A beautiful but unproved theory of particle physics is withering in the harsh light of data.

For decades, many particle physicists have devoted themselves to the beloved theory, known as supersymmetry. But it’s beginning to seem that the zoo of new particles that the theory predicts —the heavier cousins of known particles — may live only in physicists’ imaginations. Or if such particles, known as superpartners, do exist, they’re not what physicists expected.

New data from the world’s most powerful particle accelerator — the Large Hadron Collider, now operating at higher energies than ever before — show no traces of superpartners. And so the theory’s most fervent supporters have begun to pay for their overconfidence — in the form of expensive bottles of brandy. On August 22, a group of physicists who wagered that the LHC would quickly confirm the theory settled a 16-year-old bet. In a session at a physics meeting in Copenhagen, theoretical physicist Nima Arkani-Hamed ponied up, presenting a bottle of cognac to physicists who bet that the new particles would be slow to materialize, or might not exist at all.
Whether their pet theories are right or wrong, many theoretical physicists are simply excited that the new LHC data can finally anchor their ideas to reality. “Of course, in the end, nature is going to tell us what’s true,” says theoretical physicist Yonit Hochberg of Cornell University, who spoke on a panel at the meeting.

Supersymmetry is not ruled out by the new data, but if the new particles exist, they must be heavier than scientists expected. “Right now, nature is telling us that if supersymmetry is the right theory, then it doesn’t look exactly like we thought it would,” Hochberg says.
Since June 2015, the LHC, at the European particle physics lab CERN near Geneva, has been smashing protons together at higher energies than ever before: 13 trillion electron volts. Physicists had been eager to see if new particles would pop out at these energies. But the results have agreed overwhelmingly with the standard model, the established theory that describes the known particles and their interactions.

It’s a triumph for the standard model, but a letdown for physicists who hope to expose cracks in that theory. “There is a low-level panic,” says theoretical physicist Matthew Buckley of Rutgers University in Piscataway, N.J. “We had a long time without data, and during that time many theorists thought up very compelling ideas. And those ideas have turned out to be wrong.”

Physicists know that the standard model must break down somewhere. It doesn’t explain why the universe contains more matter than antimatter, and it fails to pinpoint the origins of dark matter and dark energy, which make up 95 percent of the matter and energy in the cosmos.

Even the crowning achievement of the LHC, the discovery of the Higgs boson in 2012 (SN: 7/28/2012, p. 5), hints at the sickness within the standard model. The mass of the Higgs boson, at 125 billion electron volts, is vastly smaller than theory naïvely predicts. That mass, physicists worry, is not “natural” — the factors that contribute to the Higgs mass must be finely tuned to cancel each other out and keep the mass small (SN Online: 10/22/13).

Among the many theories that attempt to fix the standard model’s woes, supersymmetry is the most celebrated. “Supersymmetry was this dominant paradigm for 30 years because it was so beautiful, and it was so perfect,” says theoretical physicist Nathaniel Craig of the University of California, Santa Barbara. But supersymmetry is becoming less appealing as the LHC collects more collisions with no signs of superpartners.

Supersymmetry solves three major problems in physics: It explains why the Higgs is so light; it provides a particle that serves as dark matter; and it implies that the three forces of the standard model (electromagnetism and the weak and strong nuclear forces) unite into one at high energies.

If a simple version of supersymmetry is correct, the LHC probably should have detected superpartners already. As the LHC rules out such particles at ever-higher masses, retaining the appealing properties of supersymmetry requires increasingly convoluted theoretical contortions, stripping the idea of some of the elegance that first persuaded scientists to embrace it.
“If supersymmetry exists, it is not my parents’ supersymmetry,” says Buckley. “That kind of means it can’t be the most compelling version.”

