Author: Christie Wilcox

Dr. Christie Wilcox is a science writer based in the greater Seattle area. Her bylines include National Geographic, Popular Science, and Quanta. Her debut book, Venomous, released August 2016 (Scientific American/FSG Books). To learn more about her life and work, check out her webpage or follow her on Twitter, Google+, or Facebook.

Is Climate Change To Blame For This Year’s West Nile Outbreak?

According to the Centers for Disease Control, there have been over 1100 reported cases of West Nile virus disease in the US this year, including 42 deaths. If these numbers seem high, they are – in fact, it’s the highest number of reported cases since West Nile was first detected in the US in 1999, and West Nile season has just begun. Given that the peak of West Nile epidemics generally occurs in mid August, and it takes a few weeks for people to fall ill, the CDC expects that number to rise dramatically. But why now?

Though the CDC doesn’t have an official response to that question, the director of the CDC’s Vector-Borne Infectious Disease Division said that ‘unusually warm weather’ may be to blame. So far, 2012 is the hottest year on record in the United States according to the National Climatic Data Center, with record-breaking temperatures and drought a national norm. It’s likely no coincidence that some of the states hit hardest by West Nile are also feeling the brunt of the heat. More than half of cases have been reported from Texas alone, where the scorching heat has left only 12% of the state drought-free. Fifteen heat records were broken in Texas just last week on August 13th.

The heat waves, droughts and other weather events are the direct effects of climate change say leading scientists. As NASA researcher James Hansen explained in a recent Washington Post editorial, “our analysis shows that, for the extreme hot weather of the recent past, there is virtually no explanation other than climate change.” He says that the European heat wave of 2003, the Russian heat wave of 2010 and catastrophic droughts in Texas and Oklahoma last year are all the repercussions of climate change. Confidently, he adds that “once the data are gathered in a few weeks’ time, it’s likely that the same will be true for the extremely hot summer the United States is suffering through right now.”

The fact that the worst US West Nile epidemic in history happens to be occurring during what will likely prove to be the hottest summer on record doesn’t surprise epidemiologists. They have been predicting the effects of climate change on West Nile for over a decade. If they’re right, the US is only headed for worse epidemics.

What Is West Nile Virus?

To understand the connection between climate change and disease, you first have to understand West Nile. First discovered in Uganda in 1937, it is what epidemiologists call a zoonotic disease, that is, one that is transmitted from animals to humans, not from humans to humans. West Nile virus mainly infects birds, which are the virus’ true hosts. We humans (as well as livestock and other animals) are accidental casualties of a bird-mosquito disease. West Nile travels via mosquitos that pick up virus particles when they bite infected birds. These particles stay in the mosquito’s salivary glands, and are transmitted into the next host when the mosquito feeds. Humans and other mammals don’t have high enough numbers of viruses in their blood for mosquitos to pick up the infection from them, which is why we are considered “dead end hosts”.

As anyone who hangs out outdoors is aware, mosquito populations pick up in the summer, when environmental conditions are just right for feeding and breeding. So, too, does West Nile. Though it sounds scary, West Nile is a fairly mild infection. Around 80% of people infected show no symptoms at all. Most of the remaining 20% will present with fever, headache and body aches, and nausea which can last for a few days or several weeks, much like getting the flu. Of course, like any illness, West Nile has the potential to be very serious. Less than 1% of infections result in a condition called West Nile meningitis or encephalitis, where the virus infects the spinal cord and even brain. Severe symptoms include high fever, headache, neck stiffness, a decreased level of consciousness (sometimes approaching near-coma), tremors, convulsions, weakness, numbness and paralysis. West Nile meningitis or encephalitis can last several weeks, and the neurological effects can be permanent. As with the flu, the elderly and anyone with a compromised immune system is at a higher risk of severe symptoms and death.

Currently there are no vaccines or antivirals with which to prevent and control West Nile virus in humans. The best offense in the case of West Nile is a good defense. To protect against illness, don’t get bitten by mosquitos in the first place. Wear protective clothing, use nets and screens, and wear insect repellent whenever you are in an area where people have gotten sick. The CDC has updated maps on where cases have occurred, though if you’re unsure if your area is suspect, caution is better than regret. Of course, if you look at that map, only one state has no West Nile activity: congrats, Vermont, on so far eluding the epidemic.

Turning Up The Heat

Higher temperatures bolster the chances of infection on many fronts. Temperature has a profound effect starting at the source: the mosquito. Studies have found that mosquitos pick up the virus more readily in higher temperatures. Higher temperatures also increase the likelihood of transmission, so the hotter it is outside, the more likely a mosquito that bites an infected bird will carry the virus and the more likely it will pass it along to an unwitting human host. In the United States, epicenters of transmission have been linked closely to above-average summer temperatures. In particular, the strain of West Nile in the US spreads better during heat waves, and the spread of West Nile westward was correlated with unseasonable warmth. High temperatures are also to blame for the virus jumping from one species of mosquito to a much more urban-loving one, leading to outbreaks across the US.

Though you might think that the droughts associated with heat waves would slow down mosquitos, it turns out to be the exact opposite. That’s because the main mosquito now involved in West Nile transmission, city-loving Culex pipiens, actually thrives in drought conditions. C. pipiens tends to breed underground in water that sits in city drains. During a drought, these pools become rich in organic material that C. pipiens needs to survive, whereas rainfall flushes the drains and dilutes the nutrients in the standing pools. Drought also has a negative effect on C. pipiens’ predators like frogs and dragonflies – and where there are less predators, there are more mosquitos. To add to the problem, drought tends to cause birds to cluster around water resources, making them easy pickings for hungry mosquitos and upping transmission rates.

