A year and a half ago, the decision to pack up shop at ScienceBlogs and begin blogging at Scientific American was an easy one. The inimitable Bora Zivkovic had assembled a blogging dream team, a group of people I respected and admired and couldn’t wait to call networkmates. Under Bora’s nurturing oversight, we all have flourished, and the SciAm blog network has become the most diverse and prolific science blogging network around. It is a supportive, successful, and safe place, full of people I am proud to call colleagues and friends, though they feel more like family. Here, I have had the freedom to write about everything from GMOs to robot babies to fake poop. I’ve played with tone and style, screaming at the top of my lungs one moment and gushing like a fangirl the next. Through it all, I have grown as a writer and person, and truly found my voice.

Like most sailors, though, I am not content to stay in port. I itch for the adventure of uncharted waters. I couldn’t have asked for a better safe harbor than SciAm, and I will always be indebted to everyone here, especially Bora for taking a chance on this young, spirited blogger. But, the time has come for me to cast off. It is with a mix of sadness, excitement, and just the right amount of fear that I wave a fond farewell to SciAm and announce that, as of today, Science Sushi is setting sail for Discover.

I am simply bubbling with excitement that I will be blogging alongside the likes of Razib Khan, Corey S. Powell, Keith Kloor, and the rest of the extraordinary crew over there. I’ve always been in awe of the high-caliber writers Discover has hosted over the years, and can hardly believe that I am becoming one of them.

Coming soonNow live! This blog’s URL is http://blogs.discovermagazine.com/science-sushi
The new feed is http://blogs.discovermagazine.com/science-sushi/rss

So, if you would like, update bookmarks and feeds accordingly. I know that some of you may not make the journey, but I sincerely hope you will join me over at Discover. If you like what I’ve done here, I’d really appreciate your help in spreading the word about this move. Whether it’s a tweet, a blog post, +1, a facebook like or a stumble—whatever you are comfortable with—every bit helps! Comments will be closed here at Scientific American, but all of my old posts are coming with me, so you can continue the conversation over at Discover when the blog launches.

All aboard, and anchors aweigh!

Title quote has been attributed to Grace Hopper and William Shedd, so I don’t know who really said it. Image taken by me of the R/V Hi’ialakai at port at Midway Atoll

"I’ve delivered lots of babies, and I know about these things" — apparently, Phil, you don't. Photo by CQ Roll Call.

It seems like every time a male republican tries to talk about women, he somehow says something stupid and misogynistic. Last year, Missouri candidate Todd Akin was torn apart for his negligent comment that, when a woman is raped, she needn’t worry about pregnancy because “the female body has ways to try to shut that whole thing down.” Akin was vilified by his own party and lost the election. But then, just when we think republicans might have learned their lesson, former OB/GYN and current congressman from Georgia Phil Gingrey makes an even more careless blunder, calling Akin’s remark “partially right.” He cites his experience as a doctor trying to aid struggling couples, and how he told them “Just relax. Drink a glass of wine. And don’t be so tense and uptight, because all that adrenaline can cause you not to ovulate.’”

I don’t care that Gingrey has since come out with a statement saying he did not mean to say he agrees with or supports Akin’s comment. That’s exactly what he did. Citing his authority as a physician, Gingrey made the dangerous and erroneous claim that rape victims are less likely to get pregnant. When you reference science using your education to create an air of authority, you don’t have the luxury of saying ‘oops’. You get no excuses.

The errors in Akin and Gingrey’s comments are beyond the issue of whether there is such a thing as so-called “legitimate” rape. Even if we overlook the fact that they made the misogynistic assertion that women frequently lie about being raped, they are, in fact, just plain wrong when it comes to the science. Make no mistake: Gingery and Akin’s assertion that rape is less likely to result in pregnancy isn’t correct—it’s not even kind of correct. Rape victims are not less likely to ovulate or get pregnant. They aren’t even equally likely to. They are more likely to.

If you carefully listen to Gingrey’s argument, he makes the assertion that the stress a woman experiences when trying and failing to get pregnant is the same as that experienced by a rape victim. He equates high over all stress—being anxious and nervous throughout a woman’s menstrual cycle—with the acute, immediate stress induced by a violent, demeaning act. This argument is fundamentally flawed. These are not the same—not even close.

As a doctor, Gingrey should be aware of the difference. Stressed individuals like couples desperately seeking a child suffer from high overall levels of serum stress hormones like cortisol, which has consequences throughout the body. I assume that Gingrey was referring to the fact that, in women, periods of prolonged physical or emotional stress can lead to reproductive difficulties. Athletes, for example, will often fail to ovulate, or have irregular menstrual cycles—a condition known as exercise-related female reproductive disfunction—which is thought to be the result of higher overall stress hormone levels from their exhausting regimen and decreased levels of estrogen. So, his advice to struggling couples has merit; relaxing and reducing day-to-day stress may indeed help promote healthy natural cycles, making pregnancy more likely (though his suggestion of drinking alcohol to reduce this stress is way off base).

That said, the stress response elicited by rape isn’t chronic; it’s acute. Rape victims aren’t more emotionally or physically stressed than their peers before their attack occurs. No, what a rape victim suffers is an immediate, strong stress response, more akin to how an animal might react when attacked by a predator.

The difference between the effects of chronic stress and acute stress on reproduction cannot be understated. During chronic stress, serum cortisol levels are elevated repeatedly and for long periods of time, but during acute stress, serum cortisol levels only rise briefly. “There appears to be little impact of short-term increases in cortisol concentrations,” explain scientists in a review of the effects of stress on reproduction. “Many short-term stresses fail to affect reproduction and there are reports of stimulatory effects.” By ‘stimulatory effects’, they mean that acute stress actually seems to have the exact opposite effects of chronic stress: it induces ovulation instead of preventing it.

This makes sense, really, when you consider that Gingrey’s comment that ‘adrenaline prevents ovulation’ is, simply put, flat-out, 100%, dead wrong. I have no idea what he was thinking when he made that statement, because decades of scientific research show the opposite. While high levels of chronic stress may prevent proper development and release of eggs, not only does adrenaline itself not prevent ovulation, it’s required for it. Adrenaline injection even forces ovulation in fish, rabbits, chickens, and rats.

From a biological standpoint, ovulation is caused by the interplay of a number of different hormones. When a woman is ready to ovulate, specialized cells in the brain are stimulated, causing the release of GnRH (gonadotrophin releasing hormone), which further triggers the release of two other hormones—LH (luteinizing hormone) and FSH (follicle stimulating hormone)—into the bloodstream. These, together, induce ovulation. The surge of LH and FSH is so well documented that scientists and doctors can use serum levels of these hormones to track ovulation in animals as well as in humans.

Lots of animals ovulate when acutely stressed. In sheep, ewes spontaneously ovulate when they are stressed by transport or medical treatments. Similarly, female fish exposed to an acutely stressful event were 9 times more likely to ovulate within 72 hours. Acute stress can cause surges in FSH and LH that could induce ovulation in species ranging from rats to monkeys and even people, especially if a female is near ovulation to begin with. Not only does stress cause LH levels to rise, the worse the stress, the more they rise. This led scientists to conclude that women “may be induced to ovulate at any point of the menstrual cycle…if exposed to an appropriate acute stressor.”

It’s likely that stress-induced ovulation is mediated by increases in stress hormones. While long-term rises in cortisol can prevent ovulation, artificially increasing stress hormones by injecting animals with cortisol kicks the ovulation mechanism into gear early, increasing LH release. Adrenaline plays a key role, too. If you block adrenaline synthesis or deplete adrenaline, the surge in LH required for ovulation is suppressed, and ovulation is prevented.

I don’t want to scare you: none of what I just told you means rape guarantees ovulation. The duration of elevated stress hormones, timing in regards to a woman’s natural cycle, intensity of the stress response and even just innate physiological variability between women can all affect how a woman’s reproductive system responds to stressful events. Furthermore, not all rape victims react the same way (emotionally or physically) to what happened to them, and these differences will affect how their body responds. But contrary to Akin and Gingrey’s assertions, science suggests that rape victims have every reason to worry about pregnancy.

Given the connection between acute stress and ovulation, it shouldn’t come as a shock that that the odds of getting pregnant from rape are significantly higher than from consensual sex. Read that sentence again. I really want this to soak in. You are more likely to get pregnant if you are raped.

The science that stands behind that statement is strong. For a while, scientists debated whether it was true. You can’t just compare the pregnancy rates from raped and unraped women because there are many factors involved, including birth control use, number of intercourse events, and the rate of rape reporting if conception doesn’t occur. But recent studies have taken into account these confounding variables, and the result is crystal clear. Based on real data on pregnancy in the United States, they estimate that percentage of pregnancies resulting from forced intercourse is around 8%—significantly higher than the 3% that result from single episodes of consensual sex.

Gingrey is just wrong on all accounts, and so is Akin. There is no evidence to support the role of adrenaline-mediated prevention of ovulation due to rape. There is no science to support their insinuations that, somehow, rape victims are less likely to get pregnant. Their statements directly contradict reproductive science, and serve only to demean women who have already undergone a terrible atrocity. There is simply no excuse for such blatant ignorance and thinly-veiled misogyny, especially coming from the mouth of someone claiming to ‘know about these things.’

Republican war on women, by Eclectablog

Here’s a tip for the GOP and republicans in general: stop citing biology to defend your misogynistic positions. At least stop claiming things to be true without a cursory look at the literature. It’s not hard to look these things up, boys, and you have a team of assistants to do such things for you. When you flap your lips without even the slightest clue as to what the science actually is on the subject, you look stupid at best. I’d say stop talking in general, but I think it’s good that the general public sees your positions for what they really are. On second thought, ignore my advice: keep on trucking. The baseless, unscientific lies that you tell will only serve to strengthen the people who run against you.

Micrograph of C. difficile bacteria from a stool sample culture

But for many, diarrhea is more than a shameful stain to be washed away in an impromptu laundry load; in the US alone, more than 500,000 suffer and 15,000 die every year from uncontrollable diarrhea caused by infection with Clostridium difficile. These rod-shaped bacteria are commonly found in the environment and even in our bodies, but have lately become a major concern in hospitals where antibiotics leave patients without the natural flora that protect their bodies. When C. difficile populations grow unchecked, toxins produced by the bacteria cause inflammation and cell death, leading to the explosive symptoms that, if not controlled, can lead to severe dehydration, kidney failure, holes in the intestines and death. Patients already weakened by other illnesses are particularly at risk of succumbing. Epidemics of C. difficile have become such a serious problem that the infection now rivals the superbug MRSA as one of the top emerging disease threats.