Still, many physicists are adopting an attitude of “keep calm and carry on.” They aren’t giving up hope that evidence for the theory — or other new particle physics phenomena — will show up soon. “I am not yet particularly worried,” says theoretical physicist Carlos Wagner of the University of Chicago. “I think it’s too early. We just started this process.” The LHC has delivered only 1 percent of the data it will collect over its lifetime. Hopes of quickly finding new phenomena were too optimistic, Wagner says.
Experimental physicists, too, maintain that there is plenty of room for new discoveries. But it could take years to uncover them. “I would be very, very happy if we were able to find some new phenomena, some new state of matter, within the first two or three years” of running the LHC at its boosted energy, Tiziano Camporesi of the LHC’s CMS experiment said during a news conference at the International Conference on High Energy Physics, held in Chicago in August. “That would mean that nature has been kind to us.”

But other LHC scientists admit they had expected new discoveries by now. “The fact that we haven’t seen something, I think, is in general quite surprising to the community,” said Guy Wilkinson, spokesperson for the LHCb experiment. “This isn’t a failure — this is perhaps telling us something.” The lack of new particles forces theoretical physicists to consider new explanations for the mass of the Higgs. To be consistent with data, those explanations can’t create new particles the LHC should already have seen.

Some physicists — particularly those of the younger generations — are ready to move on to new ideas. “I’m personally not attached to supersymmetry,” says David Kaplan of Johns Hopkins University. Kaplan and colleagues recently proposed the “relaxion” hypothesis, which allows the Higgs mass to change — or relax — as the universe evolves. Under this theory, the Higgs mass gets stuck at a small value, never reaching the high mass otherwise predicted.

Another idea, which Craig favors, is a family of theories by the name of “neutral naturalness.” Like supersymmetry, this idea proposes symmetries of nature that solve the problem of the Higgs mass, but it doesn’t predict new particles that should have been seen at the LHC. “The theories, they’re not as beautiful as just simple supersymmetry, but they’re motivated by data,” Craig says.

One particularly controversial idea is the multiverse hypothesis. There may be innumerable other universes, with different Higgs masses in each. Perhaps humans observe such a light Higgs because a small mass is necessary for heavy elements like carbon to be produced in stars. People might live in a universe with a small Higgs because it’s the only type of universe life can exist in.

It’s possible that physicists’ fears will be realized — the LHC could deliver the Higgs boson and nothing else. Such a result would leave theoretical physicists with few clues to work with. Still, says Hochberg, “if that’s the case, we’ll still be learning something very deep about nature.”

This issue marks the second year that Science News has reached out to science notables and asked: Which up-and-coming scientist is making a splash? Whose work impresses you? Tell us about early- to mid-career scientists who have the potential to change their fields and the direction of science more generally.

This year, we expanded the pool of people we asked. We reached out to Nobel laureates again and added recently elected members of the National Academy of Sciences. That allowed us to consider shining lights from a much broader array of fields, from oceanography and astronomy to cognitive psychology. Another difference this year: We spent time face-to-face with many of those selected, to get a better sense of them both as scientists and as people.
The result is the SN 10, a collection of stories not only about science, but also about making a life in science. They are stories of people succeeding because they have found what they love, be it working in the lab on new ways to probe molecular structures or staring up to the stars in search of glimmers of the early universe. In my interviews with chemist Phil Baran, I was struck by his drive to do things in new ways, whether devising chemical reactions or developing ideas about how to fund research. (If you can, he says, go private.) Laura Sanders, who met with neuroscientist Jeremy Freeman, was intrigued by his way of seeing a problem (siloed data that can’t be easily shared or analyzed) and figuring out solutions, even if those solutions were outside his area of expertise.

Of course, there are many ways to identify noteworthy scientists — and there’s plenty more fodder out there for future years. Our approach was to seek standouts, asking who deserved recognition for the skill of their methods, the insights of their thinking, the impacts of their research. Not all of the SN 10’s work has made headlines, but they all share something more important: They are participants in building the science of the future.

Notably, many of them do basic research. I think that’s because it’s the type of work that other scientists notice, even if it’s not always on the radar of the general public. But that’s where fundamental advances are often made, as scientists explore the unknown.

