It took just a 9-volt battery and a little brain zapping to turn science writer Sally Adee into a stone-cold sharpshooter.
She had flown out to California to test an experimental DARPA technology that used electric jolts to speed soldiers’ sniper training. When the juice was flowing, Adee could tell. In a desert simulation that pit her against virtual bad guys, she hit every one.
“Getting my neurons slapped around by an electric field instantly sharpened my ability to focus,” Adee writes in her new book, We Are Electric. That brain-stimulating experience ignited her 10-year quest to understand how electricity and biology intertwine. And she’s not just talking neurons. Bioelectricity, Adee makes the case, is a shockingly underexplored area of science that spans all parts of the body. Its story is one of missed opportunity, scientific threads exposed and abandoned, tantalizing clues and claims, “electroquacks” and unproven medical devices — and frogs. Oh so many frogs.
Adee takes us back to the 18th century lab of Luigi Galvani, an Italian scientist hunting for what gives animals the spark of life. His gruesome experiments on twitching frog legs offered proof that animal bodies generate their own electricity, an idea that was hotly debated at the time. (So many scientists repeated Galvani’s experiments, in fact, that Europe began to run out of frogs.)
But around the same time, Galvani critic Alessandro Volta, another Italian scientist, invented the electric battery. It was the kind of razzle-dazzle, history-shaking device that stole the spotlight from animal electricity, and the fledgling field fizzled. “The idea had been set,” Adee writes. “Electricity was not for biology. It was for machines, and telegraphs, and chemical reactions.” It took decades for scientists to pick up Galvani’s experimental threads and get the study of bioelectricity back on track. Since then, we’ve learned just how much electricity orchestrates our lives, and how much more remains to be discovered. Electricity zips through our neurons, makes our hearts tick and flows in every cell of the body. We’re made up of 40 trillion tiny rechargeable batteries, Adee writes.
She describes how cells use ion channels to usher charged molecules in and out. One thing readers might not expect from a book that illustrates the intricacies of ion channels: It’s surprisingly funny. Chloride ions, for example, are “perpetually low-key ashamed” because they carry a measly -1 charge. Bogus medical contraptions (here’s looking at you, electric penis belts) were “electro-foolery.” In her acknowledgements, Adee jokes about the “life-saving powers of Voltron” and thanks people for enduring her caffeine jitters. That energy thrums through the book, charging her storytelling like a staticky balloon.
Adee is especially electrifying in a chapter about spinal nerve regeneration and why initial experiments juddered to a halt. Decades ago, scientists tried coaxing severed nerves to link up again by applying an electric field. The controversial technique sparked scientific drama, but the idea of using electricity to heal may have been ahead of its time. Fast-forward to 2020, and DARPA has awarded $16 million to researchers with a similar concept: a bioelectric bandage that speeds wound healing.
Along with zingy Band-Aids of the future, Adee describes other sci-fi–sounding devices in the works. One day, for example, surgeons may sprinkle your brain with neurograins, neural lace or neural dust, tiny electronic implants that could help scientists monitor brain activity or even help people control robotic arms or other devices (SN: 9/3/16, p. 10).
Such implants bring many challenges — like how to marry electronics to living tissue — but Adee’s book leaves readers with a sense of excitement. Not only could bioelectricity inspire new and improved medical devices, it could also reveal a current of unexpected truths about the body.
As Adee writes: “We are electrical machines whose full dimensions we have not even yet dreamed of.”
The April 25 Nepal earthquake killed more than 8,000 people and caused several billion dollars in damage, but new research suggests the toll could have been a lot worse.
GPS readings taken during the quake indicate that most of the tremors vibrated through the ground as long shakes rather than quick pulses. That largely spared the low-lying buildings that make up much of Nepal’s capital, Kathmandu, geophysicists report online August 6 in Science. Those same low-frequency rumbles, though, toppled Kathmandu’s handful of larger buildings, such as the historic 62-meter tall Dharahara Tower.
Understanding why the fault produced a quake at such low frequencies could help seismologists better identify future seismic hazards, says Jean-Philippe Avouac of the University of Cambridge. “This could be some good news not only for this major fault, but also potentially for similar faults around the world.”
Nepal sits over a tectonic boundary where the Indian Plate slips under the Eurasian Plate. At places, the two plates snag together, building stress that abruptly releases as an earthquake (SN: 5/16/15, p. 12). Earthquakes stronger than April’s magnitude 7.8 shakedown have hit Nepal before, including a magnitude 8.0 quake in 1934. Despite the recent quake’s feebler intensity, its trembles somehow destroyed large buildings that had previously endured mightier earthquakes.
Avouac and colleagues monitored April’s quake using a network of 35 solar-powered GPS stations, the first time such an accurate system was in place during a major quake on this type of fault. The stations measured ground movements five times each second. The earthquake shook most intensely at 0.25 hertz, or one full wave every four seconds, with only moderate shaking above 1 hertz, or one or more complete waves each second.
