Young kids’ brains are especially tuned to their mothers’ voices. Teenagers’ brains, in their typical rebellious glory, are most decidedly not.
That conclusion, described April 28 in the Journal of Neuroscience, may seem laughably obvious to parents of teenagers, including neuroscientist Daniel Abrams of Stanford University School of Medicine. “I have two teenaged boys myself, and it’s a kind of funny result,” he says.
But the finding may reflect something much deeper than a punch line. As kids grow up and expand their social connections beyond their family, their brains need to be attuned to that growing world. “Just as an infant is tuned into a mom, adolescents have this whole other class of sounds and voices that they need to tune into,” Abrams says. He and his colleagues scanned the brains of 7- to 16-year-olds as they heard the voices of either their mothers or unfamiliar women. To simplify the experiment down to just the sound of a voice, the words were gibberish: teebudieshawlt, keebudieshawlt and peebudieshawlt. As the children and teenagers listened, certain parts of their brains became active.
Previous experiments by Abrams and his colleagues have shown that certain regions of the brains of kids ages 7 to 12 — particularly those parts involved in detecting rewards and paying attention — respond more strongly to mom’s voice than to a voice of an unknown woman. “In adolescence, we show the exact opposite of that,” Abrams says.
In these same brain regions in teens, unfamiliar voices elicited greater responses than the voices of their own dear mothers. The shift from mother to other seems to happen between ages 13 and 14.
It’s not that these adolescent brain areas stop responding to mom, Abrams says. Rather, the unfamiliar voices become more rewarding and worthy of attention.
And that’s exactly how it should be, Abrams says. Exploring new people and situations is a hallmark of adolescence. “What we’re seeing here is just purely a reflection of this phenomenon.”
Voices can carry powerful signals. When stressed-out girls heard their moms’ voices on the phone, the girls’ stress hormones dropped, biological anthropologist Leslie Seltzer of the University of Wisconsin–Madison and colleagues found in 2011 (SN: 8/12/11). The same was not true for texts from their mothers.
The current results support the idea that the brain changes to reflect new needs that come with time and experience, Seltzer says. “As we mature, our survival depends less and less on maternal support and more on our group affiliations with peers.”
It’s not clear how universal this neural shift is. The finding might change across various mother-child relationships, including those that have different parenting styles, or even a history of neglect or abuse, Seltzer says.
So while teenagers and parents may sometimes feel frustrated by missed messages, take heart, Abrams says. “This is the way the brain is wired, and there’s a good reason for it.”
Modern breeds are shaped around aesthetics: Chihuahuas’ batlike ears, poodles’ curly fur, dachshunds’ hot dog shape. But breeds are frequently associated with certain behaviors, too. For instance, the American Kennel Club describes border collies as “affectionate, smart, energetic” and beagles as “friendly, curious, merry.”
Now, genetic information from more than 2,000 dogs, paired with self-reported surveys from dog owners, indicates that a dog’s breed is a poor predictor of its behavior. On average, breed explains only 9 percent of the behavioral differences between individual dogs, researchers report April 28 in Science. “Everybody was assuming that breed was predictive of behavior in dogs,” geneticist Elinor Karlsson of the University of Massachusetts Chan Medical School in Worcester said in an April 26 news briefing. But “that had never really been asked particularly well.”
Geneticists had asked the question before in different ways. One study in 2019 looked at whether genetics might explain collective variation between breeds and found that genes could explain some of the differences between, say, poodles and chihuahuas (SN: 10/1/19). But Karlsson and her colleagues wanted to learn how much breed can predict variation in individual dogs’ behavior.
To study variation at the individual level, the team needed genetic and behavior data from a lot of dogs. So they developed Darwin’s Ark, an open-source database where more than 18,000 pet owners responded to surveys about their dog’s traits and behavior. The survey asked over 100 questions about observable behaviors, which the researchers grouped into eight “behavioral factors,” including human sociability (how comfortable a dog is around humans) and biddability (how responsive it is to commands).