That edge of what’s known is where Science News likes to explore, too. Such as the bet-ending, head-scratching results from the Large Hadron Collider, which have failed to reveal the particles that the equations of supersymmetry predict. As Emily Conover reports in “Supersymmetry’s absence at LHC puzzles physicists,” that means that either the theory must be more complicated than originally thought, or not true, letting down those who looked to supersymmetry to help explain a few enduring mysteries, from the nature of dark matter to the mass of the Higgs boson.

Other mysteries may be closer to a solution, as Sanders reports in “New Alzheimer’s drug shows promise in small trial.” A new potential treatment for Alzheimer’s disease reduced amyloid-beta plaques in patients. It also showed hints of improving cognition. That’s standout news, a result built on decades of basic research by many, many bright young scientists.

In smart homes of the future, computers may identify inhabitants and cater to their needs using a tool already at hand: Wi-Fi. Human bodies partially block the radio waves that carry the wireless signal between router and computer. Differences in shape, size and even gait among household members yield different patterns in the received Wi-Fi signals. A computer can analyze the signals to distinguish dad from mom, according to a report posted online August 11 at arXiv.org.

Scientists built an algorithm that was nearly 95 percent accurate when attempting to discern two adults walking between a wireless router and a computer. For six people, accuracy fell to about 89 percent. Scientists tested the setup on men and women of various sizes, but it should work with children as well, says study coauthor Bin Guo of Northwestern Polytechnical University in Xi’an, China.

In a home rigged with Wi-Fi and a receiver, the system could eventually identify family members and tailor heating and lighting to their preferences — maybe even cue up a favorite playlist.

Two trillion galaxies. That’s the latest estimate for the number of galaxies that live — or have lived — in the observable universe, researchers report online October 10 at arXiv.org. This updated headcount is roughly 10 times greater than previous estimates and suggests that there are a lot more galaxies out there for future telescopes to explore.

Hordes of relatively tiny galaxies, weighing as little as 1 million suns, are responsible for most of this tweak to the cosmic census. Astronomers haven’t directly seen these galaxies yet. Christopher Conselice, an astrophysicist at the University of Nottingham in England, and colleagues combined data from many ground- and space-based telescopes to look at how the number of galaxies in a typical volume of the universe has changed over much of cosmic history. They then calculated how many galaxies have come and gone in the universe.

The galactic population has dwindled over time, as most of those 2 trillion galaxies collided and merged to build larger galaxies such as the Milky Way, the researchers suggest. That’s in line with prevailing ideas about how massive galaxies have been assembled. Seeing many of these remote runts, however, is beyond the ability of even the next generation of telescopes. “We will have to wait at least several decades before even the majority of galaxies have basic imaging,” the researchers write.

Crucial immune system proteins that make it harder for viruses to replicate might also help the attackers avoid detection, three new studies suggest. When faced with certain viruses, the proteins can set off a cascade of cell-to-cell messages that destroy antibody-producing immune cells. With those virus-fighting cells depleted, it’s easier for the invader to persist inside the host’s body.

The finding begins to explain a longstanding conundrum: how certain chronic viral infections can dodge the immune system’s antibody response, says David Brooks, an immunologist at the University of Toronto not involved in the research. The new studies, all published October 21 in Science Immunology, pin the blame on the same set of proteins: type 1 interferons.
Normally, type 1 interferons protect the body from viral siege. They snap into action when a virus infects cells, helping to activate other parts of the immune system. And they make cells less hospitable to viruses so that the foreign invaders can’t replicate as easily.

But in three separate studies, scientists tracked mice’s immune response when infected with lymphocytic choriomeningitis virus, or LCMV. In each case, type 1 interferon proteins masterminded the loss of B cells, which produce antibodies specific to the virus that is being fought. Normally, those antibodies latch on to the target virus, flagging it for destruction by other immune cells called T cells. With fewer B cells, the virus can evade capture for longer.

The proteins’ response “is driving the immune system to do something bad to itself,” says Dorian McGavern, an immunologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Md., who led one of the studies.