A building is most vulnerable when shook near its resonance frequency, a range where even small outside forces can result in big vibrations in the structure. Because taller structures have lower resonance frequencies, the April quake’s low-frequency rumbles caused larger buildings to sway and crumble while largely sparing smaller dwellings, the researchers found.
The low frequencies resulted from the smooth and relatively long duration of the tectonic slipping that initiated the quake, the researchers propose. The low-frequency waves then echoed across the region and produced protracted violent shaking.
Determining where future low-frequency quakes will strike could save lives by identifying which building types are most vulnerable to collapse, says geologist Kristin Morell of the University of Victoria in Canada. “These are things that should be built into building codes.”
A new atlas of human genetic diversity reveals what human ancestors’ DNA may have looked like before people migrated out of Africa.
Ancestral humans carried 40.7 million more DNA base pairs than people do today, researchers report online August 6 in Science. That’s enough DNA to build a small chromosome, says study coauthor Evan Eichler, an evolutionary geneticist at the University of Washington in Seattle.
Human ancestors in Africa jettisoned 15.8 million of those DNA base pairs — information-carrying building blocks of DNA often referred to by the letters A, T, G and C — before dispersing around the globe, the researchers discovered. As people left Africa and spread to other continents, they dropped more chunks of DNA. Eichler and colleagues have followed these genetic bread crumbs to map relationships among 125 human groups worldwide. People didn’t just lose DNA. They also gained some. Compared with chimpanzees and orangutans, people have 728 extra pieces of DNA created when portions of the human genetic instruction book, the genome, were copied. Everyone has at least three copies of those duplicated bits, although the exact number varies from person to person.
Previous maps of human genetic diversity have usually not marked the yawning chasms left by deletions or the new territory created by duplications. Most diversity maps have focused on single DNA base pair changes, often called single nucleotide polymorphisms, or SNPs. But all the SNPs together comprise only 1.1 percent of the genome. Duplications and deletions, collectively known as copy number variants, have shaped more than 7 percent of the human genome.
Story continues below infographic Because duplications and deletions involve larger swaths of DNA than SNPs do, their influence on human evolution may also be bigger. Both duplications and deletions have been implicated in shaping human characteristics, such as bigger brains (SN: 3/21/15, p. 16; SN: 4/9/11, p. 15).
But researchers “can’t answer the question yet of whether what makes us human is in what was lost or what was duplicated,” says David Liberles, a computational evolutionary biologist at Temple University in Philadelphia.
Eichler’s choice is clear. “Duplications rock,” he says. “They affect more base pairs in the human genome than any other type of variation.” Duplications span 4.4 percent of the genome, while deletions represent 2.77 percent. And duplications tend to involve genes, while deletions often fall in spaces between genes, the researchers found.
His team flagged many duplications as possible medical and evolutionary points of interest. For instance, some groups of people have up to six copies of CLPS genes, which encode pancreatic enzymes that may help reduce blood sugar levels. Some African groups carry duplications of genes that may protect against sleeping sickness caused by trypanosome parasites.
Another attraction is a very large duplication of about 225,000 base pairs that Papua New Guineans inherited from Denisovans, an extinct group of hominids related to Neandertals. The colossal hunk of DNA contains two microRNA genes. MicroRNAs are small molecules that help regulate protein production. Eichler and colleagues calculate that the original duplication happened about 440,000 years ago in Denisovans. It was passed to Papuans and some other Melanesians about 40,000 years ago when their ancestors interbred with Denisovans. Now, about 80 percent of Papuans carry the duplication. Eichler speculates that the duplication may have given Papuan ancestors some evolutionary advantage, although what that advantage might be isn’t known.
While the researchers make a compelling case that duplications and deletions may play an important role in evolution, the team has provided little evidence that copy number variants really determine trait differences between groups, says Edward Hollox, a human geneticist at the University of Leicester in England. “It’s almost a paper saying, ‘Look, isn’t this interesting?’ But why it’s interesting they haven’t quite gotten to the bottom of.” Still, Hollox says the map will point other researchers to parts of the genome where evolution may have left its mark.
Memory Transfer Seen — Experiments with rats, showing how chemicals from one rat brain influence the memory of an untrained animal, indicate that tinkering with the brain of humans is also possible.
In the rat tests, brain material from an animal trained to go for food either at a light flash or at a sound signal was injected into an untrained rat. The injected animals then “remembered” whether light or sound meant food. Update: After this report, scientists from eight labs attempted to repeat the memory transplants. They failed, as they reported in Science in 1966.
Science fiction authors and futurists often predict that a person’s memories might be transferred to another person or a computer, but the idea is likely to remain speculation, says neuroscientist Eric Kandel, who won a Nobel Prize in 2000 for his work on memory. Brain wiring is too intricate and complicated to be exactly replicated, and scientists are still learning about how memories are made, stored and retrieved.
