Ruins of Saranda Kolones, Cyprus’ feces-preserving castle. Photo by Matthew Wilkinson

Cyprus, the Mediterranean island nation just south of Turkey, took centuries to gain its independence. The Greeks, Assyrians, Egyptians, Persians, Romans, Ottomans, British and others all took their turns taking over the island, and each left their mark on the archeological record. But in a ruined chamber in a castle on the western corner of the island, it may be more apt to say the invaders left a smear.

In 1191, during the Third Crusade, King Richard I of England invaded Cyprus and ordered that a castle be built on the island’s western corner in order to defend the harbor there. Called Saranda Kolones, the castle’s name refers to its many monolithic columns. But in typical tumultuous Cyprus fashion, the medieval castle was only used for thirty years before it was destroyed by an earthquake. By then, King Richard had sold Cyprus to Guy de Lusignan, the King of Jerusalem. Lusignan and his successors had other plans for expanding the island. The wrecked port was abandoned and the castle never rebuilt. 

An ancient toilet from Saranda Kolones, perched over a pit of dried human waste. Photo by Anastasiou & Mitchell, International Journal of Paleopathology

As castles go, Saranda Kolones had a pretty poor run. But two University of Cambridge researchers recently realized that, precisely thanks to the castle’s short use, a priceless treasure had been left behind in the Saranda Kolones’ bowels. One of the centuries-old castle latrines (read: ancient toilet), they found, was still full of dried-up poo. That feces, they thought, could provide valuable insight into what kind of parasites plagued the former residents’ guts. And because only 30 years’ worth of waste clogged the ancient sewage system, those parasites could provide specific insight into what ailed medieval crusaders. The researchers rolled up their sleeves and collected samples from the dessicated cesspool.

To rehydrate the ancient night soil, the team placed one gram of their sample into a chemical liquid solution. They used micro sieves, or tiny strainers to separate parasite eggs from the digested remains of the crusaders’ meals. They created 20 slides, and peeked into their microscopes to see what creatures the soldiers may have left behind.

One of the recovered whipworm eggs. Photo by Anastasiou & Mitchell, International Journal of Paleopathology

The samples revealed 118 “lemon-shaped” Trichuris trichiura eggs–a type of roundworm commonly called the whipworm–as well as 1,179 Ascaris lumbricoides, or giant roundworm, eggs. A control sample of non-toilet soil they tested did not contain any parasite eggs, confirming that the eggs did indeed come from the toilet, they report in the International Journal of Paleopathology. 

The study of ancient parasites, whether through old bones that reveal leprosy-causing pathogens or dried up leaves that elucidate the cause of the Irish potato famine, is a thriving field. In this case, the long-dead parasite eggs were pooped out by the crusaders using the toilet years ago. These species reproduce within human bodies, and go on to infect new hosts through egg-contaminated soil or food delivered courtesy of the host.

Heavy infection with either of these worms was no picnic. The authors write, first of giant roundworms:

The mature female then starts to lay about 200,000 eggs per day that can be fertile or unfertile if no male worms are present. Although a mild infection with roundworms is mostly asymptomatic, heavy burdens with Ascaris can cause intestinal blockage and abdominal pain in adults. Because children are less able to tolerate parasites that compete with them for nutrients in their diet, heavy infection with roundworms can cause nutritional impairment, vitamin deficiencies, anaemia and growth retardation.

And of whipworms:

When the females reach maturity they can release 2000–10,000 eggs per day. As with roundworm a heavy worm burden may contribute to malnutrition, stunted growth in childhood and sometimes mechanical damage of the intestinal mucosa, diarrhoea and prolapsed rectum.

The presence of these worms, the authors write, attests to the poor hygienic conditions the castle residents likely practiced and put up with. “Poor hygiene with dirty hands, contamination of the food and water supplies with faecal material, inadequate disposal of the faecal material, and consumption of unwashed vegetables fertilized with human faeces are some of the means through which roundworms and whipworms are spread.”

The worms also could have jeopardized the health of their hosts, especially during years of famine when both parasite and human competed for scarce nutrients from meals few and far between. Previous studies found that between 15 to 20 percent of nobles and the clergy died from malnutrition and infectious disease during the crusades. Although death records for poor soldiers are not available, the authors think it’s safe to assume that malnutrition probably hit the lower-ranking crusaders even harder.

“It is quite likely that a heavy load of intestinal parasites in soldiers on crusade expeditions and in castles undergoing long sieges would have predisposed to death from malnutrition,” they write. “This clearly has implications for our understanding of health and disease on mediaeval military expeditions such as the crusades.”

Before contemporary readers breathe a sign of relief that these parasites infested the guts of people living more than 800 years ago, it’s important to note that the giant roundworm infests an estimated one-sixth of all humans living today. As the authors write, “In modern times A. lumbricoides and T. trichiura are two of the most common and widespread intestinal parasites.” Other parasites continue to plague human populations worldwide, especially in developing countries. Who knows what the archaeologists of the future will find in the scum of your latrine?

DNA extracted from the skull of this leprosy victim, identified in the study as Jorgen_625, was used to sequence the genome of the medieval. Jorgen_625 lived in Odense, Denmark. Image © Ben Krause-Kyora

For centuries, millions of Europeans suffering from leprosy were shunned by society, made to wear bells that signaled to healthy citizens they were nearby. The infectious illness, also known as Hansen’s Disease, was poorly understood, often believed to be hereditary or a punishment from God. At its height, nearly one in 30 had the disease in some regions; by the 13th century, the number of leper hospitals active in Europe hit its peak at 19,000. Then, in the 16th century, the affliction fell into decline. Soon, it had virtually disappeared from the continent.

The pathogen responsible for leprosy was discovered in 1873 in Norway, squashing previous assumptions about its cause. The earliest written mention of leprosy, one of the oldest-known pathogens to plague humans, appeared in 600 B.C. in China. Historical records show it plagued ancient Greek, Egyptian and Indian civilizations. In 2009, DNA analysis of a first-century man’s remains found in a Jerusalem tomb provided the earliest proven case of leprosy.

Now, DNA sequencing technology has provided clues about the evolution of the bacteria itself. Using well-preserved DNA samples from ancient skeletons, an international team of researchers has sequenced the genome of the pathogen Mycobacterium leprae as it existed in medieval times.

Until now, scientists hadn’t even been able to sequence the pathogen from living people—the bacterium can’t be grown in cell culture in the lab, so scientists usually infect mice with it to achieve a sample big enough for sequencing. The material gleaned from human bones for this study, exhumed from medieval graves, contained a tiny amount of bacterial DNA—less than 0.1 percent, to be in fact. But thanks to extremely sensitive and precise technology, scientists were able to sequence five strains of M. leprae.

Scientists sequenced DNA found in bones excavated from Medieval graves in Denmark, Sweden and the U.K. Here, remains at the medieval leprosy hospital of  St. Mary Magdalen in Winchester, U.K., await excavation. Image courtesy of University of Winchester

Today, more than 225,000 cases of leprosy arise each year, mostly in developing countries. Using samples from some of these cases, the researchers compared the centuries-old sequences to 11 modern strains of the pathogen, extracted from recent biopsies from several geographic regions.