The researchers also collected genetic data from 2,155 purebred and mixed-breed dogs, including 1,715 dogs from Darwin’s Ark whose owners sent in dog saliva swabs. The inclusion of mixed-breed dogs, or mutts, shed light on how ancestry affects behavior while removing the purebred stereotypes that could affect the way the dog is treated — and thus behaves.
Studying mutts also makes it easier to decouple traits from one another, says Kathleen Morrill, a geneticist in Karlsson’s lab. “And that means on an individual basis, you’re going to have a better shot at mapping a gene that is actually tied to the question you’re asking.”
Then the team combined the genetic and survey data for the individual dogs to identify genes associated with particular traits. The new study revealed that the most heritable behavioral factor for dogs is human sociability, and that motor patterns — such as howling and retrieving — are generally more heritable than other behaviors.
That makes sense, Kathryn Lord, an evolutionary canine biologist in Karlsson’s lab, said during the briefing. Before modern breeding started within the last couple hundred years or so, dogs were selected for the functional roles they could provide, such as hunting or herding (SN: 4/26/17). Today, these selections still show up in breed groups. For instance, herding dogs on average tend to be more biddable and interested in toys. It also follows that, within breed groups, individual breeds are more likely to display certain motor patterns: Retrievers, unsurprisingly, are more likely to retrieve.
Still, even though breed was associated with certain behaviors, it was not a reliable predictor of individual behavior. While retrievers are less likely to howl, some owners reported that their retrievers howled often; greyhounds rarely bury toys, except some do.
The research solidifies what people have observed: Dog breeds differ on average in behavior, but there’s a lot of variation within breeds, says Adam Boyko, a canine geneticist at Cornell University who was not involved in the study.
Surprisingly, size had even less of an effect — as in, virtually none — on an individual’s behavior, despite the yappiness commonly associated with small dogs. Boyko points out that small dogs may often behave worse than large dogs, but rather than that being built into their genetics, “I think it’s that we typically tolerate poor behavior more in small dogs than we do in big dogs.”
As a dog trainer, Curtis Kelley of Pet Parent Allies in Philadelphia says that he meets a dog where it’s at. “Dogs are as individual as people are,” he says. Breed gives a loose guideline for what kind of behaviors to expect, “but it’s certainly not a hard-and-fast rule.”
If a person is looking to buy a dog, he says, they shouldn’t put too much stock in the dog’s breed. Even within a litter, dogs can show very different personalities. “A puppy will show you who they are at eight weeks old,” Kelley says. “It’s just our job to believe them.”
Pterosaurs not only had feathers, but also were flamboyantly colorful, scientists say. That could mean that feathers — and vibrant displays of mate-seeking plumage — may have originated as far back as the common ancestor of dinosaurs and pterosaurs, during the early Triassic Period around 250 million years ago. Analyses of the partial skull of a 113-million-year-old pterosaur fossil revealed that the flying reptile had two types of feathers, paleontologist Aude Cincotta of University College Cork in Ireland and colleagues report April 20 in Nature. On its head, the creature, thought to be Tupandactylus imperator, had whiskerlike, single filaments and more complicated branching structures akin to those of modern bird feathers. Because the fossil’s soft tissues were also well-preserved, the team identified a variety of different shapes of pigment-bearing melanosomes in both feathers and skin. Those shapes ranged from “very elongate cigar shapes to flattened platelike disks,” says Maria McNamara, a paleobiologist also at University College Cork. Different melanosome shapes have been linked to different colors. Short, stubby spheroidal melanosomes are usually associated with yellow to reddish-brown colors, while the longer shapes are linked to darker colors, McNamara says. The range of melanosome geometries found in this Tupandactylus specimen suggests that the creature may have been quite colorful, the team says. And that riot of color, in turn, hints that the feathers weren’t there just to keep the creatures warm, but may have been used for visual signaling, such as displays to attract a mate. Scientists have wrangled over whether pterosaurs, Earth’s first true vertebrate flyers, had true feathers, or whether their bodies were covered in something more primitive and hairlike, dubbed “pycnofibers” (SN: 