A diagram of how a stool transplant is performed

With more and more strains of C. difficile becoming resistant to antibiotics, doctors have had to find creative ways to treat the infection. One of the most promising (if not revolting) treatments that has been tested in recent years is called fecal bacteriotherapy or ‘stool transplant’, which involves taking donor poop from a healthy patient and inserting it into the gut of an infected one as a form of probiotics, seeking to replace the protective flora. I wish I was kidding. The procedure involves collecting crap from a close relative that has been screened for other microbial pathogens, mixing it with saline or milk until it reaches the right consistency, and then placing it directly in the patient’s digestive system through a tube inserted either up the anus or down from their mouths. Though it might sound gross, the dose of healthy, helpful bacteria has shown to be very effective.

Of course, most patients aren’t exactly thrilled with the suggestion of shoving someone else’s bowel movements up their rectums or down their throats. Now, University of Guelph researchers have developed a more sanitary way of achieving the same results: synthetic poop.

The researchers created fake feces, aptly named RePOOPulate, after careful examination of bacterial colonies grown from the stool of healthy volunteers. Once the right ratio of species was determined, 33 different bacteria were grown in a robotic intestine simulator affectionately called Robo-gut to create a ‘super-probiotic’ stool substitute. According to the scientists, the bacterial mixture is much more palatable than what it mimics, and smells significantly better. Two patients treated with RePOOPulate showed marked improvement after three days, remaining C. difficile-free months after treatment. Tests of their intestinal flora showed that the fake crap successfully introduced beneficial bacteria to the patients’ guts.

It’s hard to say exactly how effective the new treatment is off of such a small test, but the results are very promising. Because scientists can control the bacterial mixture in RePOOPulate, there is less risk of introducing potentially harmful bacteria than with regular stool transplants, and the treatment can be tweaked to meet the needs of different patients. This proof-of-concept paper opens the doors for future testing. In time, RePOOPulate may prove a safe and effective treatment for C. difficile infection, as well as other gut diseases caused by the imbalance of beneficial bacteria like inflammatory bowel disease.

Citation: Petrof E.O., Gloor G.B., Vanner S.J., Weese S.J., Carter D., Daigneault M.C., Brown E.M., Schroeter K. & Allen-Vercoe E. (2013). Stool substitute transplant therapy for the eradication of Clostridium difficile infection: ‘RePOOPulating’ the gut, Microbiome, 1 (1) 3. DOI: 10.1186/2049-2618-1-3

Image credits: Clostridium bacteria from the CDC’s Public Health Image Library; diagram of colonoscope from hfsimaging / 123RF Stock Photo

Just look at this face. Do you trust me? A new study in PLoS ONE says you might, even though you don't know why.

Or, more simply, what color are your eyes?

In a study published today in PLoS ONE, researchers from from Charles University in the Czech Republic had 238 participants rate the faces of 80 students for trustworthiness, attractiveness, and dominance. Not surprisingly, they found that the three measures correlated well with each other, with faces rating high on one scale rating high on the other two. Female faces were generally more trustworthy than male ones. But that’s wasn’t all. A much more peculiar correlation was discovered as they looked at the data: brown-eyed faces were deemed more trustworthy than blue-eyed ones.

It didn’t matter if the judge was male or female, blue-eyed or brown-eyed. Even accounting for attractiveness and dominance, the result was the same: brown-eyed people’s faces were rated more trustworthy. There was some evidence of in-group bias, with blue-eyed female faces receiving lower ratings from brown-eyed women than from blue or green-eyed ones, but this difference didn’t drive the phenomenon. All the participants, no matter what eye color they had or how good-looking they thought the face was agreed that brown-eyed people just appear to look more reliable.

The real question is why? Is there a cultural bias towards brown eyes? Or does eye color really correlate somehow with personality traits like accountability and honesty? Does eye color really matter that much?

To find out, the scientists used computer manipulation to take the same faces but change their eye colors. Without changing traits other than hue of the iris, the researchers swapped the eye colors of the test faces from blue to brown and vice versa. This time, the opposite effect was found. Despite the strange correlation to eye color, the team found that eye color didn’t affect a photo’s trustworthiness rating. So it isn’t the eye color itself that really matters—something else about brown-eyed faces makes them seem more dependable.

To get at what’s really going on, the researchers took the faces and analyzed their shape. They looked at the distances between 72 facial landmarks, creating a grid-like representation of each face. For men, the answer was clear: differences in face shape explained the appeal of brown eyes.

“Brown-eyed individuals tend to be perceived as more trustworthy than blue-eyed ones,” explain the authors. “But it is not brown eyes that cause this perception. It is the facial morphology linked to brown eyes.”

Brown-eyed men, on average, have bigger mouths, broader chins, bigger noses, and more prominent eyebrows positioned closer to each other, while their blue-eyed brethren are characterized by more angular and prominent lower faces, longer chins, narrower mouths with downward pointing corners, smaller eyes, and more distant eyebrows. The differences associated with trustworthiness are also how our faces naturally express happiness—an upturned mouth, for example—which may explain why we trust people who innately have these traits.

Although the trend was the same for female faces, researchers didn’t find the same correlation between trustworthiness and face shape in women. This result is puzzling, but female faces were overall much less variable than male faces, so it’s possible the statistical analyses used to test for correlation were hampered by this. Or, it’s possible that something else is in play when it comes to the trustworthiness of female faces. The researchers hope that further research can shed light on this conundrum.

Given the importance of trust in human interactions, from friendships to business partnerships or even romance, these findings pose some interesting evolutionary questions. Why would certain face shapes seem more dangerous? Why would blue-eyed face shapes persist, even when they are not deemed as trustworthy? Are our behaviors linked to our bodies in ways we have yet to understand? There are no easy answers. Face shape and other morphological traits are partially based in genetics, but also partially to environmental factors like hormone levels in the womb during development. In seeking to understand how we perceive trust, we can learn more about the interplay between physiology and behavior as well as our own evolutionary history.

Citation: Kleisner K., Priplatova L., Frost P. & Flegr J. (2013). Trustworthy-Looking Face Meets Brown Eyes., PLoS ONE, 8 (1) e53285. DOI: 10.1371/journal.pone.0053285

Female of the Emerald cockroach wasp Ampulex compressa manipulating an American cockroach, Periplaneta americana, which has been made docile by wasp venom and that will serve as food for the wasp larva. Image courtesy of Gudrun Herzner.

Glinting in shimmering shades of blue and green, the emerald cockroach wasp is surely a thing of beauty, but its shimmering exterior masks its cruel nature. The emerald cockroach wasp is one nature’s most impressive neurochemists. At its core, it is a parasite. The female wasp lays her eggs on a cockroach host, and when they hatch, the larvae eat the creature from the inside out. You’d think the cockroach would be opposed to this idea, but instead the insect patiently awaits its fate while the larvae mature. Cockroaches are much larger than even a full grown wasp, and certainly could put up a fight, but that is where the wasps’ ingenious manipulation of neurochemistry comes in. When she encounters a potential host, the female cockroach wasp first stings the cockroach in its abdomen, temporarily paralyzing its front legs and allowing the wasp to perch precisely on its head. She then stings the roach again, this time delivering venom directly into a part of the roach’s brain called the sub-esophageal ganglia. This doesn’t kill the roach. Instead, it puts the roach in a zombie-like trance. The roach is less fearful and loses the will to flee. It allows the wasp to lead it by its antennae, like a dog on a leash, to the wasp’s burrow where the roach will play the martyr for the wasp’s unborn children. Even though the roach is fully capable of locomotion during the week to month that passes from when the wasp stings the its brain until the hungry brood finish eating it alive, the zombified insect doesn’t move. Emerald cockroach wasps have elevated neural manipulation to an art form to create perfect living incubators.

But, though the roach has been rendered harmless, the wasp-to-be is threatened by other organisms. Humans aren’t the only species that have to worry about their food spoiling—so do emerald cockroach wasps. Cockroaches truly are dirty creatures, and their insides are home to a suite of bacteria that can harm the wasp’s vulnerable larvae. One of these potential threats is Serratia marcescens, a vile sort of Gram negative bacteria found in cockroach bodies. It’s the same bacteria responsible for a number of human urinary tract infections and the weird pink stains that form in our toilets and showers. In insects, its effects are much more deadly. The bacteria possess a suite of protein-degrading enzymes that cut apart fragile larval cells. The larvae aren’t entirely defenseless, though—as a new study published today in the Proceedings of the National Academy of Sciences reveals, larval wasps sterilize their food by secreting antimicrobial compounds.

For many parasitic wasps, microorganisms are a serious concern. Studies on another wasp, Microplitis croceip, found that contamination with Serratia marcescens can lead to a 25% reduction in successful parasite emergence, and even the young that do survive can be infected. When adults are exposed to the bacteria, almost 80% die. The emerald cockroach wasp must defend against this mortal enemy, or pay the ultimate price.

But how do you protect yourself against bacteria that live inside your food? Well, you do what we do to foods that house potentially harmful pathogens: you sterilize them.

Oral droplets secreted by wasp larvae, figure 1 from the paper

Gudrun Herzner and a team from the University of Regensburg in Germany noticed that larval wasps secrete droplets from their mouths that they disperse around before they feed on their cockroach meal. They suspected these secretions kill off potentially deadly bacteria, allowing the larvae to eat in peace. The researchers tested the antimicrobial activity of the oral secretions to see if they were right.

When added to bacterial cultures from the cockroach, the droplets killed off a wide variety of bacteria, including the potentially deadly Serratia marcescens. But the team wanted to know more: exactly what in the droplets killed off bacteria? So, the researchers isolated the secretions and ran them through gas chromatography–mass spectrometry to determine the nature of the substances in them. They found nine compounds previously unknown from the wasps or the cockroaches. In particular, the secretions contained a large percentage of two compounds, a kind of mellein called (R)-(-)-mellein, and micromolide, a natural product that may hold the key to treating drug-resistant tuberculosis. Both compounds showed broad-spectrum antibacterial activity, and the combination of the two was particularly effective.

As a final test, they extracted parasitized and unparasitized cockroaches and looked for these compounds. From the parasitized cockroaches, the same antimicrobial mixture could be extracted, but not from unparasitized ones. Thus, the scientists were confident that the wasp larvae produce and use these compounds to sterilize their food from the inside out.

“We found clear evidence that A. compressa larvae are capable of coping with antagonistic microbes inside their P. americana hosts by using a mixture of antimicrobials present in their oral secretion,” write the authors. While both compounds used by the larvae have been found in other animals, never before has the combination been discovered, in insects or otherwise.

The broad-spectrum nature of these antimicrobials may be key to the wasps’ success. “Food hygiene may be of vital importance, especially to the vulnerable early developmental stages of insects,” explain the authors. “The range of microbes that A. compressa larvae may encounter during their development in their hosts is unpredictable and may encompass all different kinds of microbes, such as various Gram-positive and Gram-negative bacteria, mycobacteria, viruses, yeasts, and filamentous fungi.” It would be vital, then, that the antimicrobial compounds produced by the wasps are able to fend off a wide variety of potential contaminants. “The secretion of a blend of antimicrobials with broad-spectrum activity seems to represent an essential frontline defense strategy.”