The results, published today in the journal Science, reveal that the bacterium has, in terms of genetic makeup, remained relatively the same despite the last 1,000 years. Only 800 mutations occurred among the 16 genomes in that time, the researchers write. This number means that the mysterious disappearance of the disease by the Middle Ages in Europe can’t be attributed to M. leprae losing its virulence.

“If the explanation of the drop in leprosy cases isn’t in the pathogen, then it must be in the host—that is, in us,” says Stewart Cole, co-director of the study and the head of the École Polytechnique Fédérale de Lausanne’s Global Health Institute. “So that’s where we need to look.”

The pathogen’s genetic resilience was evident in its modern strains. Researchers found that a medieval strain present in Sweden and the U.K. was nearly identical to one currently found in the Middle East. Their findings also suggest that some strains found in the Americas originated in Europe. What they can’t tell us, however, is the direction in which the epidemic spread throughout history.

This research marks a growing trend in using DNA analysis to learn more about epidemics and other devastating events in human history. Last month, scientists sampled 166-year-old Irish potato leaves using similar technology: They determined that a previously unknown strain of P. infestans caused the blight that shrunk 19th-century Ireland’s population by 25 percent. Perhaps future research could someday pinpoint the pathogen responsible for the bubonic plague, commonly known as the Black Death, which wiped out nearly half of Europe’s population between 1347 and 1351.

Languages that evolve at high elevations are more likely to include a sound that’s easier to make when the air is thinner, new research shows. Photo by Flickr user twicepix

You likely don’t give a ton of thought to the sounds and patterns that make up the language you speak everyday. But the human voice is capable making of a tremendous variety of noises, and no language includes all of them.

About 20 percent of the world’s languages, for example, make use of a type of sound called an ejective consonant, in which an intense burst of air is released suddenly. (Listen to all the ejectives here.) English, however—along with most European languages—does not include this noise.

Linguists have long assumed that the incorporation of different sounds into various languages is an entirely random process—that the fact that English includes no ejectives, for instance, is an accident of history, simply a result of the sounds arbitrarily incorporated into the language that would evolve into German, English and most other European languages. But recently, Caleb Everett, a linguist at the University of Miami, made a surprising discovery that suggests the assortment of sounds in human languages is not so random after all.

When Everett analyzed hundreds of different languages from around the world, as part of a study published today in PLOS ONE, he found that those that originally developed at higher elevations are significantly more likely to include ejective consonants. Moreover, he suggests an explanation that, at least intuitively, makes a lot of sense: The lower air pressure present at higher elevations enables speakers to make these ejective sounds with much less effort.

The finding—if it holds up when all languages are analyzed—would be the first instance in which geography is found to influence the sound patterns present in spoken words. It could open up many new avenues of inquiry for researchers seeking to understand the evolution of language throughout human history.

The origin points of each of the languages studied, with black circles representing those with ejective sounds and empty circles those without. The inset plots by latitude and longitude the high-altitude inhabitable regions, where elevations exceed 1500 meters. (1) North American cordillera, (2) Andes, (3) Southern African plateau, (4) East African rift, (5) Caucasus and Javakheti plateau, (6) Tibetan plateau and adjacent regions. Image via PLOS ONE/Caleb Everett

Everett started out by pulling a geographically diverse sampling of 567 languages from the pool of an estimated 6,909 that are currently spoken worldwide. For each language, he used one location that most accurately represented its point of origin, according to the World Atlas of Linguistic Structures. English, for example, was plotted as originating in England, even though it’s spread widely in the years since. But for most of the languages, making this determination is much less difficult than for English, since they’re typically pretty restricted in terms of geographic scope (the average number of speakers of each languageanalyzedis just 7,000).

He then compared the traits of the 475 languages that do not contain ejective consonants with the 92 that do. The ejective languages were clustered in eight geographic groups that roughly corresponded with five regions of high elevation—the North American Cordillera (which include the Cascades and the Sierra Nevadas), the Andes and the Andean altiplano, the southern African plateau, the plateau of the east African rift and the Caucasus range.

When Everett broke things down statistically, he found that 87 percent of the languages with ejectives were located in or near high altitude regions (defined as places with elevations 1500 meters or greater), compared to just 43 precent of the languages without the sound. Of all languages located far from regions with high elevation, just 4 percent contained ejectives. And when he sliced the elevation criteria more finely—rather than just high altitude versus. low altitude—he found that the odds of a given language containing ejectives kept increasing as the elevation of its origin point also increased:

Image via PLOS ONE/Caleb Everett

Everett’s explanation for this phenomenon is fairly simple: Making ejective sounds requires effort, but slightly less effort when the air is thinner, as is the case at high altitudes. This is because the sound depends upon the speaker compressing a breath of air and releasing it in a sudden burst that accompanies the sound, and compressing air is easier when it’s less dense to begin with. As a result, over the thousands of years and countless random events that shape the evolution of a language, those that developed at high altitudes became gradually more and more likely to incorporate and retain ejectives. Noticeably absent, however, are ejectives in languages that originate close to the Tibetean and Iranian plateaus, a region known colloquially as the roof of the world.

The finding could prompt linguists to look for other geographically-driven trends in the languages spoken around the world. For instance, there might be sounds that are easier to make at lower elevations, or perhaps drier air could make certain sounds trip off the tongue more readily.

Emerging research indicates that low doses of the active chemical psilocybin can have positive psychiatric effects. Image via Wikimedia Commons/Dohduhdah

In the 1960s and early 70s, researchers such as Harvard’s Timothy Leary enthusiastically promoted the study of so-called “magic” mushrooms (formally known as psilocybin mushrooms) and championed their potential benefits for psychiatry. For a brief moment, it seemed that controlled experiments with mushrooms and other psychedelics would enter the scientific mainstream.

Then, everything changed. A backlash against the 1960s’ drug culture—along with Leary himself, who was arrested for drug possession—made research nearly impossible. The federal government criminalized mushrooms, and research ground to a halt for over 30 years.

But recently, over the past few years, the pendulum has swung back in the other direction. And now, new research into the mind-altering chemical psilocybin in particular—the hallucinogenic ingredient in “magic” mushrooms—has indicated that carefully controlled, low doses of it might be an effective way of treating people with clinical depression and anxiety.

The latest study, published last week in Experimental Brain Research, showed that dosing mice with a purified form of psilocybin reduced their outward signs of fear. The rodents in the study had been conditioned to associate a particular noise with the feeling of being electrically shocked, and all the mice in the experiment kept freezing in fear when the sound was played even after the shocking apparatus was turned off. Mice who were given low doses of the drug, though, stopped freezing much earlier on, indicating that they were able to disassociate the stimuli and the negative experience of pain more easily.

Psilocybin, the active chemical in hallucinogenic mushrooms. (Black = carbon atoms, white = hydrogen, red = oxygen, blue = nitrogen, and orange = phosphorus.) Image via Wikimedia Commons/Jynto

It’s difficult to ask a tortured mouse why exactly it feels less fearful (and presumably even more difficult when that mouse is in the midst of a mushroom trip). But a handful of other recent studies have demonstrated promising effects of psilocybin on a more communicative group of subjects: humans.

In 2011, a study published in the Archives of General Psychiatry by researchers from UCLA and elsewhere found that low doses of psilocybin improved the moods and reduced the anxiety of 12 late-stage terminal cancer patients over a long period. These were patients aged 36 to 58 who suffered from depression and had failed to respond to conventional medications.