The Real Inconvenient Truth

I can’t sum it up any better than Paul Epstein did in his 2001 review of climate change and West Nile:

“We have good evidence that the conditions that amplify the life cycle of the disease are mild winters coupled with prolonged droughts and heat waves—the

long-term extreme weather phenomena associated with climate change.”

While some politicians are hesitant to accept the scientific consensus of climate change, West Nile is more than happy to reap the rewards of our poor environmental choices. It’s not the only disease benefitting from our flagrant CO2 emissions; epidemiologists predict that many vector-borne diseases, including deadly ones like malaria and dengue fever, will increase in incidence world wide as global temperatures rise.

While the CDC is hesitant to blame this year’s West Nile outbreak on climate change directly, the science is clear. Record-breaking incidences of West Nile are strongly linked to global climate patterns and the direct effects of carbon dioxide emissions. Climate change isn’t just going to screw with the environment, it will continue to have devastating public health implications. In addition to better mosquito control and virus surveillance, we need to focus our efforts on reducing and reversing climate change if we want to protect our health and our well-being.

Image credits: Disease collage by Visual Mozart / purchased from ImageZoo; Transmission cycle image from the CDC website; mosquito danger image from petrafler / 123RF Stock Photo

Even A Few Years Of Music Training Benefits The Brain

Music has a remarkable ability to affect and manipulate how we feel. Simply listening to songs we like stimulates the brain’s reward system, creating feelings of pleasure and comfort. But music goes beyond our hearts to our minds, shaping how we think. Scientific evidence suggests that even a little music training when we’re young can shape how brains develop, improving the ability to differentiate sounds and speech.

With education funding constantly on the rocks and tough economic times tightening many parents’ budgets, students often end up with only a few years of music education. Studies to date have focused on neurological benefits of sustained music training, and found many upsides. For example, researchers have found that musicians are better able to process foreign languages because of their ability to hear differences in pitch, and have incredible abilities to detect speech in noise. But what about the kids who only get sparse musical tutelage? Does picking up an instrument for a few years have any benefits?

The answer from a study just published in the Journal of Neuroscience is a resounding yes. The team of researchers from Northwestern University’s Auditory Neuroscience Laboratory tested the responses of forty-five adults to different complex sounds ranging in pitch. The adults were grouped based on how much music training they had as children, either having no experience, one to five years of training, or six to eleven years of music instruction.

Music training had a profound impact on the way the study subjects’ brains responded to sounds. The people who had studied music, even if only for a few years, had more robust neural processing of the different test sounds. Most importantly, though, the adults with music training were more effective at pulling out the fundamental frequency, or lowest frequency sound, of the test noises.

“The way you hear sound today is dictated by the experiences with sound you’ve had up until today,” explained co-author and lab head Nina Kraus. As she and her colleague wrote in an article for Nature, “akin to physical exercise and its impact on body fitness, music is a resource that tones the brain for auditory fitness.”

Bulking up the auditory brain has non-musical implications. The ability to differentiate fundamental frequencies is critical for perceiving speech, and is an integral part of how we recognize and process sounds in complex and noisy environments. Thus childhood music instruction has strong linguistic benefits and improves performance on everyday listening tasks. Since we live in an inherently noisy world, the better we are at focusing on sound and perceiving different sounds, the better. This can be particularly important for children with learning disorders or those for whom English is a second language.

There is a body of research that suggests music training not only improves hearing, it bolsters a suite of brain functions. Musically trained kids do better in school, with stronger reading skills, increased math abilities, and higher general intelligence scores. Music even seems to improve social development, as people believe music helps them be better team players and have higher self-esteem. “Based on what we already know about the ways that music helps shape the brain, the study suggests that short-term music lessons may enhance lifelong listening and learning,” said Kraus. “Our research captures a much larger section of the population with implications for educational policy makers and the development of auditory training programs that can generate long-lasting positive outcomes.”

The importance of music education is something to consider, given that election season is in full swing. According to a recent White House report, more than 300,000 education jobs have been lost since the “end” of the recession in 2009 – 7,000 were lost last month alone. As schools lose funding, arts and extracurricular programs are often first on the chopping block, meaning less music education for the nation’s youth. Given the scientific evidence supporting the importance of music both neurologically and educationally, the loss of music education seems particularly painful. Perhaps as we head to the polls this season, we should give even more thought as to how our choices of elected officials might affect the education system in this country and the brains of the children who are its future.

Citation: Skoe, E. & Kraus, N. (2012). A Little Goes a Long Way: How the Adult Brain Is Shaped by Musical Training in Childhood, Journal of Neuroscience, 32 (34) 11510. DOI: 10.1523/JNEUROSCI.1949-12.2012

Music brain image from the Department of Homeland Security

Stressed Men Like Bigger Butts

Weight is a big issue in America. More than half of Americans are unhappy with their weight, spending 33 billion on dieting and weight loss programs and products every year. This obsession starts younger than we’d like to admit, as 80 percent of 10 year old girls will say they are on a diet. But whether you count the millions dissatisfied with their looks, the percentage trying to lose weight, or the billions wasted on pills and fad diets, the message is the same: being the ideal weight matters, and it matters a lot.

But what is the ideal weight? Doctors say somewhere between a BMI of 20 to 25. Looking at runway models, you’d think it was just this side of starving, as the stick figures that grace our catwalks have an average BMI of only 16. Ask the average man and… well, actually, that will depend on a number of things, including his mood.

A number of factors affect what weight a guy prefers a woman to be, and evolution is to blame. For a long time, scientists have believed that attractiveness is really just our way of interpreting how good a person will be as a mate, starting with genes. “Good-genes theory posits that human judgments of physical attractiveness, particularly in mating contexts, have evolved to respond in part to heritable cues associated with health,” explains Jason Weeden and John Sabini in their scientific review of the topic. As the theory goes, the better someone’s genetic makeup, the more symmetrical and ideal their body becomes.

