Category: Top Posts

What is Rewilding? Scientists’ New Roadmap For Restoring Ecosystems

By Lacy Schley | April 26, 2019 4:00 pm
A river runs through the green lands and forest of Anklamer Stadtbruch, Germany.

Peene river and flooded lands near Anklamer Stadtbruch, Germany. (Credit: Solvin Zankl/Rewilding Europe)

The human imprint on Earth is undeniable. Everywhere you look, you can find traces of our species’ short time on our roughly 4.5 billion-year-old planet. Often, those stamps are visible, like roads cutting through a forest or a patchwork of farmland covering what was once prairie. These marks can hinder the natural biodiversity of ecosystems, suffocating plant and animal species that once had a happy niche.

One way to undo some of this damage is to follow a conservation practice called rewilding, which some experts have criticized, often because of the concept’s ever-evolving nature. Now, the authors of a paper out in the journal Science have outlined what they say is a framework for rewilding that addresses those concern. It also identifies key ecosystem factors for experts to home in on.

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CATEGORIZED UNDER: Environment, Living World, Top Posts

Humanity’s Early Ancestors Were Upright Walking Apes

By Bridget Alex | April 26, 2019 3:00 pm
The partial skull and jaw fragments of Sahelanthropus tchadensis are the earliest hominin finds known. (Credit: Didier Descouens/Creative Commons 4.0)

The partial skull and jaw fragments of Sahelanthropus tchadensis are the earliest hominin finds known. (Credit: Didier Descouens/Creative Commons 4.0)

Roughly 8 million years ago, some apes stood up and started human evolution.

Okay, that’s not really what happened. But it is a fair characterization of the way scientists identify the oldest fossils likely to be human ancestors. Upright walking apes mark the start of the study of human evolution in many texts and classes.

That’s because bipedalism, or two-legged locomotion, was the first major evolutionary change in human ancestors, which is evident from bones. Other distinguishing features, like big brains, small molars and handcrafted stone tools, came millions of years later. Therefore, to find early members of our lineage, anthropologists look for ancient apes with skeletal traits indicative of habitual bipedalism — they regularly walked upright.

So who were the first bipedal apes and would you recognize them as relatives?

Hominins and Panins Part Ways

Homo sapiens and our closest living relatives, chimpanzees (Pan paniscus and Pan troglodytes), both descend from the same stock of African apes. Researchers often call this creature the last common ancestor or LCA (go back far enough and you’ll have an LCA with every organism on earth, but when anthropologists say “LCA” they’re usually referring to the chimp-human one). Sometime between 6 and 9 million years ago that population split into two lineages — one eventually leading to chimps and the other leading to humans. Hominins are any living or extinct species along the human branch after the LCA. So-called “panins” are any species along the chimp branch after the LCA.

A chimpanzee gazes into the forest canopy in Uganda. (Credit: Anton_Ivanov/shutterstock)

A chimpanzee gazes into the forest canopy in Uganda. (Credit: Anton_Ivanov/shutterstock)

We can estimate how long ago this panin-hominin split happened using the DNA differences between living humans and chimpanzees and a “molecular clock” rate of genetic change over time. Logically, the LCA should be slightly older.

And while these results tell us the LCA’s approximate age, no one has ever found fossils from this elusive population, and probably never will. Their skeletal remains probably wouldn’t preserve, assuming the creatures lived in tropical forests, as most living apes do today. The same goes for the original hominins, immediately after the split. But if scientists were to find fossils from this era, it would be difficult to determine whether they represented the LCA, panins or hominins. It’s likely these creatures were physically quite similar, especially their bones.

Bipedal Apes Stand Out

Within a million years or so after hominins split onto a separate evolutionary trajectory — a relatively short amount of evolutionary time — they started traveling around on two legs, rather than four. This new locomotive strategy came with some obvious changes in skeletal anatomy. Scientists have spotted bipedal traits in three fossil species that lived between 5 and 7 million years ago: Sahelanthropus tchadensis, Orrorin tugenensis and Ardipithecus kadabba. Each of them lived a few million years before Australopiths like the Lucy fossil, who undoubtedly were upright walking hominins.

An artist’s reconstruction of Lucy. The most famous Australopithecus afarensis, a species likely ancestral to our own, appears to have died from injuries sustained in a fall, according to new research. The study reignites an old debate about how the early hominin lived. (Credit: Wikimedia Commons.)

An artist’s reconstruction of Lucy. The most famous Australopithecus afarensis, a species likely ancestral to our own, appears to have died from injuries sustained in a fall, according to new research. The study reignites an old debate about how the early hominin lived. (Credit: Wikimedia Commons.)

Let’s focus on the oldest of the three and the top contender for earliest-known hominin, Sahelanthropus, estimated to be 6.8 to 7.2 million years old.

Remains from this species were unearthed between 2001 and 2002 by a team led by French paleontologist Michel Brunet. The scientific name Sahelanthropus tchadensis refers to the location of its discovery: in Sahel, the dry region south of the Sahara, and Chad, the country in central Africa. Although today the area is a barren scape of sand dunes, when Sahelanthropus lived it seems to have been a lakeside woodland, based on other animal fossils found in the same deposits, including monkeys, crocodiles and fish. Still, the location is surprising considering most early hominins come from the East African Rift Valley, over 1,500 miles away. It shows that our ancestors were more widespread at this time than previously thought, if Sahelanthropus is indeed a hominin.

The finds included several teeth, four lower jaw fragments and a crushed skull, which was later virtually reconstructed. In many ways these bones look like an ancient ape. Most obviously, the brain is a mere 360 to 370 mL, roughly the size of a chimpanzee. However, several features are hominin-like: The face is flatter, the canine teeth are smaller and the upper canines do not sharpen against the lower premolars (as they do in chimps).