7/22/21). If the flying reptiles did have feathers, they weren’t needed for flying; pterosaurs had fibrous membranes stretched between their long, tapering wings, much like modern bats (SN: 10/22/20). In 2018, a team of researchers including McNamara reported that some of the fuzz covering two fossilized pterosaur specimens wasn’t just simple pycnofibers but showed distinct, complex, branching patterns similar to those seen in modern feathers (SN: 12/21/18). But some researchers have disputed this, saying that the branching observed in the fossils was an artifact of preservation, the appearance of branching created by overlapping fibers. The new pterosaur specimen has “turned all that on its head,” McNamara says. In this fossil, “it’s very clear. We see feathers that are separated, isolated — you can’t say it’s an overlap of structures.” The fossilized feathers show successive branches of consistent length, extending all the way along a feather’s shaft. And though the previous pterosaur fossils described in 2018 did have some preserved melanosomes, those were “middle-of-the-road shapes, little short ovoids,” McNamara says. In Tupandactylus, “for the first time we see melanosomes of different geometries” in the feathers. That all adds up to bright, colorful plumage. “To me, these fossils close the case. Pterosaurs really had feathers,” says Stephen Brusatte, a vertebrate paleontologist at the University of Edinburgh who was not involved in the study. “Not only were many famous dinosaurs actually big fluffballs,” he says, but so were many pterosaurs. Many dinosaurs, particularly theropod dinosaurs, also had colorful feathers (SN: 7/24/14). What this study shows is that feathers aren’t merely a bird thing, or even just a dinosaur thing, but that feathers evolved even deeper in time, Brusatte adds. And, as pterosaurs had wing membranes for flying, their feathers must have served other purposes, such as for insulation and communication. It’s possible that dinosaurs and pterosaurs evolved this colorful plumage independently, McNamara says. But the shared structural complexity of the pigments in both groups of reptiles makes it “much more likely that it was derived from a common ancestor in the early Triassic.” “That’s a big new implication,” says Michael Benton, a paleontologist at the University of Bristol in England. Benton, a coauthor on the 2018 paper, wrote a separate commentary on the new study in the same issue of Nature. If feathers arose in a common ancestor, Benton says, that would push back the origin of feathers by about 100 million years, to roughly 250 million years ago. And that might have other interesting implications, Benton writes. The early Triassic was a rough time for life on Earth; it was the aftermath of the mass extinction at the end of the Permian that killed off more than 90 percent of the planet’s species (SN: 12/6/18). If feathers did evolve during that time, the insulating fuzz, as well as warm-bloodedness, may have been part of an early arms race between reptilian mammal ancestors called synapsids and the pterosaur-dinosaur ancestor.
Booster shots against COVID-19 are once again on my mind. The U.S. Food and Drug Administration says that older people and immunocompromised people are eligible for a second booster shot provided it has been at least four months since their last shot. After I got over the shock of the FDA calling me “older” — meaning anyone 50 and up — I’ve been pondering whether to get a second booster (otherwise known as a fourth dose of an mRNA vaccine, or third dose of any vaccine if you initially got the Johnson & Johnson vaccine), and if so, when.
Peter, a 60-year-old acquaintance who asked me not to use his last name to protect his privacy, told me he’s going to get a second booster, but not now. He’s holding out for fall and hoping for a variant-specific version of the vaccine. Right now, he and his wife “are vaxxed out,” he says. And he worries that getting boosted too often could hurt his immune system’s ability to respond to new variants. “I just think it’s the law of diminishing returns,” he says.
Lots of scientists and policy makers are thinking about these issues, too. For instance, last week an advisory committee to the U.S. Centers for Disease Control and Prevention met to discuss boosters. And a bevy of studies about how well boosters work and how they affect the immune system have come out in recent weeks, some of them peer-reviewed, some still preliminary. In making my own decision, I wanted to know several things. First, does a second booster really provide additional protection from the coronavirus beyond what I got from my first booster (SN: 11/8/21)? Second, are there downsides to getting boosted again? And finally, if I’m going to do it, when should that be and which vaccine will I get?