But being a good potential mate isn’t just dictated by our DNA. Current health status, ability to provide for young, and other variable factors also play a role in how fit a person is as a potential husband or wife. A woman can have all the good genes in the world, for example, but if she’s starving, she won’t have the fat reserves to feed a child, let alone survive pregnancy. So, it makes sense that in times of hardship, men would prefer women better equipped to handle times of scarcity – and by better equipped, I mean with fat reserves.

“A primary function of adipose tissue is the storage of calories, which in turn suggests that body fat is a reliable predictor of food availability,” explain co-authors Viren Swami and Martin J. Tovée in their PLoS ONE paper released today. “In situations marked by resource uncertainty, therefore, individuals should come to idealise heavier individuals.”

But do times of hardship actually shift body size preferences? Science to date has supported this hypothesis, as hungrier and poorer men prefer larger women. But what Swami and Tovée wanted to know was whether the stress had to be related to food scarcity. What about other kinds of stress? Does stress in general shift preferences, or only hardship?

So, the team took college men and had half of them perform a stressful task unrelated to food or money which raised their cortisol levels. They then asked the stressed and unstressed men to take a look at some images of women, and rate their attractiveness. The images varied in body size, from underweight to obese. Finally, they recorded the participants own weight, height, and hunger status, as controlling variables.

The results were clear. The stressed out guys preferred a larger body size than their relaxed counterparts – but that was not all. “Men experiencing stress not only perceive a heavier female body size as maximally attractive, but also more positively perceive heavier female body sizes and have a wider range of body sizes considered physically attractive,” explain the authors.

The wider range of preference was notably one-sided. “This difference was driven by the shift in the experimental group’s upper limit of attractive female bodies,” the authors write. “While there was no significant difference in the lower end of the range, the experimental group appear to have shifted the maximum cut-off for attractive bodies at higher BMIs, which resulted in their wider attractiveness range.”

Why did the stressed-out guys prefer weightier women? Because, evolutionarily, more weight means better able to survive in tough times. “In contexts marked by prolonged stress as a result of resource deprivation, individuals may idealise larger body sizes because such body types are associated with better ability to handle environmental threat.” These results are consistent with cross-cultural studies on attractiveness, which found that ideal body size varies by socioeconomic status and resource scarcity. In other words, our evolutionary past has affected why different cultures throughout the world have very different ideals when it comes to beauty.

Nowadays, of course, the connection between body weight and ability to survive is uncoupled. Unlike our ancestors, Americans generally don’t worry about having the fat reserves to chase down their next meal. Modern medical technologies and an abundance of high calorie foods have made surviving and reproducing much easier. But, this evolutionary leftover does raise some interesting questions about modern life, too. What are the full implications of an economic depression, for example? I wonder if cutting taxes affects what size girls end up with modeling contracts, or if the association goes both ways, and girls on a diet become less picky. More research will have to determine if stressed women prefer larger men, too, or how chronic stress instead of acute stress affects attractiveness ratings.
 

Citation: Swami V, Tovée MJ (2012) The Impact of Psychological Stress on Men’s Judgements of Female Body Size. PLoS ONE 7(8): e42593. DOI: 10.1371/journal.pone.0042593.t001

Tape measure image c/o Fybrid Stock Photos

Fish with Melanoma – Our Enduring Environmental Legacy

We’ve all heard the horror stories. Melanoma is one of the most dangerous kinds of skin cancer, killing around 50,000 people worldwide every year. If caught early enough, it can be cured, but once it invades past the skin, it’s deadly. On the advice of doctors, we try to protect ourselves, donning floppy hats and coat upon coat of SPF 50 sunblock. We pick over our bodies in the mirror regularly, looking for dark, irregularly-shaped spots. The recent rise in the incidence of skin cancer, though, is our own fault. It is the result of our environmental hubris, a combination of a chemically-depleted ozone layer and our pathological obsession with a tanned physical appearance. Now, we’re becoming increasingly aware that our choices don’t just impact our own species. The rest of life has to deal with our poor decisions, and studies are just now determining the wide-ranging consequences of our actions.

Histology of healthy skin (left) and melanoma-

diseased skin (right) from coral trout

Unable to slather on sunscreen, the creatures on our planet are much more limited in their ability to deal with the sun’s radiation. Some, like the red seabream, are able to tan much like we do, increasing the melanin content in their skin to defend against damaging rays. But most animals are not so lucky, and are ill-equipped to deal with drastic changes in UV radiation. Yet drastic changes in UV radiation are exactly what occurred in the late 20th century, when chemicals we used as refrigerants and in aerosol sprays quickly depleted one of the most UV-protecting molecules, ozone, from our atmosphere. From 1972 to 1992, places like Australia saw a 20% increase in UV radiation levels, and colder areas like Antarctica saw ozone decreases of 50 percent or more, creating large ozone holes which allow more than double the normal level of UV radiation to pass through.

In the late 1970s, scientists began to realize that certain chemicals we were producing, called chlorofluorocarbons, or CFCs, were making their way into the stratosphere. These chemicals release chlorine atoms which, when combined with cold temperatures, begin a destructive chain reaction that turns UV-blocking ozone into oxygen. By 1987, there was so little protective ozone in the stratosphere over Antarctica that global lawmakers decided CFCs were too dangerous to go unchecked. They established the Montreal Protocol, which set strict limits on the use of CFCs. In the 25 years since, the ozone layer has rebounded some, but it is still 50 to 70 years away from returning to pre-1980s levels. Now, the ozone layer is under a new threat: climate change. Scientists predict that rising carbon dioxide levels will lead to more ozone holes, as carbon dioxide and other greenhouse gasses trap heat at the surface, chilling the stratosphere, and allowing atmospheric chlorine atoms to wreak havoc.