The interferon proteins didn’t directly destroy the B cells; they worked through middlemen instead. These intermediaries differed depending on factors including the site of infection and how much of the virus the mice received.
T cells were one intermediary. McGavern and his colleagues filmed T cells actively destroying their B cell compatriots under the direction of the interferon proteins. When the scientists deleted those T cells, the B cells didn’t die off even though the interferons were still hanging around.
Another study found that the interferons were sending messages not just through T cells, but via a cadre of other immune cells, too. Those messages told B cells to morph into cells that rapidly produce antibodies for the virus. But those cells die off within a few days instead of mounting a longer-term defense.

That strategy could be helpful for a short-term infection, but less successful against a chronic one, says Daniel Pinschewer, a virologist at the University of Basel in Switzerland who led that study. Throwing the entire defense arsenal at the virus all at once leaves the immune system shorthanded later on.

But interferon activity could prolong even short-term viral infections, a third study showed. There, scientists injected lower doses of LCMV into mice’s footpads and used high-powered microscopes to watch the infection play out in the lymph nodes. In this case, the interferon stifled B cells by working through inflammatory monocytes, white blood cells that rush to infection sites.

“The net effect is beneficial for the virus,” says Matteo Iannacone, an immunologist at San Raffaele Scientific Institute in Milan who led the third study. Sticking around even a few days longer gives the virus more time to spread to new hosts.

Since all three studies looked at the same virus, it’s not yet clear whether the mechanism extends to other viral infections. That’s a target for future research, Iannacone says. But Brooks thinks it’s likely that other viruses that dampen antibody response (like HIV and hepatitis C) could also be exploiting type 1 interferons.

Joining a gang doesn’t necessarily make a protein a killer, a new study suggests. This clumping gets dangerous only under certain circumstances.

A normally innocuous protein can be engineered to clump into fibers similar to those formed by proteins involved in Alzheimer’s, Parkinson’s and brain-wasting prion diseases such as Creutzfeldt-Jakob disease, researchers report in the Nov. 11 Science. Cells that rely on the protein’s normal function for survival die when the proteins glom together. But cells that don’t need the protein are unharmed by the gang activity, the researchers discovered. The finding may shed light on why clumping proteins that lead to degenerative brain diseases kill some cells, but leave others untouched.
Clumpy proteins known as prions or amyloids have been implicated in many nerve-cell-killing diseases (SN: 8/16/08, p. 20). Such proteins are twisted forms of normal proteins that can make other normal copies of the protein go rogue, too. The contorted proteins band together, killing brain cells and forming large clusters or plaques.

Scientists don’t fully understand why these mobs resort to violence or how they kill cells. Part of the difficulty in reconstructing the cells’ murder is that researchers aren’t sure what jobs, if any, many of the proteins normally perform (SN: 2/13/10, p. 17).

A team led by biophysicists Frederic Rousseau and Joost Schymkowitz of Catholic University Leuven in Belgium came up with a new way to dissect the problem. They started with a protein for which they already knew the function and engineered it to clump. That protein, vascular endothelial growth factor receptor 2, or VEGFR2, is involved in blood vessel growth. Rousseau and colleagues clipped off a portion of the protein that causes it to cluster with other proteins, creating an artificial amyloid.

Masses of the protein fragment, nicknamed vascin, could aggregate with and block the normal activity of VEGFR2, the researchers found. When the researchers added vascin to human umbilical vein cells grown in a lab dish, the cells died because VEGFR2 could no longer transmit hormone signals the cells need to survive. But human embryonic kidney cells and human bone cancer cells remained healthy. Those results suggest that some forms of clumpy proteins may not be generically toxic to cells, says biophysicist Priyanka Narayan of the Whitehead Institute for Biomedical Research in Cambridge, Mass. Instead, rogue clumpy proteins may target specific proteins and kill only cells that rely on those proteins for survival.

Those findings may also indicate that prion and amyloid proteins, such as Alzheimer’s nerve-killing amyloid-beta, normally play important roles in some brain cells. Those cells would be the ones vulnerable to attack from the clumpy proteins.
The newly engineered ready-to-rumble protein may open new ways to inactivate specific proteins in order to fight cancer and other diseases, says Salvador Ventura, a biophysicist at the Autonomous University of Barcelona. For instance, synthetic amyloids of overactive cancer proteins could gang up and shut down the problem protein, killing the tumor.