To get a handle on the first question, I need to know how much protection the first booster actually gave me. I’m not immunocompromised, so there’s no reason for me to get an antibody test to see if I have enough of those defenders to fend off the coronavirus. I just have to assume that my immune system is behaving normally and that what’s true for others in my age group also goes for me.
How long does COVID-19 booster immunity last? Although the exact numbers vary, several studies have found that a third dose of the Pfizer COVID-19 vaccine gave higher levels of protection against the omicron variant than two doses did (SN: 3/1/22). But that protection wanes after a few months.
Data from Israel, where some people have been getting fourth doses for months, suggest that a second booster does indeed bolster protection, but again only temporarily. In health care workers who got a fourth dose, antibody levels shot up above levels achieved after the third jab, researchers reported April 7 in the New England Journal of Medicine. Vaccine effectiveness against infection was 30 percent with the Pfizer shot and 11 percent with Moderna. Both were better at preventing symptomatic disease, with Pfizer weighing in at 43 percent and Moderna at 31 percent. But those who did get infected produced high levels of the virus, suggesting they were contagious to others.
In a separate study published in the same journal, researchers looking at people 60 and older found that a fourth dose gave protection against both infection and severe disease, but the protection against infection began to decline after about five weeks.
There’s more data on protection against severe illness from a study of more than 11,000 people admitted for COVID-19 to a hospital or emergency department in the Kaiser Permanente Southern California health care system. At nine months after the second shot, two doses of the Pfizer vaccine were 31 percent effective at keeping people out of the emergency room with omicron, researchers reported April 22 in Lancet Respiratory Medicine. The shots were 41 percent effective at preventing more severe illness resulting in hospitalizations from the omicron variant.
The third dose (first booster) bumped the effectiveness way up to 85 percent against hospitalization and 77 percent against ER visits, the team found. But the effect was temporary. By three months after the booster, effectiveness had declined to 55 percent against hospitalization and 53 percent against emergency room visits. The same jump in protection and quick waning from the first booster has also been noted in the United Kingdom and Qatar.
It’s been about six months since my first booster shot, so any extra protection I got from it is probably gone by now. But will a fourth dose restore protection?
The CDC calculates that for every million people 50 and older who get a fourth dose of vaccine, 830 hospitalizations, 183 intensive care unit admissions and 85 deaths could be prevented. Those are impressive numbers, but many people think efforts should be focused more on getting still-unvaccinated people immunized instead of worrying about additional shots for the already vaxxed. CDC’s numbers support that. Because unvaccinated people are so vulnerable to the coronavirus, you would need to vaccinate just 135 people aged 50 and older with two shots to prevent one hospitalization. But already vaccinated people still have quite a bit of immunity, so you’d need to vaccinate 1,205 older people with a fourth dose to prevent one hospitalization. How does my health factor in? Of course, that’s data concerning populations. I and millions of others are trying to make individual calculations. “People need to make decisions based on their health condition as well as their exposure levels,” says Prakash Nagarkatti, an immunologist at the University of South Carolina School of Medicine Columbia. For instance, people whose jobs or other activities put them in contact with lots of people have higher exposure risks than someone who works at home. People who are older or have underlying health conditions, such as diabetes, obesity, high blood pressure, or lung, kidney, liver and heart diseases are all at higher risk. Those people might benefit from a shot now. “But if you’re 50 to 60 and very healthy, I don’t know if you need it right away,” Nagarkatti says. “You could maybe wait a few months.”
I’ve got some health risks that may make me more likely to get severely ill, and I have a couple of big events coming up this summer where I could get exposed to the virus. So getting boosted now to get a little bump in immunity that should last for a few months seems like a good idea. I’m also basing that decision about when to get a booster on what’s happening with the virus.
Case counts in my county are on the upswing. Nationally, BA.2.12.1, a potentially even wilier subvariant of the already slippery BA.2 omicron variant, is on the rise, making up almost 29 percent of cases in the week ending April 23. South Africa is experiencing a rise in cases caused by the omicron subvariants BA.4 and BA.5. It could be the start of a fifth wave of infection in that country, something researchers thought wouldn’t happen because so many people there were previously infected and vaccinated, Jacob Lemieux, an infectious disease researcher at Massachusetts General Hospital in Boston said April 26 in a news briefing. “It has the flavor of, ‘Here we go, again,’” he said. “So much for the idea of herd immunity.”