We are only now beginning to fully document the consequences of ozone depletion. In people, the loss of ozone at the end of the 20th century was directly connected to a 16 to 60 percent increase in the incidence of skin cancer. But while we carefully documented the effects on our own species, little research has looked for health effects on other animals. Now, Australian scientists have found an entire population of fish plagued with the deadliest form of skin cancer: melanoma.

The team of researchers from Newcastle University began looking for skin cancer in the commercially and culturally important species of coral trout off Australia in 2010 when a different team of scientists studying sharks first noticed lesions. Because these other scientists from The Australian Institute of Marine Sciences were catching trout to study predator-prey dynamics, Michael Sweet and his colleagues were able to screen over a hundred coral trout (Plectropomus leopardus) for melanoma between August 2010 and February 2012. They examined lesions histologically, to determine the exact type and severity of the cancer. Lastly, they tested lesions for bacteria and viruses, to rule out a microbial cause.

A healthy coral trout (top) as compared to

trout with melanoma

A whopping 15% of the fish surveyed had melanoma. “Studying disease in wild fish populations is very time-consuming and costly so it’s hard to say how long the disease has been around,” explains lead author Michael Sweet. “What we do know is that it is now widespread in the coral trout population. We found evidence of cancer in the common coral trout, the bar-cheeked coral trout, and the blue spotted coral trout.”

While 15% sounds high, Sweet and his colleagues believe it’s only a minimum estimate. “Once the cancer spreads further you would expect the fish to become quite sick, becoming less active and possibly feeding less, hence less likely to be caught. This suggests the actual percentage affected by the cancer is likely to be higher than observed in this study.”

This isn’t the first melanoma to be found in fish, as individual cases have been identified in a wide variety of species, from catfish to nurse sharks. Never before, however, has melanoma been found population-wide. “To the best of our knowledge, cancer of any sort has never been shown in a wild marine fish population before, making this a first for science,” said Sweet

While it is a first, Sweet and his colleagues don’t think coral trout are unique. “We would not be surprised to find [melanoma] in other species as well,” he said, “including some of the smaller reef species.” So far, skin cancer in fish has likely been overlooked due to the high cost of evaluating fish for disease as well as the low likelihood of sick and weakened fish landing in fishermen’s or scientists’ hands.

Extensive laboratory analyses ruled out microbial agents as the driver of the disease, and since the fish were caught far from shore in a marine protected area, it’s unlikely that pollution factored in, either. The samples were also directly compared to UV-induced melanomas in laboratory fish, which are used as a model for human disease; the ones in coral trout looked identical to the lab-created cancers. “This combination of evidence leads us to suspect UV as the casual agent.”

If UV is the cause, then it’s really our fault. “The occurrence of this disease in today’s day and age and not before can be linked to the changes we are experiencing in our climate and the ozone hole,” explained Sweet. “It is highly likely there will be higher prevalence around areas which have these ‘ozone holes’.” While the Montreal Protocol has helped reverse some of the worst damage, Sweet is careful to note that we’re not out of the woods yet. “An increase in smaller ozone holes (other than the two large ones of the Arctic and the Antarctic) is thought to be occurring, and this has been related by other researchers to be due to climate change.”

The overall effect of skin cancer in fish populations could be devastating. In laboratory fish, melanoma cuts the lifespan of Xiphophorus species from four years to only six months, and makes them more susceptible to small changes in their environment like fluctuations in temperature. “It is unclear whether future changes in the ocean environment or climate will similarly exacerbate the effect of melanomas in wild P. leopardus populations,” write the authors, “but clearly further research is urgently needed to understand the distribution, prevalence, ecological and fisheries significance of this syndrome.”

Since lawmakers are hesitant to restrict greenhouse gasses and other pollutants, we’re stuck with whatever happens, for now – especially, as Sweet notes, when it comes to disease. “Without addressing the underlying issues, sadly, there is likely no feasible or practical cure for skin cancer in wild fish populations.” If melanoma is found in other species, too, the consequences will only magnify.

With little natural protection against UV rays, fish and most other species are at our mercy when it comes to radiation-induced disease. Skin cancer only adds to a growing list of pathological consequences to our poor ecological choices – a list which includes devastating diseases like chytridiomycosis and avian malaria. Until we change the way we treat the world around us, that list will continue to grow, while the abundance and vitality of our planet’s biodiversity shrinks.

 
Citation: “Evidence of melanoma in wild marine fish populations.” M J Sweet, N Kirkham, M Bendall, L Currey, J C Bythell, M Heupel. PLOS ONE. August 2012. DOI: 10.1371/journal.pone.0041989.g005

Histological sections from the paper; photos of coral trout by Michelle Heupel

Evolution: Out Of The Sea

Thursday 26th July saw the launch of SciLogs.com, a new English language science blog network. SciLogs.com, the brand-new home for Nature Network bloggers, forms part of the SciLogs international collection of blogs which already exist in German, Spanish and Dutch. To celebrate this addition to the NPG science blogging family, some of the NPG blogs are publishing posts focusing on “Beginnings”.

