The space shuttle Endeavour* is scheduled to blast off this afternoon at 3:47 EDT. It will be the second-to-last launch before NASA retires their shuttle fleet for good. The shuttle's commander, Mark Kelly, has spent much of the last few months at the bedside of his wife, senator Gabrielle Giffords, while she recovers from being shot in the head. It's been a long countdown, to say the least.
Now the shuttle is almost in the air, and along with its human passengers, it will be carrying some tentacled cargo: Squids in Space. No really, that's the official name of the project. (It's also referred to as Squid in Space, since the plural of "squid" is whatever you feel like.)
University of Florida scientist Jamie Foster is leading the project, which will study the development of squid embryos in the near-zero gravity of spaceflight. Her Squids in Space team also includes college students and high schoolers who, one hopes, appreciate that they are doing the coolest class project ever.
Foster's concern isn't really about the squid or squids, though; her research interest is bacteria. "Animals, including humans, are walking (or swimming) microbial ecosystems that interact daily with billions of microbes," she said in a press report. Humans' most important microbial interaction is with the bacteria that line our guts. But the Hawaiian bobtail squid, Euprymna scolopes, utilizes bacteria differently: as soon as it hatches, it absorbs a glow-in-the-dark species of bacteria from the water around it. The bacteria, Vibrio fischeri, lend the squid their bioluminescence. The squid houses the bacteria in a light organ on its body, and their glow obscures the squid's silhouette to predators lurking below.
What happens when squid embryos hatch into a low-gravity environment? "The effects of microgravity on these mutualistic associations are yet unknown," Foster said. In space, "Do good bacteria go bad?" When applied to cephalopods on a shuttle, the question has a bit of a goofy, Snakes on a Plane feel. But it's a question with serious health implications for human astronauts--whatever they're doing after the shuttles are retired.
What will they be doing, anyway? I've especially wondered about this since so many MUSE readers are space aficionados. Actually, "aficionado" might be putting it gently. One reader wrote online that she's observing today's launch by plastering her school with posters, wearing a special shuttle-launch outfit, and handing out cards to her fellow high schoolers. Some of our readers want desperately to be involved in the space program when they're older, even though they have no idea what that program will look like in 20 or 30 years.
So I'm hoping to pose the question to Mark Kelly himself and put his answer in the magazine. PBS is doing a live interview with the shuttle commander on Monday, and they're inviting questions from the public through their YouTube channel. Some of the questions with the most votes will be read during the interview (leaving out, I assume, the many iterations of "have u ever seen a ufo on ur flights, thx, anonymous"). I posted my question online, and if you'd like to vote for it, you can find it by clicking here, scrolling down to the search bar on the right-hand side of the screen, and entering "muse." Voting ends tomorrow night.
Godspeed, astronauts and cephalopods!
UPDATE: Un-shockingly, NASA has had to delay the launch until at least Monday due to technical problems. (But you should still vote for my question. Please?)
UPDATE, MAY 2: Thanks so much for your votes! My question ended up as the top rated in the "Students and Classrooms" category, which included some cute video questions from kids (who will probably get chosen anyway) as well as some hard-hitting journalistic questions ("just plz hear me out was the landing on the moon fake im relly wANT TO KNOW"). Meanwhile, NASA has again delayed the shuttle launch, this time until at least May 8. The astronauts have been sent back to Houston for more training. No word yet on the squid.
*Why the British spelling that makes your computer send up squiggly red underlines everywhere? The shuttle, christened in a nationwide student contest, is named after a ship sailed by James Cook. Even NASA has found the British affectation tricky at times; they misspelled the name of the shuttle on a giant launchpad sign in 2007.
Do mothers who diet during pregnancy predispose their children to be heavier? That's the intriguing suggestion of a new study done in the United Kingdom, and the latest addition to a field known as epigenetics.
