One of the most popular hypotheses to explain the rise in inflammatory conditions is known as the Hygiene Hypothesis, which says that our increasingly sterile lifestyle is to blame for our allergic reactions. We now live in a world of antibacterial soaps, instant hand sanitizer, vaccines, and antibiotics, all of which have taken over the job of protecting our children from dirt and germs. Left with nothing to do, kid’s immune systems get a little stir crazy, and start attacking even minor invaders like pollen with increased zeal. But Ilkka Hanski and his colleagues from the University of Helsinki in Finland suggest the Hygiene Hypothesis extends beyond how clean we keep our house. They put forward a Biodiversity Hypothesis, which suggests that less contact with the nature and biodiversity is adversely affecting the microbes on and in our bodies, leading to increased susceptibility to immune disorders.

To test this hypothesis, the research team investigated the relationship between biodiversity, allergen susceptibility, and skin microbial communities in a little over 100 randomly chosen teenagers in Finland. The kids grew up in a variety of settings, from tightly-packed villages to rural farmlands. For each participant, they measured how sensitive their skin was to allergens and what kind of microbes were living on there. Based on their skin’s immune reaction, they classified the students as allergen-sensitive (a condition known as atopy) or not. The researchers also roughly calculated the level of environmental biodiversity where the participants lived by looking at the amount of plant cover of their yards and the major land use types within 3 km of their homes, allowing comparisons between it and the participant’s allergy sensitivity and skin microorganisms.

The team found a strong, significant correlation between the diversity of a particular class of skin bacteria, called gammaproteobacteria, and allergen sensitivity. Though they only represented 3% of the skin bacterial community, gammaproteobacteria were the only class that showed a significant decrease in diversity in the atopic individuals. So, to get a closer look at this phenomenon, directly comparing the presence of different gammaproteobacteria with levels of an anti-inflamatory marker, IL-10, in the subjects’ blood. The presence of one gammaproteobacterial genus, Acinetobacter, was strongly linked to higher levels of IL-10 in healthy individuals but not in the allergen-sensitive ones. As the authors explain, this suggests that these microbes may help teach the immune system to ignore pesky allergens.

“The positive association between the abundance of the gammaproteobacterial genus Acinetobacter and IL-10 expression… in healthy individuals, but not in atopic individuals, is consistent with IL-10’s central role in maintaining immunologic tolerance to harmless substances.” Thus, the authors say, “the lack of association between Acinetobacter and IL-10 expression in atopic individuals in the present study might reflect a breakdown of the regulatory mechanisms.”

How, exactly, Actinetobacter and other gammaproteobacteria influence our immune system has yet to be determined. What the authors did show is that environment a person grows up in has a strong effect on the presence and diversity of this group of bacteria. Since gammaproteobacteria are are commonly found in soil and on plants (including flowering plants and their pollen), it may not seem that surprising to the researchers that the environmental diversity around a subject was strongly correlated to increased diversity of their skin gammaproteobacteria. But what is astounding is that this relationship held even when the researchers stepped back and looked at the overall connection between allergen sensitivity and the surrounding environment; the more natural biodiversity where the kid grew up, the less likely he or she was to be sensitive to allergens.

“The present results demonstrate that biodiversity can be surprisingly strongly associated with atopy.”

This suggests that the urban-dwelling nature of developed countries may be to blame for their increasing problem with inflammatory diseases. If so, conservation of natural spaces, including parks and other green initiatives, may be key to protecting the health of future generations. “Interactions with natural environmental features not only may increase general human well being in urban areas, but also may enrich the commensal microbiota and enhance its interaction with the immune system, with far-reaching consequences for public health.”

Since allergies cost us almost $14.5 billion annually including medical expenses, missed school and work, and over the counter drugs, there may be a strong monetary incentive to conserve our natural areas – if only for the sake of our health. That’s not even considering the other economic incentives for conservation, including water filtration and storm protection, which have been estimated at over $4.4 trillion dollars per year.

What all these studies tell us is that the cost of conservation is strongly outweighed by its benefits. Period.

Reference: Hanski, I., von Hertzen, L., Fyhrquist, N., Koskinen, K., Torppa, K., Laatikainen, T., Karisola, P., Auvinen, P., Paulin, L., Makela, M.J. & Environmental biodiversity, human microbiota, and allergy are interrelated, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.1205624109

Image of soil and hands © Soil-Net.Com under a Creative Commons License

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As a scientist, one of the most important parts of my job is outreach. I consider this blog and other outreach activities as an integral part of my profession. So every year, I wrangle grad students from the Ecology, Evolution and Conservation Biology (EECB) Specialization at the University of Hawaii to help a local elementary school teach their students about the ecology of tide pools. The partnership between EECB and Mililani-Mauka Elementary school is one of those rare gems in outreach where both sides get a tremendous amount out of the relationship. The school gets trained scientific experts that fascinate and amaze the kids with tales of slimy defenses and odd partnerships between crabs and anemones. In turn, the graduate students get to take a day off, get out of the lab, and act like kids playing in tide pools. Sometimes, I think the overworked grad students are more excited to catch critters than the kids!

What can you find in a tide pool on the coast of Oahu? Well, let’s find out…

Hexabranchus saguineus – Spanish Dancer

Kingdom: Animalia
Phylum: Mollusca
Class: Gastropoda
Family: Hexabranchidae
Genus: Hexabranchus
Species: H. sanguineus

One of my favorite finds was a Spanish Dancer nudibranch – a name that aptly fits the beautiful undulating motion of this colorful animal while it swims which looks like the swirling of a flamenco dancer’s skirt. It’s the largest species of nudibranch in Hawaii, and can get over a foot long!

The term “nudibranch” means “nude/naked gills,” and refers to the frilly, external gills found in these species (they look almost like feathers sticking out of the dancer’s back). The scientific name for this species, Hexabranchus sanguineus, refers specifically to the number of gills (six) and to its blood-like red coloring. Nudibranchs are often brilliantly colored and found in many sizes and shapes, which may serve to warn predators as many species are toxic. Unlike other sea critters, toxic nudibranchs don’t make their own defenses – they steal them from species they eat, like sponges and Portuguese man-of-war.

Dardanus gemmatus – Jeweled Anemone Crab

 
Kingdom: Animalia
Phylum: Arthropoda
Class: Malacostraca
Order: Decapoda
Family: Diogenidae
Genus: Dardanus
Species: D. gemmatus

This beautiful little crab is a specialized kind of hermit crab known as an anemone crab. The frilly bits on its shell aren’t just for show – they’re a kind of sea anemone, Calliactis polypus. For the crab, the anemones provide protection. Their painful stinging cells make the crab’s predators think twice about what they snack on. Those pretty pink strands are actually specialized stinging threads called acontia which help protect both the anemone and the crab. In turn, the crab provides the anemones with movement, thus granting them access to better food resources. This kind of you-pat-my-back-I’ll-pat-yours relationship is what is known in as symbiosis or mututalism.

Dolabella auricularia – Wedge or Eared Sea Hare

 
Kingdom: Animalia
Phylum: Mollusca
Class: Gastropoda
Family: Aplysiidae
Genus: Dolabella
Species: D. auricularia

Ok, so you can’t really see the sea hare in these pictures. But you can see what it produces when it’s scared – a thick batch of bright purple slime! Sea hares – also known as sea slugs – are relatives of snails and other shelled animals, but like slugs on land, they haven’t had a shell for millions of years, thus making them more vulnerable to predators. But the sea hares aren’t defenseless, as you can see from the goo in the pictures. When they feel threatened, they are able to produce large amounts of a thick slime which confuses their would-be predator, allowing the slug to slither away unharmed. The purple color for the slime from the red algae the hares feed on.

Echidna nebulosa – Snowflake Moray

 
Kingdom: Animalia
Phylum: Chordata
Class: Actinopterygii
Order: Anguilliformes
Family: Muraenidae
Genus: Echidna
Species: E. nebulosa

Tide pools are important nursery habitats, even for active predators like this snowflake moray. These scary hunters can grow up to 3 feet long and pack one heck of a bite, but this young eel is as vulnurable to predators as other small fish. The tide pools provide him and other young fish a place free of large predators where they can grow large enough to try and make it on their own on the exposed reefs. Snowflake morays don’t often eat fish, though they will if the opportunity arises. Their teeth are flatter than other species of eel, and are more suited to crushing shelled prey items like as shrimps, crabs, and sea urchins.

Octopus cyanea – Day Octopus

Kingdom: Animalia
Phylum: Mollusca
Class: Cephalopoda
Order: Octopoda
Family: Octopodidae
Genus: Octopus
Species: O. cyanea

By far one of the kid’s favorite finds was this small day octopus. Popular here in Hawaii as a food item (known as tako), day octopus are heavily fished. As daytime hunters, day octupus have incredible camouflage abilities. Let me point out that the two photos above are of the same octopus – those color differences are just a couple of the wide variety of elaborate color patterns and skin textures that the octopus displayed in our short time with it. Octopus have complex brains with a highly developed nervous system capable of changing their skin almost instantly as they move over different substrates. Roger Hanlon, an octopus biologist, once recorded a single day octopus changing patterns 1,000 times over a 7 hour period!

Scorpaenopsis diabolus – Devil Scorpionfish

 
Kingdom: Animalia
Phylum: Chordata
Class: Actinopterygii
Order: Scorpaeniformes
Family: Scorpaenidae
Genus: Scorpaenopsis
Species: S. diabolus

Last but not least, however, was by far my favorite catch of the week – this small devil scorpionfish, now named Stumpy. You see, this guy is one of the species that I study. I’m investigating the toxins in the entire order to get a better understanding of how toxins evolved in fish, and this little cutie is one of the many fishes whose spines possess a potent and painful sting. It’s easy to see why this particular species might be mistaken for a rock covered in algae. Because of exceptional camouflage, scorpionfish like this one are often unnoticed by tide pool goers, swimmers and divers until it’s too late and they find out the hard way exactly how strong the toxins they produce are. My goal is to better understand why other member of the order – groupers, for example – aren’t as toxic, even though they possess the ability to produce a similar protein toxin. Do they not express it? Or is the toxin itself altered to be less painful? Given that the toxins have strong effects on our bodies, it’s possible they may provide clues to new drugs or insights into how our cells work.

Stumpy here has come back with me so I can study his toxins as a part of my dissertation research. He currently resides in a tank at my house, where he has been eating like a glutton all week. The speed with which these ambush predators gulp a fish right out of the water never ceases to amaze me. Other cool fact: he glows orange in UV light. Yeah. Orange. How neat is that? I study the coolest animals EVER.

Check out more photos from this year’s tide walks on Facebook!

Studying shark populations can be tricky. As David Shiffman explains well, while there are a number of methods that can be used to study shark populations, quantifying just how far their numbers have fallen can be difficult. However, recent research out of the University of Hawaii suggests that the presence of humans has a severe and strong negative impact on sharks, driving down numbers by over 90%.

Sharks play a vital role in coral reef ecosystems. Yet every year, millions are killed for asian delicacies and disproven cancer cures. There is no question our shark fishing habits have devastated their populations; the only questions that remain are how much of an effect are we having, and can the sharks recover.

In an effort to answer the first, the research team crunched data from 1607 surveys from the NOAA Coastal Reef Ecosystem Division (CRED) to calculate the effect of human habitation on shark populations. The CRED team counted sharks throughout the Pacific using towed diver surveys, the most efficient and effective way to study open ocean creatures on a large spatial scale, and compared their counts with local human population numbers. Their results were clear – and sobering.

“Around each of the heavily populated areas we surveyed — in the main Hawaiian Islands, the Mariana Archipelago and American Samoa — reef shark numbers were greatly depressed,” said Marc Nadon, lead author of the study. “We estimate that less than 10% of the baseline numbers remain in these areas.”

The team also looked at other factors that might be affecting shark populations, including temperature and reef productivity. However, while sharks preferred warmer waters full of potential prey, the negative impact of humans dwarfed these effects. “Our results suggest humans now exert a stronger influence on the abundance of reef sharks than either habitat quality or oceanographic factors,” the authors wrote.

The team estimated that less than 100 people is enough to cut shark populations by 20%. Even 1,000 people – which is much less than the population of many small islands in the Pacific – was enough to decrease shark populations by 60%. As Nadon put it, “In short, people and sharks don’t mix.”

The findings are consistent with other research in the field. A 2003 paper, for example, found that shark populations in the Northwestern Atlantic dropped over 65% between 1986 and 2000. Similarly, a 2010 paper estimated that shark populations in the Chagos Archipelago had declined 90% since the 1970s. The more we study sharks, the worse the picture becomes, and the stronger the case becomes for conservation efforts. We simply cannot continue to treat these animals the way we do now, for all scientific evidence suggests the day is fast approaching when there will be no sharks left to exploit.