Participating in this cross-network blogging festival is nature.com’s Soapbox Science blog, Scitable’s Student Voices blog and bloggers from SciLogs.com, SciLogs.de, Scitable and Scientific American’s Blog Network. Join us as we explore the diverse interpretations of beginnings – from scientific examples such as stem cells to first time experiences such as publishing your first paper. You can also follow and contribute to the conversations on social media by using the #BeginScights hashtag. – Bora

In the beginning, the earth was without form, and void; and darkness was upon the face of the deep, as a giant cloud of gas and dust collapsed to form our solar system. The planets were forged as the nebula spun, jolted into motion by a nearby supernova, and in the center, the most rapid compression of particles ignited to become our sun. Around 4.5 billion years ago, a molten earth began to cool. Violent collisions with comets and asteroids brought the fluid of life – water – and the clouds and oceans began to take shape. It wasn’t until a billion years later that the first life was brought forth, filling the atmosphere with oxygen.

Over the next few billion years, single-celled organisms fused and became multicellular; body plans diversified and radiated, exploding into an array of invertebrates. Yet all this abundance and life was restricted to the seas, and a vast and bountiful land sat unused. Around 530 million years ago, there is evidence that centipede-like animals began to explore the world above water. Somewhere around 430 million years ago, plants and colonized the bare earth, creating a land rich in food and resources, while fish evolved from ancestral vertebrates in the sea. It was another 30 million years before those prehistoric fish crawled out of the water and began the evolutionary lineage we sit atop today. To understand life as we know it, we have to look back at where we came from, and understand how our ancestors braved a brand new world above the waves.

It was a small step for fish, but a giant leap for animalkind. Though, looking at modern fish species, it’s not so hard to envision the slow adaptation to life out of the sea. Just the other day, I was feeding my pet scorpionfish Stumpy, and he surprised me with this slow, deliberate crawl towards his food:

A number of fish exhibit traits which are not unlike those of the first tetrapods: the four-limbed vertebrates that first braved life on land, direct descendants of ancient fish. Many of Stumpy’s relatives, including the gurnards, are known for their “walking” behaviors. Similarly, mudskippers have adapted anatomically and behaviorally to survive on land. Not only can they use their fins to skip from place to place, they can breathe through their skin like amphibians do, allowing them to survive when they leave their shallow pools. Walking catfishes have modified their respiratory system so much that they can survive days out of water. But all of these are only glimpses at how the first tetrapods began, as none of these animals has fully adapted to life on land. To understand how tetrapods achieved such a feat, we must first understand the barriers that lay between their life under the sea and the land above that awaited them.

Living in air instead of water is fraught with difficulties. Locomotion is one problem, though as evolution in a number of lineages has shown, not as big a problem as you might think. Still, while mudskippers and catfish seem to walk with ease, the same cannot be said of our ancestors. Some of the earliest tetrapods, like Ichthyostega were quite cumbersome on land, and likely spent most of their time in the comfort of water. These first tetrapods came from an ancient lineages of fishes called the Sarcopterygii or Lobe-Finned Fish, of which only a few survive today. As the name implies, these animals have meaty, paddle-like fins instead of the flimsy rays of most modern day fish species. These lobe fins, covered with flesh, were ripe for adapting into limbs.

But these early tetrapods had to develop more than a new way to walk – their entire skeletons had to change to support more weight, as water supports mass in a way that air simply doesn’t. Each vertebrae had to become stronger for support. Ribs and vertebrae changed shape and evolved for extra support and to better distribute weight. Skulls disconnected, and necks evolved to allow better mobility of the head and to absorb the shock of walking. Bones were lost and shifted, streamlining the limbs and creating the five-digit pattern that is still reflected in our own hands and feet. Joints articulated for movement, and rotated forward to allow four-legged crawling. Overall, it took a long 30 million years or so to develop a body plan fit for walking on land.

At the same time, these cumbersome wanna-be land dwellers faced another obstacle: the air itself. With gills adept at drawing oxygen from water, early tetrapods were ill-equipped to breathing air. While many think that early tetrapods transformed their gills into lungs, this actually isn’t true – instead, it was the fish’s digestive system that adapted to form lungs. The first tetrapods to leave the water breathed by swallowing air and absorbing oxygen in their gut. Over time, a special pocket formed, allowing for better gas exchange. In many fish, a similar structure – called a swim bladder – exists which allows them to adjust buoyancy in the water, and thus many have hypothesized that tetrapod lungs are co-opted swim bladders. In fact, exactly when tetrapods developed lungs is unclear. While the only surviving relatives to early tetrapods – the lungfishes – also possess lungs (if their name didn’t give that away), many fossil tetrapods don’t seem to have them, suggesting that lungfish independently evolved their ability to breathe air. What we do know is that it wasn’t until around 360 million years ago that tetrapods truly breathed like their modern descendants.

The other trouble with air is that it tends to make things dry. You may have heard the statistic that our bodies are 98% water, but, as well-evolved land organisms, we have highly evolved structures which ensure that all that water doesn’t simply evaporate. The early tetrapods needed to develop these on their own. At first, like the amphibians that would arise from them, many tetrapods likely stuck to moist habitats to avoid water loss. But eventually, to conquer dry lands and deserts, animals had to find another way to keep themselves from drying out. It’s likely that many of the early tetrapods began experimenting with ways to waterproof their skin. Even more important was the issue of dry eggs. Amphibians solve the dryness issue by laying their eggs in water, but the tetrapods which conquered land didn’t have that luxury.

The solution to land’s dry nature was to encase eggs in a number of membrane layers, in what is now known as an amniote egg. Even our own children reflect this, as human babies still grow in an amniotic sac that surrounds the fetus, even though we no longer lay eggs. This crucial adaptation allowed animals to cut ties with watery habitats, and distinguishes the major lineage of tetrapods, including reptiles, birds and mammals, from amphibians.

