Cannibalism: A Perfectly Natural History

In the 1980s, British researchers, like their counterparts in New Guinea, investigated the origins and transmission of a deadly spongiform encephalopathy. Their breakthrough came when they linked the disease to the diet of dairy cows. In an effort to boost milk production, farmers were supplementing livestock feed with meat and bone meal, a processed mixture of animal byproducts, including bones, brains, spinal cords, and sick or dead animals. This practice, which began in the 1940s, unknowingly exposed cattle to infectious agents, much like the Fore people had been exposed to kuru through ritual cannibalism.

The sudden outbreak of Bovine Spongiform Encephalopathy (BSE) in the 1980s was traced to changes in the rendering process. Epidemiologist John Wilesmith discovered that in the early 1980s, rendering plants had stopped extracting tallow using solvents, a process that had inadvertently removed infectious agents. Additionally, meat and bone meal concentrations in livestock feed had increased significantly and calves were exposed to it at a younger age, shortening the disease’s incubation period. His 1988 study concluded that BSE had originated from contaminated sheep scrapie in livestock feed. However, his assumption that BSE and scrapie were identical led to dangerous consequences for British consumers in the years that followed.

Meanwhile, research into transmissible spongiform encephalopathies (TSEs) continued. In the 1940s, outbreaks of transmissible mink encephalopathy (TME) led scientists to suspect that infected feed containing sheep scrapie had transmitted the disease between species. By 1963, Daniel Carleton Gajdusek and NIH researcher Joe Gibbs conducted a groundbreaking experiment, inoculating chimpanzees with brain tissue from kuru victims. Within two years, the chimps exhibited symptoms identical to kuru, confirming that the disease was transmissible rather than genetic or psychological. The chimps’ condition deteriorated at a “frightening pace” (267).

Further research by Michael Alpers and Robert and Shirley Glasse strengthened the link between kuru and Fore mortuary cannibalism. By analyzing Fore genealogies, they noticed that kuru cases had started declining in children, coinciding with government efforts to ban ritual cannibalism in the 1950s. Since children had a shorter incubation period, the reduced consumption of infected tissue rapidly decreased the spread of kuru.

In 1966, Gajdusek, Gibbs, and Alpers published their findings in Nature, demonstrating the experimental transmission of kuru. However, Gajdusek initially hesitated to blame cannibalism, proposing instead that handling infected tissue, rather than consumption, had spread the disease. Over time, he conceded that both handling and ingestion could transmit kuru. Similar concerns about the spread of diseases through ritual handling of the dead persist today, particularly in Ebola outbreaks.

By the 1970s, interest in kuru research was “winding down” (271), but scrapie became a focus of investigation. South African biologist Tikvah Alper’s research showed that the scrapie agent was unlike any known virus: It lacked nucleic acids and was incredibly resistant to destruction. English mathematician J.S. Griffith proposed that the disease-causing agent was a self-replicating protein, an idea initially dismissed by the scientific community.

However, Stanley Prusiner at UC San Francisco pursued this idea, identifying an infectious protein that he named the prion, “an aberrant form of protein, which he claimed was responsible for the suite of neurodegenerative disorders known as Transmissible Spongiform Encephalopathies” (273). He argued that prions, unlike viruses, were misfolded proteins that could spread undetected by the immune system. In 1997, Prusiner won the Nobel Prize for his work, though critics accused him of overshadowing previous researchers and using unethical tactics to advance his career.

In 1988, despite epidemiologist John Wilesmith’s findings linking Bovine Spongiform Encephalopathy (BSE) to contaminated meat and bone meal, the British government “dragged its feet” (275). Concerned about economic consequences, officials avoided outright bans or public warnings, instead forming a panel led by zoologist Richard Southwood, who lacked experience with spongiform encephalopathies. A voluntary ban on ruminant-based protein feed was implemented, but with little enforcement, many farmers continued using the supplement to recover their financial investments.

Compensation for diseased cattle was set at only 50% of market value, incentivizing some farmers to send sick cows to slaughter rather than report them. This practice, though difficult to quantify, likely led to “significant” (277) human exposure to BSE-infected beef. The situation remained relatively hidden from the public until media coverage in 1988, including headlines like “Spongiform Fear Grows [and] Raging Cattle Attacks” (277), brought BSE to wider attention. A Nature paper further raised concerns by demonstrating that scrapie, a similar disease in sheep, could be transmitted to monkeys, lending weight to fears of cross-species infection.