Each patient was given either a pure dose of psilocybin or a placebo, and asked to report their levels of depression and anxiety several times over the next few months. Those who’d been dosed with psilocybin had lower anxiety levels at one and three months, and reduced levels of depression starting two weeks after treatment and continuing for a full six months, the entire period covered by the study. Additionally, carefully administering low doses and controlling the environment prevented any participants from having a negative experience while under the influence (colloquially, a “bad trip.”)

A research group from Johns Hopkins has conducted the longest-running controlled study of the effects of psilocybin, and their findings might be the most promising of all. In 2006, they gave 36 healthy volunteers (who’d never before tried hallucinogens) a dose of the drug, and 60 percent reported having a “full mystical experience.” 14 months later, the majority reported higher levels of overall well-being than before and ranked taking psilocybin as one of the five most personally significant experiences of their lives. In 2011, the team conducted a study with a separate group, and when members of that group were questioned a full year later, the researchers found that according to personality tests, the participants’ openness to new ideas and feelings had increased significantly—a change seldom seen in adults had increased.

As with many questions involving the functioning of the mind, scientists are still in the beginning stages of figuring out whether and how psilocybin triggers these effects. We do know that soon after psilocybin is ingested (whether in mushrooms or in a purified form), it’s broken down into psilocin, which stimulates the brain’s receptors for serotonin, a neurotransmitter believed to promote positive feelings (and also stimulated by conventional anti-depressant drugs).

Psilocybe cubensis is the most common species of psilocybin mushrooms. Image via Wikimedia Commons/Wowbobwow12

Imaging of the brain on psilocybin is in its infancy. A 2012 study in which volunteers were dosed while in an fMRI (functional magnetic resonance imaging) machine, which measures blood flow to various parts of the brain, indicated that the drug decreased activity in a pair of “hub” areas (the medial prefrontal cortex and posterior cingulate cortex), which have dense concentrations of connections with other areas in the brain. “These hubs constrain our experience of the world and keep it orderly,” David Nutt, a neurobiologist at the Imperial College London and lead author, said at the time. “We now know that deactivating these regions leads to a state in which the world is experienced as strange.” It’s unclear how this could help with depression and anxiety—or whether it’s simply an unrelated consequences of the drug that has nothing to do with its beneficial effects.

Regardless, the push for more research into the potential applications of psilocybin and other hallucinogens is clearly underway. Wired recently profiled the roughly 1,600 scientists who attended the 3rd annual Psychedelic Science meeting, many of which are studying psilocybin—along with other drugs like LSD (a.k.a. “acid”) and MDMA (a.k.a. “ecstasy”).

Of course, there’s an obvious problem with using psilocybin mushrooms as medicine—or even researching its effects in a lab setting. Currently, in the U.S., they’re listed as a “Schedule I controlled substance,” meaning that they’re illegal to buy, possess, use or sell, and can’t be prescribed by a doctor, because they have no accepted medical use. The research that has occurred went on under strict government supervision, and getting approval for new studies is notoriously difficult.

That said, the fact that research is occurring at all is an obvious sign that things are slowly changing. The idea that medicinal use of marijuana would one day be permitted in dozens of states would have once seemed far-fetched—so perhaps it’s not entirely absurd to suggest that medicinal mushrooms could be next.

A Neanderthal rib bone was discovered to have a lesion associated with a tumor (top specimen). The missing bone tissue is starkly apparent compared to a normal Neanderthal rib shown below. Image via PLOS ONE/Monge et al.

Some 120,000 years ago, in the hills of what is now Northern Croatia, an adult Neanderthal took his or her last breath. We don’t know much about this Neanderthal—his or her sex, exact age, or even what he or she died from—but new research has revealed something rather interesting present in his or her skeleton. Specifically, in the upper left rib.

As a team of researchers from the University of Pennsylvania and the Croatian National History Museum recently discovered, this Neanderthal had a tumor indicative of a disease called fibrous dysplasia—a condition in which normal bone is replaced by a fibrous, spongy tissue. Tumors of any kind are extremely rare in the human fossil record, and previously, the oldest bone tumors ever discovered were a mere 1,000–4,000 years old.

As a result, the researchers write in an article published today in PLOS ONE, “The tumor predates other evidence for these kinds of tumor by well over 100,000 years.”

CT scans of the rib bone show the cavity left behind by the tumor. Image via PLOS ONE

The rib bone that the team analyzed was originally excavated from a site called Krapina, a Croatian rock shelter that, in the late 1800s, was found to contain 876 Neanderthal fossil fragments that belonged to several dozen individuals who’d all died around 120,000 to 130,000 years ago. Scientists have proposed a range of theories to account for why the fossils are so fragmented: Some have argued that the broken and charred remains are evidence of cannibalism, while others speculate that the Neanderthals were killed and eaten by carnivorous animals.

The rib found in this bone heap is fractured and can’t be definitively paired with any other remains, but the researchers believe it matches with a right rib found nearby at the site. The first-ever detailed analysis of the bone, which included X-ray and CT scanning (right), showed a rather large lesion located at the center, which was left behind by a tumor characteristic of fibrous dysplasia. The researchers ruled out the possibility that the cavity was simply caused by a fracture because there is no evidence of trauma elsewhere on the rib—the lesion protrudes out towards the front of the bone, so if it were caused by a fracture, trauma would be visible on the back side of it.

In some cases, fibrous dysplasia causes no symptoms, while in others, the swelling produced by the tumors can cause deformity. But without the full skeleton, there’s no way of knowing what the overall effect of the disease was on the individual and whether he or she died as a result or due to entirely unrelated causes.

In either case, though, this discovery is valuable for a simple reason: Tumors, on the whole, are extremely rare in the hominid fossil record. When they occur in any tissue apart from bone, they’re unlikely to be preserved, and they also tend to develop during middle age and onwards. Because our ancient ancestors (or—in the case of Neanderthals—cousins) typically didn’t live past their thirties, they probably developed few cases of cancer or benign tumors.

However, this find shows that Neanderthals did develop this type of tumor, which tells us something about the underlying disease. The frequency of many kinds of tumors, both cancerous and benign, are generally thought to correlate with pollutants in the environment. But as the researchers note, the environment that these Neanderthals lived in was essentially pristine—meaning that, at least in some cases, the development of bone tumors has nothing to do with environmental pollution.

This discovery is part of a larger, emerging trend in which scientists are learning about the ancient history of diseases through the fossil record. Last year, analysis of the DNA extracted from hominid teeth and skulls showed that many of the viruses that infect modern humans also lived in Neanderthals and other hominids, and in February, DNA extracted from ancient human teeth helped scientists understand the evolution of oral bacteria over time.

A new system reads a user’s brain patterns to steer a toy helicopter—the first time a flight vehicle has been steered entirely by thought. Image via University of Minnesota

Think of clenching your right fist. A nimble 14-ounce helicopter flies right. Imagine clenching your left fist. The chopper veers left. Think of clenching both fists, and it ascends vertically.

This remarkable helicopter-control system is the work of a group of scientists at the University of Minnesota led by engineering professor Bin He. What sets it apart is that controlling its flight requires absolutely no actual movement for the pilot—no button-pushing or throttle-pulling. Instead of a conventional remote, users control the vehicle with a EEG (electroencephalography) cap studded with 64 electrodes, which detect electrical activity in different parts of the brain near the scalp, effectively reading their minds.