Large-scale climate patterns that can impact weather across thousands of kilometers may have a hand in synchronizing multicontinental droughts and stoking wildfires around the world, two new studies find.
These profound patterns, known as climate teleconnections, typically occur as recurring phases that can last from weeks to years. “They are a kind of complex butterfly effect, in that things that are occurring in one place have many derivatives very far away,” says Sergio de Miguel, an ecosystem scientist at Spain’s University of Lleida and the Joint Research Unit CTFC-Agrotecnio in Solsona, Spain. Major droughts arise around the same time at drought hot spots around the world, and the world’s major climate teleconnections may be behind the synchronization, researchers report in one study. What’s more, these profound patterns may also regulate the scorching of more than half of the area burned on Earth each year, de Miguel and colleagues report in the other study.
The research could help countries around the world forecast and collaborate to deal with widespread drought and fires, researchers say.
The El Niño-Southern Oscillation, or ENSO, is perhaps the most well-known climate teleconnection (SN: 8/21/19). ENSO entails phases during which weakened trade winds cause warm surface waters to amass in the eastern tropical Pacific Ocean, known as El Niño, and opposite phases of cooler tropical waters called La Niña.
These phases influence wind, temperature and precipitation patterns around the world, says climate scientist Samantha Stevenson of the University of California, Santa Barbara, who was not involved in either study. “If you change the temperature of the ocean in the tropical Pacific or the Atlantic … that energy has to go someplace,” she explains. For instance, a 1982 El Niño caused severe droughts in Indonesia and Australia and deluges and floods in parts of the United States.
Past research has predicted that human-caused climate change will provoke more intense droughts and worsen wildfire seasons in many regions (SN: 3/4/20). But few studies have investigated how shorter-lived climate variations — teleconnections — influence these events on a global scale. Such work could help countries improve forecasting efforts and share resources, says climate scientist Ashok Mishra of Clemson University in South Carolina.
In one of the new studies, Mishra and his colleagues tapped data on drought conditions from 1901 to 2018. They used a computer to simulate the world’s drought history as a network of drought events, drawing connections between events that occurred within three months of each other.
The researchers identified major drought hot spots across the globe — places in which droughts tended to appear simultaneously or within just a few months. These hot spots included the western and midwestern United States, the Amazon, the eastern slope of the Andes, South Africa, the Arabian deserts, southern Europe and Scandinavia. “When you get a drought in one, you get a drought in others,” says climate scientist Ben Kravitz of Indiana University Bloomington, who was not involved in the study. “If that’s happening all at once, it can affect things like global trade, [distribution of humanitarian] aid, pollution and numerous other factors.”
A subsequent analysis of sea surface temperatures and precipitation patterns suggested that major climate teleconnections were behind the synchronization of droughts on separate continents, the researchers report January 10 in Nature Communications. El Niño appeared to be the main driver of simultaneous droughts spanning parts of South America, Africa and Australia. ENSO is known to exert a widespread influence on precipitation patterns (SN: 4/16/20). So that finding is “a good validation of the method,” Kravitz says. “We would expect that to appear.” In the second study, published January 27 in Nature Communications, de Miguel and his colleagues investigated how climate teleconnections influence the amount of land burned around the world. Researchers knew that the climate patterns can influence the frequency and intensity of wildfires. In the new study, the researchers compared satellite data on global burned area from 1982 to 2018 with data on the strength and phase of the globe’s major climate teleconnections.
Variations in the yearly pattern of burned area strongly aligned with the phases and range of climate teleconnections. In all, these climate patterns regulate about 53 percent of the land burned worldwide each year, the team found. According to de Miguel, teleconnections directly influence the growth of vegetation and other conditions such as aridity, soil moisture and temperature that prime landscapes for fires.
The Tropical North Atlantic teleconnection, a pattern of shifting sea surface temperatures just north of the equator in the Atlantic Ocean, was associated with about one-quarter of the global burned area — making it the most powerful driver of global burning, especially in the Northern Hemisphere.
These researchers are showing that wildfire scars around the world are connected to these climate teleconnections, and that’s very useful, Stevenson says. “Studies like this can help us prepare how we might go about constructing larger scale international plans to deal with events that affect multiple places at once.”
A close look at one protein shows how it moves molecular passengers into cells in the kidneys, brain and elsewhere.
The protein LRP2 is part of a delivery service, catching certain molecules outside a cell and ferrying them in. Now, 3-D maps of LRP2 reveal the protein’s structure and how it captures and releases molecules, researchers report February 6 in Cell. The protein adopts a more open shape, like a net, at the near-neutral pH outside cells. But in the acidic environment inside cells, the protein crumples to drop off any passengers. The shape of LRP2’s structure — and how it enables so many functions — has stumped scientists for decades. The protein helps the kidneys and brain filter out toxic substances, and it operates in other places too, like the lungs and inner ears. When the protein doesn’t function properly, a host of health conditions can occur, including chronic kidney disease and Donnai-Barrow syndrome, a genetic disorder that affects the kidneys and brain.