These crucial adaptations to tetrapod skeletons and anatomy allowed them to conquer the world above the waves. Without their evolutionary ingenuity, a diverse set of animals, including all mammals, would not be where they are today. Yet still we barely understand the ecological settings that drove these early animals out of the sea. Did dry land offer an endless bounty of food not to be passed up? Perhaps, but there is evidence that our ancestors braved the dry world very early on, even before most terrestrial plants or insects, so it’s possible earth was barren. Were they escaping competition and predation in the deep? Or was land important for some yet undetermined reason? We may never know. But as we reflect upon our beginnings, we have to give credit to the daring animals that began the diverse evolutionary lineage we are a part of. While we may never understand why they left the water, we are thankful that they did.

 
Other Posts in the Evolution Series:

Photo: A model of Tiktaalik rosea, one of the earliest tetrapod ancestors. Photo courtesy of Tyler Keillor.

Biochemically, All Is Fair

There’s nothing in this world so sweet as love. And next to love the sweetest thing is hate.

– Henry Wadsworth Longfellow

I stare hard into his hazel eyes. Those damned eyes. I blink, and I’m bombarded with flashes of those eyes through lenses of love, trust, fear and anger. My blood is pumping with passion, sped on by norepinephrine and vasopressin. The neurons in a round structure at the base of my forebrain are firing like crazy, a cacophony of neural activity. I glance down at his lips. Half of me wants to kiss him – half of me wants to break his jaw.

Part of the problem is that for intense emotions, my body reacts in a similar way. Heart rate and blood pressure skyrocket, driven by stress hormones. My muscles tense. My palms sweat. My cheeks flush. Objectively, it might be hard to tell what I am feeling. Subjectively, it’s hard, too.

Love him or hate him, two regions of my brain – the putamen and the medial insula – activate when I look at his face. Some have suggested that since the putamen regulates motor functions and contains neurons that activate when we plan actions, perhaps it is helping me decide between that punch and that kiss, but there seems to be more going on. The putamen is highly regulated by dopamine, one of the neurotransmitters linked to intense romantic feelings and the messenger of our neurological reward system. I smirk at the idea that, perhaps, I just find the thought of cold-cocking him deeply rewarding.

It is the activation of the insula, though, that is most intriguing. The insula is a bit of a neurological slut, and is intimately involved in our experience of number of basic emotions, including anger, fear, disgust, happiness and sadness. Scientists believe the insula acts as a translater, connecting sensations in our bodies to emotions in our brains. The insula turns a bad taste into disgust, or a gentle touch into arousal. But what makes the insula so interesting is that many believe these connections go both ways. Not only are my feelings affecting my body, the very act of processing my body’s reaction to the situation – my fast pulse, shallow breaths, sweaty palms – is changing how I feel.

As my sensations surge, parts of my cortex responsible for judgement and reason shut down – love and hate really are blind in that way. Studies have suggested love is more blind, though, as larger areas of the cerebral cortex deactivate. I know my thoughts aren’t logical anymore. They’re at the mercy of neurotransmitter tides, waxing and waning. Confusion is an understatement.

I blink hard and try to focus.

Even my hormones are flirting with both sides of the emotional spectrum. The flushed skin, pounding heart and rapid breathing are the fault of norepinephrine and adrenaline kicking on my fight or flight instinct. Passion is passion, and the same hormonal system is triggered by fear, anger, lust and desire. Whatever the fueling emotion, my body is primed, ready to spring into action.

My other hormones are no help, either. Oxytocin, the ‘love hormone’, long touted as the chemical responsible for affection, also has a dark side. While it strengthens feelings of love and trust, it also intensifies envy and suspicion, and may even lead to strong feelings of hatred like racism and xenophobia.

Similarly, the anger-pumping hormone testosterone has a romantic side. Testosterone levels strongly control feelings of lust and desire, but more importantly, women falling in love have higher circulating testosterone. Thus even a hormone so intertwined with agression and hate is instrumental in my experience of romance and pleasure. I briefly wonder if the increased testosterone level in my body is having side effects as I clench my fist.

Sure, love and hate have their differences, too. The giddy, happy romantic feelings come from different parts of the brain than deep passion. But as the intensity of the emotion rises, the fine line between love and hate blurs. It’s no wonder philosophers have been lumping them together for centuries, two sides of the same coin. As glorified as our idea of love might be, passionate love has the same biomarkers as addiction and obsessive compulsive disorder – and like with addiction and obsession, when the stakes are high, the smallest thing can push a person over the edge.

He shouldn’t have pushed me.

My amygdala turns on. Today, the dark side wins. I close my eyes as aggression ripples through my body. I didn’t want a fight, but my body disagreed. Rage fueled by love overwhelms me. It takes everything in my power not to fly at him. Feeling my self-control waning, I clench my teeth. Then, slowly, I open my eyes to see his have hardened, too. Alright, then. Here we go.

    (lyrics)

Like this post? Check out Time – And Brain Chemistry – Heal All Wounds

Mating with the wrong species: plastics make it possible

Despite only being around for the past century or so, plastics have become ubiquitous in modern life and for good reason: the final product is incredibly versatile. From grocery bags to IV bags to the teflon on non-stick pans, plastics really do make almost everything possible.

But, such a useful product comes at a cost. One of the chemicals used in making certain plastics, BPA, has been linked to a suite of ecological and human health problems. Now, scientists have discovered that the effects of BPA are so strong, certain species of fish lose their ability to tell their own species apart from another.

BPA is the building block of polycarbonate plastics, and is used in other kinds of plastics alter their flexibility. The trouble is, BPA doesn’t stay neatly locked in – it’s known to leech out, contaminating food and liquids that come in contact with BPA containing plastics. Studies have shown that BPA is now in our lakes and rivers, affecting all kinds of creatures that rely on those water sources.