Reference: Nolan et al. Re-Creating Missing Population Baselines for Pacific Reef Sharks. Conservation Biology; DOI: 10.1111/j.1523-1739.2012.01835.x

Oil supplies the United States with approximately 40% of its energy needs. Billions upon billions of gallons are pumped out of our wells, brought in from other countries, and shipped around to refineries all over the states. 1.3 million gallons of petroleum are spilled into U.S. waters from vessels and pipelines in a typical year. Yes, it would be great if we never spilled a drop of oil. No matter how hard we may try, though, the fact is that nobody is perfect, and oil spills are an inevitable consequence of our widespread use of oil. The question is, once the oil is out there, how do we clean it up?

Nowehere is this issue more glaring than in the Gulf of Mexico right now, where 35,000 to 60,000 barrels of oil are spewing out of the remains of the Deepwater Horizon drilling rig every day. The spill has enraged an entire nation. But perhaps my grandfather put it best, when I asked him what he thought about how BP and the US is responding to the spill.

“They’re friggin’ idiots.”

My grandfather, Ralph Bianchi, knows a thing or two about oil spills. He spent thirty years in the oil spill cleanup business. His company, JBF Scientific (now a part of Slickbar), developed new technologies for cleaning up spills, including a skimming method called the Dynamic Inclined Plane (DIP). In 1970, they sold their first skimmer to the U.S. Environmental Protection Agency. The next year, the U.S. Navy purchased forty $250,000 DIP skimmers and stationed them at major naval installations throughout the world. When word of how well his designs worked for the government, private oil companies started buying DIP skimmers, too.

In 1987, my grandfather’s company, JBF Scientific, received a call from the Alyeska Pipeline Service Company. The company, based in Alaska, was formed in 1970 and charged with the duty of designing, constructing, operating and maintaining the pipeline which transports oil from the fields in Alaska. It is owned by the major oil companies that operate the Trans-Alaska Pipeline System, including a couple you may have heard of: BP and Exxon Mobil.

Part of Alyeska’s job is to clean up any spills which occur in the process of the movement of oil to, from and through the pipeline. What they wanted from my grandfather was a DIP skimmer larger than he’d ever constructed – a boat over 120 feet long. JBF drew up plans for a massive DIP skimmer capable of removing 2,500 barrels of oil per hour. But when my grandfather told them how much it would cost – an estimated $4 to $5 million at the time – Alyeska instead decided to try another company’s cheaper model, which turned out to be close to useless in the kelp-filled waters of the Northwest.

Of course, everyone knows what happened next. In 1989, the Exxon Valdez ran aground on Prince William Sound’s Bligh Reef and spilled an estimated 250,000 barrels of crude oil, creating one of the worst environmental disasters in history. The spill itself was bad enough, but Alyeska, Exxon and the country were entirely unprepared to deal with a cleanup of that nature. Despite months of cleanup efforts, less than 10% of the spilled oil was recovered, and 20 years later, the ecosystems in the area had still yet to recover.

After the spill, Alyeska bought my grandfather’s skimmer. The boat, called the Valdez Star, still operates in that area today. If another spill the size of the Exxon Valdez occurred now, picking up that volume of oil would only be a few days’ work for the Valdez Star and two aluminum oil recovery boats the company also bought. Only a few days work.

If only the cooperative in Alaska had been willing to spend a little more on their cleanup equipment! Other areas, however, were and are much better about their cleanup planning. One of the first privately owned groups to embrace the DIP skimmers was the oil cooperative in Puget Sound. Puget Sound and the Northwest Straits are among the busiest shipping lanes in the world, with billions of gallons of oil moving across the waters of Puget Sound every year. The Sound may have many environmental issues, including stormwater runoff and pollution, but it kicks butt at cleaning up oil spills.

Despite the fact that oil spills occur there fairly frequently, you don’t hear about them much. That’s because in Puget Sound, they have what my grandfather calls a “firehouse mentality.” The cooperative bought the first privately owned DIP skimmer, The North Sounder, from JBF in the late 1980s. After the Exxon spill, they purchased three more similar skimmers, and a 600 ton skimmer like the Valdez Star called The Shearwater. These skimmers are among a fleet of equipment and trained personnel ready at a moment’s notice to deal with any spill. They run drills to practice different methods of cleanup. They know the currents and wind data and predict where and when the oil will hit. They’ve identified sensitive shore areas like shell fish beds, bird feeding and nesting ground and yachting harbors, and have stationed containment and deflecting booms, storage barges, and skimmers at those areas. And all of it is funded by the state and the oil companies and other shippers whose oil could be spilled. In Washington, the state Ecology Department has a budget of $16 million, while companies spend roughly $41 million a year there preparing for spills.
Oil spill cleanup using my grandpa’s technology in 1972; my uncle Robert Bianchi on the left, a family friend Mark Mendano in the center, and my uncle Raimond Bianchi on the right.

In Puget Sound, when a spill happens, they jump into action. Just like firefighters responding to an alarm, trained teams of workers immediately assess the situation and combat the spreading problem. They contain the oil if they can, and if they can’t, they protect the areas that are most vulnerable to oil’s damaging effects. Similar oil cleanup crews are now in place in a number of harbors around the country.

So I asked my grandfather how many skimmers he sold to companies in the Gulf.

“None.”

BP now claims that 400 or so skimmers are now working to clean up the oil spilling in the gulf. One of their spokesmen, Mark Proegler, says skimmers are only able to collect about 10-15 percent of the oil. “They essentially scoop up the oil and water mix in the water for later separation,” he explained, “and that mix is about 10 percent oil and 90 percent water.”

But that’s because they aren’t using DIP skimmers, or other, better skimming technologies that have been developed over the past few decades. The resultant oil percentage of the fluids that are picked up by these skimmers is more than five times higher. When deciding how well prepared an area is for an oil spill, the government tends to operate on a 20% rule of thumb (33 CFR 155, Appendix B, Section 6) – that is, they assume that any skimmer will operate at only 20% the efficiency that the manufacturer claims. For JBF DIP models, however, they assume 74% to 94% efficiency.

What my grandfather wants to know is why the Valdez Star and the Shearwater, as well as the other large, high-quality skimmers, aren’t in the Gulf right now. Better boats are out there, which could clean up more oil and faster.

It’s not just that BP and other Gulf companies hadn’t embraced the newer, better cleanup technologies before this disaster occurred. It’s that they aren’t prepared at all for any kind of large spill. That’s what the US government discovered when they performed exercises in the early 2000s to see how companies would respond to a major spill. The After Action report of the 2004 Spill of National Significance (SONS) exercise concluded that, in the Gulf of Mexico:

Oil spill response personnel did not appear to have even a basic knowledge of the equipment required to support salvage or spill cleanup operations…. There was a shortage of personnel with experience to fill key positions. Many middle-level spill management staff had never worked a large spill and some had never been involved in an exercise.

What’s even more sobering is that of the oil spills within the Coast Guard’s jurisdiction (i.e., marine and coastal areas), approximately 50% of the incidents, both in number and the volume of oil spilled, occur in the Gulf of Mexico and its shoreline states.

Why doesn’t the Gulf have the “firehouse mentality” of areas like Puget Sound? Why haven’t they identified the most vulnerable areas and stationed cleanup equipment there, provided up to date training for cleanup personnel, and generally prepared for this kind of disaster?

The answer is simple. As my grandpa phrased it, “they’re cheap bastards.”

The lack of foresight and constant corner cutting by BP led to this disaster. But what’s worse is that they continue to botch the containment and cleanup of the billions of gallons of oil that their mistakes have spilled.

“The real issue,” my grandfather explained to me, “is that they don’t care about solving the problem.” By they, he wasn’t just referring to BP. He was referring to all of the oil companies in the Gulf and the government regulators that are supposed to be ensuring that oil drilling and transport occurs safely. “They throw dispersants on the oil. Do you know what dispersants do? They make the oil neutrally buoyant. Dispersed oil winds up in the water column and, therefore, cannot be deflected by floating booms or harvested with oil skimmers. They make the surface look cleaner, but they don’t do a damned thing to actually clean up the oil.”

Essentially, dispersants are soaps. They emulsify oil, breaking up up and allowing it to mix into water. The idea behind dispersants is that by breaking up the oil and putting it in the water column, it will be degraded faster by the microorganisms that naturally degrade oils and keeping the oil from coating the shoreline.

Starting in May, the US has been spraying oil dispersants at the spill like mad, despite concerns raised by many related to potential dispersant impact on wildlife and fisheries, environment, aquatic life, and public health. The EPA further approved injection of these dispersants directly at the the leak site to break up the oil before it reaches the surface. By the end of may, over 600,000 gallons of dispersants have been applied on the surface, with another 55,000 gallons applied underwater. The two main dispersants being used, Corexit EC9500A and EC9527A are neither the least toxic, nor the most effective, among the dispersants approved by the Environmental Protection Agency. In fact, the UK has banned their use entirely. When BP was asked why they aren’t using better dispersants, they said that Corexit was ‘what they had available.’

The bigger question, though, is why are they using dispersants at all. Multiple studies after the Exxon Valdez spill found that dispersants, detergents, and hot water cleaning of shoreline cause substantially more mortality than oil itself. Even before the Exxon spill, scientists knew that “dispersant-oil mixtures are more toxic than the dispersant alone, and many-fold more toxic than the crude oil.” While better and safer detergents are being developed, their long-term toxicity and effectiveness is still completely unknown, making them risky to use in such high quantities as BP is.

The way my grandpa sees it, the so-called cleanup of the Deepwater Horizon Oil Spill isn’t about being effective or safe, it’s about looking like they’re doing something. The goal is to make it less visible so the public forgets that it’s happening. It’s all about PR.

I think he’s right.

What needs to happen, in the Gulf of Mexico and throughout the United States, is a change of mindset. We’ve already started moving away from oil to other, more responsible and sustainable energy technologies, but that is only a small part of the solution. The truth is, we’re likely never going to have a zero demand for oil. We certainly won’t do it in the next fifty or a hundred years – it’s just not feasible. While we need to continue to research alternatives, we need to deal with how we handle and regulate oil now, too.

Oil companies have been taking advantage of loose regulations for too long. They need to be forced to prepare for the damage their products can cause. You would think that after the disaster in Alaska that we would have learned our lesson – that anywhere where oil is drilled, pumped or transported would have put in place well trained emergency response teams and extensive equipment ready to react to large spills. But apparently, we haven’t learned from our mistakes. This time, I hope that we do.

This post has been chosen as a Research Blogging Editor’s Selection, featured in the 33^rd edition of Scientia Pro Publica, and now won the Post with the Most!

PS: For amazing coverage of the oil spill in general, check out my blog-buddies over at Deep Sea News and the growing list of fantastic posts/feeds/etc from Southern Fried Science

Citations:

• Jonathan L. Ramseur (2010). Oil Spills in U.S. Coastal Waters: Background, Governance, and Issues for Congress Congressional Research Service , 7-5700 (RL33705)

• USCG Spill Compendium (2005). Cumulative Data And Graphics For Oil Spills (1973-2004)
• Ralph A. Bianchi, Edward E. Johanson, & James H. Farrell (1973). The Application of Skimmers, Piston Films,and Sorbents for Open Water Spills Offshore Technology Conference
• U.S. Department of Homeland Security, & U.S. Coast Guard (2004). California SONS 2004 After Action Report
• Paine, R., Ruesink, J., Sun, A., Soulanille, E., Wonham, M., Harley, C., Brumbaugh, D., & Secord, D. (1996). TROUBLE ON OILED WATERS: Lessons from the Exxon Valdez Oil Spill Annual Review of Ecology and Systematics, 27 (1), 197-235 DOI: 10.1146/annurev.ecolsys.27.1.197
• SWEDMARK, M., GRANMO, A., & KOLLBERG, S. (1973). Effects of oil dispersants and oil emulsions on marine animals Water Research, 7 (11), 1649-1672 DOI: 10.1016/0043-1354(73)90134-6
• CM Tarzwell (1971). Toxicity of oil and oil dispersant mixtures to aquatic life. Water pollution by oil. London, The Institute of Petroleum. P. Hepple (Ed.) , 263-272

Just this week, Gladstone researchers announced a major breakthrough in heart disease research: they successfully reprogrammed scar tissue in live mice back into functional heart muscle.

A mouse heart a month after a heart attack - scar tissue appears white

The researchers were able to use a virus-based system to deliver three key genes that guide embryonic heart development—Gata4, Mef2c and Tbx5 (GMT)—to areas of mouse hearts that were damaged in a heart attack. Within a month, cells that normally became scar tissue were beating away again as if they were not knocking on death’s door just 30 days before. By the three month mark, treated mice showed marked improvements in cardiac functioning.