The various conditions associated with LRP2 dysfunction come from the protein’s numerous responsibilities — it binds to more than 75 different molecules. That’s a huge amount for one protein, earning it the nickname “molecular flypaper,” says nephrologist Jonathan Barasch of Columbia University.
Typically, LRP2 sits at a cell membrane’s surface, waiting to snag a molecule passing by. After the protein binds to a molecule, the cell engulfs the part of its surface containing the protein, forming an internal bubble called an endosome. LRP2 then releases the molecule inside the cell, and the endosome carries the protein back to the surface.
To understand this shuttle system, Barasch and colleagues collected LRP2 from 500 mouse kidneys. The researchers put some of the protein in a solution at the extracellular pH of 7.5, and some in an endosome-mimicking solution at pH 5.2. Using a cryo-electron microscope, they captured images of the proteins and then stitched the images together in a computer, rendering 3-D maps of the protein at both open and closed formations. The researchers suggest that charged calcium atoms hold the protein open at extracellular pH. But as pH drops due to hydrogen ions flowing into the endosome, the hydrogen ions displace the calcium ions, causing the protein to contract.
You’d be forgiven for thinking that depression has a simple explanation.
The same mantra — that the mood disorder comes from a chemical imbalance in the brain — is repeated in doctors’ offices, medical textbooks and pharmaceutical advertisements. Those ads tell us that depression can be eased by tweaking the chemicals that are off-kilter in the brain. The only problem — and it’s a big one — is that this explanation isn’t true.
The phrase “chemical imbalance” is too vague to be true or false; it doesn’t mean much of anything when it comes to the brain and all its complexity. Serotonin, the chemical messenger often tied to depression, is not the one key thing that explains depression. The same goes for other brain chemicals. The hard truth is that despite decades of sophisticated research, we still don’t understand what depression is. There are no clear descriptions of it, and no obvious signs of it in the brain or blood.
The reasons we’re in this position are as complex as the disease itself. Commonly used measures of depression, created decades ago, neglect some important symptoms and overemphasize others, particularly among certain groups of people. Even if depression could be measured perfectly, the disorder exists amid myriad levels of complexity, from biological confluences of minuscule molecules in the brain all the way out to the influences of the world at large. Countless combinations of genetics, personality, history and life circumstances may all conspire to create the disorder in any one person. No wonder the science is stuck.
It’s easy to see why a simple “chemical imbalance” explanation holds appeal, even if it’s false, says Awais Aftab, a psychiatrist at Case Western Reserve University in Cleveland. What causes depression is nuanced, he says — “not something that can easily be captured in a slogan or buzzword.”
So here, up front, is your fair warning: There will be no satisfying wrap-up at the end of this story. You will not come away with a scientific explanation for depression, because one does not exist. But there is a way forward for depression researchers, Aftab says. It requires grappling with nuances, complexity and imperfect data.
Those hard examinations are under way. “There’s been some really interesting and exciting scientific and philosophical work,” Aftab says. That forward motion, however slow, gives him hope and may ultimately benefit the millions of people around the world weighed down by depression.
How is depression measured? Many people who feel depressed go into a doctor’s office and get assessed with a checklist. “Yes” to trouble sleeping, “yes” to weight loss and “yes” to a depressed mood would all yield points that get tallied into a cumulative score. A high enough score may get someone a diagnosis. The process seems straightforward. But it’s not. “Even basic issues regarding measurement of depression are actually still quite open for debate,” Aftab says.
That’s why there are dozens of methods to assess depression, including the standard description set by the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, or DSM-5. This manual is meant to standardize categories of illness.
Variety in measurement is a real problem for the field and points to the lack of understanding of the disease itself, says Eiko Fried, a clinical psychologist at Leiden University in the Netherlands. Current ways of measuring depression “leave you with a really impoverished, tiny look,” Fried says.
Scales can miss important symptoms, leaving people out. “Mental pain,” for instance, was described by patients with depression and their caregivers as an important feature of the illness, researchers reported in 2020 in Lancet Psychiatry. Yet the term doesn’t show up on standard depression measurements.
One reason for the trouble is that the experience of depression is, by its nature, deeply personal, says clinical psychologist Ioana Alina Cristea of the University of Pavia in Italy. Individual patient complaints are often the best tool for diagnosing the disorder, she says. “We can never let these elements of subjectivity go.”
In the middle of the 20th century, depression was diagnosed through subjective conversation and psychoanalysis, and considered by some to be an illness of the soul. In 1960, psychiatrist Max Hamilton attempted to course-correct toward objectivity. Working at the University of Leeds in England, he published a depression scale. Today, that scale, known by its acronyms HAM-D or HRSD, is one of the most widely used depression screening tools, often used in studies measuring depression and evaluating the promise of possible treatments. “It’s a great scheme for a scale that was made in 1960,” Fried says. Since the HRSD was published, “we have put a man on the moon, invented the internet and created powerful computers small enough to fit in people’s pockets,” Fried and his colleagues wrote in April in Nature Reviews Psychology. Yet this 60-year-old tool remains a gold standard.