Epigenetics is a funny story (though not raucously so) in biology. In my first biology textbooks in middle or high school, an 18th-century French biologist named Jean-Baptiste Lamarck was the chump of the chapters on evolution. Before Charles Darwin formulated his ideas on adaptation and natural selection, Lamarck speculated that organisms could pass down traits that they'd acquired during their lifetime. For example, if a giraffe gradually stretched out its neck by reaching for high leaves, it could pass on that stretched-out neck to its young. Poor Lamarck's theory was tragically easy to disprove. If you cut off a mouse's tail, after all, it still has babies with tails. Genes are the units of heredity. We get our DNA from our parents, and nothing we do during our lifetime changes our DNA.
Except for when it does. These days, scientists are gaining appreciation for epigenetics: factors above the level of the gene that we can pass down to our children. Sorry for all the joshing, Jean-Baptiste. Genes are still the most important unit of inheritance, but we now know that the way our DNA is coiled and packaged inside our cells affects how its instructions are carried out. Factors in our lifestyles can cause changes in that packaging, and we can pass on those changes to the next generation.
Epigenetic change can also happen in utero. A human's DNA is locked in as soon as sperm and egg combine, but factors in the womb--our first environment--can have epigenetic effects on the DNA in our rapidly multiplying cells.
That brings us back to pregnant mothers. Previous studies have shown a connection between famine in utero and obesity in adulthood. If a mother can't get enough food, does she somehow mark the genes of her fetus so that it clings to calories in later life? A slow metabolism is helpful in a time of famine, but not so much in a time of fast food. Studies in animals have suggested that epigenetic changes are responsible for the link between a pregnant mother's diet and her offspring's adult weight.
Looking at DNA from the umbilical cords of newborns, the authors of the new study set out to find epigenetic changes that were linked to the children's weight many years later--and to their mother's diets.
The authors studied two groups of women and their children living in the UK. They interviewed the women when they were 15 weeks pregnant about their diets. When the babies were born, their umbilical cords were frozen. Six or nine years later, the researchers tracked down these children (between the two groups, there were 317) and measured their body fat. They also extracted DNA from the frozen umbilical cords.
The researchers looked at a certain kind of epigenetic change called methylation--a chemical tag attached to the DNA that makes it less legible to the cellular machinery. In both groups, they found that increased methylation around one particular gene in the umbilical cord DNA was strongly correlated with higher body fat when the children were older. This marker in the newborns' DNA, that is, partly predicted what their bodies would be like as six- or nine-year-olds.
Additionally, methylation at that same gene seemed to be linked to the mothers' carbohydrate intake in early pregnancy. Mothers who reported eating low levels of carbs had babies with higher levels of methylation. The increase in methylation was not linked to higher fat or protein intake, just to low levels of (reported) carbohydrates.
It's hard to rigorously measure the nutrients in a person's diet from their answers on a questionnaire. And even if the correlation is real, it doesn't prove the mother's diet is causing the methylation or the higher fat level in her child. Furthermore, we don't know whether these children will grow up to be overweight adults. But the study's suggestion is tantalizing. Could women who follow Atkins or South Beach, or another diet sold to them in the name of health, be predisposing their unborn children to a lifetime of weight struggles?
As researchers continue to solidify the links between our lifestyles and epigenetics, new diagnostic tests and treatments may become possible. A DNA test at birth could reveal a person's risk for various diseases based on epigenetic factors--instead of, or in addition to, their genetic risk. And scientists might even develop treatments that target DNA packaging and methylation.
Or maybe someone will just start selling another fad diet. Epigenetics: the new Atkins!
Ever since they began to realize how important the vast colonies of bacteria living inside us might be to our health, scientists have been speculating that one day, people will receive medical treatments specifically tailored to their own "gut flora." That day is getting closer. An international group of researchers has found that humans fall into a few neat categories based on their gut bacteria. These categories might define us as clearly as blood types, with broad implications for our health and for medicine in general.
The easiest way for scientists to study the bacteria in people's guts is to study the bacteria that are, ah, evacuated from the gut. So the researchers obtained fecal samples from 22 people in four European countries. By sequencing the DNA in each sample and weeding out all the human bits, they were left with a set of bacterial DNA for each person. They pooled this information with previously existing data from two Americans and nine Japanese subjects to create an intercontinental set of gut microbe DNA.