“The damage from a heart attack is typically permanent because heart-muscle cells—deprived of oxygen during the attack—die and scar tissue forms,” said Dr. Deepak Srivastava, director of cardiovascular and stem cell research at Gladstone. “But our experiments in mice are a proof of concept that we can reprogram non-beating cells directly into fully functional, beating heart cells—offering an innovative and less invasive way to restore heart function after a heart attack.”

“This research may result in a much-needed alternative to heart transplants—for which donors are extremely limited,” said lead author Dr. Li Qian, a post doc at the California Institute for Regenerative Medicine. But the best part is that this method would use the person’s own cells, removing the need for stem cells or donor hearts. “Because we are reprogramming cells directly in the heart, we eliminate the need to surgically implant cells that were created in a petri dish.”

“We hope that our research will lay the foundation for initiating cardiac repair soon after a heart attack—perhaps even when the patient arrives in the emergency room,” said Srivastava. The ability to regenerate adult heart tissue from its own cells is a promising approach to treating cardiac disease because it may face fewer obstacles to clinical approval than other approaches. However, there is much to be done before this breakthrough becomes a treatment. “Our next goal is to replicate these experiments and test their safety in larger mammals, such as pigs, before considering clinical trials in humans.”

Previous work has been able to do this kind of cellular reprogramming in cultured cells, but clinically it is much more efficient if a treatment can work directly on live hearts. In 2010, coronary heart disease was projected to cost the United States $108.9 billion, including the cost of health care services, medications, and lost productivity. If research such as this can lead to improved functioning after a heart attack, it could save millions in health care costs, not to mention potentially save lives by preventing heart failure down the line. While this research’s implications for heart disease treatment is clear, this kind of in vivo reprogramming may be also useful in a variety of other diseases where tissue damage is a major cause of symptoms, including Alzheimer’s and Parkinson’s disease.

A normal and reprogrammed heart cell beating eight weeks after a heart attack

Reference: Qian, L. et al. 2012. In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytesNature DOI:10.1038/nature11044

A mouse lemur and a close-up shot of lice on its ear. Photos by Sarah Zohdy

For as long as there have been mammals, there have been lice. Though it’s hard to find lice in the fossil record, scientists have estimated that the group originated at least 130 million years ago, feeding off feathered dinosaurs, though they now live on just about all species of birds and mammals. Lice tend to be very host-specific, meaning they only live and feed on one species or a set of closely related species. Furthermore, lice can only survive a limited time without their hosts, and must quickly find a new one if they leave or are forcibly removed. This means that for lice to reproduce and spread, their hosts have to be in fairly close contact (like, as many parents know, kids in a kindergarden classroom). In wild species, lice rarely switch hosts unless the animals interact physically, whether through wrestling, nesting together or mating.

It was that requirement for close contact that made Zohdy and her colleagues think they might be an ideal proxy for investigating social interactions that can’t be viewed directly. They had already been collecting data on the mouse lemur populations in Madagascar using traps to monitor their movement. But while the researchers knew certain lemurs spent a lot of time together if they were caught together in traps, the researchers figured they were probably missing a good amount of social interaction. So, they decided to follow the lemur’s lice as well.

Mouse lemurs are parasitized by a particular species of louse, Lemurpediculus verruculosus, which feed off the lemurs’ blood. The researchers were able to track the transfer of these lice between lemurs by tagging lice with a unique color code using nail polish, so they could tell what lemur each louse started on. Over time, they continued to trap lemurs and look at their lice to see if any of the tagged ones had switched hosts.

In total, they tracked 76 transfers between 14 animals — all males — over the course of a month, which happened to be during the breeding season. The researchers hypothesized that the male-only transfers likely occurred during fights over females. But perhaps more interestingly, the lice data only supported 8 of the 28 expected social interactions predicted by trapping data, and found 13 new ones, suggesting the louse marking technique was able to uncover lemur social activity that the researchers have never observed. They also found that some animals shared more lice than others. Sarah Zohdy explained, “The youngest male in the study had the worst louse infestation, but only donated one louse, indicating a low number of interactions, while the eldest male, who also had a heavy infestation, appeared to be more sociable, collecting lice from many donors. Other males appeared to be ‘superspreaders’ donating but not collecting lice.”

The lice also revealed that lemurs travel more than the researchers had thought. “Most of the louse transfers occurred between lemurs over 100 m from each other, and one transfer spanned over 600 m,” the authors write. “The transfers therefore demonstrate a degree of lemur ranging far greater than anticipated.”

Overall, these data provide new insights into the social interaction of mouse lemurs as well as the relationship between the lice and their hosts. This isn’t the first study that used lice to look at a bigger scientific picture. Because of their host-specific nature, scientists have used them to map ancient speciation events, and even determine when humans first wore clothes. But never before have lice been used to study behavior in a living wild species, though the team hopes their study shows the usefulness of this technique. “The approach developed here has potential for application in any species parasitized by sucking lice, including the many trappable species of cryptic, nocturnal, subterraneous or otherwise elusive mammals in which host social contact and parasite exchange data are difficult to obtain.”

 
 
Reference: Sarah Zohdy, Addison D Kemp, Lance A Durden, Patricia C Wright and Jukka Jernvall (in press). Mapping the Social Network: Tracking lice in a wild primate (Microcebus rufus) population to infer social contacts and vector potential. BMC Ecology 2012, 12:4, doi: 10.1186/1472-6785-12-4.

Today, 85 percent of the world’s fisheries are either fully exploited, overexploited or have already collapsed. Combined, the world’s fishermen catch 2.5 times the sustainable number of fish every year. Scientists predict that if current trends continue, world food fisheries may collapse entirely by 2050. “We are in the situation where 40 years down the line we, effectively, are out of fish,” explains Pavan Sukhdev, special advisor to the UN Environment Programme.

What we need are better management strategies. Now, researchers from the Center for Ocean Solutions at Stanford University are turning to the past for advice. Loren McClenachan and Jack Kittinger used historical records to reconstruct fish catches for the past seven hundred years to see if earlier civilizations did a better job than we are at managing their fisheries. The authors were able to characterize historical catch rates in the Florida Keys and Hawaii by reviewing a variety of historical sources, including species-specific catch records from the 1800s and archaeological reconstructions of population densities and per-capita fish consumption.

“Seven hundred years of history clearly demonstrate that management matters,” said Loren McClenachan, co-author of the study and assistant professor of environmental studies at Colby College. In Florida, fisheries were characterized by years of boom and bust through sequential collapse of high-value species, many which are still endangered or extinct today. The Keys fisheries were set up for failure – unlike other historical island communities, the Keys were highly connected to other markets, increasing fisheries demand. Furthermore, they have historically lacked a centralized management system. But, while fisheries in the Florida Keys have always been poorly supervised, fisheries in Hawaii were once far better than they are today.

Annual fisheries catch per reef area for the Florida Keys and Hawaii over time.

“Before European contact, Native Hawaiians were catching fish at rates that far exceed what reefs currently provide society,” said Kittinger, co-author and early career fellow at the Center for Ocean Solutions. Native Hawaiians pulled in over 15,000 metric tons of fish per year, and these high yields were sustained over several hundred years, despite a dense Hawaiian population. “These results show us that fisheries can be both highly productive and sustainable, if they’re managed effectively.”

Much of the management system in Hawaii was tied to class and gender. For example, most offshore fishing was done by a professional fishing class who were familiar with their local environment. If they wanted to fish, they had to ask their chiefs, who regulated the fishing gear and canoes. The most valuable (and vulnerable) species like turtles and sharks were reserved for high chiefs and priests, reducing fishing pressure.

The key to the Hawaiian’s success lay in using a diverse suite of management measures. Many of the methods they used are similar to strategies employed in fisheries management today, including protected areas, community-based management, regulation of gear and effort, aquaculture, and restrictions on vulnerable species.

Perhaps the greatest difference between management then and now, however is that in native Hawaiian society, rules were strictly enforced. “Rules were accompanied by robust sociocultural institutions,” the authors write. The ancient Hawaiians did not hesitate, and punished transgressors with corporal punishment. “Clearly, we don’t recommend this,” said Kittinger, “but it’s easy to see there’s room to tighten up today’s enforcement efforts.”

He’eia Fishpond in Kane’ohe Bay, Hawaii. Image c/o Paepae O He’eia

 
Other differences exist as well. For example, while aquaculture was used by the native Hawaiians, these fishponds were maintained for different reasons than we farm fish today. Fishponds did not contribute substantially to total fish production, but instead served as food security during tough times. As such, Hawaiians stocked fishponds with very different species than modern farms. Fishponds contained small, algae-eating species, requiring little from the sea to support them. Modern aquaculture, in contrast, relies heavily on wild-caught feeder species to support lucrative, luxury species like salmon. Five pounds of wild-caught fish are needed to produce one pound of farmed salmon, and instead of acting as a backup for when wild fish are scarce, fish farms make up a whopping 50% of our consumed fish production.

Kittinger and McClenachan hope that understanding successful management strategies by historical societies will lead to better management of our current resources. “The evidence we present from historical reconstructions shows that reef fishery sustainability has been achieved in the past,” they write, “which can guide actions for a more sustainable future for reefs and the communities that depend on them.”
 
 

Reference: McClenachan, L & JN Kittinger (2012). Multicentury trends and the sustainability of coral reef fisheries in Hawai‘i and Florida. Fish and Fisheries, doi: 10.1111/j.1467-2979.2012.00465.x

Image of fishing c/o Flickr user dennistanay

Rejection stinks. It literally hurts. But worse, it has an immediate and negative impact on our brains, producing withdrawal symptoms as if we’re quitting a serious addiction cold turkey. It’s no wonder, then, that we are tempted to turn to drugs to make ourselves feel better. But we’re not the only species that drowns our sorrows when we’re lonely – as a new study in Science reveals, rejected Drosophila do, too. Scientists have found not only will these sexually frustrated flies choose to consume more alcohol than their happily mated peers, sex and alcohol consumption activate the same neurological pathway in their brains.

Drosophila melanogaster males sure know how to woo a lady. When placed in the same container as a potential mate, a male fly will play her a delicate love song by vibrating one wing, caress her rear end, and gently nuzzle her most private of parts with his proboiscis to convince her that he is one heck of a lover. But even the most romantic fly can’t convince an already mated female Drosophila to give up the goods, so scientists were able to use the girls’ steely resolve to see how rejection affects fly drinking behavior.

“Alcohol is one of the most widely used and abused drugs in the world,” explains lead author Galit Shohat-Ophir. “The fruit fly Drosophila melanogaster is an ideal model organism to study how the social environment modulates behavior.” Previous studies have found that Drosophila melanogaster exhibit complex addiction-like behaviors. So in the controlled setting of Ulrike Heberlein’s lab at the University of California San Francisco, researchers paired male fruit flies with three types of females: 1) unmated females, which were willing and happy to mate; 2) mated females, which actively rejected the men; and 3) decapitated females, which didn’t actively reject the guys but, well, weren’t exactly willing partners either. After the flies were satisfied or frustrated, they were offered regular food and food spiked with ethanol, and the researchers measured which type they preferred to see if there was any connection between sex and drinking.

The flies that were rejected drank significantly more than their satisfied peers, but so did the ones paired with incapacitated girls, suggesting that it wasn’t the social aspect of rejection but sexual deprivation that drives male flies to increase their ethanol consumption (see the video at the end!). This alcoholic behavior was very directly related to the guy fly ever getting laid, for even after days of blue balls, if he was allowed to spend some time with a willing woman, he no longer preferred the spiked food.

What the scientists really wanted to understand, though, was why. What drives a frustrated fly to the flask? So to look at the underlying mechanism of this phenomenon, the scientists examined the flies’ brains. A body of scientific literature has connected one particular neurotransmitter, neuropeptide F (NPF), to ethanol-related behaviors in Drosophila, so it was a logical place to start. A very similar neurotransmitter in our brains, called neuropeptide Y (NPY), is linked to alcoholism.

Increased expression of NPF in mated male brains, as shown through immunochemistry.

The team found that sexual frustration caused an immediate decrease in the expression of NPF, while sex increased expression. Furthermore, when they used genetics to artificially knock down NPF levels in the satisfied flies, they drank as much as their not-so-satisfied friends. Similarly, when the researchers artificially increased NPF levels, flies stayed sober. This is the first time NPF levels have connected sexual activity to drinking. Clearly, NPF levels controlled the flies’ desire to drink, so the team further explored how NPF works in the fly’s brain.

Many animals, including ourselves, possess a neurological reward system which reinforces good behavior. Through this system, we ascribe pleasure or positive feelings to things we do that are necessary for species survival, including sex, eating, and social interaction. Drugs tap into this system, stimulating pleasure which can lead to addiction. Previous studies have shown that flies find intoxication rewarding, so the researchers hypothesized that NPF may play a role in the reward system.

