November 25, 2013
Once upon a time, scientists thought that the human brain was a rigid, predictable organ, not tremendously different from the lungs or liver. Based on a person’s genetics, it developed in a predetermined way, endowing an individual with a particular level of learning capabilities, problem-solving abilities and baseline intelligence.
Now, though, as part of emerging research into brain plasticity, neuroscientists are recognizing that the brain is a responsive, constantly evolving organ that can change at both the cellular and large-scale levels due to environmental influences and experiences. Much of this research is hopeful: It’s shown how in people with impaired vision, for instance, areas of the brain normally devoted to processing sights can be repurposed to analyze sound.
Over the past few months, though, a series of studies have emphasized that the brain can change for worse, as well as for the better. A child’s brain, not surprisingly, is especially vulnerable to such effects—and this research has shown that growing up in difficult circumstances dictated by poverty can wreak damage to a child’s cognitive skills that last a lifetime.
An October study by researchers from the University of Michigan, for instance, used fMRI (functional magnetic resonance imaging)—which detects blood flow in various areas of the brain as a reflection of brain activity—to study the regulation of emotions in young adults who were part of a long-term study on poverty. They compared a participant’s family income at age 9 (based on survey data collected at the time) with his or her current neural activity in different brain regions, and found that those who grew up in poverty showed increased activity in the amygdala (believed to be involved in anxiety, fear and emotional disorders) and decreased activity in the prefrontal cortex (which limits the influence of the amygdala, putting long-term decision making over impulse) when the participants were shown emotionally-upsetting images.
It’s impossible to know for sure, but the researchers suspect that a range of chronic stresses that can accompany growing up in poverty—things like crowding, noise, violence, family turmoil or separation—impact the development of the brain in childhood and adolescence, potentially explaining this correlation.
Another October study, meanwhile, took a more basic approach, examining the relationship between nurturing during childhood and the growth of brain tissue in children between the ages of six and 12. In it, Washington University in St. Louis researchers found that among the 145 children studied, those whose parents had poor nurturing skills had slowed growth in white matter, grey matter and the volumes of several different areas of the brain involved with learning skills and coping with stress. Based on the differing growth rates between children who resembled each other in terms of other key factors, it seemed as though the experience of growing up with adults with less nurturing skills effectively set back their mental development a year or two. And impoverished parents, they found, were more likely to have poor nurturing skills.
Sure, attempting to objectively evaluate the parenting styles of the adults in this study might be a bit heavy-handed, but the study identified chronic stresses experienced by the children as a key element as well: Children who grew up in poverty but had fewer stressful life events (as part of a larger program, they’d gone through annual assessments from the age of three onward) demonstrated smaller reductions in neural development.
Others have even looked into very specific behavioral effects of poverty. A recent Northwestern University study found a link that children with lower socioeconomic status tended to have less efficient auditory processing abilities—that is, the area of their brains responsible for processing sound showed more response to distracting noise and less activity as a result of a speaker’s voice than control participants. This might be an effect, the researchers say, of the known correlation between low income and the amount of noise exposure in urban populations.
Of course, most of these are limited by the very nature of a longitudinal study in that they’re correlations, rather than causations—ethics aside, it’s impossible to actively alter a person’s childhood circumstances in a controlled manner and then check the results, so researchers are forced to observe what happens in the real world and draw conclusions. Additionally, in most of these cases, it’s unknown whether the effects are temporary or permanent—whether children exposed to poverty are permanently left behind their peers, or whether they’re able to catch up if given the chance.
But the fact that correlations between poverty and altered mental function when stressed has been repeatedly observed across a range of study designs, circumstances and research groups makes it likely that these effects aren’t aberrations. Additionally, even if they are temporary effects that can be resolved by changing a child’s environment, there’s other recent research that dishearteningly reveals a neurological mechanism that helps to perpetuate poverty, by making it difficult for parent to make choices that change these circumstances.
An August study in Science found that being preoccupied with the all-consuming concerns of poverty—struggling to pay medical bills, for instance—taxes the brain, leaving less extra bandwidth to solve complex cognitive problems and harming long-term decision making ability. In a pair of study groups (shoppers in a New Jersey mall and sugar cane farmers in rural India), simply getting the participants thinking about economic problems (asking them what they’d do if they had to pay $1500 to repair their car, for instance) caused them to perform more poorly on tests that measure IQ and impulse control than otherwise.