Hamilton developed his scale by observing patients who had already been diagnosed with depression. They exhibited symptoms such as weight loss and slowed speech. But those mixtures of symptoms don’t apply to everyone with depression, nor do they capture nuance in symptoms.
To spot these nuances, Fried looked at 52 depression symptoms across seven different scales for depression, including Hamilton’s scale. On average, each symptom appeared in three of the seven scales. A whopping 40 percent of the symptoms appeared in only one scale, Fried reported in 2017 in the Journal of Affective Disorders. The only specific symptom common to all seven scales? “Sad mood.”
In a study that examined depression symptoms reported by 3,703 people, Fried and Randolph Nesse, an evolutionary psychiatrist at the University of Michigan Medical School in Ann Arbor, found 1,030 unique symptom profiles. Roughly 14 percent of participants had combinations of symptoms that were not shared with anyone else, the researchers reported in 2015 in the Journal of Affective Disorders.
Before reliable thermometers, the concept of temperature was murky. How do you understand the science of hot and cold without the tools to measure it? “You don’t,” Fried says. “You make a terrible measurement, and you have a terrible theory of what it is.” Depression presents a similar challenge, he says. Without good measurements, how can you possibly diagnose depression, determine whether symptoms get better with treatments or even prevent it in the first place?
Depression differs by gender, race and culture The story gets murkier when considering who these depression scales were made for. Symptoms differ among groups of people, making the diagnosis even less relevant for certain groups. Behavioral researcher Leslie Adams of Johns Hopkins Bloomberg School of Public Health studies depression in Black men. “It’s clear that [depression] is negatively impacting their work lives, social lives and relationships. But they’re not being diagnosed at the same rate” as other groups, she says. For instance, white people have a lifetime risk of major depression disorder of almost 18 percent; Black people’s lifetime risk is 10.4 percent, researchers reported in 2007 in JAMA Psychiatry. This discrepancy led Adams to ask: “Could there be a problem with diagnostic tools?”
Turns out, there is. Black men with depression have several characteristics that common scales miss, such as feelings of internal conflict, not communicating with others and feeling the burdens of societal pressure, Adams and colleagues reported in 2021 in BMC Public Health. A lot of depression measurements are based on questions that don’t capture these symptoms, Adams says. “ ‘Are you very sad?’ ‘Are you crying?’ Some people do not emote in the same way,” she says. “You may be missing things.”
American Indian women living in the Southeast United States also experience symptoms that aren’t adequately caught by the scales, Adams and her team found in a separate study. These women also reported experiences that do not necessarily signal depression for them but generally do for wider populations.
On common scales, “there are some items that really do not capture the experience of depression for these groups,” Adams says. For instance, a common question asks how well someone agrees with the sentence: “I felt everything I did was an effort.” That “can mean a lot of things, and it’s not necessarily tied to depression,” Adams says. The same goes for items such as, “People dislike me.” A person of color faced with racism and marginalization might agree with that, regardless of depression, she says.
Our ways to measure depression capture only a tiny slice of the big picture. The same can be said about our understanding of what’s happening in the brain.
The flawed serotonin hypothesis Serotonin came into the spotlight in part because of the serendipitous discovery of drugs that affected serotonin receptors, called selective serotonin reuptake inhibitors, or SSRIs. After getting its start in the late 1960s, the “serotonin hypothesis” flourished in the late ’90s, as advertisers ran commercials that told viewers that SSRIs fixed the serotonin deficit that can accompany depression. These messages changed the way people talked and thought about depression. Having a simple biological explanation helped some people and their doctors, in part by easing the shame some people felt for not being able to snap out of it on their own. It gave doctors ways to talk with people about the mood disorder.
But it was a simplified picture. A recent review of evidence, published in July in Molecular Psychiatry, finds no consistent data supporting the idea that low serotonin causes depression. Some headlines declared that the study was a grand takedown of the serotonin hypothesis. To depression researchers, the findings weren’t a surprise. Many had already realized this simple description wasn’t helpful.
There’s plenty of data suggesting that serotonin, and other chemical messengers such as dopamine and norepinephrine, are somehow involved in depression, including a study by neuropharmacologist Gitte Moos Knudsen of the University of Copenhagen. She and colleagues recently found that 17 people who were in the midst of a depressive episode released, on average, less serotonin in certain brain areas than 20 people who weren’t depressed. The study is small, but it’s one of the first to look at serotonin release in living human brains of people with depression.
But Knudsen cautions that those results, published in October in Biological Psychiatry, don’t mean that depression is fully caused by low serotonin levels. “It’s easy to defer to simple explanations,” she says.