Preference tests showed that artificially increasing NPF levels in the absence of sex or ethanol was rewarding to the flies, confirming the scientists’ hypothesis. This was further supported by the discovery that constantly activating NPF abolished the flies’ tendency to consider ethanol rewarding.

“NPF is a currency of reward” explains Shohat-Ophir. High NPF levels signal good behavior in Drosophila brains, thus reinforcing any activities which led to that state. This is a truly novel discovery, for while NPF and the mammal version, NPY, have been linked to alcohol consumption, no animal model has ever placed NPF/NPY in the reward system.

Understanding the role of NPF in reward-seeking behaviors may lead to better treatments for addicts. “In mammals, including humans, NPY may have a similar role [as NPF],” says Shohat-Ophir. “If so, one could argue that activating the NPY system in the proper brain regions might reverse the detrimental effects of traumatic and stressful experiences, which often lead to drug abuse.” Already, NPY and drugs that affect the function of its receptors are in clinical trials for anxiety, PTSD, mood disorders and obesity. This study suggests that perhaps they should be tested as treatment for alcoholism, too, as well as other reward-based addictions.

Research: Shohat-Ophir, G, KR Kaun & R Azanchi (2012). Sexual Deprivation Increases Ethanol Intake in Drosophila. Science 335: 1351-1355.

This sequence of three videos shows a male fly courting and successfully mating with a female fly, another male fly being rejected by a female, and a male choosing to consume an alcohol-infused solution over a non-alcohol solution. Video © Science/AAAS

Images:
Fruit fly from Wikimedia Commons, posted by Thomas Wydra, edited in Photoshop.
Immunochemistry reproduced from Shohat-Ophir, G, KR Kaun & R Azanchi. Science 335: 1351-1355 (2012).

A picture of a hydra, from the Encyclopedia of Life

Upon first glance, hydra seem like remarkably simple creatures. The basic description of a hydra would be a tube closed at one end with tentacles surrounding a mouth on the other, made of fragile tissue that can be as slim as two cells thick. No gills, no heart, no brain, no eyes – of course, it would be hard to pack all those organs into a creature that you sometimes need a microscope to see, and hydra certainly seem to do well enough without them. These small relatives of jellyfish are found worldwide, and are some of the only members of the phylum Cnidaria to be found in fresh water.

Yet their modest body plan is misleading. Hydra have fascinated scientists for centuries, for they have a phenomenal capacity to regenerate and may even be immortal. In 1744, Swiss naturalist Abraham Trembly was one of the first to be entranced by these simple animals and reflected, “It seemed to me from the start of my observations that knowledge of the remarkable properties of the polyps could bring pleasure to the inquisitive and contribute something to the progress of natural history.”

The hydra’s simple nature is also belied by their tentacles, which inject a potent neurotoxin into unsuspecting prey using extremely sophisticated cells called cnidocytes. For decades, scientists have sought to understand how these specialized attack cells are triggered. Now, evidence published in BMC Biology suggests these primitive creatures may ‘see’ more than we realized, as the firing of these prey-catching stinging cells is regulated by the same chemical pathway used in our eyes.

Ever since the genome for Hydra magnipapillata was published in 2010, it was known that hydra possess the genes for opsins, the photosensitive protein family found in all animals that can see, but no one knew exactly what they do with them. Unlike other animals, hydra don’t have eyes or eye spots, or any kind of centralized visual sensory area, although they have behavioral responses to light. When David Plachetzki teamed up with Caitlin Fong and Todd Oakley’s lab at UC Santa Barbara, they found that these light-sensitive proteins were clustered on the hydra’s tentacles and around the hydra’s mouth, suggesting that they might be involved in feeding behavior.

Fluorescent picture of hydra tentacle bulbs; Musculature is stained green, neurons, including cnidocytes, are stained red and nuclei are stained blue

In hydra, potent stinging cells are grouped with other neurons in what are called “battery complexes” on the hydra’s tentacles, forming one of the most intricate systems of neurons in an organism that lacks a central nervous system. Using fluorescent molecular probes, the researchers were able to show that opsins are expressed in the same locations. They also discovered that other proteins that are part of the response to light, cyclic nucleotide gated (CNG) ion channel and arrestin, are found in these battery complexes, too. In other words, the stinging arsenals are completely equipped to react to changes in light.

Just because they have the parts, however, doesn’t mean they use them. So to see if the stinging cells themselves, the cnidocytes, are regulated by light, the researchers exposed hydra to LED lights of different intensities, then prodded the animals’ tentacles with gelatin-coated fishing wire as if they were being touched by potential prey. After, the team was able to count how many cnidocytes were embedded in the line as a way of measuring whether the stinging cells were triggered.

They found that bright light decreased the firing of stinging cells – which makes sense, really. “Cnidocytes are expensive to make for a hydra; a significant proportion of their cellular mass is comprised by these cell types. Therefore, it is important these austere animals to discharge them in an economical manner,” explains Plachetzki. Hydra and their relatives in the phylum Cnidaria are known to feed in daily patterns, becoming especially active at dawn or dusk, so it’s logical that they would be less inclined to feed in bright light, which might be perceived as day. Of course, there is an even more straightforward explanation as to why cnidocytes fire when the lights go out – shadows. “It could be that hydra use this sensory function to detect the shadows cast by prey on feeding tentacles, just when the moment is right to strike.” The researchers were able to directly connect the opsin signaling cascade to this change in feeding behavior by introducing a blocker of opsin signaling, cis-diltiazem. In the presence of the blocker, light had no affect, confirming that opsin-based signaling is required for this light-mediated change in cnidocyte firing.

Since hydra have been extensively studied for centuries, it is a bit surprising that we are only now learning how light affects their feeding. “It is strange that nobody had discovered this before,” remarked Plachetzki. “Folks have been playing around with hydra and their photobehavior for greater than 200 years, why didn’t they notice this?” But, he says, when you look at some of the older observations of these creatures, “you get the impression that others might have had this hypothesis as well, but there were until now never any data to support it.”

These findings reveal one of the earliest uses of the chemical pathways that were co-opted to create vision. By learning more about these signaling cascades, we can begin to glimpse back at the very beginnings of sight, and slowly learn more about the evolutionary steps that led to our eyes. Aside from the interesting evolutionary implications, this research may also lead to more direct benefits to humans. Cnidarians, including hydra, jellies and corals, are responsible for tens of thousands of stings every year, a handful of which are fatal. The more we know about how these stinging cells are triggered, the better we can prevent these stings, or even develop a way of protecting swimmers against them.

Reference: David C Plachetzki, Caitlin R Fong and Todd H Oakley (in press). Cnidocyte discharge is regulated by light and opsin-mediated phototransduction. BMC Biology

I truly do believe that Facebook, Twitter, and other social media are essential for every scientist to use. Not only are they the communication platforms of the future, they hold the potential to revolutionize how we do science in the first place. It seems foolish at best that in scientific circles we deride the use of these networks that, literally, two thirds of the world’s population are connecting through. I’ve laid out the arguments before (see the post list below), and will surely continue to talk about this topic until I go hoarse. Simply put, it’s not a question that scientists need to increasingly engage with new media platforms to stay relevant in this digital age. The question is how.

For that, I’m going to point you toward the freshly launched Social Media for Science Google+ Page and the workshop wiki, which is an evolving collection of information and resources, as well as the Storify of the afternoon by Jessica Rohde. You can also download my slides from slideshare, or watch the video of my talk:

More Social Media for Scientists:

• Part 1: It’s Our Job
• Part 2: You Do Have Time
• Part 2.5: Breaking Stereotypes
• Part 3: Win-Win

Other interesting posts on the topic:

• Five minutes with Patrick Dunleavy and Chris Gilson: “Blogging is quite simply, one of the most important things that an academic should be doing right now” on the LSE blog
• Social Media and the Love of Science by Brian Kateman on Eco Matters (which links a great video of a discussion at the The American Museum Natural History)
• Science and the social media by Chris Rowan for Earth Magazine
• Dialogue or Dead End? Social media for science communication a presentation by R. Andreas Kraemer
• Instant Social Media for Life Scientists a diverse set of examples and resources for scientists interested in social media collected by Mary Canady

For some species of fish, when a predator swoops in and injures one fish in a school, the rest will take off in fear. This much we know. In 1938, Austrian ethologist Karl von Frisch claimed that at the root of this behavior was a chemical alarm signal which he referred to as “Schreckstoff,” which means “scary stuff” in German. Since von Frisch’s seminal work, over 100 published studies concerning Schreckstoff have demonstrated that certain fishes have some substance in their skin cells which is released when that fish is injured and causes other fish to scatter. That much, we know, too.

This has perplexed scientists because it seems strange that any animal could evolve to give off that kind of chemical alarm. The other fish aren’t fleeing from blood or any clear signals of death, so what are they so afraid of? And if it’s not a signal of death but instead a signal of danger, as many scientists have argued, where is the benefit to the dying fish? You see, as much as we love the idea of altruism, it’s not very common in the natural world – at least not in its pure form. Doing something purely for the sake of others is of little benefit to an individual from an evolutionary perspective. So, hypotheses have been thrown around wildly to explain this kind of altruistic signaling – perhaps the alarm is to protect close kin, or, somehow, the chemical actually attracts the would-be-predator’s predators, thus giving the injured fish a chance to escape. Despite years of laboratory research, no hypothesis seems to be able to explain the presence of Schreckstoff. Furthermore, though some scientists have offered up potential compounds, what exactly Schreckstoff is has remained a mystery.

Now, a team from Singapore has identified that the elusive Schreckstoff as the same compound that we take to improve our joints and treat osteoporosis: chondroitin sulfate.

Structure of Chondroitin Sulfate (c/o Wikipedia)

Chondroitin sulfate is a specialized chain of sugars that is a major component of fish skin, just like it’s a major component of our cartilage. Using zebrafish, a common laboratory organism, the research team found chondroitin from zebrafish tissues caused other fish to turn fin and run. They even took chondroitin from shark skin – the kind we take as supplements – and found that the zebrafish were terrified by it. The fish were also more afraid when the chondroitin was broken down by an enzyme first. The team hypothesized that when a fish is injured, enzymes released by the wounding break down chondroitin sulfate into smaller sugary chunks, and these bits and pieces, as well as the larger chondroitin molecules released by the wounded cells, are the smell that serves as a chemical alarm signal.

The best part of this discovery is that it solves evolutionary issue that scientists have had with the existence of Schreckstoff. The burden of producing a fear signal while dying doesn’t make sense unless that signal is something the fish already produced for other reasons which is only released in the case of injury – akin to some being afraid of the smell of blood. That way, the evolutionary impetus isn’t on the fish producing Schreckstoff to produce an alarm, it’s on other individuals to detect a sign of danger or death to save their own tails.

Here’s how it goes: once upon an evolutionary time, fish that were sensitive to Schreckstoff were the first to run in the face of danger, and thus were more likely to survive. Over time this would lead to an entire lineage of Schreckstoff-sensitive fish. Since chondroitin is a known component of fish skin for other reasons, but wouldn’t be released into the water unless that skin is ruptured, it perfectly fits this evolutionary scenario.

Because young zebrafish are see-through, researchers were also able to specifically examine what parts of the zebrafish brain are turned on by chondroitin fragments. They found that a specialized part of the brain called the mediodorsal posterior region was responsible for the fearful reaction. What is particularly interesting about this chunk of brain matter is that it is packed with a group of neurons called crypt cells which have no other known function. Scientists have been trying to uncover what these strange neurons do for awhile, and this new discovery may hold the key. Co-author Suresh Jesuthasan thinks that these cells are a part of a special brain circuit which mediates the fish’s innate fear response.

Together, the new findings, published in Current Biology, are the pieces to the Schreckstoff puzzle that scientists have been trying to fit for decades. There are still questions to be answered, of course – how do certain species only respond to injuries by their own species and not those of others, for example? – but this new study has provided valuable insight into fear responses in fish, and perhaps opened up new doors in our understanding of how fear originates and is processed in animal brains.

Article Link: Mathuru et al., Chondroitin Fragments Are Odorants that Trigger Fear Behavior in Fish, Current Biology (2012), doi:10.1016/j.cub.2012.01.06

Here’s the researchers’ video of the fear response:
Zebrafish fear response to Schreckstoff

It’s incomprehensible, now, to think of someone writing a single volume that could equally change science as we know it. The two simple ideas that Darwin fleshed out in his first publication were earth shattering at the time. He has since been called both a genius and a heretic for these two theories – both titles equally deserved. But whatever you call him, his vision has changed the world irrevocably. Today, on what would have been his 203 birthday, we celebrate the life and scientific contributions of this man. In honor of the occasion, I am reposting my first Darwin Day post ever, from way back in 2009. Enjoy!