The bandwidth problem they identified is temporary, not permanent, but it does explain how making the difficult decisions that might allow someone to get ahead are harder for a person immersed in poverty. It also highlights yet another stressor for parents seeking to ensure that their children escape poverty—they might be inadvertently contributing to an environment that keeps their children from rising above their circumstances.
November 22, 2013
One afternoon in October 2005, neuroscientist James Fallon was looking at brain scans of serial killers. As part of a research project at UC Irvine, he was sifting through thousands of PET scans to find anatomical patterns in the brain that correlated with psychopathic tendencies in the real world.
“I was looking at many scans, scans of murderers mixed in with schizophrenics, depressives and other, normal brains,” he says. “Out of serendipity, I was also doing a study on Alzheimer’s and as part of that, had brain scans from me and everyone in my family right on my desk.”
“I got to the bottom of the stack, and saw this scan that was obviously pathological,” he says, noting that it showed low activity in certain areas of the frontal and temporal lobes linked to empathy, morality and self-control. Knowing that it belonged to a member of his family, Fallon checked his lab’s PET machine for an error (it was working perfectly fine) and then decided he simply had to break the blinding that prevented him from knowing whose brain was pictured. When he looked up the code, he was greeted by an unsettling revelation: the psychopathic brain pictured in the scan was his own.
Many of us would hide this discovery and never tell a soul, out of fear or embarrassment of being labeled a psychopath. Perhaps because boldness and disinhibition are noted psychopathic tendencies, Fallon has gone all in towards the opposite direction, telling the world about his finding in a TED Talk, an NPR interview and now a new book published last month, The Psychopath Inside. In it, Fallon seeks to reconcile how he—a happily married family man—could demonstrate the same anatomical patterns that marked the minds of serial killers.
“I’ve never killed anybody, or raped anyone,” he says. “So the first thing I thought was that maybe my hypothesis was wrong, and that these brain areas are not reflective of psychopathy or murderous behavior.”
But when he underwent a series of genetic tests, he got more bad news. “I had all these high-risk alleles for aggression, violence and low empathy,” he says, such as a variant of the MAO-A gene that has been linked with aggressive behavior. Eventually, based on further neurological and behavioral research into psychopathy, he decided he was indeed a psychopath—just a relatively good kind, what he and others call a “pro-social psychopath,” someone who has difficulty feeling true empathy for others but still keeps his behavior roughly within socially-acceptable bounds.
It wasn’t entirely a shock to Fallon, as he’d always been aware that he was someone especially motivated by power and manipulating others, he says. Additionally, his family line included seven alleged murderers, including Lizzie Borden, infamously accused of killing her father and stepmother in 1892.
But the fact that a person with the genes and brain of a psychopath could end up a non-violent, stable and successful scientist made Fallon reconsider the ambiguity of the term. Psychopathy, after all, doesn’t appear as a formal diagnosis in the Diagnostic and Statistical Manual of Mental Disorders in part because it encompasses such a wide range of symptoms. Not all psychopaths kill; some, like Fallon, exhibit other sorts of psychopathic behavior.
“I’m obnoxiously competitive. I won’t let my grandchildren win games. I’m kind of an asshole, and I do jerky things that piss people off,” he says. “But while I’m aggressive, but my aggression is sublimated. I’d rather beat someone in an argument than beat them up.”
Why has Fallon been able to temper his behavior, while other people with similar genetics and brain turn violent and end up in prison? Fallon was once a self-proclaimed genetic determinist, but his views on the influence of genes on behavior have evolved. He now believes that his childhood helped prevent him from heading down a scarier path.
“I was loved, and that protected me,” he says. Partly as a result of a series of miscarriages that preceded his birth, he was given an especially heavy amount of attention from his parents, and he thinks that played a key role.
This corresponds to recent research: His particular allele for a serotonin transporter protein present in the brain, for example, is believed to put him at higher risk for psychopathic tendencies. But further analysis has shown that it can affect the development of the ventromedial prefrontal cortex (the area with characteristically low activity in psychopaths) in complex ways: It can open up the region to be more significantly affected by environmental influences, and so a positive (or negative) childhood is especially pivotal in determining behavioral outcomes.