The system, first demonstrated in April and now fully described in an article published today in the Journal of Neural Engineering, is part of the burgeoning study of brain-computer interfaces—direct communication pathways between brains and computerized or robotic devices. In recent years, scientists have created mind-controlled robotics that can feed someone chocolate or help them drink coffee, but this is the first instance of a flight vehicle controlled entirely by thought.

The system relies upon previous EEG and other neurological research by the team, which identified which activity patterns in the brain correlated with thoughts such as “make a fist with your right hand” and “make a fist with both hands.” These sorts of movement-oriented thoughts occur mostly in the motor cortex, an area of the brain responsible for control of the body. The EEG cap is sensitive enough only to detect activity relatively close to the scalp—which is where the motor cortex is located—so the scientists were able to program their EEG software to distinguish between these relevant thought patterns in particular.

As a result, when the system senses one of the specified thoughts, it converts the thought (“make a first with my right hand”) into a command for the helicopter (“turn right”) and then sends the signal to the vehicle over Wi-Fi. With that, voilà: a thought-controlled helicopter.

The team had previously created a system that allowed users to control a virtual helicopter, and modified it for this study using an actual physical vehicle, the ARDrone Quadcopter. As part of the project, they gave five undergraduates a crack at flying the chopper, and all were able to figure out how to keep the thing aloft—and even fly it through hoops—with minimal training.

Scientists envision a range of applications for this sort of technology. Research is already underway for one of the most obvious uses: prosthetic limbs. In February, a Swiss team presented work on a mind-controlled artificial hand that allows a user to pick up objects and can even relay stimuli (such as the hand being poked by a needle) to the user’s brain. Others have worked on mind-controlled wheelchairs, which would give greater mobility to quadriplegic users.

One of the things that makes the helicopter experiment so interesting, though, is that like a few recent brain-computer interfaces (including the wheelchair), it involves brain patterns detected with a non-invasive procedure—users can simply put on or take off the EEG cap whenever they like. Compared to other sorts of brain-computer interfaces, which often rely upon surgically implanted sensors, this sort of system could be used in a much wider range of situations.

For one, paralyzed patients reluctant or unable to have costly and invasive surgery to become more autonomous can simply wear the cap. Additionally, amputees and patients who have a non-paralyzing ailment that still limits mobility—such as ALS or another neuromuscular disorder—could in theory use this sort of technology to control wheelchairs or even other vehicles, such as cars, without requiring a permanent brain implant system.

Someday, it could even be used to enhance technology use for people without related medical problems. If it becomes reliable and sensitive enough, for example, perhaps pilots could someday control full-size helicopters with their thoughts to reduce hand and arm fatigue, and surgeons could manipulate surgical instruments without having to worry about shaking hands.

A neurotransmitter called Nppb, we now know, plays a vital role in the sensation of an itch—and removing it can prevent itchiness entirely. Image via Wikimedia Commons/Orrling

There’s a lot we don’t understand about an itch. Why do itches sometimes pop up for no apparent reason? Why is itching contagious? Why can the very idea of an itch—maybe even the fact that you’re currently reading about itching—cause you to feel the actual physical sensation of one?

Given all this uncertainty, a new discovery reported today in Science should at least scratch the surface of your curiosity and answer a question you’ve been itching to ask (terrible puns intended). A pair of molecular geneticists from the National Institutes of Health, Santosh Mishra and Mark Hoon, isolated a crucial signaling molecule produced by nerve cells that is necessary for passing along the sensation of an itch to the brain.

The pair worked with mice, and started off by examining the neurotransmitter chemicals produced by a type of neuron that runs all the way from the animals’ skin into their spinal columns. These neurons are known to be involved in passing along sensory information about the outer environment, including sensations of heat and pain. They measured that one of the neurotransmitters produced by these nerve cells—a chemical called Nppb (natriuretic polypeptide b)—was secreted in excess when the mice were subjected to a range of itch-inducing substances, such as histamine (the natural compound that triggers the itchiness associated with allergies) and chloroquine (a malaria drug that’s notorious for causing itching as a side-effect).

To test whether Nppd played a role in the itching, they genetically engineered some mice so that they failed to produce the chemical. Initially, they checked to see if these engineered mice were impervious to other types of sensations also conveyed by these neurons (pain, movement and heat), but they seemed to behave just the same as the normal mice, indicating Nppb wasn’t involved in the transmission of those stimuli.

Then, they exposed them once again to the itch-inducing chemicals. The normal mice scratched away, but the genetically engineered mice were another story. “It was amazing to watch,” Mishra said in a press statement. “Nothing happened. The mice wouldn’t scratch.”

Nppb, they determined, plays a key role in passing along the sensation of an itch from these neurons to the brain—especially because, when they injected these same mice with doses of Nppb, they suddenly started scratching just like the others.

To investigate just how Nppb relays this message, they zeroed in on a spot in the mice’s spines called the dorsal horn, in which sensory information from the skin and muscles gets integrated into the spinal column and sent to the brain. In this area, they discovered a high concentration of neurons with a receptor called Npra (natriuretic peptide receptor A) that seemed likely to accept the Nppb molecules secreted when the mice encountered an itch-triggering substance.

Sure enough, when they removed the neurons with the Npra receptor from normal, non-engineered mice that produced Nppb, they too stopped scratching when exposed to the substances. This indicates that Nppb is crucial for passing along the itch sensation from the nerves that reach out into the skin to the spine, and that it fits into the Npra receptor on spinal nerve cells, which then convey the sensation to the brain. But removing these receptors didn’t impact the transmission of pain or touch, indicating that Npra is specifically involved in the itch sensation pathway. This comes as a surprise, as most previous research has indicated that the pain and itching nervous networks are intricately related.

While this chemical pathway explains part of the physical mechanism behind an itch, scientists still don’t fully understand the underlying evolutionary reason for the sensation in the first place. Some have speculated that it serves as a defense measure against insects, parasites and allergens, prompting us to scratch—and, ideally, remove the offending item from our skin—before it causes further damage.

Regardless of the evolutionary reason, our nervous system is similar enough to that of mice that the finding could help us better understand itching patterns in humans—perhaps people who are more prone to itching naturally produce higher levels of Nppb, compared to those who get biten by a mosquito and find the itchiness easy to ignore. On a practical level, the discovery could eventually help us develop anti-itch drugs for people with chronic itching ailments, such as allergic reactions or skin conditions like eczema, which affects an estimated 30 million people.

The problem, though, is that Nppb plays several other important roles in the body (it was originally discovered due to its role in the regulation of blood circulation and pressure) so simply creating a drug that disables Nppb is likely to cause disruptive side-effects that go way beyond itching. But looking more closely into the way the Nppb molecule acts as a “start switch” for itching in humans—and perhaps figuring out a way to safely turn the switch off—could potentially provide relief for itchiness caused by all sorts of triggers, because in the mice, at least, the molecule was found to be involved in the whole range of itch-inducing substances the team tested.