These beguiling wasps not only have mastered neurochemistry, they have aced microbiology to become proficient parasites. Already, this tiny wasp has given us great insights into brains through the study of its particularly effective zombification strategy. Now, it is shedding light on another field of science. This study is one of the first to suggest that larval parasites possess the ability to protect themselves against microbial pathogens, but the authors suspect many species of insects may have similar strategies. These small creatures may prove a vital new resource for natural products to fight against human diseases. Who knows what other pharmaceutical secrets are being kept by insects like the emerald cockroach wasp, and what ailments we might be able to treat with their chemical arsenal.

Citation: Herzner G., Schlecht A., Dollhofer V., Parzefall C., Harrar K., Kreuzer A., Pilsl L. & Ruther J. (2013). Larvae of the parasitoid wasp Ampulex compressa sanitize their host, the American cockroach, with a blend of antimicrobials. PNAS Early Edition, DOI: 10.1073/pnas.1213384110

One of the most interesting evolutionary hypotheses about brain size is The Expensive Tissue Hypothesis. Back in the early 1990s, scientists were looking to explain how brain size evolves. Brains are exceedingly useful organs; more brain cells allows for more behavioral flexibility, better control of larger bodies, and, of course, intelligence. But if bigger brains were always better, every animal would have them. Thus, scientists reasoned, there must be a downside. The hypothesis suggests that while brains are great and all, their extreme energetic cost limits their size and tempers their growth. When it comes to humans, for example, though our brains are only 2% of our bodies, they take up a whopping 20% of our energy requirements. And you have to wonder: with all that energy being used by our brains, what body parts have paid the price? The hypothesis suggested our guts took the hit, but that intelligence made for more efficient foraging and hunting, thus overcoming the obstacle. This makes sense, but despite over a century of research on the evolution of brain size, there is still controversy, largely stemming from the fact that evidence for the expensive tissue hypothesis is based entirely on between species comparisons and correlations, with no empirical tests.

With beauty and brains, Poecilia reticulata help give insights into cognitive evolution

A unique study published this month in Current Biology has taken a new approach to examining this age old question. Rather than comparing species with bigger brain-to-body ratios to smaller-brained relatives, they exploited the natural variation of brain size in guppies (Poecilia reticulata). Guppies, as it turns out, aren’t as dumb as they look. They’re able to learn, and show rudimentary ability to count. Researchers from Uppsala University in Sweden were able to use their numerical abilities to test whether brain size affects intelligence in these simple fish.

Fig. 2 from the paper; Large-brained females outperform small-brained females in a numerical learning task. Depicted are the mean and standard error values for the number of times, out of eight tests, that an individual chose the correct option of either two or four objects in females and males selected for large and small brain size.

First, the team selected for larger and smaller brains from the natural variation in guppies. They successfully created smarty-pants guppies that had brains about 9% larger than their counterparts through artificial selection. Then, they put them to the test. While the males seemed to gain no benefits from possessing larger noggins, the females with bigger brains were significantly better at the task.

But what was really remarkable was the cost of these larger brains. Gut size was 20% smaller in large-brained males and 8% smaller in large-brained females. The shrunken digestive system seemed to have serious consequences reproductively, as the smarter fish produced 19% fewer offspring in their first clutch, even though they started breeding at the same age as their dumber counterparts. And, the authors noted, this was in an idealized tank setting with an plenty of food—what about in the wild, where resources are harder to come by? How much of a cost does a reduced gut have when meals aren’t guaranteed?

“Because cognitive abilities are important to facilitate behaviors such as finding food, avoiding predation, and obtaining a mate, individuals with increased cognitive abilities are likely to have higher reproductive success in the wild,” explain the authors. These benefits, though, don’t come cheap. “Our demonstration of a reduction in gut size and offspring number in the experimental populations selected for larger relative brain size provides compelling experimental evidence for the cost of increased brain size.”

There are still many questions to be answered. For example, the authors aren’t entirely sure why females were the only ones to show cognitive improvement with larger brains. They suggest that, perhaps, the researcher’s measure of intelligence (the numerical task presented to the guppies) may be be geared toward female behaviors. “In the guppy, females are more active and innovative while foraging,” they explain. “Because females feed more, they may thus have had more time to associate the cue with food in our experimental design.”

The clear trade-off between brains and guts, though, is an important finding. By providing empirical evidence for the physiological costs of brains, this study provides the first direct support for the expensive-tissue hypothesis, and can provide us with insights into how our own big brains evolved. One of the prevailing hypothesis for our own brain growth is that the incorporation of more animal products into our diets, through hunting or cooking or however, allowed us to obtain more energy from less food, thus offsetting the cost of a reduced gut. The less food we needed to eat for the same amount of energy, the more our brains could grow even if our guts suffered for it. The debate, however, is far from over. Comparative analyses in primates don’t support a gut-brain tradeoff, and there are certainly plenty of other hypothesis as to how and why we developed our massive lobes, and what prices our bodies paid for them.

Kotrschal A., Rogell B., Bundsen A., Svensson B., Zajitschek S., Brännström I., Immler S., Maklakov A. & Kolm N. (2013). Artificial Selection on Relative Brain Size in the Guppy Reveals Costs and Benefits of Evolving a Larger Brain, Current Biology, DOI: 10.1016/j.cub.2012.11.058

Photo credit: Guppies from gucio_55 / 123RF Stock Photo

It’s been a good year here at Science Sushi. In the past year…
…I have posted 60 posts
…with several hundred thousand views
…from more than 25 countries
…with 269 comments

Most popular posts of the year? Well, controversy swirled around my posts related to organic farming, including why the failure of Prop 37 was a good thing, how bad reporting turns to fearmongering, and pesticides might not be as scary as we think, with added attention to my 2011 posts. Sharks were a hot topic, too, with my posts on the myth of bull shark testosterone and how shark populations are dwindling drawing in a lot of readers. Brain boosts from music and damages from Toxoplasmosa also ranked high on the list. My readers were intrigued by medical topics, from jellyfish sting treatments to reprogrammed heart muscle and the part played by scientists in bad reporting. Not surprisingly, sex was popular, from posts on big butts, Wild Sex (definitely worth watching!) and sex-deprived flies making the short list. I was most happy to see that some of my more creative posts also fared well; my heartfelt weavings of personal experience, science, and music, Taking Einstein’s Advice, Biochemically, All Is Fair and my 2011 post Time—And Brain Chemistry—Heal All Wounds were also among the most-read posts of 2012.

I’m thankful for the wonderful year that I have had here at Scientific American, and am excited to start 2013 on such a high note. Thank you to all of you who read this blog: let’s keep this bio-nerdy party going all through 2013!

Stumpy (devil scorpionfish, Scorpaenopsis diabolus) and Ginny (Hawaiian green lionfish, Dendrochirus barberi) wishing you the best this holiday season!

Biochemist and venom expert Angel Yanagihara

Nothing can turn a fun day at the beach into a nightmare faster than a jellyfish sting, as Angel Yanagihara, researcher at the University of Hawaii, learned firsthand when she was swimming off Kaimana beach in 1997. She had never heard of the nastiest group of jellyfish, the cubozoans (better known as box jellies), until she was badly stung. “I made it back to the beach in excruciating pain but then lost consciousness,” she recounts. “I was bed ridden for days in great pain and none of the approaches I tried brought any relief.” While the encounter was devastating, as a biochemist, Yanagihara was intrigued. She began scouring the scientific literature to find out what caused her traumatic ordeal, only to find out no one knew what was in box jelly venom. She has been studying the animals ever since.

When human flesh brushes up against a jellyfish tentacle, the tiny stinging cells jellies carry, called cnidocytes, can discharge their painful venom in as little as 700 nanoseconds. During the winter months, Australian waters are home to an abundance of the deadliest jellyfish in the world, the box jelly Chironex fleckeri, which has been known to kill a person in less than five minutes.

The deadly but beautiful Chironex fleckeri

Chironex even looks scary, with a bell that can be large as a basketball and tentacles up to ten feet long carrying millions upon millions of stinging cells. But Chironex didn’t earn its title as the deadliest jellyifish in the world based on looks. Anyone who has come in contact with Chironex knows its fearsome reputation is justified, as even mild stings are excruciating. Yet despite decades of research, exactly how Chironex and other jellies deal their sometimes-fatal blows has remained a fearsome mystery.

“For over 60 years researchers have sought to understand the horrifying speed and potency of the venom of the Australian box jellyfish, arguably the most venomous animal in the world,” explains Yanagihara. It’s not that scientists have been unable to isolate any toxins. Yanagihara’s initial work discovered pore-forming toxins called porins in a related species, Carybdea alata, capable of tearing holes in blood cells, and since scientists have found similar porins in every jellyfish species they’ve looked at. The conundrum is that severe sting victims don’t suffer from profound destruction of red blood cells, seemingly counting out the porins as the cause of fatal stings. But if it’s not the porins, what in jellyfish venom is to blame? How does it act so quickly, leading to such sudden cardiovascular collapse? And is there anything we can do to slow or stop its deadly activity?

Now, in a new paper published today in PLOS ONE, Yanagihara and her colleagues from the University of Hawaii have revealed the key mechanism by which Chironex venom—and, specifically, the overlooked porins—quickly dismantle the cardiovascular system. Armed with physiology, the team was able to find a safe treatment that could be used to improve survival in sting victims.

Yanagihara collecting Hawaiian box jellies

It’s virtually impossible to find a good treatment for a toxin without first knowing what it is. So, the first step for Yanagihara was to isolate jellyfish venom and figure out if the porins were the real culprits. For species like snakes and spiders, this is a straightforward process, as they possess glands with large volumes of venom. But you can’t just have a jelly bite a container or pull venom from a cnidocyte using a syringe; minuscule amounts of venom components are stored in microscopic compartments amongst a plethora of other body parts—deadly needles in haystacks of cellular debris. Yanagihara spent years troubleshooting and perfecting a new method of venom extraction to yield potent venom free of as much junk as possible. With this in hand, she was able develop assays to visualize how the venom acts both on red blood cells and in live animal models.

Ring-shaped pores in the wall of a red blood cell from jelly porins

Yanagihara used electron microscopy to visualize the venom’s affects on blood cells, and as suspected, found that venom porins create holes that lead to cell rupture. But as previous clinical research had shown, the cells bursting wasn’t the real issue; Yanagihara found that instead, for several minutes before they break apart, red blood cells leaked potassium. Animal models confirmed that this sudden spike of potassium in the blood stream, termed hyperkalemia, is what leads to rapid changes in heart rate and function and, ultimately, the cardiovascular collapse that causes death by jellyfish. With the physiology of stings revealed, Yanagihara could finally start the laborious task of finding a way to stop the venom in its tracks.