If I ask you what group of organisms is an exhibition of evolution at its finest, what would you say? Most people, I think, would say human beings, or at least apex predators. After all, we have staggering intellect compared to our prey items and clearly dominate the planet, eat what we will, etc. Not only that, we’re insanely complex. Ask some scientists, and they might give you any number of answers. Cockroaches are likely to exist long after we do, as are rodents, so maybe they get the title. Or, being scientists, they might be biased to whatever organism they study. Maybe algae and plants, as the sustenance for all other life. But all of you, in my humble opinion, are wrong. That is, unless you choose parasites.

It’s ok if you don’t believe me yet. Darwin wouldn’t have, either. He and his contemporaries viewed parasites as degenerates who, at best, violated the progressive nature of evolution. Even in The Origin of Species, Darwin refers to parasites as regressive instead of progressive. But truly, no group of species is a better choice for evolution’s finest.

First off, let’s talk numbers. Parasitism is the most popular lifestyle on earth – over 40% of all known species are parasitic, and the number of parasitic species rises daily¹. Sure, you might say, but they tend to be small. In that case, let’s talk biomass – weight, just to be clear. One group of parasites, the flukes, have been found to be equal in weight to fish in estuarine habitats, and three to nine times the weight of the top predators, the birds – estimates which are thought to be conservative for the earth as a whole². Though they’re largely ignored when we study food webs, they’ve been estimated to be involved in over 75% of inter-species interactions¹. Clearly, by the numbers, they are the most prolific and successful organisms on earth.

But even that is not why I would argue they are evolution’s finest. They, more than any other group out there, both exhibit extreme evolutionary adaptations and spur them onward in other species.

No matter how complex or how impressive any other species may be, it has parasites. We do – lots, actually. Every species we might hold as a masterpiece of evolutionary complexity cannot out maneuver their parasites. Not one. Even parasites, marvelous as some are, have parasites – like a crazy russian doll. They have evolved amazing abilities to survive host defense systems, manipulate host behavior and boost heir own reproductive success. They’ve even been implicated in major cultural differences in people. It turns out that a rat parasite, Toxoplasma gondii, needs to be eaten by a cat to complete its lifestyle. Somehow it developed a trick to make rats unafraid of cat smells. When it accidentally ends up in people, it does the same kind of mind-altering, making people more guilty and insecure, even more frugal, mild-tempered, and complacent³. Other parasites do far more intricate manipulations of behavior, turning males into females, creating walking zombies, even forcing suicide. If parasites can not only break into and survive the most complex assortments of systems available, even with modern medicine fighting against them, and manipulate those complex organisms to slave to their bidding, how can we not credit them as masters at what they do?

But even more impressively, I would argue, is that no other group has so dramatically impacted how other species have evolved. They don’t just affect their hosts immune systems, either. If you read much into evolutionary theory, you realize it’s riddled with parasites. Why are some birds very colorful? Oh, because if they’ve got a lot of parasites they can’t be, so it’s a signal of a healthy male⁴. Why are we attracted to certain people? Because their immune genes are different from ours, giving our children the best chance to fight off the next generation of parasites. Almost everywhere you look, evolutionary changes are spurred on by parasites. It’s even suggested that sex itself evolved as a response to parasites. It’s a way of better shuffling our genes so that we have better odds at fighting off parasites.

Even we, as “ideal” or “complex” as we are, owe much to parasites. Some even argue that we are worse off without them. The argument, as it goes, is that our immune system evolved in the presence of unkillable parasites, particularly the parasitic worms. These worms, or Helminths as they are called as a group, were too costly to try and eradicate. Attacking foreign invaders, after all, is energetically expensive, and always runs the risk of over-activating our immune system, leading to self-inflicted injuries and diseases. So the best strategy, instead, was to have an immune system that functioned optimally against other issues, like the fatal viruses or bacteria, despite the mostly benign worm infections⁵. Since worms secrete anti-inflammatory compounds to fight off our defenses, we were better off with systems that overcompensated for that. Now, since we have drugs which kill them off, our immune system is out of balance. Many cite the rising rates of auto-immune and inflammatory diseases like allergies, arthritis, irritable bowel, type 1 diabetes, and even cancer in developed nations as evidence that ridding ourselves of helminths has damaged our health⁶. They’re backed up with multiple studies that show unexpected results, like that mice genetically predisposed to diabetes never develop it if infected with flukes at an early enough age.⁷

Parasites are uniquely capable of out-evolving their hosts and adapting to whatever changes go on in them. Simply put, they evolve better. They change their genes faster and keep up with a barrage of host defense systems, often like it’s effortless, spurring onward dramatic changes in other species. If Darwin had only known how amazingly complex the barriers these creatures have to overcome and the extent to which they have affected the species he’d encountered on his travels, he would not have labeled them “degenerates”.

As far as evolution is concerned, no group of species demonstrates it, causes it, and is so capable of it as the parasites. While disgusting or even cruel, they are truly evolutionary masterpieces. So while you may find them vile or detestable, you have to admit they’re good at it. Can you really argue that some other group is more deserving of the title of Evolution’s Finest?

Cited:
1. A. Dobson, K. D. Lafferty, A. M. Kuris, R. F. Hechinger, W. Jetz (2008). Colloquium Paper: Homage to Linnaeus: How many parasites? How many hosts? Proceedings of the National Academy of Sciences, 105 (Supplement_1), 11482-11489 DOI: 10.1073/pnas.0803232105

7. Anne Cooke (2009). Review series on helminths, immune modulation and the hygiene hypothesis: How might infection modulate the onset of type 1 diabetes? Immunology, 126 (1), 12-17 DOI: 10.1111/j.1365-2567.2008.03009.x

Only 17% of Americans can name a living scientist. If you ask middle school students what a scientists looks like, they’ll tell you he’s a an old white guy with crazy hair, glasses and a lab coat. More often than not, he’s depicted inside and playing with chemicals. This stereotype is pervasive – and completely, totally wrong.

All of this is why I completely and totally love the new tumblr This Is What A Scientist Looks Like started by sci-comm guru Allie Wilkinson. Scientists from all kinds of fields are asked to submit photos of themselves and write a brief bit about who they are. The pictures are incredible; scientists are depicted everywhere from Antarctica to the tropics, on the tops of mountains or under the sea. The pics express personality, intelligence, and even a little humor.

Anyhow, if you’re a scientist, I strongly encourage you to add yourself. And if you’re not, go check out what scientists really look like, including a few goofballs like this:

A Marine Biologist’s Story

The air felt thick and heavy in my lungs. As I drove further down the narrow strip of beach, my throat closed and my eyes burned. It wasn’t normal sea air – it was toxic. Red tide was hitting the area in full force, killing off thousands of marine animals and filling the air with the neurotoxic compounds the algae Karenia brevis is known for. As the waves crash on shore, they break open the delicate algal cells, aerosolizing the odorless but noxious brevatoxins.

Many people have heard of red tide, but if you haven’t experienced it, you should consider yourself lucky. A few years ago I was driving an ATV on Casey Key late at night looking for nesting turtles to tag during one of the worst red tide seasons in recent history. Everything was dying. You couldn’t go near a beach without coughing and wheezing, and you probably didn’t want to anyhow, since they were covered in dead fish and other marine life.

But there I was, 2:30 in the morning, holding my breath as much as I could and scanning relentlessly for nesting turtles as a part of a summer internship at Mote Marine Laboratory in Sarasota, FL. I hadn’t slept much in days, and I was going to be out there until sunrise. I was exhausted. I couldn’t breathe. And it was in that moment that I started thinking about how I ended up in this situation in the first place.

You know, no one ever asks me why I am a marine biologist. I still expect that people will, and that I’ll get to tell these elaborate stories of the great things I get to do as if they had anything to do with my choice to follow this career path. But no one ever asks. I think most people assume that they know why someone becomes a marine biologist. They think “ooo, she gets to be like those people at SeaWorld riding the dolphins.” Everyone has this fanatasy of what a marine biologist is, and they think that all marine biologists have known their whole lives they would end up that way.

First off, they’re completely wrong about what it means to be a marine biologist. Being a marine biologist isn’t all playful dolphins and spectacular diving. It’s driving an ATV up and down a beach littered with dead fish – and spending an hour pulling a 200 lb dead sea turtle high enough out of the water so that the stranding crew could find it in the morning, even though you can barely breathe. It’s never, ever being able to look at seafood the same way again. It’s getting up at a god-awful hour to make it to your field site for sampling when the tide is at just the right height, where you can pull water from the ground but still count the crab burrows on the surface, then staying out there all day even though it’s 100 degrees out with no clouds and you feel like you’re being baked alive. It’s cleaning the bones of a manatee so that it can be used as a teaching tool, which requires placing the putrid rotting skeleton in a vat of water in the sun to rot, and then going back once a week, dumping the fetid water and pulling whatever decomposed flesh you can off, until the bones are picked clean. It’s counting the 53 dead baby sea turles from a nest that was raided by fire ants (who aren’t exactly pleased that you’re disturbing their hard-earned meal). It’s staring into a microscope for hours picking the miniature, formaldehyde-pickled marine life from a mud sample to catalog the fauna in a riverbed. It’s always feeling like you smell of dead creatures or harmful chemicals, and being so used to it you actually kind of like the smell.

In other words, it’s gruesome. It’s a little grotesque. And to be honest, there’s got to be something kind of off with you to begin with to enjoy it enough to make a living doing it.

Secondly, I haven’t always known I would be a marine biologist. Looking back it might be obvious to the casual observer, but that doesn’t mean it was obvious to me. I didn’t really figure it out until I had to pick a college and a major to go with it. Let me explain:

I was born in Boston, Massachusetts in the summer of 1985. I was happy in New England. I liked being a little kid. And I was a smart kid, too, which made being a little kid all the more fun. I didn’t really have much of a choice about being nerdy. Just look at my dad, who designed the first computer go program – I was screwed. Neither of my parents, though, were biologists, and in Boston the ocean is cold and unwelcoming. Of course, when I was about four years old, my parents decided they didn’t want to live in the frozen northeast any more, and they moved me and my brother to Hawai’i. I know – how awful.

It’s in Hawai’i that the first signs of my future career began to show. At the ripe age of 5 years old, my parents decided to send me to a special school for gifted kids (I said I was smart, didn’t I?).

I liked tongues.

To do so, they had to have my IQ tested. I passed. But the most interesting part of my IQ report isn’t the score, it’s the commentary from my examiner. She said I was a “poised, cooperative young child.” I was friendly and quick to talk, and even better, in my chatty childish way, I talked about what I liked:

The student spoke briefly about her interest in animals and bugs, noting that she likes to “find dead geckos and open their mouths to see their tongues.“

Oh yeah. I was a biologist when I was five – not that I knew this until much later. I loved animals of all kinds, and couldn’t get enough of museums and zoos. I also fell in love with the sea. I loved tide pools and whatever creatures I could find in them. I thrived in the ocean, learning to swim at a very young age and spending as much time as I could underwater instead of on land. Hawai’i became my home, and I felt like I had lived there all my life (I still say “Hawai’i” and certain Hawaiian and Asian words with an accent that never ceases amuses my non-local friends).

Then my parents divorced. My mom moved to Vermont, of all possible places. So I spent most of the year in the artic world of New England, and only my summers back in the wet and salty world I loved. But being in Vermont gave me the opportunity to explore a whole range of interests. Being an outgoing person, I took well to the stage, and loved every facet of the theater. I loved art and painting, and always had a creative streak in me that I still nurture. I learned to play guitar and sing, and wrote my own songs. By high school, in fact, you probably would have expected me to end up a starving artist of some kind.

In high school, I was a jack of all trades. I took the highest level courses in math, science, theater, art, history, and english. My senior year I was granted independent studies in History, Theater and English. I took all kinds of AP courses, walking away with APs in English Lit, English Language, U.S. History, Calculus BC, Physics B and Advanced Physics. Note, for the record, that not one of the things I just mentioned has the word “biology” in it.

You see, I loved animals – I had cats and dogs and odd pets like hedgehogs my whole life, I loved searching the woods for living creatures, adopting anything injured or sick – but I didn’t think of myself as a biologist. Not yet, anyhow. I was an actress, musician, artist, writer, historian, and even physicist, but I wasn’t a biologist. Then, of course, I had to think about where I wanted to go to college. There was one thing I wanted above all else – I wanted to live in Hawai’i.

I missed it. I missed the water and the waves. I missed the sun and the beach. I missed everything about the islands. I felt like a fish out of water in New England – all I wanted was to go home.

Somehow, in my homesick, 16-year-old mind, I came up with a brilliant idea. I would study the physics of cetacean (whale and dolphin) communication. I could double major in Marine Biology and Physics, ending up in Hawai’i for graduate school, and I would get to be where I belonged. So I found out which colleges had good science programs, particularly marine ones (the whole getting back to Hawai’i bit hinged on me being a marine-centered physicist), and applied. And through a twist of fate, I ended up in Florida at Eckerd College.