Of course, there’s also a third ingredient, in addition to genetics and environment: free will. “Since finding all this out and looking into it, I’ve made an effort to try to change my behavior,” Fallon says. “I’ve more consciously been doing things that are considered ‘the right thing to do,’ and thinking more about other people’s feelings.”
But he added, “At the same time, I’m not doing this because I’m suddenly nice, I’m doing it because of pride—because I want to show to everyone and myself that I can pull it off.”
November 21, 2013
Over the course of 1700 miles, they sampled the water for small pieces of plastic more than 100 times. Every single time, they found a high concentration of tiny plastic particles. “It doesn’t look like a garbage dump. It looks like beautiful ocean,” Miriam Goldstein, the chief scientist of the vessel sent by Scripps Institution of Oceanography, said afterward. “But then when you put the nets in the water, you see all the little pieces.”
In the years since, a lot of public attention has been justifiably paid to the physical effects of this debris on animals’ bodies. Nearly all of the dead albatrosses sampled on Midway island, for instance, were found to have stomachs filled with plastic objects that likely killed them.
But surprisingly little attention has been paid to the more insidious chemical consequences of this plastic on food webs—including our own. “We’d look over the bow of the boat and try to count how many visible pieces of plastic were there, but eventually, we got to the point that there were so many pieces that we simply couldn’t count them,” says Chelsea Rochman, who was aboard the expedition’s Scripps vessel and is now a PhD student at San Diego State University. “And one time, I was standing there and thinking about how they’re small enough that many organisms can eat them, and the toxins in them, and at that point I suddenly got goosebumps and had to sit down.”
“This problem is completely different from how it’s portrayed,” she remembers thinking. “And, from my perspective, potentially much worse.”
In the years since, Rochman has shown how plastics can absorb dangerous water-borne toxins, such as industrial byproducts like PCB (a coolant) and PBDE (a flame retardant). Consequently, even plastics that contain no toxic substances themselves, such as polyethylene—the most widely used plastic, found in packaging and tons of other products—can serve as a medium for poisons to coalesce from the marine environment.
But what happens to these toxin-saturated plastics when they’re eaten by small fish? In a study published today in Scientific Reports, Rochman and colleagues fill in the picture, showing that the toxins readily transfer to small fish through plastics they ingest and cause liver stress.This is an unsettling development, given that we already know such pollutants concentrate further the more you move up the food chain, from these fish to the larger predatory fish that we eat on a regular basis.
In the study, researchers soaked small pellets of polyethylene in the waters of San Diego Bay for three months, then tested them and discovered that they’d absorbed toxins leached into the water from nearby industrial and military activities. Next, they put the pollution-soaked pellets in tanks (at concentrations lower than those found in the Great Pacific garbage patch) with a small, roughly one-inch-long species called Japanese rice fish. As a control, they also exposed some of the fish to virgin plastic pellets that hadn’t marinated in the Bay, and a third group of fish got no plastic in their tanks at all.
Researchers still aren’t sure why, but many small fish species will eat these sort of small plastic particles—perhaps because, when covered in bacteria, they resemble food, or perhaps because the fish simply aren’t very selective about what they put in their mouths. In either case, over the course of two months, the fish in the experiment consumed many plastic particles, and their health suffered as a result.
“We saw significantly greater concentrations of many toxic chemicals in the fish that were fed the plastic that had been in the ocean, compared to the fish that got either clean plastic or no plastic at all,” Rochman says. “So, is plastic a vector for these chemicals to transfer to fish or to our food chain? We’re now fairly confident that the answer is yes.”
These chemicals, of course, directly affected the fishes’ health. When the researchers examined the tiny creatures’ livers (which filter out toxins in the blood) they found that the animals exposed to the San Diego Bay-soaked plastic had significantly more indications of physiological stress: 74 percent showed severe depletion of glycogen, an energy store (compared to 46 percent of fish who’d eaten virgin plastic and zero percent of those not exposed to plastic), and 11 percent exhibited widespread death of individual liver cells. By contrast, the fish in the other treatments showed no widespread death of liver cells. One particular plastic-fed fish had even developed a liver tumor during the experimental period.