Jellies aren’t the only animals that create porins. “The structural motif of the cubozoan porin reminded me of the bacterial porins,” said Yanagihara. “I scoured that literature to look for inhibitors of the self assembly of those pore forming toxins and discovered studies from the 1940s even as far back as the 1890′s citing zinc ion as useful in the inhibition of bacterial driven lytic reactions.” Yanagihara tested over 100 compounds to see if they inhibited jellyfish venom, and found that one of the safest—zinc gluconate—worked well.

Scientists aren’t 100% sure how zinc compounds inhibit the porins, but they believe that the zinc disrupts the binding domains necessary for the proteins to assemble to form pores. In in vitro models, Yanagihara found that a low dose of zinc gluconate completely prevented the venom’s blood cell busting effect. She then tested the compound in animal models, and found it worked better than the commercially available antivenom for box jelly stings, keeping the mice alive more than twice as long as the antivenom.

Yanagihara preparing the topical treatment for Nyad

Yanagihara is now investigating how to turn the compound into a treatment for human stings. She has created a topical version, which was tested on extreme swimmer Diana Nyad when she attempted to swim a record-breaking 103 miles from Cuba to Florida. Nyad attempted the swim in 2011, but was stung so severely by box jellies on the first day in the water that she had to stop after 29 hours. This time, armed with Yanagihara’s treatment, she swam three nights through dense jelly aggregations, and kept at the swim for a total of 51 hours covering over 60 miles of the trek before she gave in. Nyad reported that the treatment blunted the stings to her exposed lips and face enough to keep her going.

Zinc gluconate isn’t a cure-all; it won’t stop all of the excruciating pain associated with severe stings, and victims are still at risk of going into shock and cardiovascular failure. But, Yanagihara is hopeful that treatment with zinc gluconate might be effective enough at prolonging survival in severe sting victims long enough to get them to medical professionals that can save their lives, and may provide welcome relief to mild sting victims. Currently, vinegar is used to treat jellyfish stings, though it only prevents unfired cnidocytes from contributing to the sting and doesn’t act on the venom itself. Hot water can provide temporary relief, but Yanagihara is hopeful that zinc treatment will prove a more viable solution.

In Australia and other areas of the Pacific where Chironex roams, such a solution is desperately needed. Despite being home to ten of the worlds deadliest snakes, since 1980, there have been more deaths due to jellies than snakebites in Australia, and it’s estimated that 20-50 people die annually from box jelly stings in the Philippines. Worse, in recent years, scientists have reported that expanding ranges for many jellyfish species due to changing ocean currents, over-fishing of other species, and warmer ocean temperatures from climate change. The Nation Science Foundation estimates that jellies cost hundreds of millions or even billions of dollars in medical damages, fisheries effects and tourism loss. This breakthrough treatment is more important than ever, and hopefully, will help relieve the thousands of stings worldwide every year.

Citation: Yanagihara AA, Shohet RV (2012) Cubozoan Venom-Induced Cardiovascular Collapse Is Caused by Hyperkalemia and Prevented by Zinc Gluconate in Mice. PLoS ONE 7(12): e51368. DOI: 10.1371/journal.pone.0051368.t002

Photo credits: Angel Yanagihara taken by Laura Aguon; Chironex fleckeri by Dr. Robert Harwick; Box jelly collecting by Keoki Stender; Pores in RBC from the paper itself; Yanagihara prepping treatment by Christi Barli (all images provided by Angel Yanagihara)

Lysibia nana parasitizing cocoons of Cotesia glomerata

But, as Dutch scientists have discovered, the story doesn’t end there. What goes around comes around for the C. glomerata, as there are other wasps that use them as hosts, laying eggs in the wasp larvae that grew in the caterpillar, like a parasitic Russian doll. Researchers have discovered that these hyperparasitoids (parasitoids of parasitoids) can smell the call being broadcast by the plant, too.

After all, the world is a large place. Parasites that need to find a very specific, small host benefit from having a way of finding what they need without wasting tons of energy searching. So it makes sense that Cotesia glomerata and other parasitoid wasps with caterpillar hosts are drawn to the chemical compounds emitted by damaged plants. If they’re drawn, the wasps that parasitize them should be drawn, too. So the team tested this hypothesis by collecting air from undamaged plants, plants damaged by uninfected caterpillars, and plants damaged by caterpillars already infected with parasitiod wasp larvae, then presented those scents to hyperparasitoid wasps to see if they were attracted to them.

Not only were the wasps attracted to the smell of caterpillar damage in general, “we found that they preferentially detected odours of plants damaged by infected caterpillars,” explained Dr Erik Poelman, lead author of the study published today in PLoS Biology. The wasps were nearly five times more attracted to the damage done by infected caterpillars. “We were excited by these results as they indicate that hyperparasitoids rely on a network of interactions among plant, herbivore and parasitoids to locate their host”.

But how did the wasps detected whether the caterpillars were infected? Poelman and his team wanted to find out. It’s known that infection can change the saliva contents of caterpillars, so they took the saliva from uninfected and infected caterpillars and presented those scents to the wasps, but the wasps didn’t care. So while the infection is altering the caterpillar’s saliva, the change in attractive chemicals had to be coming from the plant. They then tested the different air collections for volatile compounds, and found the ones damaged by caterpillars infected with Cotesia glomerata were only 40% similar to the ones damaged by uninfected caterpillars. Something about infection changes the saliva in a caterpillar, which in turn affects what volatile compounds a plant emits when it gets damaged by that saliva.

This complex web of interactions calls in to question the role of the plant compounds in the first place. Though they are often thought of as a ‘cry for help,’ the team noted that this may not be the case at all. “Although plant volatiles may function as a ‘‘cue’’ to parasitoids, they may not be a specific ‘‘signal’’ released by the plant (implying a selective benefit),” write the authors. “It is important to emphasize that volatile cues may provide many community members with information and thereby may not necessarily result in a fitness benefit to plants.”

These findings also call into question the use of parasitoid wasps as biocontrol for managing pests. Cotesia glomarata has been introduced and intentionally released in a number of agricultural areas to control caterpillars like Pieris rapae. Recently, some have suggested that farmers might be able to spray the volatile compounds emitted by damaged plants to attract more parasitoids, as a way of reducing pest populations without using pesticides. But the authors think that this strategy might not be so clear-cut. “Our results show that hyperparasitoids may parasitize up to 55% of the parasitoid offspring, therefore potentially playing a major role in parasitoid population dynamics,” they caution. “Overexpression of herbivore-induced plant volatiles [HIPVs] in crops or field application of synthetic parasitoid attractants may not benefit pest control in conditions where the responses of hyperparasitoids to HIPVs cause major mortality to parasitoids.”

In other words, the interactions between species are far more complex than we once thought, and we can’t assume we can predict how our manipulations will affect a community—which is generally the trouble we’ve gotten into when trying to use biocontrol mechanisms. The more we try to tinker with interspecies interactions, the more unintended consequences we seem to have.

Research: Poelman E., Bruinsma M., Zhu F., Boursault A. & et al (2012). Hyperparasitoids Use Herbivore-Induced Plant Volatiles to Locate Their Parasitoid Host., PLoS Biology, 10 (11) e1001435. DOI: 10.1371/journal.pbio.1001435.t005

Image: Nina Fatouros, www.bugsinthepicture.com

So, I had a little free time this holiday weekend and re-recorded another old song of mine. This one goes way, way back to when I was in high school—and of course, it’s about a boy, as many of my songs are, and certainly many were at that age. But, it was a particularly insightful one for little 14 year old me, about how sometimes letting go is harder than it should be. Enjoy!

“I have been writing and talking about animal sex for the better part of 5 years,” explains Carin, who received her PhD in Freshwater Ecology from the University of British Columbia. “We hit topics hard, and not just for the quirk factor, but because there is a lot of cool science behind so many strange mating rituals.”

When it comes to salacity, this series has it all. The show looks at the spicy sex lives of all sorts of animals, from insects to elephants, outing each for their kinkiest traits. It has your basic fetishes from bondage to orgies, prostitution, and even a little sexual cannibalism. I was fortunate enough to preview the first three episodes, and I am more than impressed with the accuracy, indecency, intelligence and humor with which Carin and her team have tackled these, uh, sticky topics. They make no apologies for the straightforward style—this is a show that gets down and dirty with nature’s deviants. “The show is all about sex, and I was not shy about it,” says Carin. “I approached it from a go big or go home standpoint. I feel like it could have come across as really drab if I played it too safe.”

And go big she does. This is no surprise to anyone who has met Carin in person. Her slogan “biologist with a twist” is spot on, and her bold yet charming personality is immediately apparent when you meet her. On screen, it is even more captivating. She has a way of drawing you right into the room with her, which, given the titillating subject matter, may be a little uncomfortable at times—in a good way. The second episode (which is about getting stuck during copulation) had me wincing and cringing throughout, yet like the soapberry bugs Carin describes, I was totally hooked. From sex toys to half-naked men, Carin wasn’t afraid to choose the right tool to get across the science—which is, of course, the show’s ultimate goal.

“I think that the person who would normally watch a science show will love it,” says Carin, “but people who would not normally watch science shows will have their attention piqued and will love watching it (and learning it!) too.” She giddily explained to me how even the actors and crew got a lot out of filming. “While we were shooting there were so many learning moments with members of the crew…people would say things like ‘Wow! I didn’t know that—that’s so interesting’. ‘I had no idea that…’ ‘I’m so glad I learned that…’”

Carin’s passion for the science behind the sex is what really makes this series work. Anyone who reads my blog knows I’m not shy about these things, but Carin’s knowledge is impressive and disarming, even for a shameless girl like me. In my interview with her, she easily made me blush. It was my fault, really. She mentioned that working with elephants was one of her favorite moments of filming, and I made the mistake of asking how they fit into a sex show. “Surely you must know about the penile clitoris?!” Actually, I don’t, but I’m looking forward to that episode, titled “You Can’t Rape An Elephant.”

Carin is well aware that not everyone will respond kindly to her bold approach to a series about animal sex. “I will (and already have) received feedback along the lines of : oh she sold out to using her looks instead of her brain, oh she’s desperate for attention, etc,” said Carin. It’s sad that any time an attractive woman talks about an even remotely racy topic, she gets these kinds of comments. But Wild Sex isn’t gratuitous; it’s an intelligent, well done scientific program that happens to be about fornication. “So yes, there is sex,” Carin says confidently. “And graphic language. And me being sexy. Take it or leave it, I stand behind my work 100%.”

I’m standing with her. This series is amazing. Carin is a smart, strong, beautiful woman with four kids who isn’t afraid to bust out of puritanical norms and discuss the darkest of animal desires with wit and sex appeal. She is the epitome of a modern feminist, unafraid of and unapologetic about being true to herself and to the science that inspires her. Besides, you have to give props to anyone who can say “detachable swimming penis”, “penis snapping” and “vaginal plugging” with a straight face.