SSRIs essentially form a molecular blockade, stopping serotonin from being reabsorbed into nerve cells and keeping the levels high between the cells. Those high levels are thought to influence nerve cell activity in ways that help people feel better.
Because the drugs can ease symptoms in about half of people with depression, it seemed to make sense that depression was caused by problems with serotonin. But just because a treatment works by doing something doesn’t mean the disease works in the opposite way. That’s backward logic, psychiatrist Nassir Ghaemi of Tufts University School of Medicine in Boston wrote in October in a Psychology Today essay. Aspirin can ease a headache, but a headache isn’t caused by low aspirin.
“We think we have a much more nuanced picture of what depression is today,” Knudsen says. The trouble is figuring out the many details. “We need to be honest with patients, to say that we don’t know everything about this,” she says.
The brain contains seven distinct classes of receptors that sense serotonin. That’s not even accounting for sensors for other messengers such as dopamine and norepinephrine. And these receptors sit on a wide variety of nerve cells, some that send signals when they sense serotonin, some that dampen signals. And serotonin, dopamine and norepinephrine are just a few of dozens of chemicals that carry information throughout a multitude of interconnected brain circuits. This complexity is so great that it renders the phrase “chemical imbalance” meaningless.
Overly simple claims — low serotonin causes depression, or low serotonin isn’t involved — serve only to keep us stymied, Aftab says. “[It] just keeps up that unhelpful binary.” Depression research can’t ignore the world In the 1990s, Aftab says, depression researchers got intensely focused on the brain. “They were trying to find the broken part of the brain that causes depression.” That limited view “really hurt depression research,” Aftab says. In the last 10 years or so, “there’s a general recognition that that sort of mind-set is not going to give us the answers.”
Reducing depression to specific problems of biology in the brain didn’t work, Cristea says. “If you were a doctor 10 years ago, the dream was that the neuroscience would give us the markers. We would look at the markers and say, ‘OK. You [get] this drug. You, this kind of therapy.’ But it hasn’t happened.” Part of that, she says, is because depression is an “existentially complicated disorder” that’s tough to simplify, quantify and study in a lab.
Our friendships, our loves, our setbacks and our stress can all influence our health. Take a recent study of first-year doctors in the United States. The more these doctors worked, the higher the rate of depression, scientists reported in October in the New England Journal of Medicine. Similar trends exist for caregivers of people with dementia and health care workers who kept emergency departments open during the COVID-19 pandemic. Their high-stress experiences may have prompted depression in some way.
“Depression is linked to the state of the world — and there is no denying it,” Aftab says. Today’s research on depression ought to be more pluralistic, Adams says. “There are so many factors at play that we can’t just rest on one solution,” she says. Research from neuroscience and genetics has helped identify brain circuits, chemical messengers, cell types, molecules and genes that all may be involved in the disorder. But researchers aren’t satisfied with that. “There is other evidence that remains unexplored,” Adams says. “With our neuroscience advances, there should be similar advances in public health and psychiatric work.”
That’s happening. For her part, Adams and colleagues have just begun a study looking at moment-to-moment stressors in the lives of Black adolescents, ages 12 to 18, as measured by cell phone questionnaires. Responses, she hopes, will yield clues about depression and risk of suicide.
Other researchers are trying to fit together all of these different ways of seeing the problem. Fried, for example, is developing new concepts of depression that acknowledge the interacting systems. You tug on one aspect of it — using an antidepressant for instance, or changing sleep patterns — and see how the rest of the system reacts.
Approaches like these recognize the complexity of the problem and aim to figure out ways to handle it. We will never have a simple explanation for depression; we are now learning that one cannot possibly exist. That may sound like cold comfort to people in depression’s grip. But seeing the challenge with clear eyes may be the thing that moves us forward.
Some fish can recognize their own faces in photos and mirrors, an ability usually attributed to humans and other animals considered particularly brainy, such as chimpanzees, scientists report. Finding the ability in fish suggests that self-awareness may be far more widespread among animals than scientists once thought.
“It is believed widely that the animals that have larger brains will be more intelligent than animals of the small brain,” such as fish, says animal sociologist Masanori Kohda of Osaka Metropolitan University in Japan. It may be time to rethink that assumption, Kohda says. Kohda’s previous research showed that bluestreak cleaner wrasses can pass the mirror test, a controversial cognitive assessment that purportedly reveals self-awareness, or the ability to be the object of one’s own thoughts. The test involves exposing an animal to a mirror and then surreptitiously putting a mark on the animal’s face or body to see if they will notice it on their reflection and try to touch it on their body. Previously only a handful of large-brained species, including chimpanzees and other great apes, dolphins, elephants and magpies, have passed the test.
In a new study, cleaner fish that passed the mirror test were then able to distinguish their own faces from those of other cleaner fish in still photographs. This suggests that the fish identify themselves the same way humans are thought to — by forming a mental image of one’s face, Kohda and colleagues report February 6 in the Proceedings of the National Academy of Sciences.