By combing through these DNA sequences for matches to previously published bacterial genomes, the scientists assembled a list of bacterial types in each subject. Then they looked for relationships among these diverse casts of gut bacteria. They found a startlingly clear pattern: There were three distinct bacterial ecosystems, and each person fell into just one of these three categories.
Each category--the researchers dubbed them enterotypes--was characterized by one dominant bacterial type, coexisting with up to a dozen other main bacterial players. This led the authors to believe that the bacteria inside you aren't a random grouping. Instead, they make up a stable and discrete ecosystem. Your gut might be a desert or a tundra or a wetland, but it's not a zoo.
How do we come to house one of these bacterial ecosystems? The researchers found that people's enterotypes didn't correspond to their age, gender, body mass index (BMI), or nationality. Perhaps whatever types of bacteria are the first to colonize us when we're sterile newborns--some random accident of the hospital or house where we're delivered--determine our microbial fate.
And to what degree is our microbiome our fate? It's not clear yet. We rely on our gut bacteria to help us digest our foods and to produce certain vitamins. The researchers found that each enterotype was especially good at producing a certain necessary vitamin--but no enterotype was lacking in any vitamin production.
While there was no pattern to who fell into what enterotype (except that one type was somewhat more frequent in Japan), there were correlations between human features and the genes of their gut bacteria. Some types of bacterial genes corresponded to nationality, gender, age, or BMI. This might reflect the demands that we make on our gut bacteria. We don't determine which ecosystem populates us, but our diet and lifestyle could affect the balance of species in their population.
The researchers also looked at a larger set of data from American and Danish subjects, and found that their gut microbe DNA seemed to fit into the same three clusters. But further research might reveal more enterotypes, or subcategories among them. Individuals from less westernized societies, or from remote rural areas, might reveal new patterns. Additionally, fecal bacteria don't represent all the bacteria living in our guts. But these three enterotypes represent an exciting step toward defining our individual microbiomes.
Scientists are only beginning to understand how our gut bacteria affect our overall health, tendency toward diseases or obesity, and even mental health. As more of their functions become clear, doctors may be able to offer diagnoses--or treatments--specific to our enterotypes. Medicine based on the the non-human organisms living inside us, strange as it seems, might be more personalized than ever before.
Once the new federal budget, which has already been passed by the House of Representatives, makes it through the Senate and across the President's desk, a familiar animal species will have undergone an identity change: in the western United States, the gray wolf will no longer be endangered.
Before humans got involved, gray wolves ranged all over North America:
Then we hunted them until their range looked like this:
In 1978, on the brink of extinction, the gray wolf was listed as endangered in the lower 48 states. The one exception was in Minnesota, where it was only "threatened." (See that gray spot?) We stopped hunting them and started trying to save them instead.
In the mid-1990s, small populations of gray wolves were reintroduced in the Southwest and in Yellowstone National Park. The Yellowstone population began as just 66 animals captured in Canada. The reintroduction was controversial, but today the wolves are considered a success story because of how their population has rebounded:
Now that there are about 1,650 wolves living in the western United States, hunters and ranchers would really like to be allowed to shoot them again.
It was 2003 when the Fish and Wildlife Service first tried to "downlist" most gray wolves in the U.S., moving them from the endangered category to merely threatened. This would make it easier for people to legally manage the wolf population. (In this context, "manage" is a nicer way to say "sometimes shoot.") But conservation groups challenged the new rules, arguing that the FWS had jerrymandered the ranges of wolf populations to make them appear healthier than they really were. Federal district courts in Vermont and Oregon overturned the downlisting in 2005, and wolves stayed protected.
A new rule in 2005 made it permissible to kill wolves anywhere they had an "unacceptable impact" on wild animals such as deer, bison, or moose. In 2008, the FWS loosened the rule, removing the term "unacceptable." People would be allowed to kill wolves as long as the population stayed above 20 breeding pairs per state. (For more details on gray wolf laws through 2008, see here.)