Engineers and doctors 3D printed this custom-made splint that currently holds open the airway of a six-week-old infant and will be gradually absorbed into the body over time. Image via University of Michigan

For most of human history, any baby who suffered a collapsed trachea or bronchi faced a tragic fate: suffocation. These tubes convey air from the mouth to the lungs, and some infants are born with congenitally weakened cartilage surrounding them, a condition known as tracheomalacia. In severe cases, this can lead the trachea or bronchi to collapse completely, blocking the flow or air and causing a newborn to suddenly stop breathing.

To the amazingly wide-ranging list of accomplishments attributed to 3D printing technology, we can now add one more: a custom-made tracheal splint that saved the life of an infant with tracheomalacia and will be safely absorbed into his tissue over the next two years. A team of doctors and engineers from the University of Michigan printed the splint and implanted it into six-week-old Kaiba Gionfriddo last year, and announced the feat in a letter published today in the New England Journal of Medicine.

In December of 2011, Giondriddo was born with tracheomalacia, a condition that affects roughly 1 in 2200 American babies. Typically, the weakened cartilage causes some difficulty breathing, but children grow out of it by age 2 or 3 as the trachea naturally strengthens over time. His case, though, was particularly severe, and in February 2012, his parents April and Bryan were out to dinner when they noticed that he suddenly stopped breathing and was turning blue.

He was rushed to a hospital and kept alive with a ventilator, but doctors said there was a good chance he wouldn’t be able to survive long-term. Several weeks later, a team of Michigan engineers led by Scott Hollister began designing the device, based off prior research, in which they’d 3D printed splints and other prostheses but hadn’t implanted them in clinical patients. For this splint, they used a CT scan of Giondriddo’s trachea and left bronchus to create a 3D digital representation that was then printed, allowing them to produce a splint that would perfectly match his airway’s size and contours.

The CT scan of Giondriddo’s trachea and bronchi. Image via New England Journal of Medicine

The 3D printed cast of Giondriddo’s trachea and bronchi, which the splint implanted in the image at right. Image via New England Journal of Medicine

On February 21, 2012, the splint was surgically sewn around Giondriddo’s failed bronchus; almost immediately, it held open his air passages and allowed him to breathe normally. “It was amazing. As soon as the splint was put in, the lungs started going up and down for the first time,” Glenn Green, the doctor who performed the surgery and helped design the splint, said in a press statement.

21 days later, Giondriddo was taken off the ventilator and has had no breathing problems in the 14 months since the surgery.  In addition to holding open the bronchus, the splint also provides a skeleton upon which natural cartilage tissue can grow, and because it was printed using a biopolymer called polycaprolactone, it will gradually be absorbed into this body tissue over time.

Previously, severe tracheomalacia was treated by extended periods of time using a ventilator, or the implantation of mesh tubes around the trachea or bronchus to keep the airway open. By custom-designing the splint based off a CT scan, though, the team created a treatment method that they say is more effective. Additionally, the dissolvable material means Giondriddo won’t need invasive surgery later to remove the device.

The team has also worked on using this same CT scanning and 3D printing process to produce custom-made ear, nose, skull and bone prostheses that are currently in experimental phases. Other research groups have successfully implanted 3D printed ears, noses and skulls in clinical patients, while last month, an Oxford team figured out how to print microscopic droplets that behave like human tissue.

Could this gator’s teeth hold clues for regenerating humans’ pearly whites? Photo by Flickr user montuschi

Humans drew the short end of the toothbrush when it comes to our pearly whites’ longevity. Other animals such as reptiles and fish frequently lose and replace their teeth by growing new ones, but people are stuck with the same set of mature adult teeth their entire lives. If they lose a tooth–or all 32–dentures are usually the only option.

Oddly enough, alligators’ deadly chomps may hold a clue for how scientists could coax humans into regrowing teeth. These reptiles belong to the order Crocodilia, who, with their famous cheerful grins, caused songwriters to warn that you should never smile at a crocodile. To the bane of Captain Hook and other victims of gator and croc attacks, the large reptiles often regrow their razor teeth multiple times. Researchers think that, given time, technology may advance so that we can borrow these reptilian smiles. But first, scientists need to understand just how these animals keep their smiles toothy.

In a paper published this week in the Proceedings of the National Academy of Sciences, an international team of researchers attempted to get at the mechanisms behind the superior tooth regenerating abilities of one species of Crocodilia–the American alligator–in the hopes of applying the results to humans.

In humans, organs such as hair, scales, nails and teeth “are at the interface between an organism and its external environment and therefore, face constant wear and tear,” the researchers write. But alligators have evolved ways to deal with these challenges. The carnivores can replace any of their 80 teeth up to 50 times throughout their 35 to 75-year lives. Small replacement teeth grow under each mature alligator tooth, ready to spring into action the moment a gator loses a tooth.

To figure out the molecules and cells responsible for replacement, the researchers used X-rays and small tissue samples from alligator embryos, hatchlings and 3-year old juveniles’ developing teeth. They also grew tooth cells in the laboratory and created computer models of the process. Alligator teeth appear to cycle continuously, they write, but in fact the animals’ teeth seem to go through three distinct phases: pre-initiation, initiation and growth.

Once an alligator loses a tooth, these three phases kick off. The dental lamina, or a band of tissue associated with the initial stages of tooth formation in many animals, begins to bulge. This triggers stem cells and an array of signaling molecules that direct the process of forming a new tooth.

These results may be applicable to humans’ pearly whites. Alligators’ flesh-chomping incisors are surprisingly similar to well-organized, complex vertebrate teeth such as ours. In humans, a remnant of the dental lamina–the structure crucial to tooth formation–still exists and sometimes wrongly activates and begins forming toothy tumors. If the researchers could better tease out the molecular signaling pathways behind alligator tooth replacement, they reason, they they may be able to induce those same chemical instructions in humans to coax the body into forming a new tooth after one gets kicked out in a soccer game or has to be removed after becoming infected.

Alternatively, doctors may be able to shut off the molecules responsible for conditions that cause uncontrolled tooth formation. Individuals suffering from cleidocranial dysplasia syndrome grow many unusually shaped, peg-like teeth, for example, and people with Gardner syndrome also grow supernumerary, or extra, teeth.

While the researchers still need to clarify more molecular details behind alligator tooth growth, this initial study does hint that doctors and dentists may someday be able to selectively bestow patients with the reptiles’ tooth-regenerating abilities.

“Based on our study, it may be possible to identify the regulatory network for tooth cycling,” the researchers conclude. “This knowledge will enable us to either arouse latent stem cells in the human dental lamina remnant to restart a normal renewal process in adults who have lost teeth or stop uncontrolled tooth generation in patients with supernumerary teeth.”

Either way, they note that “Nature is a rich resource from which to learn how to engineer stem cells for application to regenerative medicine.”

New research shows our brains have a specialized system to anticipate the location of moving objects, located in V5 region of the visual cortex. Image via Wikimedia Commons/Calebrw

Throwing a baseball is hard. As xkcd pointed out just yesterday, accurately throwing a strike requires that a pitcher release the ball at an extremely precise moment—doing so more than half a millisecond too early or too late causes it to miss the strike zone entirely. Because it takes far longer (a full five milliseconds) just for our nerve impulses to cover the distance of our arm, this feat requires the brain to send a signal to to the hand to release the ball well before the arm has reached its proper throwing position.