“I think it’s truly remarkable that they can do this,” says primatologist Frans de Waal of Emory University in Atlanta who was not involved in the research. “I think it’s an incredible study.”
De Waal is quick to point out that failing the mirror test should not be considered evidence of a lack of self-awareness. Still, scientists have struggled to understand why some species that are known to have complex cognitive abilities, such as monkeys and ravens, have not passed. Researchers have also questioned whether the test is appropriate for species like dogs that rely more on scent, or like pigs that may not care enough about a mark on their bodies to try to touch it.
The mixed results in other animals make it all the more astonishing that a small fish can pass. In their first mirror test studies, published in 2019 and 2022, Kohda’s team exposed wild-caught cleaner fish in separate tanks to mirrors for a week. The researchers then injected brown dye just beneath the scales on the fish’s throats, making a mark that resembles the parasites these fish eat off the skin of larger fish in the wild. When the marked fish saw themselves in a mirror, they began striking their throats on rocks or sand in the bottom of the tank, apparently trying to scrape off the marks.
In the new study, 10 fish that passed the mirror test were then shown a photo of their own face and a photo of an unfamiliar cleaner fish face. All the fish acted aggressively toward the unfamiliar photo, as if it were a stranger, but were not aggressive toward the photo of their own face.
When another eight fish that had spent a week with a mirror but had not previously been marked were shown a photo of their own face with a brown mark on the throat, six of them began scraping their throats just like the fish that passed the mirror test. But they did not scrape when shown a photo of another fish with a mark. Animals that recognize their reflection in the mirror most likely first learn to identify themselves by seeing that the movement of the animal in the mirror matches their own movement, researchers think. Because the cleaner fish were also able to recognize their own faces in still images, they, and possibly other animals that have passed the mirror test, may be able to identify themselves by developing a mental image of their own face that they can compare to what they see in the mirror or photos, the authors say.
“I think it’s a great next step,” says comparative cognitive psychologist Jennifer Vonk of Oakland University in Rochester, Mich., who wasn’t involved in the study. But she would like to see more research before drawing conclusions about what’s being represented in the mind of a nonverbal being like a fish. “As with most other studies, it still leaves some room for further follow-up.”
Kohda’s lab has more experiments planned to continue to probe what’s going on in the brain of the cleaner fish, and to try the new photo-recognition method on another popular research fish, the three-spined stickleback (Gasterosteus aculeatus).
Animal behaviorist Jonathan Balcombe, author of the book What a Fish Knows, is already convinced, describing the new study as “robust and quite brilliant.” People shouldn’t be surprised that fish could be self-aware given that they have already been shown to have complex behavior including tool use, planning and collaboration, Balcombe says. “It’s time we stopped thinking of fishes as somehow lesser members of the vertebrate pantheon.”
In the early morning of February 6, a devastating magnitude 7.8 earthquake struck southern Turkey, near the border with Syria. Numerous aftershocks followed, the strongest nearly rivaling the power of the main quake, at magnitude 7.5. By evening, the death toll had climbed to more than 3,700 across both countries, according to Reuters, and was expected to continue to rise.
Most of Turkey sits on a small tectonic plate that is sandwiched between two slowly colliding behemoths: the vast Eurasian Plate to the north and the Arabian Plate to the south. As those two plates push together, Turkey is being squeezed out sideways, like a watermelon seed snapped between two fingers, says seismologist Susan Hough of the U.S. Geological Survey. The entire country is hemmed in by strike-slip, or sideways-sliding, fault zones: the North Anatolian Fault that runs roughly parallel to the Black Sea, and the East Anatolian Fault, near the border with Syria. As a result, Turkey is highly seismically active. Even so, Monday’s quake, which occurred on the East Anatolian Fault, was the strongest to strike the region since 1939, when a magnitude 7.8 quake killed 30,000 people.
Science News talked with Hough, who is based in Pasadena, Calif., about the quake, its aftershocks and building codes. The conversation has been edited for length and clarity.
SN: You say on Twitter that this was a powerful quake for a strike-slip fault. Can you explain?
Hough: The world has seen bigger earthquakes. Subduction zones generate the biggest earthquakes, as much as magnitude 9 (SN: 1/13/21). But quakes close to magnitude 8 are not common on strike-slip faults. But because they’re on land and tend to be shallow, you can get severe … shaking close to the fault that’s moving.
SN: Some of the aftershocks were very strong, at magnitudes 7.5 and 6.7. Is that unusual?
Hough: As with a lot of things, there’s what’s expected on average, and there’s what’s possible. On average, the largest aftershocks are a full unit smaller than the main shock. But that’s just average; for any individual main shock, the largest aftershock can have a lot of variability.