The real trouble with BPA is that it looks a lot like one of the most potent animal hormones: estrogen. It tricks animal cells. Because estrogen controls a number of very important bodily functions, the potential affects of BPA on animals – including us – are severe and range widely.

In animals like mice and rats, doses as low as 0.025 µg/kg/day can causes permanent changes to the genital tract and predispose breast cells to cancerous activity. Between 1 and 30 µg/kg/day can lead to long-term reproductive changes like earlier puberty and longer periods, decline in testicular testosterone, and prostate cell changes indicative of cancer, as well as behavioral effects like decreased maternal instincts and even reversed sex roles.

Jessica Ward and her colleagues were particularly concerned with how BPA is affecting fish in contaminated waters. In Georgia waters, an introduced species of fish – the red shiner (Cyprinella lutrensis) – is encroaching upon the habitat of a native species, the blacktail shiner (Cyprinella venusta). To determine the short term effects of BPA exposure on these two species, the research team placed male and female fish in BPA and control treatments for two weeks, then looked for physical and behavioral changes.

Males that were exposed to BPA changed color, losing some of their distinctive coloring that females use in mate choice (image from the paper on the right). This loss of color affected the females’ behavior: they were less choosy when it came to their mates. Exposure to BPA led to more mixed-species pairings.

“This can have severe ecological and evolutionary consequences,” said Ward, “including the potential for the decline of our native species.” Already, hybridization with red shiners is altering the community composition of native shiners in southern waterways and facilitating the invasion. With BPA and other hormone-mimicking pollutants speeding up the process of invasion, our native species are in for the fight of their life.

While we knew BPA was a problem, this is one of the first studies to reveal how broad its effects really are. “Until now studies have primarily focused on the impact to individual fish, but our study demonstrates the impact of BPA on a population level,” said Ward. Additional studies like this one on other species, from insects to mammals, will help us better understand how BPA and other hormone-mimicking chemicals are affecting our ecosystems. Given the dire situation many of our ecosystems currently face, such knowledge is vital in the effort to protect what biodiversity we have left for further generations.

 

Citation: Ward, J.L. & Blum, M.J. (2012). Exposure to an environmental estrogen breaks down sexual isolation between native and invasive species, Evolutionary Applications, n/a. DOI: 10.1111/j.1752-4571.2012.00283.x

A Birthday Wish

On Sunday, I celebrated my 27th birthday. But today is an even more special birthday: today, the entire Scientific American Blog Network celebrates its first birthday. One year ago, this rag-tag team of bloggers began this network under the wise guidance of Bora. Today, we celebrate, as the network blows out its first candle.

But what is a birthday party without presents? No, I’m not asking for money or trinkets – just your voice, in the tradition of Ed Yong. You have been lurking in the shadows, reading posts here and on other SciAm blogs. What I want for my blog birthday is for you to tell me a bit about yourself and why you read this blog in the comment thread of this post.

Who are you? What is your relationship to science? How did you end up at this blog – what drew you in? Are you a regular reader or a casual encounter? Do you also follow on Twitter, Facebook, etc? What other blogs do you follow, and how do you follow them (RSS, Social Media, etc)? And, always the hard question: how am I doing? What do you like, and what could be improved?

Say as much or as little as you want: these questions are a guide, not a strict format to be followed. What I want, above anything else, is for you to express yourself. So be yourself!

Last but not least, the real gift: tell someone else about this blog. Ideally, pick someone who’s not a scientist but who might be interested in what is written here. Encourage them to poke around, read a few articles, then also come here and comment.

Note: If you’re a first-time commenter, there may be a small delay before your comment is approved (can’t be online 24/7!). Once it’s approved, you can comment freely.

First birthday photo c/o Jerad Hill on Flickr

Toxoplasma’s Dark Side: The Link Between Parasite and Suicide

We human beings are very attached to our brains. We’re proud of them – of their size and their complexity. We think our brains set us apart, make us special. We scare our children with tales of monsters that eat them, and obsessively study how they work, even when these efforts are often fruitless. So, of course, we are downright offended that a simple, single-celled organism can manipulate our favorite organ, influencing the way we think and act.

Toxoplasma gondii is arguably the most interesting parasite on the planet. In the guts of cats, this single-celled protozoan lives and breeds, producing egg-like cells which pass with the cats bowel movements. These find their way into other animals that come in contact with cat crap. Once in this new host, the parasite changes and migrates, eventually settling as cysts in various tissues including the host’s brain, where the real fun begins. Toxoplasma can only continue its life cycle and end up a happy adult in a cat’s gut if it can find its way into a cat’s gut, and the fastest way to a cat’s gut, of course, is to be eaten by a cat. Incredibly, the parasite has evolved to help ensure that this occurs. For example, Toxoplasma infection alters rat behavior with surgical precision, making them lose their fear of (and even become sexually aroused by!) the smell of cats by hijacking neurochemical pathways in the rat’s brain.

Of course, rats aren’t the only animals that Toxoplasma ends up in. Around 1/3 of people on Earth carry these parasites in their heads. Since Toxoplasma has no trouble affecting rats, whose brains are similar in many ways to our own, scientists wonder how much the parasite affects the big, complex brains we love so much. For over a decade, researchers have investigated how this single-celled creature affects the way we think, finding that indeed, Toxoplasma alters our behavior and may even play a role in cultural differences beween nations.

The idea that this tiny protozoan parasite can influence our minds is old news. Some of the greatest science writers of our time have waxed poetic about how it sneaks its way into our brains and affects our personalities. Overall, though, the side effects of infection are thought to be minor and relatively harmless. Recently, however, evidence has been mounting that suggests the psychological consequences of infection are much darker than we once thought.