So do yourself a favor: grab some chocolate-dipped strawberries or some oysters, light some candles, and sit down and watch Wild Sex from Earth Touch TV. I can definitely promise things will get wild, but hopefully, you’ll find your brain as aroused as other areas. Carin, Benjamin and Richard have truly nailed it—pun intended.

I only hope that I can find a way to slip in for a cameo when she films season two… What do you say, Carin? What does a girl have to do to get on an episode of Wild Sex?

…Uh, on second thought, maybe I don’t want to know.

Episode 1!

Photo of Dr. Bondar c/o Kim Mallory Photography

Before I get started, though, let me explain where I am in this whole process. Right now I’m still in the thick of it. I’m three and a half years into my doctorate degree, with an approved proposal and my comprehensive exams looming around the corner. So this isn’t advice from a veteran, per se—it’s advice from a fellow soldier, down in the trenches right now, still fighting the good fight. Maybe I’ll have different advice in a few years, but for now, this is what I know.

First off: don’t start until you’re ready. I remember feeling the pressure junior and senior year of undergrad. Everyone was talking about what programs were best for what, what advisors to chase or avoid, what GPA you needed to get in—it was all anyone talked about. Have you figured out what schools you’re applying to yet? Have you contacted potential advisors? What research do you think you’re going to do? The worst was one day senior year when I went to the movies, and upon presenting my student ID to get a discount, the teller said “I went to Eckerd, too! Graduated two years ago. What are you majoring in?” When I said Marine Science, she cheerfully replied “ME TOO!” It was like a punch in the stomach. It really felt like those were my options: either get into grad school somewhere, or look forward to a dazzling future selling movie tickets. The pressure was on.

Trouble was, I was still very much lost. Yes, I had research experience, but of all the things my undergraduate research project taught me, the most obvious was that I hated counting mangrove leaves. I was not the extreme field biologist that my advisors were. Similarly, while I’d dabbled in a few other research experiences through volunteering and internships, nothing felt like it fit. I liked a few things, but did I like them enough to spend the next five years doing them? To bet my career on them? As senior year came and went, I made the scariest decision of my life: I didn’t apply to grad school.

Instead, I applied to jobs. I hoped that getting a little more experience before committing myself to a degree program would help me figure out what kind of scientist I wanted to be. The little tastes of molecular biology that I had gotten in my lab courses was enough for me to think maybe, just maybe, that was the field for me. In the end, I spent two years as a research assistant studying adenosine signaling in heart cells. Guess what? The biomedical field wasn’t right for me either. But by the end of it, I figured out where I did fit. I had found my scientific niche, somewhere in between field biologist and lab lackey. When I applied to grad schools, I did so with confidence and conviction. Keep in mind that through grad school, you become the world expert on something—make sure it’s something you want to be the world expert on.

Which brings me to my second piece of advice: find your niche. I was lucky enough to be in a program that required three rotations, which means I spent my first year at UH bouncing between three very different labs. Most people in the natural sciences start with an advisor, and stay with them until dissertation do they part. That’s ok and all, but before you make that kind of lasting commitment, spend a little time and get to know the lab you’re assigning yourself to. At minimum, fly out to your prospective university, meet the man or woman in charge, and talk to their grad students. While people often joke about the similarities between grad school and marriage, there’s a lot of truth in jest. Getting a PhD in particular is a huge commitment, and you don’t want to get several years in and realize you want a divorce.

Yes, you can deal with a bad advisor or an unsupportive lab, but do you want to? Are you the kind of person with an iron will that pushes through at all costs? Some people are. Some people are tenacious, headstrong, and absolutely amazing, and they barrel through no matter how bad things get. I’m not that kind of person, which is why I’m so glad that I got those three rotations to give my potential advisors a thorough screening. Simply put, without those rotations, I wouldn’t be in the lab I am in now, and I would probably be worse off for it. My advisor is a perfect fit. He lets me be creative and come up with insane project ideas, then reels me in and pushes me to actually get things done when it’s time. His co-PI is an amazing mentor, always there with the advice, aid, or encouragement I need even though I’m not his student. And the rest of my lab: well, to put it bluntly, my lab f*cking rocks. As cliche as it might sound, they really are like family to me. Sure, we don’t all get along all the time, but when push comes to shove we have each other’s backs, and support and drive each other to be the best scientists we can be. I have no doubt that my lab mates will be my friends and colleagues for years to come. The other people I have surrounded myself with—my committee members, other graduate students and post-docs—have been my champions, drinking buddies, guides and rocks to cling to when I feel like I’m about to drown. Without the generous support I’ve received to date from my advisor, other mentors, and fellow grad students, I don’t think I would have made it this far. Honestly, I don’t think I would have made it at all. This perfect mix of camaraderie, encouragement and occasional butt-kicking was exactly what I needed.

Figure out what you need. The best way to do that is to follow your passions and instincts. Maybe the lab dynamic isn’t as important to you as having a supportive group of family nearby. Or cats. Or gardening. Find what keeps you sane and helps you keep going forward, at work and at home. Get into good, healthy routines like eating well and sleeping enough. You can break these when you need to, like when that big grant deadline approaches too quickly, but then get back into them. For me, getting a place with a real kitchen was key. I needed to cook, and when I first moved to Hawaii, all I had was a hot plate. It’s funny how something as simple as an oven can make a world of difference.

I’m not going to tell you that grad school is easy. Maybe it will be for you. Most likely, it won’t. Learn to be flexible and adapt, because things rarely go as planned. You’ll be all ready for field season, and your target species will be MIA. Your genius experiment won’t work, or you’ll spend months in the lab trying to figure out the right protocol. It’ll take an extra six months to get the permits you need. Your key piece of equipment will break. You’ll be on the verge of the discovery of a lifetime, and someone else will beat you to publication. Or, if you work where I do, your lab will get randomly shut down for construction for ambiguous and often unreliable amounts of time. These things happen to everyone, and they can feel like impenetrable walls keeping you from your degree. They’re not. You’ll find a way around them if you’re willing to bend in the right ways, ask for help when you need it, and keep your head in the game.

You’re not necessarily going to feel like you know what you’re doing all the time. Hell, I haven’t. I spent the first couple years of my dissertation wondering why anyone let me into grad school in the first place. Couldn’t they see I was far dumber than the rest of these people? Had I really tricked them all into thinking I’m good enough for this? What is going to happen when they finally figure me out, and realize that I can’t cut it?

It’s called impostor syndrome. I wish I had some magic formula for how to shake those cancerous feelings of unworthiness. I don’t. But what I do know is that over the past year, I’ve really come to own my dissertation. I’ve buckled down, focused my research, gotten things done, and crossed that hidden threshold between newbie and senior grad student. Sometime in the past six months or so, when I wasn’t looking, my impostor syndrome went into remission. If I had to guess, I would say that I finally convinced myself, through actions, that I am the scientist I kept feeling like I wasn’t. I didn’t mean to, really. It all kind of happened by accident, a side effect of really making my dissertation my own. Maybe that was the magic cure all along.

So, that’s my last and best advice to you: Be confident. Take charge. It’s your project. It’s your degree. Choose it. Love it. Own it. And guess what? You can not choose it, too. There’s no shame in deciding that grad school isn’t right for you, or that you’re in the wrong lab, program, field, career—whatever. Trust yourself to make the right call. After all, the one thing you are definitely the world expert on is you.

Finally, there are some great scientific projects in need of a little cash-y love on SciFund right now. Want to help support research on chemical warfare in the intertidal (with a RAP VIDEO)? How about sexy shrimp or butterfly STDs? You can be an integral part of real scientific research! There are tons of great research projects that need your help, so head on over to the SciFund page and see what tickles your fancy.

Remember, ’tis the season of giving, so open your hearts and empty your wallets!

Well, now I want to be more explicit in my sharing. I don’t have fancy blog posts to go with every song I’ve ever written; I’ve been writing songs since I was a kid. So, I’ve decided to start a new series: Musical Mondays. Surely I won’t manage to post one every Monday, but on some Mondays, I’ll post songs of mine to share with all of you. I’ll try and write a little backstory on the songs, just to give some perspective.

This is a song I wrote over a decade ago (gosh, has it really been that long?!), and have always played for myself when I need comfort. It’s probably the most honest and soul-searching I’ve ever been in a song, which is why I’ve kept it to myself for so many years. But talking to awesome people like David Kroll—hearing, firsthand, how much music can make an impact, even on us science types (neurologically!)—has got me thinking a lot about songwriting and what it means to me, and I think it’s time I shared more, especially the songs I guard most vehemently. So, enjoy.

Coral under siege by the seaweed Chlorodesmis fastigiata

Just below the ocean’s surface, a war is being waged. Coral reefs are under constant assault by seaweeds which seek to take control, stealing the coral’s prime sunlit location for themselves. Many of these plant invaders come equipped with deadly chemical weapons that knock down the coral’s metabolism, which might come off as an unfair fight against a seemingly unarmed foe. But corals aren’t defenseless; as a new paper in Science shows, corals have fish bodyguards at the ready to mount a defense.

Coral reefs are one of the most productive ecosystems on Earth. They’re also one of the most threatened. While managers and scientists struggle to find ways to protect these precious habitats, coral cover has decreased by 50% along the Great Barrier Reef and 80% in the Caribbean. The losses ripple up the food chain, causing declines in fisheries and ecosystem services. But not all organisms mourn coral declines—when corals struggle, seaweeds reap the benefits.

Corals and seaweeds are in a constant struggle for dominance. On healthy reefs, seaweeds are kept in check by plant-eating fishes and invertebrates which keep the algae from overtaking their coral homes. When these herbivores are lost, like when sea urchins underwent a massive die off in the Caribbean in the 1980s, the algae run rampant, reducing habitat complexity and leaving many fish homeless. Up until recently, it appeared that corals are relatively passive in this ongoing battle. But now, scientists from Georgia Tech have found that corals actively recruit defenders to fight algal invasions.

“We had been studying coral-seaweed interactions to determine which seaweeds were most damaging to which corals and the mechanisms involved,” explains study co-author and professor in the School of Biology at Georgia Tech, Mark Hay. He and his post-doc Danielle Dixson discovered that the seaweed Chlorodesmis fastigiata is particularly chemically toxic to corals, emitting lipid toxins that harm corals that they come in contact with. Yet in Fiji, where the experiment was conducted, corals seemed to be holding their own. Given the important role of herbivores, the team decided to see if the fishes living in the corals might be fighting back on behalf of their homes. So, they took Acropora nasuta colonies (an important reef-building coral) that had resident gobies and removed the fishes from some of them. They then placed algae or an algae mimic made of nylon line on the corals and watched the corals over a few days to see what happened.