After my first semester of courses at Eckerd, though, I knew that I wasn’t a physicist. I loved physics, but the advanced, theoretical stuff just wasn’t my cup of tea – I liked the hands on, applied physics. I did, however, adore my marine science classes. I liked learning about the physiology of marine inverts, and playing with them in labs. Once, I spent an entire hour flipping an upside-down jellyfish upside-down then right-side-up again until my hand actually went numb. I met my undergraduate mentor, Dr. Nancy Smith, who I quickly came to aspire to be like. And from that time onward, there was no doubt in my mind that although I didn’t know it until then, I was a biologist all along.

I believe the phrase is, “duh”

In truth, I should have seen it earlier. Heck, I was never squeamish or easily grossed out by things. When I took freshman biology in high school I was the only person who actually got a bit of a kick out of dissecting the fetal pig. I stayed after class to carefully remove its brain so that I could look at it close-up. I loved the natural world. I really, really loved animals, often to my parents’ dismay when I would attempt to make “pets” out of every creature I could get my hands on. When I was writing my PhD applications this year, I asked my dad when he knew that I would end up in biology. “Are you kidding me?” he responded. “You’ve been like this since you were born!”

But I didn’t become a marine biologist because I wanted to since birth. I didn’t even want to since I was in high school. In some ways, I became a marine biologist by accident. Or maybe it was fate, if such a thing exists.

Now, I can’t imagine a life other than this. I love what I do. You see, it was that thought, not some self-doubting “why am I doing this?”, which went though my head as I breathed in the thick, noxious air while riding that ATV. It was a thought of wonder, asking the world how I got to be so lucky as to do what I do. In truth, I was barely paying attention to the toxic fumes. I was too intrigued by the fact that the dead fish I drove over started to glow after my tires crunched their bones – the beach, in fact, was glowing bluish-green. Some kind of bioluminescent algae or bacteria was all over the rotting corpses and in the water, and it glowed whenever it was disturbed. It was one of the coolest things I’d ever seen. I remember stopping just to step on dead fish and watch them light up (I did say you have to be a little sick to do what I do, right?).

Of course, the best part was tagging the turtles. That night I sat quietly and watched massive female green sea turtles dig their nests and drop hundreds of eggs into the sand. While they did, of course, I calmly checked their flippers for tags and tagged any that didn’t have them already. They didn’t run or flee as I touched them – once a female sea turtle has begun laying her eggs, she’s intent on finishing the job, and just about nothing will deter her from that task. To this day, the sight of those beautiful girls laying their precious eggs is still one of my favorite memories.

The point, I guess, of this long and self-indulgent monologue is that you should always follow your passions, and eventually, you’ll end up where you want to be. Or where you want to be will be where you end up – as Douglas Adams says, “I may not have ended up where I intended to go, but I know I’ve ended up where I’m intended to be.” For me, in the end, I even get to fulfill my 16-year-old me’s dream – in the fall, I start my PhD at the University of Hawaii.

This story is also in part to explain what it means to be a marine biologist. It’s not all cliches and playful creatures, and we’re all a little weird to even like what we do. And in part, I wanted you all to get to know me a bit better.

But mostly, it’s because no one ever asks why I’m a marine biologist. I have all these fun stories and anecdotes about being nerdy. And, damn it, I really wanted to tell some of them.

Anyhow, I was at Science Online not only to engage with other scientists and journalists, but also to co-moderate a session titled “Blogging Science While Female.” Here’s the session description:

The session on women in science blogging at Science Online 2011 sparked internet-wide discussion about sexism, discrimination and gender representation in science and science blogging. Now here we are, a year later. How have we, as a community, faced the issues brought up by last year’s discussion? What has changed? What have we learned, and what challenges still lie ahead? Moderators and attendees will assess the current state of women in the science blogosphere and discuss the best way we can support and encourage gender representation in science blogging.

Rather than rehash the session here, I’ll instead give you Tanya Lewis’ storify of the session (below). Also, be sure to read Kate Clancy’s epically awesome post: Blogging While Female, and Why We Need A Posse

The creatures which dared to arise are called cyanobacteria, or blue-green algae. They were the pioneers of photosynthesis, transforming the toxic atmosphere by producing oxygen and eventually paving the way for the plants and animals of today. But what is even more incredible is that they were the first to do something extraordinary – they were the first cells to join forces and create multicellular life.

It’s a big step for evolution, going from a single cell focused solely on its own survival to a multicellular organism where cells coordinate and work together. Creationists often cite this jump as evidence of God’s influence, because it seems impossible that creatures could make such a brazen leap unaided. But scientists have shown that multicellularity can arise in the lab, given strong enough selective pressure.

Just ask William Ratcliff and his colleagues at the University of Minnesota. In a PNAS paper published online this week, they show how multicellular yeast can arise in less than two months in the lab. To achieve this leap, they took brewer’s yeast – a common, single celled lab organism – and grew them in a liquid medium. Once a day, they gently spun the yeast in the culture, starting the next batch with whichever cells ended up at the bottom of the tube. Because the force of spinning pulls larger things down first, clumps of cells were more likely to be at the bottom than single ones, thus setting up a strong selective pressure for multicellularity.

Images of the snowflake-like pattern that arose in all of the experimental cell cultures from Ratcliff et al. 2012

All of their cultures went from single cells to snowflake-like clumps in less than 60 days. “Although known transitions to complex multicellularity, with clearly differentiated cell types, occurred over millions of years, we have shown that the first crucial steps in the transition from unicellularity to multicellularity can evolve remarkably quickly under appropriate selective conditions,” write the authors. These clumps weren’t just independent cells sticking together for the sake of it – they acted as rudimentary multicellular creatures. They were formed not by random cells attaching but by genetically identical cells not fully separating after division. Furthermore, there was division of labor between cells. As the groups reached a certain size, some cells underwent programmed cell death, providing places for daughter clumps to break from. Since individual cells acting as autonomous organisms would value their own survival, this intentional culling suggests that the cells acted instead in the interest of the group as a whole organism.

Given how easily multicellular creatures can arise in test tubes, it might then come as no surprise that multicellularity has arisen at least a dozen times in the history of life, independently in bacteria, plants and of course, animals, beginning the evolutionary tree that we sit atop today. Our evolutionary history is littered with leaps of complexity. While such intricacies might seem impossible, study after study has shown that even the most complex structures can arise through the meandering path of evolution. In Evolution’s Witness, Ivan Schwab explains how one of the most complex organs in our body, our eyes, evolved. Often touted by Intelligent Designers as ‘irreducibly complex’, eyes are highly intricate machines that require a number of parts working together to function. But not even the labyrinthine structures in the eye present an insurmountable barrier to evolution.

Our ability to see began to evolve long before animals radiated. Visual pigments, like retinal, are found in all animal lineages, and were first harnessed by prokaryotes to respond to changes in light more than 2.5 billion years ago. But the first complex eyes can be found about 540 million years ago, during a time of rapid diversification colloquially referred to as the Cambrian Explosion. It all began when comb jellies, sponges and jellyfish, along with clonal bacteria, were the first to group photoreceptive cells and create light-sensitive ‘eyespots’. These primitive visual centers could detect light intensity, but lacked the ability to define objects. That’s not to say, though, that eyespots aren’t important – eyespots are such an asset that they arose independently in at least 40 different lineages. But it was the other invertebrate lineages that would take the simple eyespot and turn it into something incredible.

According to Schwab, the transition from eyespot to eye is quite small. “Once an eyespot is established, the ability to recognize spatial characteristics – our eye definition – takes one of two mechanisms: invagination (a pit) or evagination (a bulge).” Those pits or bulges can then be focused with any clear material forming a lens (different lineages use a wide variety of molecules for their lenses). Add more pigments or more cells, and the vision becomes sharper. Each alteration is just a slight change from the one before, a minor improvement well within bounds of evolution’s toolkit, but over time these small adjustments led to intricate complexity.

Fossilized compound eyes from Cambrian arthropods (Lee et al. 2011)

In the Cambrian, eyes were all the rage. Arthropods were visual trendsetters, creating compound eyes by using the latter approach, that of bulging, then combining many little bulges together. One of the era’s top predators, Anomalocaris, had over 16,000 lenses! So many creatures arose with eyes during the Cambrian that Andrew Parker, a visiting member of the Zoology Department at the University of Oxford, believes that the development of vision was the driver behind the evolutionary explosion. His ‘Light-Switch’ hypothesis postulates that vision opened the doors for animal innovation, allowing rapid diversification in modes and mechanisms for a wide set of ecological traits. Even if eyes didn’t spur the Cambrian explosion, their development certainly irrevocably altered the course of evolution.

Our eyes, as well as those of octopuses and fish, took a different approach than those of the arthropods, putting photo receptors into a pit, thus creating what is referred to as a camera-style eye. In the fossil record, eyes seem to emerge from eyeless predecessors rapidly, in less than 5 million years. But is it really possible that an eye like ours arose so suddenly? Yes, say biologists Dan-E. Nilsson and Susanne Pelger. They calculated a pessimistic guess as to how long it would take for small changes – just 1% improvements in length, depth, etc per generation – to turn a flat eyespot into an eye like our own. Their conclusion? It would only take about 400,000 years – a geological instant.

But how does complexity arise in the first place? How did cells get photoreceptors, or any of the first steps towards innovations such as vision? Well, complexity can arise a number of ways.

An illustration of the endosymbiont hypothesis

Each and every one of our cells is a testament to the simplest way that complexity can arise: have one simple thing combine with a different one. The powerhouses of our cells, called mitochondria, are complex organelles that are thought to have arisen in a very simple way. Some time around 3 billion years ago, certain bacteria had figured out how to create energy using electrons from oxygen, thus becoming aerobic. Our ancient ancestors thought this was quite a neat trick, and, as single cells tend to do, they ate these much smaller energy-producing bacteria. But instead of digesting their meal, our ancestors allowed the bacteria to live inside them as an endosymbiont, and so the deal was struck: our ancestor provides the fuel for the chemical reactions that the bacteria perform, and the bacteria, in turn, produces ATP for both of them. Even today we can see evidence of this early agreement – mitochondria, unlike other organelles, have their own DNA, reproduce independently of the cell’s reproduction, and are enclosed in a double membrane (the bacterium’s original membrane and the membrane capsule used by our ancestor to engulf it). Over time the mitochondria lost other parts of their biology they didn’t need, like the ability to move around, blending into their new home as if they never lived on their own. The end result of all of this, of course, was a much more complex cell, with specialized intracellular compartments devoted to different functions: what we now refer to as a eukaryote.

Complexity can arise within a cell, too, because our molecular machinery makes mistakes. On occasion, it duplicates sections of DNA, entire genes, and even whole chromosomes, and these small changes to our genetic material can have dramatic effects. We saw how mutations can lead to a wide variety of phenotypic traits when we looked at how artificial selection has shaped dogs. These molecular accidents can even lead to complete innovation, like the various adaptations of flowering plants that I talked about in my last Evolution post. And as these innovations accumulate, species diverge, losing the ability to reproduce with each other and filling new roles in the ecosystem. While the creatures we know now might seem unfathomably intricate, they are the product of billions of years of slight variations accumulating.

Of course, while I focused this post on how complexity arose, it’s important to note that more complex doesn’t necessarily mean better. While we might notice the eye and marvel at its detail, success, from the viewpoint of an evolutionary lineage, isn’t about being the most elaborate. Evolution only leads to increases in complexity when complexity is beneficial to survival and reproduction. Indeed, simplicity has its perks: the more simple you are, the faster you can reproduce, and thus the more offspring you can have. Many bacteria live happy simple lives, produce billions of offspring, and continue to thrive, representatives of lineages that have survived billions of years. Even complex organisms may favor less complexity – parasites, for example, are known for their loss of unnecessary traits and even whole organ systems, keeping only what they need to get inside and survive in their host. Darwin referred to them as regressive for seemingly violating the unspoken rule that more complex arises from less complex, not the other way around. But by not making body parts they don’t need, parasites conserve energy, which they can invest in other efforts like reproduction.

When we look back in an attempt to grasp evolution, it may instead be the lack of complexity, not the rise of it, that is most intriguing.

Other Posts in the Evolution Series:

• The Curious Case of Dogs
• Watching Speciation Occur
• A Game Of Chance

References

• Ratcliff, W. C., Denison, R. F., Borello, M., & Travisano, M. (2012). Experimental evolution of multicellularity. PNAS Early Edition, 1–6. doi:10.1073/pnas.1115323109
• Schwab, I. R. (2012). Evolution’s Witness: How Eyes Evolved. Oxford University Press, 297 pp.
• Parker, A. (2003). In the blink of an eye. Basic Books, 352 pp.
• Nilsson, D.-E. & Pelger, S. (1994). A Pessimistic Estimate of the Time Required for an Eye to Evolve. Proceedings: Biological Sciences Vol. 256, No. 1345, pp. 53-58
• Reijnders, L. (1975). The origin of mitochondria. Journal of Molecular Evolution Vol. 5, No. 3, pp. 167-176. DOI: 10.1007/BF01741239

Every plant and animal out there produces miRNAs. We, for example, are thought to produce thousands. These teeny-tiny snippets of RNA serve regulatory roles in our cells, attaching to bits of messenger RNA and causing changes in expression of different proteins. They are far from evil: indeed, miRNAs are necessary for cells to function properly.