All this is bad news for the entire food webs that rest upon these small fish, which include us. “If these small fish are eating the plastic directly and getting exposed to these chemicals, and then a bigger fish comes up and eat five of them, they’re getting five times the dose, and then the next fish—say, a tuna—eats five of those and they have twenty-five times the dose,” Rochman explains. “This is called biomagnification, and it’s very well-known and well-understood.”
This is the same reason why the EPA advises people to limit their consumption of large predatory fish like tuna. Plastic pollution, whether found in high concentrations in the Great Pacific garbage patch or in the waters surrounding any coastal city, appears to be central to the problem, serving as a vehicle that carries toxins into the food chain in the first place.
November 20, 2013
In 1834, Charles Darwin discovered a strange animal during his exploration of Chile’s southern coast. The creature, a small frog, was shaped like a leaf with a pointed nose, but appeared puffed up as if had been blown full of air, like a balloon. As it turned out, those fat male frogs hadn’t been gorging themselves on too many mosquitoes, but instead were enacting duties that earn them distinction as one of nature’s best dads. They were incubating several of their squirming babies in their vocal sac.
These peculiar animals, known as Darwin’s frogs, are today divided into two species, one that occurs in northern Chile, and another that lives in southern Chile and Argentina. When a female Darwin’s frogs lay her eggs, her mate keep a careful watch until the tadpoles hatch. The eager dad then swallows his young, allowing the babies to safely grow within his vocal sac until they turn into frogs and are ready to strike out on their own. Here, you can see a dutiful papa frog seemingly vomit up his living young:
Northerly Darwin’s frogs, however, have not been spotted in the wild since 1980. Researchers are nearly certain the species is extinct. Meanwhile, their southerly cousins are in steep decline and seem to be heading down extinction’s death row as well. For once, it seems that humans are not entirely to blame for these biodiversity disasters (unlike the western black rhino, which bit the dust a couple years ago after enduring decades of poaching for its valuable but medicinally worthless horn, used as an ingredient in traditional Chinese medicine). Instead, the deadly amphibian chytrid fungus, researchers report today in PLoS One, is likely to blame.
The chytrid fungus has popped up in amphibians in North and South America, Europe and Australia. The fungus infects the animals’ skin, preventing them from absorbing water and other nutrients. The fungus can rapidly decimate amphibian populations it comes into contact with, and has been called (pdf) “the worst infectious disease ever recorded among vertebrates in terms of the number of species impacted, and its propensity to drive them to extinction” by the International Union for Conservation of Nature.
To identify chytrid as the likely culprit behind the Darwin’s frogs disappearance and decline, researchers from Chile, the UK and Germany conducted a bit of historical sleuthing. They dug up hundreds of archived specimens of Darwin’s frogs and closely related species dating from 1835 until 1989, and then tested them all for fungal spores (the problematic form of chytrid fungus was first recorded in the 1930s and reached epidemic-status around 1993, but researchers aren’t certain of when it first emerged). They also took around 800 skin swabs between 2008 and 2012 from 26 populations of still-living southern Darwin’s frogs and other similar frog species that live nearby.
Six of the old museum specimens, all collected between 1970 and 1978–just before the northern Darwin’s frog’s disappearance–tested positive for the disease. More than 12 percent of the living frogs tested positive for the fungal spores. In places where the Darwin’s frog has gone extinct or is experiencing drastic declines, however, rates of infection jumped to 30 percent in other amphibian species. Although these events don’t prove that the fungus killed the northern Darwin’s frogs and are now wiping out the southern species, the researchers strongly suspect that is the case.
Despite evidence that the disease has spread throughout the Darwin’s frog’s range, the researchers are not giving up on hope to save one of the world’s greatest dads from extinction. “We may have already lost one species, the Northern Darwin’s frog, but we cannot risk losing the other one,” Claudio Soto-Azat, the study’s lead author, said in a statement. ”There is still time to protect this incredible species.”
About a month ago, I suffered my first-ever concussion, when I was (accidentally) kicked in the head playing ultimate frisbee. Over the next few weeks, I dutifully followed medical instructions to avoid intense physical activity. For a little while, I noticed a bit of mental fogginess—I had trouble remembering words and staying focused—but eventually, these symptoms faded away, and I now feel essentially the same as before.