The Southwood Committee’s 1989 report downplayed risks, asserting that human transmission of BSE was “remote” and unrelated to Creutzfeldt-Jakob Disease (CJD). The government relied on these conclusions, projecting that BSE would fade by 1996 without further intervention. However, dissenting scientists, including Yale’s Dr. Laura Manuelidis, challenged the prevailing theory that prions—self-replicating misfolded proteins—were the cause of BSE and kuru. Instead, she argued that a still-unidentified virus was responsible for transmissible spongiform encephalopathies (TSEs), as misfolded proteins were found in various diseases without necessarily being infectious.

Public trust in British beef was further shaken in the 1990s. In 1990, Agriculture Minister John Gummer made an infamous televised attempt to reassure the public by feeding his four-year-old daughter a hamburger. However, troubling cases soon emerged. In 1993, two dairy farmers died of CJD, an unlikely statistical occurrence. Then in 1994, a 15-year-old girl named Victoria Rimmer exhibited kuru-like symptoms and a government investigator urged her family to remain silent to avoid damaging “the economy” (281). By 1995, several more young people were diagnosed with CJD, a disease previously rare in individuals under 30. In 1996, government advisor Dr. Eileen Rubery officially acknowledged that a new form of the disease, Variant Creutzfeldt-Jakob Disease (vCJD), was transmitted via infected beef, marking the start of a human BSE epidemic.

By 2013, vCJD had caused 177 deaths in the UK. While some believed the epidemic was over, others feared that cases could continue appearing decades later, similar to kuru’s long incubation period. A study testing 32,000 appendix samples found that one in 2,000 UK residents carried the abnormal prion protein, suggesting widespread exposure. However, research by scientists like Simon Mead and John Collinge revealed a genetic variant in Fore survivors that conferred resistance to kuru, raising hope that some people exposed to prion-contaminated meat might never develop the disease. If Manuelidis’s viral theory proves correct, TSEs may be more mutable than previously believed, challenging the dominant prion hypothesis. The scientific debate continues, with implications for both disease prevention and public health policies.

Cannibalism, in an evolutionary sense, can be beneficial or detrimental depending on environmental conditions. In species like spiders, consuming excess males can improve reproductive success, but in populations where mates are scarce, it can reduce survival chances. This logical, predictable behavior contrasts with the moral and cultural complexities surrounding cannibalism in human societies.

Sigmund Freud theorized that “cultural or societal rules” (288) against cannibalism helped shape modern civilization, but historical evidence suggests that some cultures openly practiced it without the associated guilt. Societies such as the Fore of New Guinea and ancient Chinese communities incorporated cannibalism into rituals, sometimes as an act of respect. However, due to Western cultural influence, ritual cannibalism has likely disappeared from contemporary societies.

Despite its rarity, human fascination with cannibalism persists. This is evident in popular culture, from The Road to The Walking Dead, as well as in media sensationalism around cases like the “Cannibal Cop” Gilberto Valle. Cannibalistic crimes are often linked to psychological disorders, with experts suggesting that cannibal killers harbor deep-seated aggression. Yet, public intrigue fuels books, films, and sensational news coverage.

Some researchers argue that growing overpopulation and environmental stress could lead to widespread cannibalism, as it does among animals. Historical evidence shows that famine-induced cannibalism has occurred throughout history, particularly in times of crisis. Today, desertification and climate change threaten food and water supplies in regions like Africa and the Middle East, potentially setting the stage for future occurrences of cannibalism.

The dystopian film Soylent Green imagines “just such an environmental disaster scenario” (292) where overpopulation and resource depletion lead to government-sanctioned cannibalism. While fictional, this scenario raises real concerns about food scarcity. If mass starvation were to occur, historical patterns suggest that cannibalism could resurface as a survival strategy. Additionally, large-scale cannibalism could trigger outbreaks of diseases like kuru, a fatal neurological disorder previously linked to cannibalistic practices in New Guinea.

Anthropologist Simon Underdown proposes that “widespread practice of cannibalism and a kuru-like epidemic” (294) may have contributed to Neanderthal extinction. Small, isolated populations engaging in cannibalism might have unknowingly spread transmissible spongiform encephalopathies, gradually reducing their numbers. His model suggests that such a disease could have rendered Neanderthal populations non-viable within 250 years.

The ongoing scientific debate over whether TSEs are caused by prions or viruses remains unresolved. If future environmental crises lead to outbreaks of cannibalism, new neurological diseases could emerge, warranting further research. Given humanity’s history, it is likely that such a disease—should it arise—will be given a sensational name, “something lurid” (296), continuing society’s morbid fascination with cannibalism.