Can miRNAs we eat alter our gene expression? Well, yes. That was the incredible scientific discovery made by the Chinese research team that was recently published in Cell Research. But to make the leap from ‘miRNAs we eat can alter gene expression’ to ‘GMOs are dangerous’ requires unbelievable gaps in understanding about GMOs and miRNAs.

First off, there’s no reason to think that the DNA being introduced into GMOs is going to produce more/different miRNAs than it did in the original organism. Ari’s claim that “new DNA can have dangerous implications far beyond the products it codes for” simply isn’t true because miRNAs are coded for. These small RNA fragments aren’t random or accidental – they are explicitly detailed within the genome. So a stretch of DNA that didn’t code any miRNAs before isn’t going to suddenly code for a ton of them when it’s placed in a different genome. If we’re worried about potential miRNA effects, we can screen genes we are considering transferring and determine if there is any chance they produce miRNAs before we shuffle around which organism they are in. Indeed, GMOs are tested genetically, to ensure that the target gene has incorporated properly and that the organism is producing the desired protein, and not unexpected products. Genetic modification is a very precise process, and there is no reason to think it would cause a sudden burst of miRNAs.

But perhaps more fundamentally, miRNAs are found in all kinds of life, including every single species that we currently eat. There’s no logical reason that a new miRNA being produced by a GM plant is going to be more dangerous than the multitude of miRNAs we ingest when we eat the non-GM version.

In fact, the potential side effects of non-GM food is, very explicitly, what the Chinese research team showed: that of the millions of miRNAs we eat every day, at least a few make it from our stomachs into our blood, and that a specific one from ordinary rice can change the expression of genes in mice. So if miRNAs are dangerous – guess what? – you’re already ingesting them every time you eat. And, to get a little gross, let’s be clear: when we eat something, we don’t just ingest the miRNAs from the species we intentionally eat. Did you know, for example, that foods you eat are allowed to contain mold, hair, insect parts, and even rat poop? All of those bits of organisms which we inadvertently eat have DNA, and – you guessed it! – miRNAs, too. If miRNAs are so dangerous, we would never have been able to eat anything previously alive in the first place.

But we can eat other organisms, and we will continue to, because, simply put, miRNAs aren’t that dangerous.

Perhaps what ticks me off most, though, is that Ari’s scaremongering overshadows the very real and interesting implications of the science he failed to cover. The notion that miRNAs may drive some of the interaction between us and our food is incredibly new and totally cool. As the authors write, their research suggests that “miRNAs may represent a novel class of universal modulators that play an important role in mediating animal-plant interactions at the molecular level. Like vitamins, minerals and other essential nutrients derived from food sources, plant miRNAs may serve as a novel functional component of food and make a critical contribution to maintaining and shaping animal body structure and function.”

What if some of the benefits of drinking wine aren’t from the antioxidants, but from the miRNAs present in grapes? What if we can produce beneficial miRNAs, and take them like we do vitamins? Or reduce the expression of harmful ones? Suddenly, we have been given a sneak peek at a whole new facet of nutrition science that we didn’t even know existed. The amazing implications of this research – not some ludicrous and tenuous connection to anti-GMO propaganda – should have been what The Atlantic highlighted. Instead, they made a fool of themselves by allowing Ari Levaux to expose just how poorly he understands genetics.

Evolution isn’t predictable, and randomness is key in determining how things change. But that’s not the same as saying life evolves by chance. That’s because while the cause of evolution is random (mutations in our genes) the processes of evolution (selection) is not. It’s kind of like playing poker – the hand you receive is random, but the odds of you winning with it aren’t. And like poker, it’s about much more than just what you’re dealt. Outside factors – your friend’s ability to bluff you in your poker game, or changing environmental conditions in the game of life – also come into play. So while evolution isn’t random, it is a game of chance, and given how many species go extinct, it’s one where the house almost always wins.

Of course chance is important in evolution. Evolution occurs because nothing is perfect, not even the enzymes which replicate our DNA. All cells proliferate and divide, and to do so, they have to duplicate their genetic information each time. The enzymes which do this do their best to proof-read and ensure that they’re faithful to the original code, but they make mistakes. They put in a guanine instead of an adenine or a thymine, and suddenly, the gene is changed. Most of these changes are silent, and don’t affect the final protein that each gene encodes. But every once in awhile these changes have a bigger impact, subbing in different amino acids whose chemical properties alter the protein (usually for the worse, but not always).Or our cells make bigger mistakes – extra copies of entire genes or chromosomes, etc.

These genetic changes don’t anticipate an individual’s needs in any way. Giraffes didn’t “evolve” longer necks because they wanted to reach higher leaves. We didn’t “evolve” bigger brains to be better problem solvers, social creatures, or hunters. The changes themselves are random*. The mechanisms which influence their frequency in a population, however, aren’t. When a change allows you (a mutated animal) to survive and reproduce more than your peers, it’s likely to stay and spread through the population. This is selection, the mechanism that drives evolution. This can mean either natural selection (because it makes you run faster or do something to survive in your environment) or sexual selection (because even if it makes you less likely to survive, the chicks dig it). Either way the selection isn’t random: there’s a reason you got busier than your best friend and produced more offspring. But the mutation occurring in the first place – now that was luck of the draw.

Mistakes made by genetic machinery can lead to huge differences in organisms. Take flowering plants, for example. Flowering plants have a single gene that makes male and female parts of the flower. But in many species, this gene was accidentally duplicated about 120 million years ago. This gene has mutated and undergone selection, and has ended up modified in different species in very different ways. In rockcress (Arabidopsis), the extra copy now causes seed pods to shatter open. But it’s in snap dragons that we see how the smallest changes can have huge consequences. They, too, have two copies of the gene to make reproductive organs. But in these flowers, each copy fairly exclusively makes either male or female parts. This kind of male/female separation is the first step towards the sexes split into individual organisms, like we do. Why? It turns out that mutations causing the addition of a single amino acid in the final protein makes it so that one copy of the gene can only make male bits. That’s it. A single amino acid makes a gene male-only instead of both male and female.

Or, take something as specialized as flight. We like to think that flight evolved because some animals realized (in some sense of the word) the incredible advantage it would be to take to the air. But when you look at the evolution of flight, instead, it seems it evolved, in a sense, by accident. Take the masters of flight – birds – for example.

There are a few key alterations to bird bodies that make it so they can fly. The most obvious, of course, are their feathers. While feathers appear to be so ideally designed for flight, we are able to look back and realize that feathers didn’t start out that way. Through amazing fossil finds, we’re able to glimpse at how feathers arose, and it’s clear that at first, they were used for anything but airborne travel. These protofeathers were little more than hollow filaments, perhaps more akin to hairs, that may have been used in a similar fashion. More mutations occurred, and these filaments began to branch, join together. Indeed, as we might expect for a structure that is undergoing selection and change, there are dinosaurs with feather-like coverings of all kinds, showing that there was a lot of genetic experimentation and variety when it came to early feathers. Not all of these protofeathers were selected for, though, and in the end only one of these many forms ended up looking like the modern feather, thus giving a unique group of animals the chance to fly.

There’s a lot of variety in what scientists think these early feathers were used for, too. Modern birds use feathers for a variety of functions, including mate selection, thermoregulation and camouflage, all of which have been implicated in the evolution of feathers. There was no plan from the beginning, nor did feathers arise overnight to suddenly allow dinosaurs to fly. Instead, accumulations of mutations led to a structure that happened to give birds the chance to take to the air, even though that wasn’t its original use.

The same is true for flying insects. Back in the 19^th century, when evolution was fledging as a science, St. George Jackson Mivart asked “What use is half a wing?” At the time he intended to humiliate the idea that wings could have developed without a creator. But studies on insects have shown that half a wing is actually quite useful, particularly for aquatic insects like stoneflies (close relatives of mayflies). Scientists experimentally chopped down the wings of stoneflies to see what happened, and it turned out that though they couldn’t fly, they could sail across the water much more quickly while using less energy to do so. Indeed, early insect wings may have functioned in gliding, only later allowing the creatures to take to the air. Birds can use half a wing, too – undeveloped wings help chicks run up steeper hills – so half a wing is quite a useful thing.

But what’s really key is that if you rewound time and took one of the ancestors of modern birds, a dino with proto-feathers, or a half-winged insect and placed it in the same environment with the same ecological pressures, its decedents wouldn’t necessarily fly.

That’s because if you do replay evolution, you never know what will happen. Recently, scientists have shown this experimentally in the lab with E. coli bacteria. They took a strain of E. coli and separated it into 12 identical petri dishes containing a novel food source that the bacteria could not digest, thus starting with 12 identical colonies in an environment with strong selective pressure. They grew them for some 50,000 generations. Every 500 generations, they froze some of the bacteria. Some 31,500 generations later, one of the twelve colonies developed the ability to feed off of the new nutrient, showing that despite the fact that all of them started the same, were maintained in the same conditions and exposed to the exact same pressures, developing the ability to metabolize the new nutrient was not a guarantee. But even more shocking was that when they replayed that colony’s history, they found that it didn’t always develop the ability, either. In fact, when replayed anywhere from the first to the 19,999th generation, no luck. Some change occurring in the 20,000 generation or so – a good 11,500 generations before they were able to metabolize the new nutrient – had to be in place for the colony to gain its advantageous ability later on.

There’s two reasons for this. The first is that the mutations themselves are random, and the odds of the same mutations occurring in the same order are slim. But there’s another reason we can’t predict evolution: genetic alterations don’t have to be ‘good’ (from a selection standpoint) to stick around, because selection isn’t the only evolutionary mechanism in play. Yes, selection is a big one, but there can be changes in the frequency of a given mutation in a population without selection, too. Genetic drift occurs when events change the gene frequencies in a population for no reason whatsoever. A massive hurricane just happens to wipe out the vast majority of a kind of lizard, for example, leaving the one weird colored male to mate with all the girls. Later, that color may end up being a good thing and allowing the lizards to blend in a new habitat, or it may make them more vulnerable to predators. Genetic drift doesn’t care one bit.

Every mutation is a gamble. Even the smallest mutations – a change of a single nucleotide, called a point mutation – matter. They can lead to terrible diseases in people like sickle cell anemia and cystic fibrosis. Of course, point mutations also lead to antibiotic resistance in bacteria.

What does the role of chance mean for our species? Well, it has to do with how well we can adapt to the changing world. Since we can’t force our bodies to mutate beneficial adaptations (no matter what Marvel tells you), we rely on chance to help our species continue to evolve. And believe me, we as a species need to continue to evolve. Our bodies store fat because in the past, food was sporadic, and storing fat was the best solution to surviving periods of starvation. But now that trait has led to an epidemic of obesity, and related diseases like diabetes. As diseases evolve, too, our treatments fail, leaving us vulnerable to mass casualties on the scale of the bubonic plague. We may very well be on the cusp of the end of the age of man, if random mutations can’t solve the problems presented by our rapidly changing environment. What is the likelihood that man will continue to dominate, proliferate, and stick around when other species go extinct? Well, like any game of chance, you have to look at the odds:

99.99% of all the species that have ever existed are now extinct.

But then again – maybe our species is feeling lucky.

* If you want to get into more detail, actually, mutations aren’t completely random. They, too, are governed by natural laws – our machinery is more likely to sub an adenine for a guanine than for a thymine, for example. Certain sections are more likely to be invaded by transposons… etc. But from the viewpoint of selection, these changes are random – as in, a mutation’s potential selective advantage or disadvantage has no effect on how likely it is to occur.

Originally posted Nov 1st, 2010.