If this is sounding like an endless legal slog, you've got the right idea. Wolves in the Rocky Mountain region were delisted altogether in 2008, then re-listed in 2010. Delisting the wolves would mean turning over their stewardship to the individual states. But while Montana and Idaho had come up with plans to monitor the wolf population and regulate wolf kills, Wyoming couldn't commit to any plan besides killing all wolves on sight.
This brings us back to the present day. In a bid to circumvent the ongoing legal struggle--and perhaps to boost his own chances for reelection--Democratic Montana senator Jon Tester attached a gray wolf provision to the new budget. The addendum will "roll back the clock" to 2008 and remove protections on wolves in Montana and Idaho.
If the wolves are really recovered, is this a problem? One issue is that the wolves, of course, don't care about state lines, so treating one population as three distinct ones doesn't make sense. Another is that scientific assumptions about how many wolves can be killed without destabilizing the whole population may be unfounded. And though Montana and Idaho claim they'll responsibly manage the wolf population, the governor of Montana recently made it clear that he won't investigate or prosecute any wolf killings. Anywhere livestock are attacked, he said, entire packs of wolves should be destroyed.
Furthermore, Tester's budget add-on sets a precedent. Never before has Congress intervened to remove a species from the protection of the Endangered Species Act. "Science should dictate which plants and animals will be protected, not the whims of politicians," says Andrew Wetzler of the Natural Resources Defense Council. If other endangered species are in the way of drilling or development projects, will they show up on the congressional agenda?
The wolf population in the Rocky Mountains may be safely regulated by the states, finally ending the long legal battle. It also might end up back on the endangered species list--either as a result of further litigation, or because its population is truly, once again, in danger.
In September and October of 2001, five giant squid washed up in one area of the coast of Spain. In October 2003, another four giant squid were found dead. Both incidents occurred near boats that were using air guns for geophysical research, producing high-intensity, low-frequency sound waves.
It can get pretty loud in the ocean, between shipping, operations to explore and drill for oil, and naval activities. In the past, naval sonar blasts have been linked to large-scale whale strandings; the beached whales had bleeding in their ears and brains.
So could sound be to blame for the strandings of giant squid? Whales are mysterious enough; there's a lot we don't know about their behavior, including what exactly leads them to beach themselves after a so-called acoustic trauma. But giant squid are even more mysterious--they're rarely spotted alive. It was only recently confirmed that squid can hear.
Nevertheless, a group of Spanish scientists set out to study acoustic trauma in cephalopods (squid, octopuses, and cuttlefish--which is to say, inkfish). They captured 187 common (non-giant) cephalopods. Of these, 87 were put in tanks and blasted with sound at around 157 decibels for 2 hours. For reference, 160 decibels can rupture a human eardrum.
After the noise exposure, the squid were decapitated--some immediately, and the rest at intervals up to 96 hours later. The scientists then microscopically examined the animals' statocysts. These are complex structures that help squid control their position and keep their balance. The statocysts may also be involved in hearing, just as our own sense of balance is controlled by a system inside our ears.
Across all four cephalopod species in the study, every animal that had been blasted with noise showed damage in its statocysts. And the damage hadn't stopped when the noise stopped: lesions in their statocysts grew worse over time, with the most damage appearing in the squid killed 96 hours later. The 100 un-blasted squid that had been kept as controls showed no damage.
There are a few disappointing omissions in this study. The authors only used one narrow decibel range, rather than testing different levels of sound, and they don't speculate as to what kind of underwater noise it approximates. Is this what a squid hears when it's two miles from a drilling operation? When it's three feet from a navy submarine? And though the authors describe the statocyst damage as "not compatible with life," they didn't leave any of the squid alone to see if they would die, or observe their behaviors after their statocysts were damaged. Would they have stopped eating? Become disoriented? Floated to the surface of the tank? (With a 100% decapitation rate, being a subject in this study was "not compatible with life.")