The mutualistic fish Gobidon histrio in its home coral Acropora nausuta, coming out to investigate the presence of the toxic green alga Chlorodesmis fastigiata

While the fake algae (which physically covered the coral but lacked the chemical weaponry of the algae itself) had no effect, the corals where algae was transplanted were all damaged by the introduction of the competitive plant. But, the scientists noted, the corals that retained their fish residents were much better off. After three days, the amount of seaweed left on the corals was reduced by 30%, and the corals themselves suffered only 20% – 30% the damage of the corals without their fish colonies.

Assured of the important role of the fishes living in the corals, the team further investigated the interplay between the fish, coral and algae. The team introduced Chlorodesmis fastigiata to corals again, but this time they watched how the fish reacted. Within minutes, small gobies—only inches in size—emerged from their hiding places to pick at and eat the seaweed. “These little fish would come out and mow the seaweed off so it didn’t touch the coral,” said Hay.

But to really understand what was going on, the scientists took water samples from next to undamaged corals, corals damaged by algae while the algae was still present, corals damaged by algae after the algae was removed, and the algae alone away from coral. They exposed gobies to these water samples and watched how they responded. In less than 15 minutes, gobies were drawn to the water from damaged corals, but didn’t react to the chemical signature of algae by itself. “We found that the gobies were being “called to” the area damaged by the algae, and that the “call” was coming from the damaged coral, not from the seaweed.”

“This species of coral is recruiting inch-long bodyguards,” explained Hay. “This takes place very rapidly, which means it must be very important to both the coral and the fish. The coral releases a chemical and the fish respond right away.” The scientists even tested the gobies by using water from seaweed damage of a different but closely related coral species, but the fish didn’t react. “The gobies came to the rescue of their host coral but did not respond to a related coral’s chemical cues,” said Hay.

The gobies aren’t being entirely selfless. Gobies don’t just eat seaweed—they also eat mucus from the coral itself. “The fish are getting protection in a safe place to live and food from the coral,” explains Hay. “The coral gets a bodyguard in exchange for a small amount of food. It’s kind of like paying taxes in exchange for police protection.”

In addition to defending their homes, the team found that one of the little fish species gets an extra defensive boost from eating the invading seaweed. “One of the gobies was known to produce a toxic skin secretion,” explained Hay. “This goby consumed the toxic seaweed and became more toxic,” thus helping to protect it from potential predators. The other main species of goby found in the coral doesn’t have this defense, but it still fought off the attacker. “It trimmed back the seaweed from its host coral but did not consume the seaweed – it apparently just trimmed it and spit it out.”

The scientists were even able to narrow down what in the seaweed is causing the coral’s cry for help. The team took different fractions of seaweed chemicals and applied them to fake nylon mimics. Only the extract containing the known lipid chemical weapon triggered the fish defense system.

“I’m an ecologist that studies chemically-mediated interactions, but the wonderfully subtle, nuanced, and specific chemical dance being conducted here is still shocking to me,” said Hay. He noted that these findings highlight the significance of mutualistic interactions on coral reefs. “Competition among some seaweeds and corals has been important enough to drive the evolution of this wonderfully well-tuned signaling among a coral and its mutualistic fishes.” While similar mutualistic defense systems are well described in terrestrial species, this is the first time such an interaction has been shown in a marine environment.

Hay also emphasized that, at least when it comes to ecosystems, size really doesn’t matter. “Organisms need not be large or abundant to be ecologically important,” said Hay. “These tiny, inconspicuous fishes are important in slowing, or preventing, the damage that seaweeds do to corals and thus are important, but unappreciated, in stabalizing reef corals and preventing coral loss and reef decline.”

Citation: Dixson D.L. & Hay M.E. (2012). Corals Chemically Cue Mutualistic Fishes to Remove Competing Seaweeds, Science, 338 (6108) 804-807. DOI: 10.1126/science.1225748

Photos: Coral and seaweed © Paul Asman and Jill Lenoble, under creative commons license from Gaia Guide; Goby defending coral by Danielle Dixon c/o Georgia Tech; Juvenile goby by Joao Paulo Krajewski c/o Georgia Tech

The rallying cry for supporters of this proposition has been “The Right To Know.” It sounds so simple: why shouldn’t people know if their food is genetically modified? What does Monsanto have to hide? But couching the issue in terms of knowledge assumes one thing: that labeling will be in any way informative. In the case of Prop 37, it simply wouldn’t have been. Michael Eisen put it perfectly:

This language reflects the belief of its backers that GMOs are intrinsically bad and deserve to be labeled – and avoided – en masse, no matter what modification they contain or towards what end they were produced. This is not a quest for knowledge – it is a an attempt to reify ignorance.

The simple fact is that there is no evidence that GMOs, as a blanket group, are dangerous. There’s a simple reason for this: not all GMOs are the same. Every plant created with genetic technology contains a different modification. More to the point, if the goal is to know more about what’s in your food, a generic GMO label won’t tell you. Adding Bt toxin to corn is different than adding Vitamin A to rice or vaccines to potatoes or heart-protective peptides to tomatoes. If Prop 37 was really about informed decisions, it would have sought accurate labeling of different types of GMOs so consumers can choose to avoid those that they disapprove of or are worried about. Instead, anti-GMO activists put forward a sloppily written mandate in a attempt to discredit all genetic engineering as a single entity. The legislation was considered so poorly worded that most Californian newspapers rallied against it, with the LA Times calling Prop 37 “problematic on a number of levels”.

By all means, boycott Monsanto, or any food containing their products. Despite rumors to the contrary, I do not support Monsanto in any way (nor do they, in any way, support me). Like many big companies, I think they have had shady business practices at times and are more concerned with their own bottom line than the good of the people or the environment. I’ve already come out strong against RoundUp Ready crops. But my lack of love for Monsanto doesn’t tarnish the fact that GMOs have the potential to dramatically benefit people across the world by providing balanced nutrition and enhancing production in struggling areas. GMOs aren’t inherently evil, and they have the potential to address many of the very real concerns about our current and future food supply.

There’s also another reason that GMOs aren’t considered dangerous: decades of scientific research support their safety. As Pamela Ronald, a UC-Davis plant geneticist, phrased it last year in Scientific American: “There is broad scientific consensus that genetically engineered crops currently on the market are safe to eat. After 14 years of cultivation and a cumulative total of 2 billion acres planted, no adverse health or environmental effects have resulted from commercialization of genetically engineered crops.” Or, as Ingo Potrykus, career plant scientist, put it in a review article for the Journal of Plant Biochemistry and Biotechnology, “GE-technology has an unprecedented safety record and it is far more precise and predictable than any other “traditional” and unregulated breeding technology.”

And, despite the call to arms against GMOs on environmental grounds, a 20 year study published in Nature found that some GM crops can actually improve biodiversity. Because Bt crops reduce pesticide spraying, scientists saw increases in populations of ladybugs, lacewings and spiders. Even more impressive, these benefits weren’t just seen in Bt fields—these upsides spread to the fields near them. And it’s just one of many studies refuting the ecological argument against GMOs.

Based on the growing body of scientific literature, numerous scientists and scientific organizations have come out in defense of genetic engineering technologies and against labeling initiatives like Proposition 37, including the American Association for the Advancement of Science (AAAS), the American Medical Association, the National Academy of Sciences and the World Health Organization. The AAAS statement put it succinctly: “Legally mandating such a label can only serve to mislead and falsely alarm consumers.”

The proponents of Prop 37 sought to use rhetoric and language to sway against science. They used the word “right” to smother dissent—after all, how can anyone debate against someone’s “rights”? They tried to capitalize on people’s lack of knowledge of the science of genetic engineering to push their own political agenda. Instead of stimulating discussion and understanding of genetically modified foods, they sought to guilt or scare people into making rash decisions. So yes, I’m happy to see that they have failed. Californians have stood in defense of science, and should be applauded for it.

In retrospect, I feel like a fool. As I sit at the edge of my bed fumbling with my guitar, I can’t help but blame myself. Why did I choose time and again to trust a person whose actions have always betrayed it? Blinded by love, I had a slew of reasons, a variety of parameters I could change that I thought might affect the outcome. But now, with 20-20 hindsight, I cannot find any. I should have known better, I chide myself. I failed the scientist in me.

Yet still at the slightest mention of him, I flush with anger, jealousy and regret, and heart pounding, I fantasize about retaliation and justice. Evolutionary psychologists would tell me that the physiological experience of betrayal stems from the fact that humans, at our core, are a social species. Personal bonds were vital to our ancestors, and thus natural selection has reinforced emotional mechanisms that evaluate the connections we form with others. In a dangerous world, our ancestors had to know whom they could trust with their lives. Anyone who threatened the relationships we have with one another didn’t just wound pride or break hearts, they threatened our predacessors very survival. The reaction is strong and visceral: stress hormones spike, leading to twisting pain in our gut and heightened sensitivity. But at the same time, areas of our brain involved in deception detection activate. While we feel the rush of cortisol and adrenaline clouding our thinking, brain regions like the anterior insula process our physical and emotional state to make judgements of trustworthiness to inform future interactions.

My desire for retribution is primal, too. When we feel betrayed, our brains light up in areas associated with agression and testosterone levels rise. Scientists have found that other primates get upset when they feel that have been treated unjustly, and that people, when trust is broken, often will choose to punish the transgressor even if that punishment comes at a high cost to themselves. We want to lash out, to make things equal by returning the wrongs inflicted upon us. But instead of acting on instinct, I start to play. As calming notes pour from my fingertips, I feel the burning pain in my chest subside.

If only my previous judgements had been more permanent. A friend of mine likes to say “monkeys learn,” but clearly, I didn’t the first time. Though the rest of our evolutionary lineage seems to be quick to categorize friends from foes, I could not.

What’s done is done, though, and I am left to collect the pieces of my heart that they shattered so effortlessly. While I might not have learned my lesson as quickly as I should have, I have learned it now. I know that this time is different. There will be no more replicates, no more re-runs with the hope of a different result. There are no variables I can change to get what I want. The data are clear, and it’s time to stop trying to bias them toward the end I prefer. All that is left is to document what happened, so like a good scientist, I write and record my final results.

Like this post? Check out Time—And Brain Chemistry—Heal All Wounds and Biochemically, All Is Fair

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I have been to Raleigh thrice before, and each and every time I have tried desperately to go to the Duke Lemur Center. Each and every time, I have failed. Friends and colleagues would regale me with furry tales (we all know what you did, Ed Yong) while I jealously listened, trying and failing to imagine what they experienced. No photo or video was enough—I knew that, like with most good things in life, I simply had to be there. So when I hopped on the tour bus on a cold, wet Friday morning, it didn’t matter that it had been more than 30 hours since I’d slept in a bed. I was ready for lemurs.