Are there any downsides to a second booster? But would I be harming my immune system if I get a booster shot now? Previous experience with vaccines against other viruses suggests repeated boosting isn’t always a good thing, Galit Alter, codirector of the Harvard University Center for AIDS Research said in the news briefing. For instance, in one HIV vaccine trial, people were boosted six times with the same protein. Each time their antibody levels went up, but the researchers found that the immune system was making nonfunctional, unhelpful antibodies that blocked the action of good ones. So far, that hasn’t happened with the COVID-19 vaccines, but it could be important to space out doses to prevent such a scenario.
Another worry for immunologists is original antigenic sin. That has nothing to do with apples, serpents and gardens. Instead it happens when the immune system sees a virus or portion of the virus for the first time and trains memory cells to make antibodies against the virus. The next time the person encounters the virus or another version of it, instead of adding to the antibody arsenal, it continues to make only those original antibodies.
With the coronavirus, though, “what’s happened is the opposite of antigenic sin,” says Michel Nussenzweig, an immunologist and Howard Hughes Medical Institute investigator at Rockefeller University in New York City. He and colleagues examined what happens to the immune response after a third dose of vaccine, focusing especially on very long-lived immune cells called memory B cells. Those memory cells still made new antibodies when they got a third look at the vaccine, Nussenzweig and colleagues reported April 21 in Nature. That wouldn’t happen if antigenic sin were a problem. And it’s great news since an ever-growing repertoire of antibodies may help defend against future variants.
A separate Nature Immunology study found that other immune cells called T cells also learn new tricks after a booster dose or a breakthrough infection. Those and other studies seem to indicate that getting a booster isn’t bad for my immune system and could help me against future variants.
Is it okay to mix and match COVID-19 booster shots? Now the question is, which booster to get? Mixing vaccines doesn’t seem to push the immune system toward making the unhelpful antibodies, Alter said. It “tantalizes the immune system with different flavors of vaccines, and seems to reawaken it,” she said. “Even mixing and matching mRNAs may be highly advantageous to the immune system.” She and colleagues found that the Moderna vaccine may make more IgA antibodies, the type that help protect mucous membranes in the nose, mouth and other slick surfaces in the body from infection, than the Pfizer vaccine does. Pfizer’s makes more of the IgM and IgG antibodies that circulate in the blood, data published March 29 in Science Translational Medicine show.
Since I got the Pfizer vaccine for my first three doses, it seems wise to shake things up with Moderna this time. I’ve already booked my shot.
As for Peter, after I laid out the evidence, he said he was convinced that he should probably get a shot now, as his doctor recommends. But he admitted he might just wait to see if Moderna comes out with an updated version of its vaccine.
What’s really needed, all the experts tell me, is to better understand how the immune system operates so researchers can build better vaccines with longer-lasting protection so we won’t be facing needles multiple times per year.
Roughly 400 million years before the founding father invented bifocals, the now extinct trilobite Dalmanitina socialis already had a superior version (SN: 2/2/74). Not only could the sea critter see things both near and far, it could also see both distances in focus at the same time — an ability that eludes most eyes and cameras.
Now, a new type of camera sees the world the way this trilobite did. Inspired by D. socialis’s eyes, the camera can simultaneously focus on two points anywhere between three centimeters and nearly two kilometers away, researchers report April 19 in Nature Communications. “In optics, there was a problem,” says Amit Agrawal, a physicist at the National Institute of Standards and Technology in Gaithersburg, Md. If you wanted to focus a single lens to two different points, you just simply could not do it, he says.
If a camera could see like a trilobite, Agrawal figured, it could capture high-quality images with higher depths of field. A high depth of field — the distance between the nearest and farthest points that a camera can bring into focus — is important for the relatively new technique of light-field photography, which uses many tiny lenses to produce 3-D photos.