The one feat even more difficult than throwing a fastball, though, might be hitting one. There’s a 100 millisecond delay between the moment your eyes see an object and the moment your brain registers it. As a result, when a batter sees a fastball flying by at 100 mph, it’s already moved an additional 12.5 feet by the time his or her brain has actually registered its location.

How, then, do batters ever manage to make contact with 100 mph fastballs—or, for that matter, 75 mph change-ups?

In a study published today in the journal Neuron, UC Berkeley researchers used fMRI (functional magnetic resonance imaging) to pinpoint the prediction mechanisms in the brain that enable hitters to track pitches (and enable all sorts of people to envision the paths of moving objects in general). They found that the brain is capable of effectively “pushing” forward objects along in their trajectory from the moment it first sees them, simulating their path based on their direction and speed and allowing us to unconsciously project where they’ll be a moment later.

The research team put participants in an fMRI machine (which measures blood flow to various parts of the brain in real time) and had them watch a screen showing the “flash-drag effect” (below), a visual illusion in which a moving background causes the brain to mistakenly interpret briefly flashed stationary objects as moving. “The brain interprets the flashes as part of the moving background, and therefore engages its prediction mechanism to compensate for processing delays,” said Gerrit Maus, the paper’s lead author, in a press statement.

Because the participants’ brains thought these briefly flashing boxes were moving, the researchers hypothesized, the area of their brain responsible for predicting the motion of objects would show increased activity. Similarly, when shown a video where the background didn’t move but the flashing objects actually did, the same motion-prediction mechanism would cause similar neuron activity to occur. In both cases, the V5 region of their visual cortex showed distinctive activity, suggesting this area is home to the motion-prediction capabilities that allow us to track fast-moving objects.

Previously, in another study, the same team had zeroed in on the V5 region by using transcranial magnetic stimulation (which interferes with brain activity) to disrupt the area and found that participants were less effective at predicting the movement of objects. “Now not only can we see the outcome of prediction in area V5, but we can also show that it is causally involved in enabling us to see objects accurately in predicted positions,” Maus said.

It’s not much of a leap to suppose that this prediction mechanism is more sophisticated in some people than others—which is why most of us would whiff when trying to hit the fastball of a major league pitcher.

A failure in this mechanism might be at work, the researchers say, in people who have motion perception disorders such as akinetopsia, which leaves the ability to see stationary objects completely intact but renders a person essentially blind to anything in motion. Better understanding how neurological activity in the V5 region—along with other areas of the brain—allows us to track and predict movement could, in the long-term, help us develop treatments for these sorts of disorders.

Recent testing shows that, contrary to prior findings, new plastic helmets reduce the risk of concussions by 45 to 96 percent. Image via Journal of Neurosurgery, Rowson et. al.

In the past century or so, football helmets have come a long way, evolving from crude “leatherheads” crafted by shoemakers to plastic-and-rubber hybrids that can be customized to fit a player’s head and have radios built in.

Nevertheless, the sport currently faces a serious and growing problem: brain injuries. Studies have shown that former NFL players are about three times more likely to die from Alzheimer’s, Parkinson’s and Lou Gehrig’s diseases as the general population, a result of the alarming number of concussions they experience over the course of their careers. The NFL has responded by changing its rules to minimize head impacts, instituting stricter guidelines for concussed players returning to games and pouring money into attempts to develop safer helmets.

But some critics argue that, no matter how much research we undertake, there’s simply no way to create a concussion-proof helmet—no technology can stop a fundamentally violent game from inflicting harm. A 2011 study, in fact, found that with many types of impacts, modern helmets were no better than vintage leather ones at protecting players’ heads.

But now, fans who find their desire for a safe game at odds with their love of it can take comfort in a new study, published today in the Journal of Neurosurgery, that determines otherwise: Compared to “leatherheads,” new helmets are indeed much more effective at protecting the human head. Researchers from Virginia Tech came to the finding by using an automated head impact simulation system to test the effectiveness of a pair of vintage Hutch H-18 leather helmets from the 1930s against 10 plastic helmets currently in use, and found that, depending on the force of impact, modern helmets reduced the concussion risk by anywhere from 45 to 96 percent.

The impact system used in the study, simulating a frontal impact (A) and a side impact (B). Image via Journal of Neurosurgery, Rowson et. al.

The team used the system to measure four different types of head impacts (on the front, side, rear and top of the head), and dropped the head from a range of heights (12, 24, 36, 48 and 60 inches) with each helmet on to simulate in-game impacts of a variety of intensities. Sensors inside the head were used to measure the force of each type of impact. This same type of testing, developed by the Virginia Tech team, has been used extensively to classify the safety of modern helmets on a 1 through 5-star scale.

The researchers found that there was some difference in the performance of the modern helmets—but, as you’d probably expect just from looking at them, the vintage leather helmets performed significantly more poorly than any of the plastic ones. At the lowest intensity impacts (from a 12 inch drop height), the modern helmets reduced the impact on the head by by 59 to 63 percent, and at the medium-intensity impacts (from 36 inches), they provided a 67 to 73 percent reduction. The researchers didn’t even try dropping the head with the leather helmets on from 48 or 60 inches for fear of damaging them.

At the same time, it’s worth noting that the vintage helmets tested were each about 80 years old, so their age might have meant weaker leather fibers than if pristine leatherheads had been tested. Additionally, the leather helmets had presumably taken some beating during their years of use, while the plastic ones were unused before being subjected to the drops, which might have further skewed the results.

Still, both these factors were also included in the previous 2011 finding that leather helmets were just as effective as modern ones—so what accounts for the fact that this experiment so thoroughly contradicted it? The authors of this study say that the experimental setup used in the previous one—in which two helmeted heads were smashed together, one with a modern helmet and the other with either a modern or leather one—distorted the findings and masked the differences between helmet types. Some of the impact, they say, was actually absorbed by the padding in the modern plastic helmet even when the leather one was being tested.

Of course, given the distressing numbers on the concussions suffered by football players even with the latest helmets, this sort of testing shouldn’t suggest that the goal of designing safer head gear has been achieved. But it should give us a bit of hope in showing that 100 years of helmet design has provided some benefits—and future efforts to create and rigorously test new helmet technologies might be able to cut down on concussions long-term.

The creamy sticks of color seen here are just the latest in a long history of lipsticks—historical records suggest that humans have been artificially coloring their lips since 4,000 B.C. Photo by Flickr user ookikioo

Lipstick has seen a fair share of funky ingredients in its long history of more than 6,000 years, from seaweed and beetles to modern synthetic chemicals and deer fat. In recent years, traces of lead have been found in numerous brands of the popular handbag staple, prompting some manufacturers to go the organic route. This week, more dangerous substances joined the roster.

Researchers at Berkeley’s School of Public Health at the University of California tested 32 different types of lipstick and lip gloss commonly found in the brightly lit aisles of grocery and convenience stores. They detected traces of cadmium, chromium, aluminum, manganese and other metals, which are usually found in industrial workplaces, including make-up factories. The report, published in the journal Environmental Health Perspectives, indicated that some of these metals reached potentially health-hazardous levels.

Lipstick is usually ingested little by little as wearers lick or bite their lips throughout the day. On average, the study found, lipstick-clad women consume 24 milligrams of the stuff a day. Those who reapply several times a day take in 87 milligrams.