For those of you who aren’t familiar with it, the Duke Lemur Center is the world’s largest sanctuary for lemurs, rare and endangered primates endemic to the island of Madagascar. It covers a massive 85 acres of Duke Forest in Durham, NC, and is home to around 250 animals, including 15 species of lemurs and some of their prosimian relatives, the lorises and bushbabies. Many of the lemurs are “free range,” as they are given access to acres of forest to call their own. As Education Specialist for the center and my tour guide of the day Chris Smith explained, it is the second most incredible place on Earth, falling just short of the lemur’s native habitat.

Chris’ passion for these quirky relatives of ours is instantly evident. The tall, lanky blonde with just enough of a southern accent to hint at his Tennesseean roots couldn’t help but spend the entire bus ride gushing over the animals he’s been helping the Center take care of for the past three years. “Lemurs are entrancing. They have these big, expressive eyes that pull you in.” But to Chris, what makes lemurs even more bewitching is that they have so many human features, too. “They have this sort of basal mammal quality that makes them absolutely adorable… [but] they have hands, feet, fingerprints, and complex social behaviors just like we do.”

He’s not alone in being captivated by lemurs; all of the staff I met at the center seem to be fueled by their love for the furry little creatures. “Having had several roles at the DLC—work-study, volunteer tech, full-time paid tech, and educator—I honestly have to say that the best thing at the Center is the people,” explained Chris. The small staff of around 30 people pour their hearts and souls into caring for the animals, he says. It’s no wonder the center is known worldwide for its excellence.

The Duke Lemur Center has been caring for lemurs for over half a century. More than 85% of the animals were born on site, as a part of ongoing breeding efforts to support conservation. The center was the first in the world to reintroduce lemurs back into the wild through their breeding program, and has collaborations with scientists and communities in Madagascar to promote lemur conservation half a world away. Lemurs need all the help they can get; as a report just this year revealed, lemurs are the world’s most endangered primates, with over 91% of species listed as vulnerable to extinction by the IUCN Red List, including twenty-three listed as critically endangered. Without the efforts of dedicated organizations like the Duke Lemur Center, most lemur species don’t stand a chance.

As soon as we neared the animal enclosures, I could feel my heart beat faster. I’d never seen a lemur in person before. I mean, sure, I’ve seen pictures and Discovery Channel specials, but never had I laid eyes upon a living, breathing lemur. Before we could see them, we could hear them, and they were all around us. The forests were filled with alarm calls, responding to the sight of large vultures in the sky. Though these birds pose no real threat to the animals, the lemurs weren’t taking any chances, and their eerie, echoing calls set the stage for the sights to come.

Once inside, I found myself face to face with more lemurs than I could count. There were Coquerel sifakas, blue-eyed black lemurs, red ruffed lemurs, ring tailed lemurs, black and white ruffed lemurs, mongoose lemurs, bamboo lemurs – the list goes on and on! I was introduced to many lemurs, and yet they were only a small portion of the animals on site, as many were free ranging in the forests around us. As we walked though, Chris explained little details about their unique biology, like how blue-eyed black lemurs are one of a very small number of primates (including us) to possess blue eyes, or how Coquerel sifakas can jump 30 feet in a single leap, though they seem to prefer a strange sidewards shuffle when moving around on the ground.

As a highlight of our tour, we not only got to see the lemurs—we got to take a glimpse at the kind of research they are involved with. The Duke Lemur Center is proud to be the best place in the world other than Madagascar to study lemurs. In truth, they may be the best place period, for even in Madagascar, it would be impossible to do the kind of up close behavioral research that scientists do at the Center. Scientists can come to the Center to study all aspects of lemur biology. Undergraduate students from Duke University showed us how they test the cognitive abilities of lemurs by seeing if they realize to take advantage of food placed behind a researcher’s back, while some grad students showed us how they test lemurs’ amazing sense of smell using sticks.

As much as lemurs need us, we need them, too. Lemurs represent one of the earliest lineages of primates, splitting from our ancestors some 60 million years ago. They are a unique glimpse at our own evolutionary history, and provide insights into how we developed into the super-smart primates we are today. Not only are they our relatives, they represent one of the most impressive adaptive radiations on Earth. Some twenty million years ago, a handful of lemur ancestors arrived on the shored of Madagascar by hitching a ride on floating debris. They then diversified to fill just about every niche the island had to offer. From the finger-sized mouse lemurs to the dog-sized Aye-Aye, lemurs dominated the forests of Madagascar for millions of years, until their bigger-brained relatives arrived on more well-constructed rafts and began clear cutting the only home the lemurs had ever known.

As cool as the science was, my favorite part of the tour by far was when Chris took us outside into one of the free-ranging enclosures. As I crossed the little bridge to the outer area, I stopped dead when out of nowhere came a ring-tailed lemur. He hopped up on the railing only inches from me. Suddenly, lured by the sound of a keeper shaking a food box, we were surrounded by lemurs. As incredible as any part of the tour had been up to that point, nothing prepared me to be in the midst of so many lemurs, scampering and jumping around as if I wasn’t even there. I was frozen, overwhelmed by a mix of fear, fascination and joy. When I saw the smug look on Chris’ face, I knew he gets this reaction from people all the time. “I get to share these incredibly amazing and endangered animals with people,” he explained later. “When people leave the Center totally stoked about lemurs, that makes my day. I was on cloud nine after the tours Friday because the positive response we received from everyone was so huge.” I would say ‘huge’ is a gross understatement.

As we boarded the bus to go home, black and white ruffed lemurs swung from the branches to send us off. I watched for a moment as they effortlessly lept from tree to tree, still amazed, even after everything I had experienced, that I was just standing by a road staring at lemurs. The Duke Lemur Center is a magical place, where even a seasoned biologist like me can be star struck by such rare and beautiful animals. Chris was right. Lemurs are entrancing—so foreign and mysterious, yet so undeniably familiar. If you’re ever in the Raleigh/Durham area, I strongly suggest you make the time stop by the Duke Lemur Center and see for yourself. You can bet that I will be back again whenever I can.

For more information on the lemurs, head over to the Duke Lemur Center website, or keep tabs on them on Twitter and Facebook. Like what you see? Donate to help the lemurs!

All photos of lemurs taken by me using my iPhone, with the exception of the photo of Chris Smith painting with a lemur, which was provided by Chris himself (he also provided the LOL caption for the blue-eyed black lemur photo)

It’s that time of the year again: time to give what you can to help students get the education they deserve.

Every year, science bloggers from around the interwebs team up with DonorsChoose.org to help teachers. Science blogging networks battle to raise the most money to buy supplies for needy classrooms across the country.

The challenge runs from now until November 5th. I sincerely hope you’ll follow this link here and join the crusade. I chose to focus my fundraising on projects here in Hawaii because the education system here is dismal – the teachers here need all the help they can get to rise above some of the worst public education infrastructure I’ve ever seen. You should also check out all the other SciAm bloggers and their projects – let’s show the other networks that our readers are the most giving!

Please consider making a donation, even if it’s small. And if you can’t afford to donate, you can still help out by spreading the word on Facebook, Twitter and beyond!

Donate through my Science Sushi giving page, or any of the other science blogs!

The scientists found that female opihi live higher up on the shore than male opihi. Why? Well, we don’t know yet, but Chris is determined to find out. He thinks it likely has to do with spawning, and may prove valuable information for managers of the opihi fishery. The recent discovery was even featured on the local news – alongside some fantastic visuals of the perils these scientists undergo to conduct their research:

Hawaii News Now – KGMB and KHNL

Learn more about the ongoing opihi research though the Bird lab’s facebook page!

Yes, conventional foods have more synthetic pesticide residues than organic ones, on average. And yes, pesticides are dangerous chemicals. But does the science support paying significantly more for organic foods just to avoid synthetic pesticides? No.

A Pesticide Is A Pesticide

I’m not saying that pesticides, herbicides, and insect repellants aren’t toxic. I certainly wouldn’t recommend drinking cocktails laced with insect-repelling chemicals, for without a doubt, they can be bad for you. Pesticide exposure has been linked to all kinds of diseases and conditions, from neurodegenerative diseases like Parkinson’s to cancer. What we do know, though, is that natural isn’t synonymous with harmless. As a 2003 review of food safety concluded, “what should be made clear to consumers is that ‘organic’ does not equal ‘safe’.”

I’ve said it before and I’ll say it again: there is nothing safe about the chemicals used in organic agriculture. Period. This shouldn’t be that shocking – after all, a pesticide is a pesticide. “Virtually all chemicals can be shown to be dangerous at high doses,” explain scientists, “and this includes the thousands of natural chemicals that are consumed every day in food but most particularly in fruit and vegetables.”

There’s a reason we have an abundance of natural pesticides: plants and animals produce tens of thousands of chemicals to try and deter insects and herbivores from eating them. Most of these haven’t been tested for their toxic potential, as the Reduced Risk Program of the US Environmental Protection Agency (EPA) applies to synthetic pesticides only. As more research is done into their toxicity, however, we find they are just as bad as synthetic pesticides, sometimes worse. Many natural pesticides have been found to be potential – or serious – health risks, including those used commonly in organic farming.

In head-to-head comparisons, natural pesticides don’t fare any better than synthetic ones. When I compared the organic chemicals copper sulfate and pyrethrum to the top synthetics, chlorpyrifos and chlorothalonil, I found that not only were the organic ones more acutely toxic, studies have found that they are more chronically toxic as well, and have higher negative impacts on non-target species. My results match with other scientific comparisons. In their recommendations to Parliament in 1999, the Committee on European Communities noted that copper sulfate, in particular, was far more dangerous than the synthetic alternative. A review of their findings can be seen in the table on the right (from a recent review paper). Similarly, head to head comparisons have found that organic pesticides aren’t better for the environment, either.

Organic pesticides pose the same health risks as non-organic ones. No matter what anyone tells you, organic pesticides don’t just disappear. Rotenone is notorious for its lack of degradation, and copper sticks around for a long, long time. Studies have shown that copper sulfate, pyrethrins, and rotenone all can be detected on plants after harvest—for copper sulfate and rotenone, those levels exceeded safe limits. One study found such significant rotenone residues in olives and olive oil to warrant “serious doubts…about the safety and healthiness of oils extracted from drupes treated with rotenone.” Just like with certain synthetic pesticides, organic pesticide exposure has health implications—a study in Texas found that rotenone exposure correlated to a significantly higher risk of Parkinson’s disease. The increased risk due to Rotenone was five times higher than the risk posed by the synthetic alternative, chlorpyrifos. Similarly, the FDA has known for a while that chronic exposure to copper sulfate can lead to anemia and liver disease.