To mimic the trilobite’s ability, the team constructed a metalens, a type of flat lens made up of millions of differently-sized rectangular nanopillars arranged like a cityscape — if skyscrapers were one two-hundredth the width of a human hair. The nanopillars act as obstacles that bend light in different ways depending on their shape, size and arrangement. The researchers arranged the pillars so some light traveled through one part of the lens and some light through another, creating two different focal points. To use the device in a light-field camera, the team then built an array of identical metalenses that could capture thousands of tiny images. When combined, the result is an image that’s in focus closeup and far away, but blurry in between. The blurry bits are then sharpened with a type of machine learning computer program.
Achieving a large depth of field can help the program recover depth information, says Ivo Ihrke, a computational imaging scientist at the University of Siegen in Germany who was not involved with this research. Standard images don’t contain information about the distances to objects in the photo, but 3-D images do. So the more depth information that can be captured, the better.
The trilobite approach isn’t the only way to boost the range of visual acuity. Other cameras using a different method have accomplished a similar depth of field, Ihrke says. For instance, a light-field camera made by the company Raytrix contains an array of tiny glass lenses of three different types that work in concert, with each type tailored to focus light from a particular distance. The trilobite way also uses an array of lenses, but all the lenses are the same, each one capable of doing all the depth-of-focus work on its own — which helps achieve a slightly higher resolution than using different types of lenses.
Regardless of how it’s done, all the recent advances in capturing depth with light-field cameras will improve imaging techniques that depend on that depth, Agrawal says. These techniques could someday help self-driving cars to track distances to other vehicles, for example, or Mars rovers to gauge distances to and sizes of landmarks in their vicinity.
Taking antibiotics in the first two years of life can prevent babies from developing a robust immune response to certain vaccines. The new finding provides another cautionary tale against overusing antibiotics, researchers say.
Babies get immunized in their first six months, and receive booster doses in their second year, to protect against certain infectious diseases. Antibiotic use during that time was associated with subpar immune responses to four vaccines babies receive to ward off whooping cough, polio and other diseases, researchers report online April 27 in Pediatrics.
And the more rounds of antibiotics a child received, the more antibody levels to the vaccines dropped below what’s considered protective. Levels induced by the primary series of shots for the polio, diphtheria-tetanus-pertussis, Haemophilus influenzae type b and pneumococcal vaccines fell 5 to 11 percent with each antibiotic course. In the children’s second year, antibody levels generated by booster shots of these vaccines dropped 12 to 21 percent per course. “If anyone needed yet another reason why overprescription of antibiotics is not a good thing, this paper offers that reason,” says immunologist Bali Pulendran of Stanford University School of Medicine, who was not involved in the study.
Taking antibiotics disrupts the population of bacteria that live in the gut. That’s well known, but researchers are still learning about how that disruption can affect a person’s health. The new study adds to evidence that diminishing the amount and diversity of gut bacteria impacts vaccination. In studies in mice, antibiotics hampered the immune system’s response to vaccines. And a small study in humans found that antibiotics dampened adults’ response to the flu vaccine in those whose prior immune memory for influenza had waned, Pulendran and colleagues reported in 2019.
The study in Pediatrics is the first to report an association between antibiotic use and compromised vaccine responses in children. Michael Pichichero, a pediatric infectious diseases specialist at the Rochester General Hospital Research Institute in New York, and colleagues collected blood samples taken from 560 children during routine visits with their pediatricians. Of those, 342 children had been prescribed close to 1,700 courses of antibiotics and 218 children had not gotten the drugs. The team analyzed whether antibody levels induced by the four vaccines met the threshold considered protective and found levels more often fell short for the kids who had gotten antibiotics.
The type and length of antibiotic treatment also made a difference. Broad spectrum drugs were associated with antibody levels below what is protective, while a more targeted antibiotic was not. Furthermore, a 10-day course, but not a five-day course, reduced vaccine-induced antibody levels.