The researchers estimated risk by comparing consumers’ daily intake of these metals through lip makeup with health guidelines. They report that an average use of some lipsticks and lip glosses results in “excessive exposure” to chromium, and frequent use can lead to overexposure to aluminum, cadmium and manganese.

Minor exposure to cadmium, which is used in batteries, can result in flu-like symptoms such as fever, chills and achy muscles. In the worst cases, the metal is linked to cancer, attacking the cardiovascular, respiratory and other systems in the body. Chromium is a carcinogen linked to stomach ulcers and lung cancer, and aluminum can be toxic to the lungs. Long-term exposure to manganese in high doses is associated with problems in the nervous system. There are no safe levels of chromium, and federal labor regulations require industrial workers to limit exposure to the metal in the workplace. We naturally inhale tiny levels of aluminum present in the air, and many FDA-approved antacids contain the metal in safe levels.

Despite the presence of these metals in lipstick, there’s no need to start abandoning lipstick altogether—rather, the authors call for more oversight when it comes to cosmetics, for which there are no industry standards regulating their metal content if produced in the United States. 

After all, cadmium and other metals aren’t an intended ingredient in lipstick—they’re considered a contaminant. They seep into lipstick when the machinery or dyes used to create the product contain the metals themselves. This means trace amounts are not listed on the tiny stickers on lipstick tubes, so there’s no way to know which brands might be contaminated.

Concern about metals in cosmetics came to the forefront of American media in 2007, when an analysis of 33 popular brands of lipstick by the Campaign for Safe Cosmetics showed that 61 percent of them contained lead. The report eventually led the Food and Drug Administration (FDA), which doesn’t regulate cosmetics, to look into the issue, and what it found wasn’t any better: it found lead in all of the samples tested, with levels four times higher than the earlier study, ranging from 0.09 parts per million to 3.06 parts per million. According to the Centers for Disease Control and Prevention, there is no safe level of lead for humans.

So we’ve got cadmium, chromium, aluminum, manganese and lead in our lipstick. What else? Today, most lipstick is made with beeswax, which creates a base for pigments, and castor oil, which gives it a shiny, waxy quality. Beeswax has been the base for lipstick for at least 400 years–England’s Queen Elizabeth I popularized a deep lip rouge derived from beeswax and plants.

Lipstick as we know it appeared in 1884 in Paris, wrapped in silk paper and made from beeswax, castor oil and deer tallow, the solid rendered fat of the animal. At the time, lipstick was often colored using carmine dye. The dye combined aluminum and carminic acid, a chemical produced by cochineals–tiny cacti-dwelling insects–to ward off other insect predators.

That early lipstick wasn’t the first attempt at using insects or to stain women’s mouths. Cleopatra’s recipe for homemade lipstick called for red pigments drawn out from mashed-up beetles and ants.

But really, any natural substance with color was fair game for cosmetics, regardless of its health effects: Historians believe women first starting coloring their lips in ancient Mesopotamia, dotting them with dust from crushed semi-precious jewels—these lovely ancients were eating tiny bits of rocks whenever they licked their lips. Ancient Egyptians used lip color too, mixing seaweed, iodine and bromine mannite, a highly toxic plant-derived chemical that sickened its users.

From mannite to heavy metals, humanity’s quest for painted beauty doesn’t seem to have progressed far from toxic roots. The sacrifices we make for fashion!

Our bodies convert asparagusic acid into sulfur-containing chemicals that stink—but some of us are spared from the pungent aroma. Photo by Gunnar Magnusson

If you’ve ever noticed a strange, not-entirely-pleasant scent coming from your urine after you eat asparagus, you’re definitely not alone.

Distinguished thinkers as varied as Scottish mathematician and physician John Arbuthnot (who wrote in a 1731 book that “asparagus…affects the urine with a foetid smell”) and Marcel Proust (who wrote how the vegetable “transforms my chamber-pot into a flask of perfume”) have commented on the phenomenon.

Even Benjamin Franklin took note, stating in a 1781 letter to the Royal Academy of Brussels that “A few Stems of Asparagus eaten, shall give our Urine a disagreable Odour” (he was trying to convince the academy to “To discover some Drug…that shall render the natural Discharges of Wind from our Bodies, not only inoffensive, but agreable as Perfumes”—a goal that, alas, modern science has still not achieved).

But modern science has, at least, shed some light on why this one particular vegetable has such an unusual and potent impact on the scent of urine. Scientists tell us that the asparagus-urine link all comes down to one chemical: asparagusic acid.

Asparagusic acid, as the name implies, is (to our knowledge) only found in asparagus. When our bodies digest the vegetable, they break down this chemical into a group of related sulfur-containing compounds with long, complicated names (including dimethyl sulfide, dimethyl disulfide, dimethyl sulfoxide and dimethyl sulfone). As with many other substances that include sulfur—such as garlic, skunk spray and odorized natural gas—these sulfur-containing molecules convey a powerful, typically unpleasant scent.

All of these molecules also share another key characteristic: They’re volatile, meaning that have a low enough boiling point that they can vaporize and enter a gaseous state at room temperature, which allows them to travel from urine into the air and up your nose. Asparagusic acid, on the other hand, isn’t volatile, so asparagus itself doesn’t convey the same rotten smell. But once your body converts asparagusic acid into these volatile, sulfur-bearing compounds, the distinctive aroma can be generated quite quickly—in some cases, it’s been detected in the urine of people who ate asparagus just 15-30 minutes earlier.

Of course, the whole asparagus-urine scent issue is complicated by an entire separate issue: Some people simply don’t smell anything different when urinate after they eat asparagus. Scientists have long been divided into two camps in explaining this issue. Some believe that, for physiological reasons, these people (which constitute anywhere from 20 to 40 percent of the population) don’t produce the aroma in their urine when they digest asparagus, while others think that they produce the exact same scent, but somehow lack the ability to smell it.

On the whole, the evidence is mixed. Initially, a pair of studies conducted in the 1980s with participants from France and Israel found that everyone produced the characteristic scent, and that a minority of people were simply unable to smell it. People with the ability to detect the scent, though, were able to smell it even in the urine of those who couldn’t smell it, indicating that the differences were rooted in perception, not production.

More recent studies, though, suggest the issue is a bit more complicated. The most recent study, from 2010, found that differences existed between individuals in both the production and detection of the scent.

Overall, scientists now conclude that most of the difference is in perception—that is, if your urine doesn’t seem to smell any differently after you eat asparagus, it’s likely that you simply can’t perceive the sulfurous compounds’ foul odor, but there’s a small chance it’s because your body digests asparagus in a way that reduces the concentration of these chemicals in your urine.

It’s still unclear why some people don’t produce the smell, but we do seem to have a clear explanation of why some people don’t perceive it. In 2010, the genetic sequencing company 23andMe conducted a study in which they asked nearly 10,000 customers if they noticed any scent in their urine after eating asparagus, and looked for genetic similarities among those who couldn’t. This peculiarity—which you might consider useful if you eat asparagus frequently—appears to stem from a single genetic mutation, a switched base-pair among a cluster of 50 different genes that code for olfactory receptors.

We’re still waiting for some enterprising team of scientists to attempt gene therapy to convert smellers into non-smellers—but given other priorities to use genetic modification to cure blindness and breast cancer, it seems likely that those suffering from asparagus-scented urine might have to wait a while.