Artificial amyloids might also be used to screen potential drugs for anticlumping activity that could be used to combat brain-degenerating diseases, Rousseau suggests.

It was barely more than half a century ago that the Nobel Prize–winning virologist Sir Frank Macfarlane Burnet mused about the demise of contagions. “To write about infectious disease,” he wrote in 1962, “is almost to write of something that has passed into history.”

If only. In the past several decades, over 300 infectious pathogens have either newly emerged or emerged in new places, causing a steady drumbeat of outbreaks and global pandemic scares.

Over the course of 2016, their exploits reached a crescendo. Just as the unprecedented outbreak of Ebola in West Africa was collapsing in early 2016, the World Health Organization declared Zika virus, newly erupted in the Americas, an international public health emergency. What would balloon into the largest outbreak of yellow fever in Angola in 30 years had just begun. A few months later, scientists reported the just-discovered “superbug” mcr-1 gene in microbes collected from humans and pigs in the United States (SN Online: 5/27/16). The gene allows bacteria to resist the last-ditch antibiotic colistin, bringing us one step closer to a looming era of untreatable infections that would transform the practice of medicine. Its arrival presaged yet another unprecedented event: the convening of the United Nations General Assembly to consider the global problem of antibiotic-resistant bugs. It was only the fourth time over its 70-plus-year history that the assembly had been compelled to consider a health challenge. It’s “huge,” says University of Toronto epidemiologist David Fisman.
But even as UN delegates arrived for their meeting in New York City in September, another dreaded infection was making headlines again. The international community’s decades-long effort to end the transmission of polio had unraveled. In 2015, the WHO had declared Nigeria, one of the three last countries in the world that suffered the infection, free of wild polio. By August 2016, it was back. Millions would have to be vaccinated to keep the infection from establishing a foothold.
Three fundamental, interrelated factors fuel the microbial comeback, experts say. Across the globe, people are abandoning the countryside for life in the city, leading to rapid, unplanned urban expansions. In crowded conditions with limited access to health care and poor sanitation, pathogens like Ebola, Zika and influenza enjoy lush opportunities to spread. With more infections mingling, there are also more opportunities for pathogens to share their virulence genes.

At the same time, global demand for meat has quadrupled over the last five decades by some estimates, driving the spread of industrial livestock farming techniques that can allow benign microbes to become more virulent. The use of colistin in livestock agriculture in China, for example, has been associated with the emergence of mcr-1, which was first discovered during routine surveillance of food animals there. Genetic analyses suggest that siting factory farms full of chickens and pigs in proximity to wild waterfowl has played a role in the emergence of highly virulent strains of avian influenza. Crosses of Asian and North American strains of avian influenza caused the biggest outbreak of animal disease in U.S. history in 2014–2015. Containing that virus required the slaughter of nearly 50 million domesticated birds and cost over $950 million. Worryingly, some strains of avian influenza, such as H5N1, can infect humans.
The thickening blanket of carbon dioxide in the atmosphere resulting from booming populations of people and livestock provides yet another opportunity for pathogens to exploit. Scientists around the world have documented the movement of disease-carrying creatures including mosquitoes and ticks into new regions in association with newly amenable climatic conditions. Climate scientists predict range changes for bats and other animals as well. As the organisms spread into new ranges, they carry pathogens such as Ebola, Zika and Borrelia burgdorferi(a bacterium responsible for Lyme disease) along with them.
Since we can rarely develop drugs and vaccines fast enough to stanch the most dangerous waves of disease, early detection will be key moving forward. Researchers have developed a welter of models and pilot programs showing how environmental cues such as temperature and precipitation fluctuations and the insights of wildlife and livestock experts can help pinpoint pathogens with pandemic potential before they cause outbreaks in people. Chlorophyll signatures, a proxy for the plankton concentrations that are associated with cholera bacteria, can be detected from satellite data, potentially providing advance notice of cholera outbreaks.