Except, it turns out, that if doctors were to look inside my head using a type of brain scanning technology called diffusion MRI, there’s a good chance that they’d notice lingering abnormalities in the gray matter of my left prefrontal cortex. These abnormalities, in fact, could persist up to four months after the injury, even after my behavioral symptoms are long gone. This news, from a study published today in the journal Neurology, underlines just how much more prolonged and complex the healing process from even a mild concussion is than we’ve previously thought.
“These results suggest that there are potentially two different modes of recovery for concussion, with the memory, thinking and behavioral symptoms improving more quickly than the physiological injuries in the brain,” Andrew R. Mayer, a neuroscientist at the University of New Mexico and lead author of the study, explained in a press statement issued with the paper.
The abnormalities that Mayer’s team detected, they say, are so subtle that they can’t be detected by standard MRI or CT scans. Instead, they found them using the diffusion MRI technology, which measures the movement of molecules (mostly water) through different areas of the brain, reflecting the tissue’s underlying architecture and structure.
Mayer and colleagues performed these scans on 26 people who’d suffered mild concussions four months earlier, in addition to scanning them 14 days after the injuries. They also gave them behavioral and memory tests at both times, and then compared all the results to 26 healthy participants.
In the initial round, the people with concussions performed slightly worse than the healthy participants on tests that measure memory and attention, consistent with prior findings on concussions. Using the diffusion MRI, the researchers also found structural changes in the prefrontal cortex of both hemispheres of the subjects with recent concussions.
Four months later, the behavioral tests showed that the gap between the two groups had significantly narrowed, and the concussion patients’ self-reported symptoms were less significant too. But interestingly, when they averaged the scans of all 26 people, the neurological changes were still detectable in the left hemisphere of their brains.
What were these abnormalities? Specifically, their gray matter—the squishy outer layer of brain tissue in the cortex—showed ten percent more fractional anisotrophy (FA) than the controls’. This value is a measure of how likely water molecules located in this area are to travel in one direction, along the same axis, rather than scattering in all directions. It’s believed to reflect the density and thickness of neurons: the thicker and denser these brain cells are, the more likely water molecules are to flow in the direction of the cells’ fibers.
In other words, in this one particular area of the brain, people who’d suffered concussions four months earlier may have denser, thicker neurons than before. But it’s hard to say what these abnormalities reflect, and if they’re even a bad thing. As I found during my semi-obsessive post-concussion research, there are bigger gaps in scientists’ understanding of the brain than any other part of our bodies, and knowledge of the healing process after a concussion is no exception.
The scientists speculate that the increased FA could be a lingering effect of edema (the accumulation of fluid with the brain as a result of concussion) or gliosis (a change in the shape of the brain’s structural cells, rather than neurons).
But it’s even possible that this increased FA could be a sign of healing. A 2012 study found that in people who’d suffered mild concussions, higher FA scores right after the injury were correlated with fewer post-concussive symptoms, such as memory loss, a year after the injury. Similarly, a study published this past summer found a correlation between low FA scores and the incidence of severe symptoms right after a concussion. Interestingly, the researchers noted similar correlations in studies of Alzheimer’s—people with the disease tend to also demonstrate lower FA scores, in the same areas of the brain as those with most severe concussions, underscoring the link to memory performance.
If that’s the case, then the thicker, denser neurons in the brain of people with concussions might be something like the tough scabs that form after your skin gets burned, scabs that linger long after the pain has dissipated. As Mayer points out, during the recovery process after a burn “reported symptoms like pain are greatly reduced before the body is finished healing, when the tissue scabs.” In a similar way, the symptoms of a concussion—memory loss and difficulty maintaining attention, for instance—may disappear after a few weeks, while the nerve tissue continues forming its own type of scab four months later.
It’s possible that this scab, though, might be vulnerable. Scientific research is increasingly revealing just how devastating the impact of repeated concussions—the type suffered by football players—can be in the long term. “These findings may have important implications about when it is truly safe to resume physical activities that could produce a second concussion, potentially further injuring an already vulnerable brain,” Mayer said. The fact that the brain’s healing process is more prolonged than previously assumed could help explain why returning to the field a few weeks after a concussion and experiencing another is so dangerous.