Still, the study shows that loud underwater noises can cause dramatic physical damage to the statocysts of squid, and that these organs are probably responsible for hearing, in addition to balance and positioning. Though most cephalopods aren't as cute or endangered as most whales, the types used for food are economically important--and it's nice, in general, to avoid needless mass killings. If cephalopods are this vulnerable to noise pollution, there could be countless other species suffering that aren't as visible to us as a washed-up giant squid.
Image: C. Lozano/Cepemsa/The Ecological Society of America
Modern life in a developed nation has plenty of perks. We drink clean water and bathe with it as often as we like. We use flush toilets. Our insides are free of parasites, and children almost never die of infectious diseases. There are downsides, too: stress, obesity, depression. But we recognize these as tradeoffs for our contemporary lifestyle.
There's one catch: A recent paper says that no part of this tradeoff is a coincidence. Eliminating certain microorganisms from our environment, the authors suggest, has thrown our immune systems, finely calibrated by millions of years of evolution, off kilter. The results include ailments ranging from multiple sclerosis to mental illness.
This idea may remind you of the "hygiene hypothesis," the theory that overly hygienic modern living makes us more susceptible to allergies and asthma. The hygiene hypothesis originally focused on childhood infections: kids who were allowed to get sick now and then, it said, would have properly developed immune systems and wouldn't react to harmless allergens. But the theory has now expanded to include many kinds of microorganisms that live around and inside us, not just those that can make us sick. These companions are euphemistically called the "old friends."
The old friends historically included three groups of microorganisms, the authors say: bacteria from mud and unclean water or food that pass through our bodies harmlessly; the mostly-bacterial microorganisms that live in our gut; and--sorry--worms. More on them in a moment. We still have a host of microbes living inside us, though doubtless a different complement than what was there in earlier centuries, since our environment and diet affect which species colonize us. As for the other two groups of old friends? We don't eat much dirt these days, and we avoid worms if at all possible (though people in developing nations don't have that luxury).
Numerous studies, according to the authors, have shown that the old friends have a positive impact on our immune systems. You might expect your body to object to so many inhabitants. But in fact, those inhabitants trigger the release of anti-inflammatory agents in our bodies. Perhaps the microorganisms learned this trick over the course of evolution, to protect themselves; or perhaps we learned that it wasn't worth fighting them. Either way, our gut microbes and other microorganisms seem to dampen our immune systems and discourage inflammation.
Inflammation is the body trying to protect itself. But it's not always necessary or productive. Many illnesses stem from chronic inflammation, and it's even been linked to obesity. Asthma, Crohn's disease, multiple sclerosis, and type I diabetes all stem from an immune system that overreacts--whether it's to allergens, foods, or the body's own cells.
Depression, though the steps of its development are less easy to trace, has also been linked to inflammation. The authors think depression might be another overreaction by the body's defenses; instead of an allergen, the trigger is some psychological stressor. There are genes that can make a person more vulnerable to depression, or to any of these other conditions (including obesity), but genes aren't fate--a person's environment always plays a role.
Given all these factors, the authors suggest that since parting ways with our old friends in the middle of the 20th century, we have paid a price. We had grown dependent on these microorganisms to "train" our immune systems, and in their absence, our bodies are liable to overreact. Depending on our genetic vulnerabilities, this can lead to various illnesses. And sure enough, certain conditions related to a jumpy immune system have "increased dramatically in the developed world" since 1950 or so, including asthma, hay fever, type I diabetes, and multiple sclerosis. Depression seems to have increased, too, though it's hard to separate a real increase from a cultural change that encourages it to be diagnosed.
The next step in testing this hypothesis would be to treat depressed patients with the old friends themselves, or with some medication derived from them. There hasn't been much research in this area yet. One intriguing study showed that lung cancer patients receiving chemotherapy were significantly less depressed and anxious after being treated with Mycobacterium vaccae, one of the dirt bacteria.
There has been more interest, surprisingly, in the worms. "Helminthic therapy," in which doctors infest patients with parasitic worms, is being used to treat autoimmune conditions, IBS, and even food allergies. You'd have to be a pretty good sport to voluntarily take on parasitic worms. But these patients are on the cutting edge; while modern living means cleanliness, dirt and worms might be the future.