Even social media chatter can be helpful. Innovative financing methods, such as the World Bank’s recently launched Pandemic Emergency Financing Facility — a kind of global pandemic insurance policy funded by donor countries, the reinsurance market and the World Bank — could help ensure that resources to isolate and contain new pathogens are readily available, wherever they take hold. Right now, emerging disease expert Peter Daszak points out, “we wait for epidemics to emerge and then spend billions on developing vaccines and drugs.” The nonprofit organization that Daszak directs, EcoHealth Alliance, is one of a handful that instead aim to detect new pathogens at their source and proactively minimize the risk of their spread.

Burnet died in 1985, two years after the discovery of HIV, one of the first of the latest wave of new pathogens. His vision of a contagion-free society was that of a climber atop a foothill surrounded by peaks, mistakenly thinking he’d reached the summit. The challenge of surviving in a world of pathogens is far from over. In many ways, it’s only just begun.

Thousands of years ago, it didn’t just rain on the Sahara Desert. It poured.

Grasslands, trees, lakes and rivers once covered North Africa’s now arid, unforgiving landscape. From about 11,000 to 5,000 years ago, much higher rainfall rates than previously estimated created that “Green Sahara,” say geologist Jessica Tierney of the University of Arizona in Tucson and her colleagues. Extensive ground cover, combined with reductions of airborne dust, intensified water evaporation into the atmosphere, leading to monsoonlike conditions, the scientists report January 18 in Science Advances.
Tierney’s team reconstructed western Saharan rainfall patterns over the last 25,000 years. Estimates relied on measurements of forms of carbon and hydrogen in leaf wax recovered from ocean sediment cores collected off the Sahara’s west coast. Concentrations of these substances reflected ancient rainfall rates.

Rainfall ranged from 250 to 1,670 millimeters annually during Green Sahara times, the researchers say. Previous estimates — based on studies of ancient pollen that did not account for dust declines — reached no higher than about 900 millimeters. Saharan rainfall rates currently range from 35 to 100 millimeters annually.

Leaf-wax evidence indicates that the Green Sahara dried out from about 8,000 to at least 7,000 years ago before rebounding. That’s consistent with other ancient climate simulations and with excavations suggesting that humans temporarily left the area around 8,000 years ago. Hunter-gatherers departed for friendlier locales, leaving cattle herders to spread across North Africa once the Green Sahara returned (SN Online: 6/20/12), the investigators propose.

Hunter-gatherers and farming villagers who live in worlds without lightbulbs or thermostats sleep slightly less at night than smartphone-toting city slickers, researchers say.

“Contrary to conventional wisdom, people in societies without electricity do not sleep more than those in industrial societies like ours,” says UCLA psychiatrist and sleep researcher Jerome Siegel, who was not involved in the new research.

Different patterns of slumber and wakefulness in each of these groups highlight the flexibility of human sleep — and also point to potential health dangers in how members of Western societies sleep, conclude evolutionary biologist David Samson of Duke University and colleagues. Compared with other primates, human evolution featured a shift toward sleeping more deeply over shorter time periods, providing more time for learning new skills and knowledge as cultures expanded, the researchers propose. Humans also evolved an ability to revise sleep schedules based on daily work schedules and environmental factors such as temperature.
Samson’s team describes sleep patterns in 33 East African Hadza hunter-gatherers over a total of 393 days in a paper published online January 7 in the American Journal of Physical Anthropology. The team’s separate report on slumber among 21 rural farmers in Madagascar over 292 days will appear later this year in the American Journal of Human Biology.