Read more: Everything Worth Knowing About Human Origins


But, having only bones from the head, why do scientists think Sahelanthropus was bipedal? That brings us to the most relevant hominin-like feature, the position of the foramen magnum. This is the hole in the skull for the spine. In four-legged primates it’s found near the back of the head. In two-legged hominins, including Homo sapiens, it’s at the base of the skull, forming a near-right angle with the eye sockets. Both anatomies allow animals to point their eyes straight ahead without straining their necks, in the respective quadrapedal or bipedal stances.

You guessed it. The foramen magnum of Sahelanthropus is positioned like a hominin, suggesting the species spent more time on two legs than four.

But before you go honoring Sahelanthropus as your great-great… great grandparent, keep in mind two caveats. First, the species could be a hominin without being a direct ancestor of Homo sapiens. Rather, it could belong to a hominin side-branch that died off without continuous descendants to present-day humans.

Second, while many scholars and textbooks include Sahelanthropus as a bipedal hominin (or at least a “putative” one), some researchers disagree. Among other critiques, they argue that proving bipedalism requires lower limb bones, like the pelvis and femur. Allegedly a femur was found along with the skull (here, here, here), although it has not been published.

The remains remain to be seen.

CATEGORIZED UNDER: Living World, Top Posts

A Familiar Fungus May Help Us Defeat a Deadly One

candida albicans

The fungus Candida albicans causes candidiasis, or thrush. (Credit: Kateryna Kon/Shutterstock)

It seems like every few years there’s a virus or bacterium that threatens human health in a new way. But a new fungus that is a threat to humans? That doesn’t happen very often. That’s why we in the medical mycology community – the people who study dangerous fungi – are so intrigued and concerned by news reports about a new, deadly fungus called Candida auris.

C. auris is believed to have been first identified in 2009 in the ear canal of a patient in Japan, but has taken the medical community by surprise with its rapid spread across the globe in the last decade. C. auris has now been detected in about 20 countries and shows no evidence of stopping. Read More

Off Planet Hikes: The Backpacker’s Guide to the Solar System

By John Wenz | April 23, 2019 1:30 pm

Grab a spacesuit and a few months of provisions. We’re taking you on a tour of the Interplanetary Parks Service.

Saturn rises over Iapetus' ridge in this still from a computer-animated film released by NASA's Cassini team. (Credit: NASA)

The Ringed Planet rises over the strange ridge of its moon Iapetus in this still from a computer-animated film released by NASA’s Cassini team. (Credit: NASA)

Space is harsh. From damaging radiation to deadly gases and drastic temperature changes, pretty much any environment beyond Earth can kill you at a moment’s notice. Yet our cosmic backyard boasts natural wonders that rival the greatest found on terra firma.

And, one day, when we have the technology for deep-space rocket launches, suitable protective gear, enough provisions to last the average hiker — and any number of X factors — lucky adventurers may get to hike these solar system monuments.

It’s a far-future vision, a sort of Interplanetary Parks Service, where an extraterrestrial great outdoors beckons you toward adventure.

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CATEGORIZED UNDER: Space & Physics, Top Posts

How Does the Impossible Burger Look and Taste Like Real Beef?

By Mark R. O'Brian, University at Buffalo | April 22, 2019 1:58 pm
impossible burger

A sign advertising the Impossible Burger. (Credit: NTL Photography)

This is a guest post from Mark R. O’Brien, University at Buffalo, State University of New York. This piece reflects the views of the author.

People eat animals that eat plants. If we just eliminate that middle step and eat plants directly, we would diminish our carbon footprint, decrease agricultural land usage, eliminate health risks associated with red meat and alleviate ethical concerns over animal welfare. For many of us, the major hurdle to executing this plan is that meat tastes good. Really good. By contrast, a veggie burger tastes like, well, a veggie burger. It does not satisfy the craving because it does not look, smell or taste like beef. It does not bleed like beef.

Impossible Foods, a California-based company, seeks to change this by adding a plant product to their veggie burger with properties people normally associate with animals and give it the desired qualities of beef. The Impossible Burger has been sold in local restaurants since 2016 and is now expanding its market nationwide by teaming up with Burger King to create the Impossible Whopper. The Impossible Whopper is currently being test marketed in St. Louis, with plans to expand nationally if things go well there.

But what exactly is being added to this veggie burger? Does it make the burger less vegan? Is the additive from a GMO? Does it prevent the burger from being labeled organic?

I am a molecular biologist and biochemist interested in understanding how plants and bacteria interact with each other and with the environment, and how that relates to human health. This knowledge has been applied in a way that I did not anticipate to develop the Impossible Burger.

What On Earth Is Leghemoglobin?

The Impossible Burger includes an ingredient from soybeans called leghemoglobin, which is a protein that is chemically bound to a non-protein molecule called heme that gives leghemoglobin its blood-red color. In fact, a heme – an iron-containing molecule – is what gives blood and red meat their color. Leghemoglobin is evolutionarily related to animal myoglobin found in muscle and hemoglobin in blood, and serves to regulate oxygen supply to cells.

Heme gives the Impossible Burger the appearance, cooking aroma and taste of beef. I recruited a scientific colleague in St. Louis to try out the Impossible Whopper, and he could not distinguish it from its meaty counterpart. Although he was quick to qualify this by noting all of the other stuff on the Whopper may mask any differences.

soybean nodule

A cross section of a soybean root nodule. The red color is due to leghemoglobin. (Credit: CSIRO, CC BY)

So, why aren’t soybean plants red? Leghemoglobin is found in many legumes, hence its name, and is highly abundant within specialized structures on the roots called nodules. If you cut open a nodule with your thumbnail, you will see that it is very red due to leghemoglobin. The soybean nodule forms as a response to its interaction with the symbiotic bacterium Bradyrhizobium japonicum.