So why do we keep hearing that organic foods have fewer pesticide residues? Well, because they have lower levels of synthetic pesticide residues. Most of our data on pesticide residues in food comes from surveys like the USDA’s Pesticide Data Program (PDP). But the while the PDP has been looking at the residues of over 300 pesticides in foods for decades, rotenone and copper sulfate aren’t among the usual pesticides tested for—maybe, because for several organic pesticides, fast, reliable methods for detecting them were only developed recently. And, since there isn’t any public data on the use of organic pesticides in organic farming (like there is for conventional farms), we’re left guessing what levels of organic pesticides are on and in organic foods.

So, if you’re going to worry about pesticides, worry about all of them, organic and synthetic. But, really, should you worry at all?

You Are What You Eat? Maybe Not.

We know, quite assuredly, that conventionally produced foods do contain higher levels of synthetic chemicals. But do these residues matter?

While study after study can find pesticide residues on foods, they are almost always well below safety standards. Almost all pesticides detected on foods by the USDA and independent scientific studies are at levels below 1% of the Acceptable Daily Intake (ADI) set by government regulators. This level isn’t random – the ADI is based on animal exposure studies in a wide variety of species. First, scientists give animals different amounts of pesticides on a daily basis throughout their lifetimes and monitor those animals for toxic effects. Through this, they determine the highest dose at which no effects can be found. The ADI is then typically set 100 times lower than that level. So a typical human exposure that is 1% of the ADI is equivalent to an exposure 10,000 times lower than levels that are safe in animal models.

Systematic reviews of dietary pesticide exposure all come to the same conclusion: that typical dietary exposure to pesticide residues in foods poses minimal risks to humans. As the book Health Benefits of Organic Food explains, “while there is some evidence that consuming organic produce will lead to lower exposure of pesticides compared to the consumption of conventional produce, there is no evidence of effect at contemporary concentrations.” Or, as a recent review states, “from a practical standpoint, the marginal benefits of reducing human exposure to pesticides in the diet through increased consumption of organic produce appear to be insignificant.”

Reviews of the negative health effects of pesticides find that dangerous exposure levels don’t come from food. Instead, non-dietary routes make for the vast majority of toxin exposures, in particular the use of pesticides around the home and workplace. A review of the worldwide disease burden caused by chemicals found that 70% can be attributed to air pollution, with acute poisonings and occupational exposures coming in second and third. Similarly, studies have found that indoor air concentrations of pesticides, not the amount on foodstuffs, correlate strongly to the amount of residues found in pregnant women (and even still, there was no strong correlation between exposure and health effects). Similarly, other studies have found that exposures to toxic pyrethroids come primarily from the environment. Children on organic diets routeinely had pyrethroids in their systems, and the organic group actually had higher levels of several pyrethroid metabolites than the conventional one. In other words, you have more to fear from your home than from your food.

Your home probably contains more pesticides than you ever imagined. Plastics and paints often contain fungicides to prevent mold—fungi that, by the way, can kill you. Your walls, carpets and floors also contain pesticides. Cleaning products and disenfectants contains pesticides and fungicides so they can do their job. Ever used an exterminator to get rid of mice, termites, fleas or cockroaches? That stuff can linger for months. Step outside your house, and just about everything you touch has come in contact with a pesticide. Insecticides are used in processing, manufacturing, and packaging, not to mention that even grocery stores use pesticides to keep insects and rodents at bay. These chemicals are all around you, every day, fighting off the pests that destroy our buildings and our food. It’s not surprising that most pesticide exposures doesn’t come from your food.

That said, there are some studies that have found a link between diet and exposure to specific pesticides, particularly synthetic organophosphorus pesticides. Lu et al. found that switching children from a conventional food diet to an entirely organic one dropped the urinary levels of specific metabolites for malathion and chlorpyrifos to nondetectable levels in a matter of days. But, it’s important to note that even the levels they detected during the conventional diet are three orders of magnitude lower than the levels needed in animal experiments to cause neurodevelopmental or other adverse health effects.

While it might seem that decreasing exposure to pesticides in any way could only be good for you, toxicologists would differ. Contrary to what you might think, lower exposure isn’t necessarily better. It’s what’s known as hormesis, or a hormetic dose response curve. There is evidence that exposure to most chemicals at doses significantly below danger thresholds, even pesticides, is beneficial when compared to no exposure at all. Why? Perhaps because it kick starts our immune system. Or, perhaps, because pesticides activate beneficial biological pathways. For most chemicals, we simply don’t know. What we do know is that data collected from 5000 dose response measurements (abstracted from over 20,000 studies) found that low doses of many supposedly toxic chemicals, metals, pesticides and fungicides either reduced cancer rates below controls or increased longevity or growth in a variety of animals. So while high acute and chronic exposures are bad, the levels we see in food that are well below danger thresholds may even be good for us. This isn’t as surprising as you might think—just look at most pharmaceuticals. People take low doses of aspirin daily to improve their heart health, but at high chronic doses, it can cause anything from vomiting to seizures and even death. Similarly, a glass of red wine every day might be good for you. But ten glasses a day? Definitely not.

No Need To Fear

To date, there is no scientific evidence that eating an organic diet leads to better health.

What of all those studies I just mentioned linking pesticides to disorders? Well, exactly none of them looked at pesticides from dietary intake and health in people. Instead, they involve people with high occupational exposure (like farmers who spray pesticides) or household exposure (from gardening, etc). Judging the safety of dietary pesticide intake by high exposures is like judging the health impacts of red wine based on alcoholics. A systematic review of the literature found only three studies to date have looked at clinical outcomes of eating organic – and none found any difference between an organic and conventional diet. My question is: if organic foods are so much healthier, why aren’t there any studies that show people on an organic diet are healthier than people eating conventionally grown produce instead?

More to the point, if conventional pesticide residues on food (and not other, high exposure routes) are leading to rampant disease, we should be able to find evidence of the connection in longitudinal epidemiological studies—but we don’t. The epidemiological evidence for the danger of pesticide residues simply isn’t there.

If dietary exposure to pesticides was a significant factor in cancer rates, we would expect to see that people who eat more conventionally grown fruits and vegetable have higher rates of cancer. But instead, we see the opposite. People who eat more fruits and vegetables have significantly lower incidences of cancers, and those who eat the most are two times less likely to develop cancer than those who eat the least. While high doses of pesticides over time have been linked to cancer in lab animals and in vitro studies, “epidemiological studies do not support the idea that synthetic pesticide residues are important for human cancer.” Even the exposure to the persistent and villainized pesticide DDT has not been consistently linked to cancer. As a recent review of the literature summarized, “no hard evidence currently exists that toxic hazards such as pesticides have had a major impact on total cancer incidence and mortality, and this is especially true for diet-related exposures.”

The closest we have to studying the effects of diet on health are studies looking at farmers. However, farmers in general have high occupational pesticide exposures, and thus it’s impossible to tease out occupational versus dietary exposure. Even still, in this high-risk group, studies simply don’t find health differences between organic and conventional farmers. A UK study found that conventional farmers were just as healthy as organic ones, though the organic ones were happier. Similarly, while test-tube studies of high levels of pesticides are known to cause reproductive disorders, a comparison of sperm quality from organic and conventional farmers was unable to connect dietary intake of over 40 different pesticides to any kind of reproductive impairment. Instead, the two groups showed no statistical difference in their sperm quality.

In a review of the evidence for choosing organic food, Christine Williams said it simply: “There are virtually no studies of any size that have evaluated the effects of organic v. conventionally-grown foods.” Thus, she explains, “conclusions cannot be drawn regarding potentially beneficial or adverse nutritional consequences, to the consumer, of increased consumption of organic food.”

“There is currently no evidence to support or refute claims that organic food is safer and thus, healthier, than conventional food, or vice versa. Assertions of such kind are inappropriate and not justified,” explain scientists. Neither organic nor conventional food is dangerous to eat, they say, and the constant attention to safety is unwarranted. Worse, it does more harm than good. The scientists chastise the media and industry alike for scaremongering tactics, saying that “the selective and partial presentation of evidence serves no useful purpose and does not promote public health. Rather, it raises fears about unsafe food.”

Furthermore, the focus on pesticides is misleading, as pesticide residues are the lowest food hazard when it comes to human health (as the figure from the paper on the right shows). They conclude that as far as the scientific evidence is concerned, “it seems that other factors, if any, rather than safety aspects speak in favor of organic food.”

If you don’t want to listen to those people or me, listen to the toxicologists, who study this stuff for a living. When probed about the risk that different toxins pose, over 85% rejected the notion that organic or “natural” products are safer than others. They felt that smoking, sun exposure and mercury were of much higher concern than pesticides. Over 90% agreed that the media does a terrible job of reporting the about toxic substances, mostly by overstating the risks. They slammed down hard on non-governmental organizations, too, for overstating risk.

What’s in a Name?

There’s good reason we can’t detect differences between organic and conventional diets: the labels don’t mean that much. Sure, organic farms have to follow a certain set of USDA guidelines, but farm to farm variability is huge for both conventional and organic practices. As a review of organic practices concluded: “variation within organic and conventional farming systems is likely as large as differences between the two systems.”

The false dichotomy between conventional and organic isn’t just misleading, it’s dangerous. Our constant attention to natural versus synthetic only causes fear and distrust, when in actuality, our food has never been safer. Eating less fruits and vegetables due to fear of pesticides or the high price of organics does far more harm to our health than any of the pesticide residues on our food.

Let me be clear about one thing: I’m all for reducing pesticide use. But we can’t forget that pesticides are used for a reason, too. We have been reaping the rewards of pesticide use for decades. Higher yields due to less crop destruction. Safer food because of reduced fungal and bacterial contamination. Lower prices as a result of increased supply and longer shelf life. Protection from pests that carry deadly diseases. Invasive species control, saving billions of dollars in damages—and the list goes on. Yes, we need to manage the way we use pesticides, scrutinize the chemicals involved and monitor their effects to ensure safety, and Big Ag (conventional and organic) needs to be kept in check. But without a doubt, our lives have been vastly improved by the chemicals we so quickly villainize.

If we want to achieve the balance between sustainability, production outputs, and health benefits, we have to stop focusing on brand names. Instead of emphasizing labels, we need to look at different farming practices and the chemicals involved and judge them independently of whether they fall under organic standards.

In the meantime, buy fresh, locally farmed produce, whether it’s organic or not; if you can talk to the farmers, you’ll know exactly what is and isn’t on your food. Wash it well, and you’ll get rid of most of whatever pesticides are on there, organic or synthetic. And eat lots and lots of fruits and vegetables—if there is anything that will improve your health, it’s that.

 

Before you say otherwise and get mad at me for mentioning it, rotenone is currently a USDA approved organic pesticide. It was temporarily banned, but reapproved in 2010. Before it was banned, it was the most commonly used organic pesticide, and now—well, without public data on pesticide use on organic farms, we have no idea how much it is being used today.

Food picture from FreeFoto.Com