Sleep patterns in these groups were tracked with wrist devices that measure a person’s activity levels. Both Hadza and Malagasy volunteers slept an average of about 6.5 hours nightly, less than the about seven-hour average for most U.S. adults. Foragers and villagers, who slept in areas with various family and group members, awoke more frequently during the night than has been reported among Westerners. Scalp electrodes worn at night by nine villagers during nine nights revealed biological signs of relatively light sleep compared with Westerners, including shorter periods of slow-wave and rapid eye movement sleep.
But Hadza and Malagasy individuals often supplemented nighttime sleep with one or two daytime naps. Shut-eye breaks averaged 47.5 minutes for the Hadza and about 55 minutes for villagers. Critically, Samson says, foragers and villagers displayed more consistent daily cycles of sleep and wakefulness than are characteristic of Westerners. Hadza adults tended to hit the sack — or, more commonly, the mat — shortly after midnight and nap in the early afternoon. Malagasy villagers napped once or twice during the day’s hottest hours, usually starting around noon, and retired in the early evening. At night, they slept in two phases, awakening for around an hour shortly after midnight. Historical accounts describe a similar sleep pattern among Western Europeans between 500 and 200 years ago — two sleep segments, divided by a period of activity or reflection (SN: 9/25/99, p. 205).
Nighttime sleep in both populations became deeper and less fragmented as tropical humidity dipped.

Researchers also noted that hunter-gatherers and villagers got plenty of direct sunlight, unlike many Westerners. Several studies have linked inconsistent sleep-wake cycles and lack of sun exposure to health problems, including inflammation and heart problems, Samson says. “People in modern societies can take lessons from this research by attempting to get lots of light exposure during the day while reducing blue-wave light exposure after dark and dropping inside temperatures by a few degrees at night.” Smartphones and other digital devices emit blue-wave light, which can suppress melatonin production and delay sleep.

Effects of wayward sleep patterns or too little sleep on health vary across cultures and regions, says biomedical anthropologist Kristen Knutson of Northwestern University Feinberg School of Medicine in Chicago. For instance, sleeping less than six hours per night may increase appetite, as some studies suggest, but a sleep-deprived office worker surrounded by fast-food joints is more likely to become obese than a physically active hunter-gatherer faced with a limited food supply.

Samson’s research aligns with previous evidence, conducted by Knutson, that rural Haitians living without electricity sleep an average of about seven hours nightly. In addition, Siegel’s team recently reported that nightly sleep averages 5.7 to 7.1 hours in three hunter-gatherer societies, including the Hadza (SN: 11/14/15, p. 10).

Until recently, researchers thought cannibalism took place only among a few species in the animal kingdom and only under extraordinary circumstances. But as zoologist Bill Schutt chronicles in Cannibalism, plenty of creatures inhabit their own version of a dog-eat-dog world.

Over the last few decades, scientists have observed cannibalism — defined by Schutt as eating all or part of another individual of the same species — among all major groups of vertebrates. The practice seems to be even more prevalent, and less discriminating, among invertebrates such as mollusks, insects and spiders, whose eggs, larvae and young are often produced in profusion and are therefore readily available, not to mention nutritious.
Cannibalism, Schutt contends, makes perfect evolutionary sense, and not merely as a feeding strategy. When food supplies are low or living conditions are crowded, some mammals and birds may eat some or all of their offspring to terminate an expenditure of effort with poor chances of paying off. For birds, eating a dead or dying hatchling also is a way to get rid of a carcass that could spread infection or whose scent could attract flies or predators to the nest.

Switching to a historical and cultural perspective, Schutt tackles the various forms of human cannibalism, where, he admits, “the ick factor is high.” That includes medicinal cannibalism, from 17th and 18th century Europeans’ consumption of powdered mummies to modern moms’ ingestion of their newborns’ placentas to purportedly restore nutrients lost during childbirth. The author also explores survival cannibalism (think famine victims, people under siege, plane-crash survivors and the ill-fated Donner Party) and briefly addresses our natural shock and seemingly unnatural fascination with criminal cannibalism (à la Jeffrey Dahmer).

As Schutt explains, ritual cannibalism — the consumption of a foe or loved one to acquire the decedent’s strength, courage or wisdom — is a practice that has apparently taken place in different cultures throughout history. In an interesting aside, Schutt ponders whether people who consume wafers and wine during Communion, especially those who firmly believe these items are literally converted into the body and blood of Christ, are engaging in a form of ritual cannibalism.

Cannibalism is a wide-ranging, engaging and thoroughly fun read. The author’s numerous field trips and lab visits with scientists who study the phenomenon heartily enrich this captivating book.