The researchers didn’t look at whether children in the study with diminished antibody levels were more likely to develop vaccine-preventable diseases. But there has been concern about outbreaks of whooping cough, says Pichichero, which have occurred in the the United States despite vaccination (SN: 4/4/14). Perhaps antibiotic use can help explain these outbreaks, he says.
To see what kinds of changes are occurring in the gut bacteria, Pichichero and colleagues are beginning a study with a new group of children. The researchers will collect stool samples along with blood draws and antibiotic use records. They’d like to follow the children past age 5, beyond the time kids receive another round of booster shots, to learn whether antibiotics also interfere with this next opportunity to develop antibodies.
“Antibiotics are miracle medicines,” says Pichichero. “In no way does this study imply that children who need an antibiotic shouldn’t get it.” But if possible, it should be a narrowly targeted antibiotic for a shorter course, he says. Along with the risk of antibiotic resistance that comes with overuse of the drugs (SN: 1/24/22), the impact antibiotics could have on vaccine-induced immunity “has clinical implications for every individual child.”
The multitalented, Renaissance genius wrote down his “rule of trees” over 500 years ago. It described the way he thought that trees branch. Though it was a brilliant insight that helped him to draw realistic landscapes, Leonardo’s rule breaks down for many types of trees. Now, a new branching rule — dubbed “Leonardo-like” — works for virtually any leafy tree, researchers report in a paper accepted April 13 in Physical Review E.
“The older Leonardo rule describes the thickness of the branches, while the length of the branch was not taken into account,” says physicist Sergey Grigoriev of the Petersburg Nuclear Physics Institute in Gatchina, Russia. “Therefore, the description using the older rule is not complete.” Leonardo’s rule says that the thickness of a limb before it branches into smaller ones is the same as the combined thickness of the limbs sprouting from it (SN: 6/1/11). But according to Grigoriev and his colleagues, it’s the surface area that stays the same.
Using surface area as a guide, the new rule incorporates limb widths and lengths, and predicts that long branches end up being thinner than short ones. Unlike Leonardo’s guess, the updated rule works for slender birches as well as it does for sturdy oaks, the team reports.
The connection between the surface area of branches and overall tree structure shows that it’s the living, outer layers that guide tree structure, the researchers say. “The life of a tree flows according to the laws of conservation of area in two-dimensional space,” the authors write in their study, “as if the tree were a two-dimensional object.” In other words, it’s as if just two dimensions — the width of each limb and the distance between branchings on a limb — determine any tree’s structure. As a result, when trees are rendered in two dimensions in a painting or on a screen, the new rule describes them particularly well. The new Leonardo-like rule is an improvement, says Katherine McCulloh, a botanist at the University of Wisconsin–Madison who was not involved with this study. But she has her doubts about the Russian group’s rationale for it. In most trees, she says, the living portion extends much deeper than the thin surface layer.
“It’s really species-dependent, and even age-dependent,” McCulloh says. “A giant, old oak tree might have a centimeter of living wood … [but] there are certainly tropical tree species that have very deep sapwood and may have living wood for most of their cross sections.”
Still, the fact that the Leonardo-like rule appears to hold for many trees intrigues McCulloh. “To me, it drives home the question of why are [trees] conserving this geometry for their external tissue, and how is that related to the microscopic level differences that we observe in wood,” she says. “It’s a really interesting question.”
To test their rule, Grigoriev and colleagues took photographs of trees from a variety of species and analyzed the branches to confirm that the real-world patterns matched the predictions. The photos offer “a direct measurement of the characteristics of a tree without touching it, which can be important when dealing with a living object,” Grigoriev says.
Though the team hasn’t studied evergreens yet, the rule holds for all of the deciduous trees that the researchers have looked at. “We have applied our methodology to maple, linden, apple,” Grigoriev says, in addition to oak, birch and chestnut. “They show the same general structure and obey the Leonardo-like rule.”
While it’s possible to confirm the rule by measuring branches by hand, it would require climbing into trees and checking all the limbs — a risky exercise for trees and scientists alike. “Note,” the researchers write, “that not a single tree was harmed during these experiments.”