Swedish researchers are developing a system that tests for 12 different drugs on your breath, including cocaine, marijuana and amphetamines. Image via SensAbues

Your breath says a lot about you. Recent research has found that the chemicals present in each person’s breath can provide a unique “breathprint” that differs from person to person, while other scientists have worked on breathalyzer-like tests that can indicate the presence of a bacterial infection inside someone’s body.

In the decades since the 1960s, though, when the first electronic breathalyzer for blood alcohol content was developed, research has led to relatively little advancement in the use of chemical breath analysis for law enforcement purposes. Police have long been able to instantly test a person’s level of alcoholic intoxication by the side of a road, but testing for other drugs has required blood or saliva—substances that are more invasive acquire and that typically have to be sent to a crime lab for processing. Both factors make it difficult to figure out who’s under the influence at, say, the scene of a car accident right after it occurs.

But new research suggests that the status quo might be changing in a hurry. A study published yesterday in the Journal of Breath Research reveals that scientists can now use breath analysis to test for the presence of 12 different drugs in the body, including cocaine, marijuana and amphetamines. Previous work has shown that such technology can reliably test for several of these drugs, and this new study is the first time the drugs alprazolam (commercially known as Xanax, useful for treating anxiety disorders) and benzoylecgonine (a topical pain killer) have been detected. Members of the research group, from Sweden’s Karolinska Institutet, have already created a commercially-available breath testing system, called SensAbues—and it’s easy to speculate that law enforcement across the U.S. (and around the world) would love to get their hands on such technology as soon as possible.

Tiny amounts of microparticles in your breath reflect the substances in your bloodstream—and can be trapped and preserved for analysis. Image via SensAbues

The research team, led by Olof Beck, conducted the new study by testing the breath of 46 individuals who were checked into a drug addiction emergency clinic, had taken drugs about 24 hours earlier and volunteered to participate in the study. Each participant exhaled about 20 deep breaths into the SensAbues filter (which takes 2-3 minutes), and the solid and liquid microparticles suspended in their breath were trapped on a disk for analysis.

These tiny quantities of microparticles reflect the substances in a person’s bloodstream, because small amounts of the molecules from our blood diffuse into the fluid that lines our lungs’ bronchioles and then into our breath. By isolating these particles and analyzing them with liquid chromatography and mass spectrometry, the research team was able to determine the drugs present in each person’s body with a decent level of accuracy.

They compared the results to blood and urine samples taken from each of the participants, as well as their own reports of what drugs they’d taken in the previous 24 hours, and on the whole, the tests performed pretty well—although some progress clearly still needs to be made. All 46 people had reported taking one of the 12 detectable illegal substances, and drugs were detected in the breath of 40 of them (87 percent). Most of the particular drugs detected matched with self-reports and blood tests, but 23 percent of the time, the breath tests also indicated the presence of a drug that hadn’t actually been taken. This level of accuracy was higher than previous studies the team has done, as they’ve slowly refined the system to cut down on false positives and improve the detection rate.

Currently, using the SensAbues system would only allow officials to collect a sample and send it elsewhere for analysis. But the researchers say that advances in the cost and portability of chemical analysis could eventually allow for the same sort of roadside breath testing for drugs that we currently have for alcohol.

Another scientific hurdle is data: Unlike for alcohol, we still don’t know what a given quantity of drug molecules detected on someone’s breath means in terms of how much of the drug is actually in their bloodstream (although an accurate detection of any illegal substance might be all law enforcement officials may be after). We also don’t know how long traces of these drugs remain on a person’s breath, and how quickly they degrade.

If scientists are able to make some progress in figuring this all out, though—and if they can make the testing procedure more accurate—roadside drug tests could become a routine part of law enforcement protocol.

We find different pitches attractive because of the body size they signal—and a touch of breathiness is crucial to take the edge off a man’s deep voice. Image via Flickr user linda

Who you’re physically attracted to might seem like a frivolous, random preference. In recent years, though, science has told us that our seemingly arbitrary tastes often reflect unconscious choices that are based upon very relevant biological traits.

In general, we find symmetric faces more attractive, likely because they reflect a healthy underlying genome. Women typically prefer men with more distinctively masculine facial features because they indicate high testosterone levels and physical strength, while men prefer women with exaggerated youthful features, possibly because of the evolutionary advantages a male gets when coupling with a younger mate.

Despite all this research into our visual appearances, though, scientists have done relatively little digging into our auditory preferences when it comes to sexual attraction. Why do we find certain peoples’ voices attractive–and why do we sometimes find other types of voices such a turn-off? Specifically, why do women generally prefer men with deep voices, and men prefer women with higher ones?

At least according to a paper published today in PLOS ONE, the explanation is relatively simple: It’s all about body size. Researchers from University College London found that, at least among a sample of 32 participants, high-pitched female voices females were found to be attractive because they indicated the speaker had a small body. Deep male voices, on the other hand, were judged as more attractive because they conveyed that the speaker had a large frame—but were found to be most attractive when tempered by a touch of “breathiness,” suggesting the speaker had a low level of aggression despite his large size.

The group, led by Yi Xu, figured this out by playing recordings of digitally manipulated voices to the participants. The males in the study heard a computer-generated female voice saying phrases such as “I owe you a yo-yo” in which the voice was manipulated with a number of digital alterations in terms of pitch, formant (the particular peaks and valleys in a sound’s frequency spectrum) and other qualities.

The specific manipulations either conveyed a smaller body size or a larger one, based upon previous research that matched various voice qualities with different body sizes in humans. When asked to rate the voice’s attractiveness on a 1 to 5 scale, the men preferred the voices that suggested a smaller female. Past a certain point, though, higher voices were judged as no more attractive that slightly deeper ones. Listen to the most and least attractive (both, admittedly creepy) voices below:

The female participants’ voice preferences were similar, but slightly more nuanced. On the whole, they preferred deeper voices, which signaled a large body size, but another trait was also crucial: “breathiness.” The researchers hypothesized that this breathiness effectively takes the edge off a voice, making a man with a presumed large frame seem less aggressive and angry. They also polled the participants on whether they thought the simulated voices sounded angry or happy, and the breathy deep males voices were generally perceived as much happier and less angry than the less breathy (i.e. “pressed”) deep ones. Listen to the most and least attractive male voices below:

Beyond explaining the popularity of Barry White, the researchers say these findings correspond to much of what we know about voice preferences in the rest of the animal kingdom. Birds and other mammals, it turns out, have long been known to advertise their physical characteristics via the sound qualities in their mating calls.

All this points to an obvious question, though: Why would males prefer smaller females, and females prefer larger males in the first place? The researchers don’t attempt to address this question, but this duality reflects the sexual dimorphism present in most animal species. These differences generally result from sexual selection giving incentive to different mating strategies—so in this case, our voice preferences suggest that women benefit, in evolutionary terms, by mating with larger, but less aggressive men, while males benefit from mating with smaller females.

As the same time, what we commonly consider attractive varies dramatically over time and location—for example, dozens of prehistoric “Venus figurines,” discovered all over the world, portray extremely voluptuous female figures. So, if we tested the preferences of all humans throughout history, we might find a less obvious trend. This preference for small-voiced females and big-voiced males, then, might simply be an artifact of our contemporary cultural concepts of “attractiveness,” rather than a deep-seated evolutionary choice after all.