In 2003, E. Fuller Torrey of the Stanley Medical Research Institute in Bethesda, Maryland his colleagues noted a link between Toxoplasma and schizophrenia – specifically, that women with high levels of the parasite were more likely to give birth to schizophrenics-to-be. The hypothesis given for this phenomenon is that while for most people who are infected, Toxoplasma has minor effects, for some, the changes are much more pronounced. The idea has gained traction – a later paper found, for example, that anti-psychotics worked just as well as parasite-killing drugs in restoring normal behaviors in infected rats, affirming the similarities between psychological disorders and Toxoplasma infection.

Continuing to work with mental patients, scientists later discovered a link between suicide and parasite infection. But, of course, this link was in people who already have mental illness. Similarly, a study found that countries with high Toxoplasma infection rates also had high suicide rates – but the connection between the two was weak, and there was no direct evidence that the women who committed suicide were infected.

What scientists really wanted to understand is whether Toxoplasma affects people with no prior disposition to psychological problems. They were in luck: in Denmark, serum antibody levels for Toxoplasma gondii were taken from the children of over 45,000 women as a part of a neonatal screening study to better understand how the parasite is transmitted from mother to child. Since children do not form their own antibodies until three months after birth, the antibody levels reflect the mother’s immune response. Thus the scientists were both able to passively screen women not only for infection status, but degree of infection, as high levels of antibodies are indicative of worse infections. They were then able to use the Danish Cause of Death Register, the Danish National Hospital Register and the Danish Psychiatric Central Research Register to investigate the correlation between infection and self-directed violence, including suicide.

The results were clear. Women with Toxoplasma infections were 54% more likely to attempt suicide – and twice as likely to succeed. In particular, these women were more likely to attempt violent suicides (using a knife or gun, for example, instead of overdosing on pills). But even more disturbing: suicide attempt risk was positively correlated with the level of infection. Those with the highest levels of antibodies were 91% more likely to attempt suicide than uninfected women. The connection between parasite and suicide held even for women who had no history of mental illness: among them, infected women were 56% more likely to commit self-directed violence.

While these results might seem frightening, they make sense when you think about how Toxoplasma is known to affect our personalities. In 2006, researchers linked Toxoplasma infection to neuroticism in both men and women. Neuroticism – as defined by psychology – is the “an enduring tendency to experience negative emotional states,” including depression, guilt and insecurity. The link between neuroticism and suicide is well established, thus if the parasite does make people more neurotic, it’s not surprising that it influences rates of self-violence.

How does a parasite affect how we think? The authors suggest that our immune system may actually be to blame. When we are infected with a parasite like Toxoplasma gondii, our immune system goes on the offensive, producing a group of molecules called cytokines that activate various immune cell types. The trouble is, recent research has connected high levels of cytokines to depression and violent suicide attempts. The exact mechanism by which cytokines cause depression and other mental illnesses is poorly understood, but we do know they are able to pass the blood-brain barrier and alter neurotransmitters like serotonin and dopamine in the brain.

But the authors caution that even with the evidence, correlation is not causation. “Is the suicide attempt a direct effect of the parasite on the function of the brain or an exaggerated immune response induced by the parasite affecting the brain? We do not know,” said Teodor T. Postolache, the senior author and an associate professor of psychiatry and director of the Mood and Anxiety Program at the University of Maryland School of Medicine, in a press release. “We can’t say with certainty that T. gondii caused the women to try to kill themselves.”

“In fact, we have not excluded reverse causality as there might be risk factors for suicidal behavior that also make people more susceptible to infection with T. gondii,” Postolache explained. But given the strong link between the two, there is real potential for therapeutic intervention. “If we can identify a causal relationship, we may be able to predict those at increased risk for attempting suicide and find ways to intervene and offer treatment.” The next step will be for scientists to affirm if and how these parasites cause negative thoughts. Not only could such research help target at-risk individuals, it may help scientists understand the dark neurological pathways that lead to depression and suicide that the sinister protozoan has tapped into. But even more disconcerting is that scientists predict that Toxoplasma prevalence is on the rise, both due to how we live and climate change. The increase and spread of this parasitic puppeteer cannot be good for the mental health of generations to come.

 

Citation: Pedersen, M.G., Mortensen, P.B., Norgaard-Pedersen, B. & Postolache, T.T. Toxoplasma gondii Infection and Self-directed Violence in Mothers, Archives of General Psychiatry, DOI: 10.1001/archgenpsychiatry.2012.668

Photos: Toxoplasma gondii parasites in rat ascitic fluid from the CDC’s Public Health Image Library; Brain MRI Scan in Patient with Toxoplasma Encephalitis from the University of Washington’s HIV Web Study

Social Media for Scientists Part 6: The Wiki

I just returned from a wonderful week in Washington DC, where I gave workshops on social networking to scientists at the Fourth Biennial National IDeA Symposium of Biomedical Research Excellence (NISBRE). I was delightfully surprised that so many of the scientists there came to my workshop not only to learn, but to support the use of social networking in science – what a good sign!

Anyhow, as a part of the workshop, I created a wiki jam-packed with just every resource I could find on social networking for researchers and educators. I shared it with the NISBRE folks, and now I want to share it with you.

The wiki is broken down into sub-categories, with pages for each of the major networks as well as general resources on the topic. I hope it will become not only a resource, but a place of discussion – somewhere scientists from all backgrounds share their experiences and discuss how to use Web 2.0 tools effectively.

But, like any wiki, it needs input. What links have I missed? What other specific topics should I include? Whether you’re a scientist who is contemplating jumping into the social media world, or an online guru with advice for beginners, your opinions are valued and desired. So head over to the wiki, become a member, and add your thoughts/links!

More Social Media for Scientists: