

Our results confirmed the presence of L-canavanine (an antimetabolite with demonstrated toxicity in mammals) as a significant component of H. alpinum seeds…. In the case of Christopher McCandless, there is evidence that H. alpinum seeds constituted a significant portion of his meager diet during a period before his death. Based on this and what is known about the toxic effects of L-canavanine, we make the logical conclusion that under these conditions, it is highly likely that the ingestion of relatively large amounts of this antimetabolite was a contributing factor to his death.
The death of Chris McCandless should serve as a caveat to other foragers: Even when some parts of a plant are known to be edible, other parts of the same species may contain dangerous concentrations of toxic compounds. Additionally, there may be seasonal, as well as ecotypic, variations in the concentrations of L-canavanine between various communities of H. alpinum. Further studies are needed to determine the range of L-canavanine concentrations among different populations of the plant. Given the known toxic properties of L-canavanine and its established presence in H. alpinum seeds, it seems prudent to use caution before ingesting these seeds, especially as a significant part of the diet.

Although Ron Hamilton was wrong about ODAP’s role in the death of McCandless, he was correct that H. alpinum seeds are poisonous, and that an amino acid, rather than an alkaloid, is the toxic constituent. I am tremendously grateful to Hamilton for publishing “The Silent Fire: ODAP and the Death of Christopher McCandless,” because if he hadn’t, it is unlikely I would have stumbled upon Birdsong’s article, and thus would never have learned about the presence of L-canavanine in H. alpinum seeds. Near the end of “The Silent Fire,” Hamilton mused,

It might be said that Christopher McCandless did indeed starve to death in the Alaskan wild, but this only because he’d been poisoned, and the poison had rendered him too weak to move about, to hunt or forage, and, toward the end, “extremely weak,” “too weak to walk out,” and, having “much trouble just to stand up.” He wasn’t truly starving in the most technical sense of that condition…. [But] it wasn’t arrogance that had killed him, it was ignorance…, which must be forgiven, for the facts underlying his death were to remain unrecognized to all, scientists and lay people alike, literally for decades.
Chris McCandless took this selfie in the meadow outside the bus shortly before he died. The note in his left hand reads, “I HAVE HAD A HAPPY LIFE AND THANK THE LORD. GOODBYE AND MAY GOD BLESS ALL!” Photo courtesy of the Chris McCandless Memorial Foundation

Confirmation that toxic seeds were at least partly responsible for McCandless’s death is unlikely to persuade many Alaskans to regard him in a more sympathetic light, but it may prevent other backcountry foragers from accidentally poisoning themselves. Had McCandless’s guidebook to edible plants warned that H. alpinum seeds contain a “highly toxic secondary plant constituent,” as L-canavanine is described in the scientific literature, he probably would have walked out of the wild in late August with no more difficulty than when he walked into it in April, and would still be alive today.


A version of this post was published as the afterword to a new edition of Into the Wild, released in 2015.