The other thing people noted was the distance [between the main shock and some aftershocks over a hundred kilometers away]. Aftershock as a term isn’t precise. What is an aftershock isn’t something that seismologists are always clear on. The fault that produced the main shock is 200 kilometers long, and that’s going to change the stress in a lot of areas. Mostly it releases stress, but it does increase stress in some areas. So you can get aftershocks along that fault, but also some distance away. It’s a little bit unusual, but not unheard of.
SN: People have wondered whether Monday’s magnitude 3 earthquake near Buffalo, N.Y., might be related.
Hough: A magnitude 7.8 quake generates [seismic] waves that you can record all around Earth, so it’s technically disrupting every point on Earth. So it’s not a completely outlandish idea, but it’s statistically exceedingly unlikely. Maybe if a seismic wave passed through a fault that was just ready to go in just the right way, it’s possible.
An interesting [and completely separate] idea is that you might get earthquakes around the perimeter of the Great Lakes [such as near Buffalo] because as the lake levels go up and down, you’re stressing the Earth’s crust, putting weight on one side or the other. That’s a source of stress that could give you these pretty small quakes.
SN: The images emerging from this deadly disaster are devastating.
Hough: It’s hard to watch. And it hammers home the importance of building codes. One of the problems that any place is up against is that building codes improve over time, and you’ve always got the problem of older structures. It’s really expensive to retrofit. I expect that earthquake engineers will be looking at the damage, and it will illuminate where the vulnerabilities are [in the area]. The hope is that with proper engineering, we can make the built environment safe.
For mammals, one secret to a long life may be spending it living with friends and family.
An analysis of the life spans and social lives of nearly 1,000 mammal species shows that species that live in groups, such as horses and chimpanzees, tend to live longer than solitary beasts, like weasels and hedgehogs. The finding suggests that life span and social traits are evolutionarily entwined in mammals, researchers report January 31 in Nature Communications. The maximum life span of mammals ranges widely. The shortest-lived shrews, for example, survive about two years, while bowhead whales (Balaena mysticetus) can reach roughly 200 years of age (SN: 1/6/15).
When evolutionary biologist Xuming Zhou of the Chinese Academy of Sciences in Beijing was studying the longest-lived mammals to understand the evolution of longevity, he took particular note of naked mole-rats (Heterocephalus glaber). The rodents are exceptionally long-lived, sometimes reaching over 30 years of age. They also live in huge, complex, subterranean societies. In contrast, other rodents like golden hamsters (Mesocricetus auratus), which are solitary, live to only about four years.
Some previous research on specific mammal species showed an effect of social behavior on longevity, Zhou says. For instance, female chacma baboons (Papio ursinus) with strong, stable social bonds live longer than females without them.
Zhou and his colleagues decided to see if there were any links between longevity and social habits shared across a wide range of mammal species.
The researchers compiled information from the scientific literature on the social organization of 974 mammal species. They then split these species into three categories: solitary, pair-living and group-living. When the researchers compared these three groups with data on the mammals’ known longevity, they found that group-living mammals tended to live longer than the solitary species — roughly 22 years compared with nearly 12 years in solitary mammals.
Zhou and his colleagues then accounted for body mass — bigger mammals tend to live longer than smaller ones — and the effect of social bonds held. A stark example comes from shrews and bats. Both are similarly tiny mammals, but the loner shrews live only a few years, while some far more social bat species can live for 30 or 40 years.
“We were so surprised, because individuals who live in groups also face a lot of costs, such as competition for potential mating partners and food,” Zhou says. Frequent social contact in group settings can also encourage the spread of infectious disease. But there are benefits to living in a group too, he says, such as banding together for protection against predators. Living together may also reduce the risk of starvation if, for instance, group members increase foraging efficiency by finding and gathering food together. These factors may allow social mammals to live longer.
The evolution of a long life may also be more likely in group-living species: Living in a group allows animals to potentially aid the survival of their family members, which carry their genes.
Evolutionary biologist Laurent Keller of the University of Lausanne in Switzerland lauds the study for the sheer size of the sampling effort. “But it would have been useful to be a bit more precise about different levels of sociality.” There are more variations of social organization within the three categories used in the study, he says, and the relative degree of sociality could influence any patterns you see.
Still, fine tuning the social categories “is not an easy task,” Keller notes.
To get an idea of how genes might produce the link between longevity and group living, Zhou and his team took brain tissue samples from 94 mammal species and analyzed the transcriptome — the full complement of RNA — giving insights into different genes’ activity levels. This can reveal whether genes are turned on or off, or how much protein the genes may be instructing cells to produce.
The researchers found 31 genes whose relative activity levels were correlated with both longevity and one of the three prescribed social categories. Many of these genes appear to have roles in the immune system, which may have importance when countering pathogens spreading through the social group. Other genes were associated with hormone regulation, including some thought to influence social behaviors.
In studying these genes in more detail, Zhou envisions uncovering more about how mammals’ social habits and life spans have evolved together.