I suspect that Impossible Foods depicts a soybean without nodules on their website because people tend to be creeped out by bacteria even though Bradyrhizobium is beneficial.

My research group’s interest in the symbiotic relationship between the soybean and its bacterial sidekick Bradyrhizobium japonicum is motivated by the goal of reducing humanity’s carbon footprint, but not by creating palatable veggie burgers.

The bacteria within root nodules take nitrogen from the air and convert it to a nutrient form that the plant can use for growth and sustenance – a process called nitrogen fixation. The symbiosis lessens the reliance on chemical nitrogen fertilizers, which consume a lot of fossil fuel energy to manufacture, and which also pollute the water supply.

Some research groups are interested in extending the symbiosis by genetically engineering crops such as corn and wheat so that they can reap the benefits of nitrogen fixation, which only some plants, including legumes, can do now.

I am pleasantly surprised and a little amused that esoteric terms of my vocation such as heme and leghemoglobin have found their way into the public lexicon and on the wrapper of a fast-food sandwich.

soybeans

Root nodules occur on the roots of legumes associated with symbiotic nitrogen-fixing bacteria. Within legume nodules, nitrogen gas in the air is converted into ammonia. (Credit: Kelly Marken/Shutterstock)

Is Leghemoglobin Vegan? A Non-GMO? Organic?

Leghemoglobin is the ingredient that defines the Impossible Burger, but it is also the additive most closely scrutinized by those seeking assurances of it being organic, non-GMO or vegan.

The leghemoglobin used in the burgers comes from a genetically engineered yeast that harbors the DNA instructions from the soybean plant to manufacture the protein. Adding the soybean gene into the yeast then makes it a GMO. The U.S. Food and Drug Administration agrees with the “generally recognized as safe” (GRAS) designation of soybean leghemoglobin. Nevertheless, the U.S. Department of Agriculture prohibits the “organic” label for foods derived from genetically modified organisms. It is ironic that an innovation that may be eco-friendly and sustainable must be readily dismissed by groups that claim to share those goals.

Not all vegans are delighted by this new burger. Some insist that a GMO product cannot be vegan for various reasons, including animal testing of products such as leghemoglobin. In my view, the moral certitude of that position can be challenged because it does not take into account the cattle that are spared. Other vegans view GMOs as a solution to problems that are important to them.

Judging from its website, Impossible Foods is keenly aware of the constituencies that weigh in on their product. It includes a link describing how GMOs are saving civilization. But they also make the misleading claim that “Here at Impossible Foods, heme is made directly from plants.” In reality, it comes directly from yeast.

The commercialization of leghemoglobin represents an unanticipated consequence of inquiry into an interesting biological phenomenon. The benefits of scientific research are often unforeseen at the time of their discovery. Whether or not the Impossible Burger venture succeeds on a large scale remains to be seen, but surely food technology will continue to evolve to accommodate human needs as it has since the advent of agriculture 10,000 years ago.The Conversation

 

Mark R. O’Brian, Professor and Chair of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York. Mark R. O’Brian receives funding from the National Institutes of Health.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

H.M.S. Challenger: Humanity’s First Real Glimpse of the Deep Oceans

By Kate Golembiewski | April 19, 2019 2:48 pm
HMS Challenger

A painting of the HMS Challenger by William Frederick Mitchell. (Credit: Wikimedia Commons)

We know more about the surface of the moon than about the ocean floor. Scientists estimate that 91 percent of life under the sea hasn’t been discovered yet and more than 80 percent of the ocean has never been explored. What we do know about the ocean makes it almost more mysterious. It’s an alien landscape, complete with undersea mountain ranges and trenches deeper than Mount Everest is tall, home to a glorious nightmare carnival of weird, often glowing animals.

And most of what we know has only come to light in the last 150 years, starting with the expedition of HMS Challenger. From 1872 to 1876, the 200-foot-long warship was repurposed as a floating lab for the world’s first large-scale oceanographic expedition, circumnavigating the globe and dredging up samples of never-before-seen creatures from the ocean floor. The Challenger explorers brought to light thousands of new species and revealed the oceans to be a place of startling depths and untold wonders. Scientists today still rely on the Challenger findings to study everything from seashells to climate change. Read More

CATEGORIZED UNDER: Environment, Living World, Top Posts

The Quest For the Roots of Autism — and What It Says About Us All

By Emily Willingham | April 18, 2019 9:33 am
autism brain banner

(Credit: Brian Stauffer/brianstauffer.com)

As alarm grew over autism prevalence at the turn of this century, there was much public talk of a growing “epidemic.” That language has since softened, and it is now clear that many autistic people were there all along, their condition unrecognized until relatively recently.

But what is the cause? The emerging narrative today is that there is no single cause — rather, multiple factors, roughly sorted into the categories of genetics and environment, work together in complex ways. Because of this complexity and the hundreds of gene variants that have been implicated, developing human brains may follow many possible paths to arrive at a place on the autism spectrum.

And this may help explain something true about autism: It varies greatly from one person to the next.

As clinicians view it, autism involves communication deficits and formulaic, repetitive behaviors that present obstacles to establishing conventional relationships. The soft borders of that definition — where does communication difficulty cross over into communication deficit? — suggest blurred margins between people who are diagnosed with autism and those who approach, but never quite cross, the line into diagnostic territory.

Those who do have diagnoses display behaviors on a continuum of intensity. Their use of spoken language ranges from not speaking at all to being hyperverbal. They can have a unique interest in the finer details of window blinds or an intense but more socially tolerated fascination with dinosaurs. As with many human behaviors, each feature exists on a spectrum, and these spectra blend in a person to create what clinicians call autism.

By pinpointing risk-associated genes and uncovering their roles, studying the roots of autism also is providing new insights into the development of all human brains, autistic or not. Here is a taste of what we now know, and what we don’t, about autism’s causes — and what that search is teaching us about everybody’s neurology.

They Know It When They See It

Despite the many and varied threads that may interweave to cause autism, the condition is largely identifiable. What clinicians are really saying when they diagnose autism, says James McPartland, a clinical psychologist at the Yale Child Study Center, is that they see a recognizable, if broadly defined, constellation of behaviors. “So really, there is something true about autism, and everyone who meets the diagnosis of autism shows these kinds of behaviors.”

Autism Diagnosis

US rates of autism diagnoses have increased over the years, as shown in this graph. Numbers are averages of prevalence among 8-year-old children from several reporting sites of the CDC’s Autism and Developmental Disabilities Monitoring Network. Not all sites reported in each year shown, and the ranges can be broad (for example, in 2000 the average was 6.7 per 1,000 children, but the range from different reporting sites was 4.5 to 9.9). At least part of the increase is due to heightened awareness and shifting diagnostic criteria

At the same time, the subtle differences in how each autistic person manifests the telltale features make it highly individual, says Pauline Chaste, a child psychiatrist at Inserm U 894, the Centre de Psychiatrie et Neurosciences, in Paris. “We describe a specific behavior that exists — that kind of social impairment and rigidity. You can have more or less of it, but it definitely exists.”

The more or less of autism could trace, in part, to the types of gene variants that contribute to it in a given person. Some of these variants have a big effect by themselves, while others make tiny contributions, and any autistic person could have their own unique mix of both. One thing seems clear: Though there may be something true about autism, as McPartland puts it, the existence of “one true autism gene” or even one gene for each autism feature is unlikely.

Instead, there will be patterns of gene combinations and the results they produce, says epidemiologist Elise Robinson of the Harvard T.H. Chan School of Public Health and an associate member of the Broad Institute. People who have both autism and intellectual disability, for example, tend to have more big-effect gene mutations than people with autism alone.

Facial Communication

Looking for these contributing gene variants isn’t simply an exercise in scientific curiosity or in finding potential targets for drug treatments. Because most of these genes direct how human brains develop and nerve cells communicate, learning about how they lead to autism can also reveal a lot about how everyone’s brain works.

For example, a key autism trait is atypical social behaviors, such as, sometimes, not focusing on “social” facial features like the eyes. Although the tendency to look into another person’s eyes seems like something we might learn simply from being around other people, autism research has revealed that genes underlie the instinct.

In a 2017 study, the authors first showed that identical twins are similar in how they look at a video with social content, such as faces. When viewing the same video, the identical twin pairs shifted their eyes with the same timing and focused on the same things far more than did two non-identical siblings or unrelated children. The fact that almost all twin pairs shared this tendency suggests solid genetic underpinnings for the behavior.

Having established a strong genetic contribution to this trait, the investigators, from Emory University and the Marcus Autism Center in Georgia and Washington University in St. Louis, then showed that the tendency to look at the eye and mouth areas of a human face is decreased in autistic children. They concluded that while not all of the inclination to look at certain parts of a face is genetic, much of it is.

Twin studies like this are powerful tools for evaluating how much genes dictate a feature, and such investigations reveal that the genetic contribution to autism is substantial. Autism also tends to cluster in non-twin family members: One in five infants who has an older sibling with autism also develops it.

Genetic Determinants

Overall, genetics accounts for about 70 to 80 percent of factors contributing to autism, says neurologist Daniel Geschwind, director of UCLA’s autism research and treatment center. By comparison, a condition like depression has an underlying genetic contribution of about 50 percent, he says. Alessandro Gozzi, neuroscientist and group leader at the Istituto Italiano di Tecnologia, weights the power of genes even more, placing the shared diagnosis rate between twins as high as 95 percent, depending on how strict the diagnostic boundaries are. But regardless of the precise value, he says that the “wide consensus” among autism researchers is that genetics is a powerful determinant of autism.

Going the next step — finding the specific genes involved — is a monumental task. It’s also one that yields dividends for understanding brain function more broadly.

The candidate gene variants are today very numerous, but a few stand out for their potential to exert a large effect. Chaste cites fragile X syndrome and Rett syndrome as examples — both are genetic conditions (termed syndromes because they are defined by a cluster of traits) that are tied to variants of a single gene or chromosome region and are closely associated with autism.

Fragile X Syndrome

Children with fragile X syndrome carry X chromosomes with an abnormality at the tip of one of the chromosome arms, as shown in this illustration (normal X on the left, abnormal X on the right). This affects a gene called FMR1, which carries instructions for a protein important for brain activity, such that little or none of the protein is made. Fragile X is associated with a range of developmental disabilities, often including autism. (Credit: Soleil Nordic/Shhutterstock)

The gene linked to fragile X syndrome lies on the X chromosome. Its name, FMR1, is easily forgettable, but the effects of its variants are not. Studies on the causes of fragile X reveal that the protein this gene encodes, FMRP, acts as a cellular shuttle for RNA molecules that are crucial for nerve-cell communication and plasticity of connections in the brain. In people with fragile X, cells don’t produce the protein, or make very little of it. The FMR1 variants underlying fragile X are the most common known genetic cause of intellectual disability and are implicated in 1 to 6 percent of autism cases.

Like FMR1, the genetic changes involved in Rett syndrome also affect brain development. A gene called methyl CpG binding protein 2, or MECP2, oversees the activity of many brain-related genes, turning them off or on. Because of this pivotal role for MECP2, mutations that affect its function can lead to broad effects. Some of the resulting features look so much like autism that Rett syndrome was categorized as an autism spectrum disorder until 2013.

Other genetic syndromes also include autism as a feature. Some are caused by variants in a gene called SHANK3 which, like most genes implicated in autism, is involved in brain development and function. The protein that it encodes helps to coax nerve extensions to form and take shape so that a nerve cell can communicate with others. The SHANK3 protein also provides a physical scaffold for those cells to link up. In populations of people with mutations that prevent SHANK3 protein production or who are missing the segment of chromosome 22 that contains the gene, most will have autism or Phelan-McDermid syndrome, which often includes autism.

Yet another syndrome arises from the loss or duplication of a chunk of chromosome 16. Researchers linked this chromosomal change to autism in studies comparing the DNA of people with and without the condition, singling out sequence alterations found only in autistic participants.

Despite their clear ties to autism, these syndromes are rare. “Collectively, they are found in about 5 percent of the total population of patients with autism,” Gozzi says. That leaves a great deal to explain.

Inheritance on a Spectrum

So where do the other autistic people come from, genetically speaking? Robinson says that their genetics don’t neatly fall into two types of buckets, of either a few genes with big effects or many genes with small effects. “It’s been well established at this point that it’s not either–or,” she says.

In fact, says Gozzi, varying combinations of big-effect mutations and lots of different, smaller-effect ones could explain the wide spectrum of differences observed among autistic people. The evidence supports such a range, he says: everything from a few heavy-hitting variations in some people, to an additive dose from many variants in others, and with overlap between the two patterns in still others.

autism proteins

Scientists have identified many genetic variants that are linked to a raised risk of autism. Often, these variants affect the function of genes involved in the development and activity of brain cells. Here are four such genes, each of which carries instructions for a protein (called MECP2, PTEN, FMRP and SHANK3) that has an important function in neurons. Studies like this, of autism’s genetic causes, are teaching scientists more about brain biology.

Geschwind adds yet another layer of complexity: the role of the cellular environment that all the other gene variants in a person create, known as the background effect. For example, someone could have a mutation conferring high risk that is either enhanced or diminished by the background input from other genes not directly related to autism, to create a gradation of autism intensity.

Environmental Influences

When researchers speak of environmental inputs to traits, diseases and disorders, they are referring to everything from pollutants in the air to subtle perturbations inside cells to cues from other cells. Finding such causative candidates for autism generally involves epidemiological studies that look for correlations between autism rates in a population and an environmental factor of interest.

These connections aren’t easy to locate. In the case of genes, if a study involves enough people, even rare genetic differences that make small contributions to autism can often be plucked from the pile. Not so for environmental influences if their effects are significant but small, says Robinson. Within those epidemiological studies, you have to be able to detect that slight signal and assess its power against the larger, background noise of lots of other variations in the cell, body or outside environment that you might not even be aware of and might not be relevant. “We don’t live in a simple, single-exposure world,” says Kristen Lyall, an epidemiologist at Drexel University in Philadelphia.

And even when a connection is made, its basis is still just math. That is certainly the first step in evaluating a link between an environmental factor and a condition such as autism: As one thing goes up, does the other follow? But two things that track together don’t necessarily share a biological association. (One of the silliest examples to illustrate how misleading correlation can be is how tightly the number of people killed by venomous spiders each year tracks with the number of letters in the winning word of the same year’s Scripps National Spelling Bee.)

In the case of genetic studies, gene changes with tiny effects can still be considered plausible if their usual role relates to brain function in some way. Environmental factors aren’t as well catalogued, measured and tracked. But the better epidemiological studies do look for correlations with credible and pre-identified factors of interest (so, not Scripps Spelling Bee words).

For feasibility’s sake, work on environmental factors in autism has tended to focus on inputs that have broad effects on brain development. Robinson points to extreme preterm birth, which is related to many kinds of neurodevelopmental disorders — autism among them.

Eventually, studies can add up to connect dots and arrive at a plausible story of cause and effect. For example, along with preterm birth, air pollution also has been linked to autism risk. Another recent study found that when oil and power plants close down, preterm births in the region drop. It’s therefore a reasonable hypothesis that very preterm birth operates as an intermediate between air pollution exposure and autism.

spectrum news interactive map

View this interactive map created by the team at Spectrum News. The map displays autism prevalence studies conducted at different times and places around the world. Each dot refers to a study. Clicking on the dots reveals granular information such as the country, sample size, years studied, autism prevalence, age of children, diagnostic criteria and sex ratio. (Credit SpectrumNews.org)

Lyall believes that prenatal exposures to environmental pollutants that can behave like hormones are particularly strong candidates for involvement in autism risk. These chemicals, collectively known as endocrine-disrupting compounds, include pesticides and even heavy metals, and they are pretty much everywhere — in air, land, water, food and us.

Some research suggests, for example, that exposure to the endocrine disruptor mercury in air pollution raises autism odds. The studies are few and the data haven’t overwhelmingly showed increases in risk, Lyall acknowledges, “but I think that it’s an interesting and important area for future research given the lack of regulation around these chemicals, their ubiquity in the environment and their known adverse effects on broader neurodevelopment.”

Researchers have also homed in on plausible biological bases for a couple of other potential environmental effects. Gozzi points to animal studies, mostly in mice, that bolster human work linking autism in a child with prenatal exposure to a mother’s ramped-up immune responses as a result of infections. Again, Gozzi stresses that the findings are far from definitive, and most studies involving humans have focused on infections severe enough to require hospitalization.

Another unearthed link is to paternal age at conception: Studies find that autism risk increases with the age of the father, usually starting in the thirties or forties, although the age range and magnitude of the increase vary among different studies. The cells that give rise to sperm tend to accumulate new mutations over the years, so the sperm contain sequence changes that pass to offspring but aren’t present in the father’s own body cells. Some of these changes involve regions or genes already implicated in autism risk. Sperm also show changes in the chemical tagging of DNA that controls the activity of genes.

sperm

One of the more plausible environmental links to autism is age of the father. Over a man’s lifetime, genetic changes accrue in the cells that give rise to sperm, shown here in a scanning electron microscopy image. Among them are alterations in genes that can raise the risk of autism. (Credit: Sebastian Kaulitzki/Shutterstock)

Establishing environmental cause unequivocally is almost impossible, because of ethical constraints. It’s one thing to examine blood or tissue samples for genetic variants that track with autism diagnoses. It’s another thing entirely to manipulate factors to see if they induce autism or not. No one’s going to deliberately infect a pregnant woman or have a group of men specifically delay fatherhood just to test how these factors influence autism odds.

Researchers instead are stuck finding correlations between these factors and then looking at available measures, such as changes in gene activity, accrual of mutations over the lifespan and studies of autism-like behavior in animal models. And as they look at these associations, they often make discoveries that are relevant beyond autism — ones that have now been extended to studies of schizophrenia, aging and even human evolution. The link between autism and having an older father, for example, has led to studies examining how changes in sperm over time affect brain development in later generations.

While most environmental candidates remain just that — candidates — Lyall says emphatically that one factor is out of the running: vaccines. “That’s pretty conclusively been shown to have no association with autism,” she says, noting the numerous large epidemiological studies that have reached that conclusion.

The settled vaccine question is a small point of clarity in an otherwise blurred landscape of autism cause-and-effect research. Every new finding seems to open up yet more pathways, some leading toward autism, and some toward broader revelations about the brain and how hormones, the immune system, the air we breathe and more add up to make their mark on neural development. The network of genetic and environmental factors that converge and diverge to produce autism may reflect not only the multiplicity of ways of being autistic — but also, more broadly, of being human.

 

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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NASA’s Twins Study: How Spaceflight (Temporarily) Changes the Body

By Jake Parks | April 17, 2019 11:00 am
Retired astronaut Mark Kelly (left) cracks a slight smile while posing with his identical twin brother, astronaut Scott Kelly (right). As part of NASA's Twins Study, Scott took a long trip to space, while Mark remained on Earth. Researchers then monitored how their bodies reacted to their differing environments. (Credit: NASA)

Retired astronaut Mark Kelly (left) poses with his identical twin brother, astronaut Scott Kelly (right). As part of NASA’s Twins Study, Scott took a long trip to space, while Mark remained on Earth. Researchers then monitored how their bodies reacted to their differing environments. (Credit: NASA)

Brothers compete. So in 2016, when astronaut Scott Kelly returned to Earth after spending a year in space, it must have really annoyed his identical twin brother — retired astronaut Mark Kelly — that Scott was two inches taller than when he left. However, Scott’s temporary increase in height was not the only thing that changed during his trip.

As part of NASA’s Twins Study, while Scott was in space, Mark went about his daily life on Earth. Over the course of the year-long mission, researchers tracked changes in both brothers’ biological markers to pinpoint any variances. Because the twins share the same genetic code, researchers reasoned that any observed differences could tentatively — though not definitively — be linked to Scott’s time aboard the International Space Station (ISS). This allowed them to take advantage of a unique opportunity and explore how an extended stay in space may impact the human body.

Based on their results, which were published last week in the journal Sciencespaceflight can definitely trigger changes in the human body. But the vast majority of these changes disappear within just a few short months of returning to Earth. Read More

Meet the Snake That Hunts Birds With a Spider On Its Tail

By Troy Farah | April 16, 2019 5:06 pm
The spider-tailed viper. (Credit: reptiles4all/shutterstock)

The spider-tailed viper. (Credit: reptiles4all/shutterstock)

When Steven Anderson first examined a specimen of the Iranian spider-tailed viper, he, of course, noticed the arachnid-shaped lump on the dead snake’s tail. It was 1970, and the herpetologist was at the Field Museum in Chicago examining what the museum assumed to be a Persian horned viper, a snake common throughout the Middle East.

But this one had such a bizarre growth on its tail. To Anderson, a biologist who studies reptiles in Southeast Asia, it resembled “an oval knob-like structure,” with long scales resembling appendages or legs. But with only a single specimen, it was impossible to say if this tail modification was due to genes or something else, like a parasite or cancerous growth. For nearly four decades, the snake lurked in the back of Anderson’s mind.

“All of a sudden, a few years ago this Iranian amateur naturalist Hamid Bostanchi found another one,” says Anderson, now an emeritus professor at the University of the Pacific in Stockton, California. “And so then I realized there is something going on here.”

spider-tailed viper

The spider-tailed viper and its strange tail. (Credit: Omid Mozaffari/Wikimedia Commons)

Unbeknownst to Anderson, the snake’s weird accessory was a caudal lure — an aggressive form of animal mimicry where a tail evolves to resemble the prey of another organism. When something like, say a frog, tries to gobble this fake food, it becomes food itself. In this case, the spider-tailed viper uses its caudal lure to capture birds.

Bostanchi’s second specimen was also dead and badly preserved — but the tails were similar. In 2006, Anderson and his colleagues published evidence that this was indeed a new snake species. They called it Pseudocerastes urarachnoides, meaning “fake horned with a spider-like tail.” Because the newer snake had a half-digested bird in its stomach, they believed that the viper might use the weird spider-shaped bulge on its tail as a way to attract prey.

Many animals, including a species of shark and some lizards, waggle their tails as a decoy that trick prey into coming near. Other snakes, especially vipers, employ this technique as well — but the spider-tailed viper stood in a league of its own. Still, to see just how deceptive the snake actually was, the researchers would have to find one alive in the wild.

Spider-Tails Snatch Birds

It’s easy to miss the spider-tailed viper. Its skin is rippled with rough, corrugated scales that resemble the glittering hills of gypsum and limestone where it is often found. These are the Zagros Mountains and the snake blends right into this range that bleeds into Turkey and Kurdistan, although it’s only been found in western Iran. We still don’t know much about the snake, but you often won’t see one until it strikes, which can happen in less than a second.

In April 2008, a team tracked a pair of the vipers in the Ilam Province in Western Iran, and watched as one slithered into a cracked rock. When they illuminated the burrow with a torch, the snake hissed back. After cleaving the rock apart with a crowbar, they pinned the snake to the ground with a forked stick and captured it.

spider-tailed viper

A close-up of the spider-like tail. (Credit: Bostanchi et al.)

The viper was transported to a cage in a lab that resembled the semi-arid land of scrub and forest the snakes normally inhabit. A few birds were released in the enclosure, and a video camera set up. The researchers watched as the snake gently swooshed its tail along the ground, the swollen bulb and frilly scales perfectly recreating the skittering motions of a tasty spider. The illusion is eerily accurate; several birds became instant meals after trying to attack what appeared to be a meal for them. Anderson and his team were right.

“It’s one of those things that makes me feel awe in the power of natural selection,” says Kurt Schwenk, an evolutionary biology professor at the University of Connecticut, who specializes in the feeding and chemosensory systems of lizards and snakes. “The evolution of luring is more complex than contrasting color or simple shaking — the movement is precisely adapted to duplicate prey movement frequencies, amplitudes and directions, at least in specialized cases.”

It’s not uncommon for many snakes to do something similar with their tails to deceive prey. The common death adder of Australia buries itself in leaves, then writhes its tail like a worm to catch lizards and frogs. The Saharan sand viper conceals itself in sand with only its eyes and nostrils visible. When a lizard comes along, it sticks its tail out from the dirt, making it squirm like an insect larvae.

The behavior — and the elaborate body modifications that can accompany it — likely arose from a behavior common to many reptiles, Schwenk explains. When they are about to strike prey, any lizards and snakes enter a hyper-alert pose. The reptiles will focus their vision by cocking their heads to the side, arching their backs, and certain species will commonly vibrate their tail tip against the ground. This can distract the prey, which will shift its attention to the vibrating tail, ignoring the reptile mouth opening to grab them.

“This simple pattern leads to selection causing refining of the tail form and motion to be more attractive to such prey by more accurately mimicking actual prey movements,” Schwenk theorizes. “The other ancestral condition that could have led to caudal luring, or possibly an intermediate step in the process, is the use of tail vibration for prey distraction rather than for luring.”

Indeed, those most famous tail shakers, the rattlesnakes, sometimes also use caudal luring. For example, juvenile dusky pygmy rattlesnakes, whose rattle is so small it barely makes noise, wiggle their tails to attract prey. The behavior, in fact, may be key to how rattlesnakes evolved their distinctive rears, although this theory is somewhat controversial.

“Like many other apparently simple things in biology, there is a lot of complexity to caudal luring that has barely been explored,” Schwenk says. “Much of this has been considered in a piecemeal fashion, but a thorough review and synthesis … has not been attempted.”

The spider-tailed viper’s distinctive caboose might also be leading it into trouble. Not long after this snake was first formally described, it became a matter of concern for the Iranians, Anderson says. Zoos and professional collectors have been looking for spider-tailed vipers, but the Iranian government has been reluctant to give any up, which Anderson says has likely led to poaching.

“I’m sure it’s worth a lot of money,” Anderson says. “You can pay thousands of dollars just for odd mutations of various snakes … There’s people who just collect venomous snakes because they like to live dangerously, I guess. I’m sure there’s a demand out there.”

Luring From Both Ends

Spider-tailed vipers may be the flashiest caudal lurers, but the behavior is so common it’s presumed other snakes probably use it, too — it just hasn’t been recorded yet. There are even several snakes that use so-called lingual luring, such as the mangrove saltmarsh, which catches fish by looping its tongue in a way that likely resembles fish food. But only one snake uses both its tail and its tongue to lure prey: the African puff adder.

This literal tongue-twister was discovered by Xavier Glaudas and Graham Alexander, two researchers at the University of the Witwatersrand in South Africa. They surgically implanted 86 puff adders with radio transmitters and set them loose near where they were captured in the Dinokeng Game Reserve.

For two years, they used fixed cameras to film the snakes, ending up with 193 continuous days of footage. They noticed snakes used their tails as lures, but the researchers observed that wasn’t the only trick up their nonexistent sleeves. They were using their tongues, too. And they were using them for a totally different prey, suggesting they can tell their targets apart by species. This kind of behavioral segmentation had never been observed before, which the researchers say is odd given how common the puff adder is throughout Africa and is frequently kept in captivity.

“We observed puff adders lingual luring only in the presence of amphibians, indicating that they have the ability to discriminate between prey types,” the researchers wrote, adding, “[This] indicates that snakes may have higher cognitive abilities than those usually afforded to them.”

Schwenk, though, downplays suggestions that caudal luring means that snakes must necessarily be more clever than thought. “This requires sophisticated sensory processing, but not a lot in the way of cognition or higher level processing,” he says. “Don’t get me wrong — it’s amazing! But snakes are very unlikely to be aware of their prey as other thinking entities.”

In other words, snakes may have no conscious idea why they wiggle their tails about suggestively just that it helps them eat. The spider-tailed viper probably doesn’t realize what its tail resembles or that birds eat spiders. Nonetheless, studying caudal lures is a fascinating case study of the transformative powers of natural selection, as well as a reminder to look again if you ever happen to see a spider while hiking in western Iran.

CATEGORIZED UNDER: Living World, Top Posts

Running Made Us Human: How We Evolved to Run Marathons

By Bridget Alex | April 12, 2019 4:54 pm
boston marathon

Runners taking part in the Boston Marathon. (Credit: Marcio Jose Bastos Silva/Shutterstock)

This Monday the 123rd annual Boston Marathon will take place, with an expected 30,000 participants and a half million spectators. The top finishers should complete the grueling 26.2-mile course in just over 2 hours by clocking a pace of under five minutes per mile.

I know. It’s painful to imagine. Most of us couldn’t maintain that speed for one mile — forget 26 of them.

But take heart, recreational runners of the world. Your endurance abilities are actually extraordinary, when compared to the rest of the animal kingdom. True, other creatures boast greater strength, agility and raw speed. Homo sapiens are relatively pathetic athletes by all measures. But when it comes to long distance locomotion, we’re remarkable. After 15 minutes of sustained running, fit humans can outlast nearly all mammals, especially in hot weather.

That’s more than a useful tip for betting on a hypothetical Interspecies Marathon (or the actual Man vs. Horse Marathon). Rather, it’s the basis for an important idea in human evolution studies.

Let’s call it the “running made us human” hypothesis: According to some scientists, distance running was key to our ancestors’ evolutionary success. They say adaptations for endurance allowed early members of the genus Homo to hunt long before the invention of complex weapons. Regular access to meat spurred brain growth, and ultimately, humanity as we know it.

How Running Made Us Human

The role of running in human evolution has been most intensely investigated by Daniel Lieberman, a Harvard University evolutionary biologist and 9-time Boston Marathon runner. Lieberman and others hypothesize that roughly 2 million years ago Homo erectus ancestors, armed with sharpened sticks and stones, were able to kill prey by persistence hunting. This strategy, practiced in some recent forager societies, entails pursing a tasty herbivore in midday sun until the animal collapses from exhaustion and heat stroke. Hunters can then finish it off with simple weapons.

This scenario could solve a major puzzle in human evolution: how did Homo erectus get meat? Researchers assume these hominins hunted because archaeological sites, between 2 and 1 million years old, have yielded plenty of butchered animal bones. Yet stone tools back then were hefty implements, like the Acheulean handaxe — technology better suited for processing carcasses than impaling moving targets. Projectile weapons, like the bow and arrow, were probably not invented until the past 80,000 years. It’s hard to imagine handaxe-wielding hominins catching much prey, especially since they would have been competing with lions, hyena and other African carnivores.

But persistence hunting might have been the secret. To avoid overheating, most predators forgo hunting during the hottest hours. Humans — and potentially earlier Homo species — can handle heat thanks to adaptations such as furless bodies and increased sweat glands. Around high noon while most carnivores napped, human ancestors could have hunted by persistently chasing and tracking prey.

Proof of Their Persistence

Ethnographic studies have noted persistence hunts in some recent hunter-gatherer societies, including Kalahari Bushmen, Aboriginal Australians and Native American groups in the American Southwest and Mexico. A 2006 Current Anthropology paper provided the first real data on the matter, based on 10 persistence hunts in the Kalahari of Botswana (one was filmed for David Attenborough’s docu-series Life of Mammals).

These hunts, which were successful five out of 10 times, lasted up to 6 hours and covered 10-20 miles in temperatures over 100°F. During the chases, prey would sprint ahead in short bursts punctuated by resting bouts. Meanwhile the humans slowly and steadily pursued, averaging paces of 9.6 to 15 minutes per mile. Though the hunters periodically lost sight of the animal, signs like footprints and indented grass indicated its path.

The ethnographic studies prove that persistence hunting works, but only in hot, grassland-like environments. Even then, the practice is rare among hunter-gatherers today. To some anthropologists, these points are enough to refute the hypothesis. They argue that persistence hunting is too uncommon, and effective in too few habitats, to have been an important force in human evolution. Others counter that just because the strategy is rare today it doesn’t mean that was the case 2 million years in our ancestral environments.

Homo erectus as Marathon Runners?

So let’s say that human ancestors did run down their prey. What is the evidence that Homo erectus was the first species to embrace this strategy?

In a 2004 Nature paper Lieberman and biologist Dennis Bramble, now an emeritus professor at the University of Utah, identified skeletal features in hominin fossils that indicate running abilities. These include a narrow pelvis, short toes, expanded attachment for the gluteus maximus (butt muscle) and large semicircular canals, fluid-filled ear chambers that help us stay balanced while moving.

Most of these adaptations for running appeared around 2 million years ago in the species Homo erectus, rather than earlier hominins such as the Australopiths. This suggests H. erectus was the first endurance athlete in our lineage.

But certainly not the last, as the Boston Marathon’s 30,000 competitors will remind you.

CATEGORIZED UNDER: Living World, Top Posts
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