Orcas are good-looking creatures. Their distinct black-and-white features lend themselves well to stuffed animal versions, and might make you think these animals are the pandas of the sea. But there's a reason they're also called killer whales. Hint: this is not a photo of interspecies friendship.
Scientists from the National Marine Fisheries Service (part of NOAA, the National Oceanic and Atmospheric Administration) studied killer whales off the coast of Antarctica. They report that a certain group, which they've dubbed pack ice (PI) killer whales, are specialized hunters. They use a clever cooperative hunting technique to kill seals, such as the hapless fellow above who's doing an impression of a burrito on a plate.
The group hunting technique is called "wave washing," and it works like this: After identifying their target sitting on a piece of pack ice, a group of killer whales swims a little ways away from it. Then they turn and swim in formation toward the ice floe, beating their tails to make a wave. The wave reaches the ice and splashes over the seal, washing it into the ocean, where it rapidly becomes lunch.
At the ScienceNow site, you can watch a step-by-step slideshow of one of these seal hunts. If you have a weak stomach, or much sympathy for big-eyed marine mammals, you'll probably want to stop after slide 8. (After the whales ate this seal, the authors recovered the carcass and thoroughly documented the precision with which the whales had "butchered" it.)
Just like humans and other smart, social mammals, killer whales can develop new behaviors within their communities. The PI killer whales have figured out a resourceful hunting technique that they share within their group. And they're persistent about it: if the seal doesn't come off the ice floe with the first wave, the whales will keep swimming back and forth, for half an hour or more, until it does.
There's another curious consistency within the PI killer whales. They seem to have a taste for one particular species of seal, the Weddell seal. The authors report that these seals were not the most common item on the buffet; in fact, they represented just 15% of the hundreds of seals observed on ice floes in the area. But Weddell seals represented 14 out of 15 kills. The reason for the whales' taste preference is a mystery.
If you have a fear of heights, called acrophobia, you probably consider activities such as standing on a glass ledge 103 stories high to be stressful. But a scientist in Switzerland says that cortisol, the stress hormone, can actually help banish your fear.
A team of researchers led by Dominique de Quervain at the University of Basel recruited 40 patients with serious acrophobia. All the patients received a series of virtual reality sessions, in which they traveled across virtual bridges and stood on virtual platforms, to treat their phobia.
This is a standard and effective treatment called exposure therapy. It assumes that the patient's phobia is a "conditioned response." Just like good old Pavlov's drooly dogs, a person reacts automatically to a specific stimulus (say, being up high) with a specific response (say, panic). But if you repeatedly expose patients to the stimulus in a safe environment, and help them tone down their fear reaction, they learn a new association. If Pavlov had started giving his dogs empty bowls after ringing his bell, they would have eventually stopped drooling.
The patients in the study responded well to the virtual-reality treatments. Their acrophobia was reduced, according to both questionnaires and skin-conductance measurements. (Your skin gets sweaty when you're worked up; this is how lie detectors work.)
But there was another factor in the study: half the patients, before each of their treatment sessions, had been given a dose of cortisol. The other half had taken a placebo. The patients who received cortisol had a greater reduction in their phobia than the placebo patients, both a few days after treatment and a whole month later.
It seems like a counterintuitive result. Why would stress make you less afraid? The answer may have to do with memory. Cortisol can impair your ability to retrieve memories, especially emotionally powerful ones. This could include your memories of previous panic attacks--or a memory of a traumatic event that inspired your fear in the first place. Additionally, cortisol helps you to store new memories. In general, the stress hormone tells your body and brain that what's happening right now is vitally important. In exposure therapy, cortisol may give extra weight to new memories of experiencing a stimulus in a safe setting, while simultaneously damping down fearful memories.
The paper's authors are also studying the use of cortisol in treating social phobia, a condition that causes some people to avoid all social interaction. For the rest of us, the results may not be as life-changing. But they tell us that it's OK to feel stressed when we face our fears. If this inspires you to go up the Sears/Willis Tower, just make sure to bring a camera so you can prove you did it.