References:
Airoldi, C., Bergonzi, S., & Davies, B. (2010). Single amino acid change alters the ability to specify male or female organ identity Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1009050107

XU Xing, & GUO Yu (2009). THE ORIGIN AND EARLY EVOLUTION OF FEATHERS: INSIGHTS
FROM RECENT PALEONTOLOGICAL AND NEONTOLOGICAL DATA Verbrata PalAsiatica, 47 (4), 311-329

Perrichot, V., Marion, L., Neraudeau, D., Vullo, R., & Tafforeau, P. (2008). The early evolution of feathers: fossil evidence from Cretaceous amber of France Proceedings of the Royal Society B: Biological Sciences, 275 (1639), 1197-1202 DOI: 10.1098/rspb.2008.0003

Marden, J., & Kramer, M. (1994). Surface-Skimming Stoneflies: A Possible Intermediate Stage in Insect Flight Evolution Science, 266 (5184), 427-430 DOI: 10.1126/science.266.5184.427

DIAL, K., RANDALL, R., & DIAL, T. (2006). What Use Is Half a Wing in the Ecology and Evolution of Birds? BioScience, 56 (5) DOI: 10.1641/0006-3568(2006)056[0437:WUIHAW]2.0.CO;2

Blount, Z., Borland, C., & Lenski, R. (2008). Inaugural Article: Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli Proceedings of the National Academy of Sciences, 105 (23), 7899-7906 DOI: 10.1073/pnas.0803151105

Well, here I am anyway. I’ve spent the past few days reflecting on the past year, and thinking about my hopes for the next one. In accordance with proper US traditions, I feel obliged to write down some resolutions. It’s probably a silly endeavor – the science has found that new year’s resolutions are indifferent at best. Still, it can’t hurt to try. So here are my hopes and goals for 2012:

• Take at least 10 minutes every week to reflect on the positive. No matter how bad things are, or how stressful life might get, studies have shown that taking time to focus on what you’re thankful for can improve your health and happiness. So I resolve to take that time and truly contemplate the things in my life that make me happy.
• Read. I have a number of books that have been gathering dust on my bookshelf for the past few months because I ‘don’t have time’ or ‘have so many more important things to do.’ Well screw it. I love reading – it’s my personal escape from the rest of the world. So, I resolve to read more. A lot more.
• There’s this great song by Sara Bareilles, and in it, she has this line that always hits me: “I’m not the girl that I intend to be. But I dare you darlin’, just you wait and see.” I think we all are like that to some extent; we have all these high hopes or ideals that we strive to live up to, and end up falling short because we simply don’t care enough to push for it. Well, I resolve to be the person I intend to be, at least as much as I can. Nothing extraordinary, just the best version of me that I can be.

So there you have it. My three new year’s resolutions. What about you? What are your hopes for the new year?

Happy 2012 everyone, and have a wonderful year.

…I have posted 33 posts
…which have gotten 269 comments
…with visitors from more than 15 countries across the globe
…and have been syndicated at BlogHer, Ecology.com and more

The three most popular posts of the year:
3. Instant Zombie: Just Add Salt
2. Time – And Brain Chemistry – Heal All Wounds
1. Mythbusting 101: Organic Farming > Conventional Agriculture

…and last, but certainly not least, my post Why Do Women Cry? Obviously, It’s So They Don’t Get Laid was chosen to be published in Open Lab 2012

Overall, I’d say it’s been a pretty good year – especially since it’s only been six months here at SciAm. Here’s to next year being even better!

We saw that the littlest differences can lead to dramatic variations when we looked at the wide variety in dogs. But despite their differences, all breeds of dogs are still the same species as each other and their ancestor. How do species split? What causes speciation? And what evidence do we have that speciation has ever occurred?

Critics of evolution often fall back on the maxim that no one has ever seen one species split into two. While that’s clearly a straw man, because most speciation takes far longer than our lifespan to occur, it’s also not true. We have seen species split, and we continue to see species diverging every day.

For example, there were the two new species of American goatsbeards (or salsifies, genus Tragopogon) that sprung into existence in the past century. In the early 1900s, three species of these wildflowers – the western salsify (T. dubius), the meadow salsify (T. pratensis), and the oyster plant (T. porrifolius) – were introduced to the United States from Europe. As their populations expanded, the species interacted, often producing sterile hybrids. But by the 1950s, scientists realized that there were two new variations of goatsbeard growing. While they looked like hybrids, they weren’t sterile. They were perfectly capable of reproducing with their own kind but not with any of the original three species – the classic definition of a new species.

How did this happen? It turns out that the parental plants made mistakes when they created their gametes (analogous to our sperm and eggs). Instead of making gametes with only one copy of each chromosome, they created ones with two or more, a state called polyploidy. Two polyploid gametes from different species, each with double the genetic information they were supposed to have, fused, and created a tetraploid: an creature with 4 sets of chromosomes. Because of the difference in chromosome number, the tetrapoid couldn’t mate with either of its parent species, but it wasn’t prevented from reproducing with fellow accidents.

This process, known as Hybrid Speciation, has been documented a number of times in different plants. But plants aren’t the only ones speciating through hybridization: Heliconius butterflies, too, have split in a similar way.

It doesn’t take a mass of mutations accumulating over generations to create a different species – all it takes is some event that reproductively isolates one group of individuals from another. This can happen very rapidly, in cases like these of polyploidy. A single mutation can be enough. Or it can happen at a much, much slower pace. This is the speciation that evolution is known for – the gradual changes over time that separate species.

But just because we can’t see all speciation events from start to finish doesn’t mean we can’t see species splitting. If the theory of evolution is true, we would expect to find species in various stages of separation all over the globe. There would be ones that have just begun to split, showing reproductive isolation, and those that might still look like one species but haven’t interbred for thousands of years. Indeed, that is exactly what we find.

The apple maggot fly, Rhagoletis pomonella is a prime example of a species just beginning to diverge. These flies are native to the United States, and up until the discovery of the Americas by Europeans, fed solely on hawthorns. But with the arrival of new people came a new potential food source to its habitat: apples. At first, the flies ignored the tasty treats. But over time, some flies realized they could eat the apples, too, and began switching trees. While alone this doesn’t explain why the flies would speciate, a curious quirk of their biology does: apple maggot flies mate on the tree they’re born on. As a few flies jumped trees, they cut themselves off from the rest of their species, even though they were but a few feet away. When geneticists took a closer look in the late 20th century, they found that the two types – those that feed on apples and those that feed on hawthorns – have different allele frequencies. Indeed, right under our noses, Rhagoletis pomonella began the long journey of speciation.

As we would expect, other animals are much further along in the process – although we don’t always realize it until we look at their genes.

Orcas (Orcinus orca), better known as killer whales, all look fairly similar. They’re big dolphins with black and white patches that hunt in packs and perform neat tricks at Sea World. But for several decades now, marine mammalogists have thought that there was more to the story. Behavioral studies have revealed that different groups of orcas have different behavioral traits. They feed on different animals, act differently, and even talk differently. But without a way to follow the whales underwater to see who they mate with, the scientists couldn’t be sure if the different whale cultures were simply quirks passed on from generation to generation or a hint at much more.

Now, geneticists have done what the behavioral researchers could not. They looked at how the whales breed. When they looked at the entire mitochondrial genome from 139 different whales throughout the globe, they found dramatic differences. These data suggested there are indeed at least three different species of killer whale. Phylogenetic analysis indicated that the different species of orca have been separated for 150,000 to 700,000 years.

Why did the orcas split? The truth is, we don’t know. Perhaps it was a side effect of modifications for hunting different prey sources, or perhaps there was some kind of physical barrier between populations that has since disappeared. All we know is that while we were busy painting cave walls, something caused groups of orcas to split, creating multiple species.

There are many different reasons why species diverge. The easiest, and most obvious, is some kind of physical barrier – a phenomenon called Allopatric Speciation. If you look at fish species in the Gulf of Mexico and off the coast of California, you’ll find there are a lot of similarities between them. Indeed, some of the species look almost identical. Scientists have looked at their genes, and species on either side of that thin land bridge are more closely related to each other than they are to other species, even ones in their area. What happened is that a long time ago, the continents of North and South America were separated, and the oceans were connected. When the two land masses merged, populations of species were isolated on either side. Over time, these fish have diverged enough to be separate species.

Species can split without such clear boundaries, too. When species diverge like the apple maggot flies – without a complete, physical barrier – it’s called Sympatric Speciation. Sympatric speciation can occur for all kinds of reasons. All it takes is something that makes one group have less sex with another.

For one species of Monarch flycatchers (Monarcha castaneiventris), it was all about looks. These little insectivores live on Solomon Islands, east of Papua New Guinea. At some point, a small group of them developed a single amino acid mutation in the gene for a protein called melanin, which dictates the bird’s color pattern. Some flycatchers are all black, while others have chestnut colored bellies. Even though the two groups are perfectly capable of producing viable offspring, they don’t mix in the wild. Researchers found that the birds already see the other group as a different species. The males, which are fiercely territorial, don’t react when a differently colored male enters their turf. Like the apple maggot flies, the flycatchers are no longer interbreeding, and have thus taken the first step towards becoming two different species.

These might seem like little changes, but remember, as we learned with dogs, little changes can add up. Because they’re not interbreeding, these different groups will accumulate even more differences over time. As they do, they will start to look less and less alike. The resultant animals will be like the species we clearly see today. Perhaps some will adapt to a lifestyle entirely different from their sister species – the orcas, for example, may diverge dramatically as small changes allow them to be better suited to their unique prey types. Others may stay fairly similar, even hard to tell apart, like various species of squirrels are today.

The point is that all kinds of creatures, from the smallest insects to the largest mammals, are undergoing speciation right now. We have watched species split, and we continue to see them diverge. Speciation is occurring all around us. Evolution didn’t just happen in the past; it’s happening right now, and will continue on long after we stop looking for it.

1. Soltis, D., & Soltis, P. (1989). Allopolyploid Speciation in Tragopogon: Insights from Chloroplast DNA American Journal of Botany, 76 (8) DOI: 10.2307/2444824
2. McPheron, B., Smith, D., & Berlocher, S. (1988). Genetic differences between host races of Rhagoletis pomonella Nature, 336 (6194), 64-66 DOI: 10.1038/336064a0
3. Uy, J., Moyle, R., Filardi, C., & Cheviron, Z. (2009). Difference in Plumage Color Used in Species Recognition between Incipient Species Is Linked to a Single Amino Acid Substitution in the Melanocortin‐1 Receptor The American Naturalist, 174 (2), 244-254 DOI: 10.1086/600084
4. Phillip A Morin1, Frederick I Archer, Andrew D Foote, Julie Vilstrup, Eric E Allen, Paul Wade, John Durban, Kim Parsons, Robert Pitman, Lewyn Li, Pascal Bouffard, Sandra C Abel Nielsen, Morten Rasmussen, Eske Willerslev, M. Thomas P Gilbert, & Timothy Harkins (2010). Complete mitochondrial genome phylogeographic analysis of killer whales (Orcinus orca) indicates multiple species Genome Research

Image Credits:
Salsify plate showing two new species from the New Zealand Plant Radiation Network (taken from Ownbey, 1950 in which the species were described)
Flycatchers image by Robert Boyle, as featured on Science Now

Gratitude. By definition, it is the state of being grateful or thankful. It is universally seen as a positive human attribute. You can hear how highly gratitude is thought of over and over again in sayings from all over the world:

A thankful heart is not only the greatest virtue, but the parent of all the other virtues. -Roman saying
The truly rich are those who enjoy what they have. – Yiddish proverb
If you’re not thankful then you’re a wizard. – African Proverb

Perhaps the merits of gratitude have been parised for centuries in so many cultures for good reason. Studies have shown that expressing gratitude is connected to a wide variety of positive outcomes.

Gratitude may help us deal with stress, for example. Over the past decade, evidence has been mounting to show that gratitude mitigates the negative consequences of traumatic events. Studies have found that soldiers who score higher on dispositional gratitude are less likely to develop post-traumatic stress disorder (PTSD). Similarly, another study found an inverse correlation between gratitude and PTSD symptom levels in college women who experienced trauma.

Of course, the benefits of gratitude extend far beyond serious traumatic events. Simply expressing gratitude has positive effects on our daily lives. In one study, Kent State researchers had students write one letter every two weeks with the simple ground rules that it had to be positively expressive, require some insight and reflection, be nontrivial and contain a high level of appreciation or gratitude. After each letter, students completed a survey to gauge their moods, satisfaction with life and feelings of gratitude and happiness – all of which increased after each letter – the more they wrote, the happier they were.

Similar results have been found in a number of other studies. Middle school students that counted their blessings expressed enhanced self-reported gratitude, optimism, life satisfaction, and decreased negative feelings. In adults, the keeping of gratitude journals led to overall happier thoughts. Not only were the journal keepers in a better mood, they also were more likely to to report having helped someone with a personal problem or offered emotional support to another, suggesting that the positive affects of gratitude expand outward.

Given the benefits of expressing thanks, I decided to do so myself. Yesterday, I sat on my couch with a pad of paper and my favorite purple sharpie pen and wrote out all the little things in my life that I am thankful for. It turned out to be quite a long list – about 8 pages long, actually. So rather than bore you with the whole thing, I’ve included a few of my favorite highlights:

• I am thankful for all of the people in my life who have made me smile. If you have ever been my friend, then you have surely made me smile a lot, so I am extra grateful for you.
• I am thankful for my family, who helped me become the woman I am today.
• I am thankful for Bora, for the term ‘BlogFather’ is more fitting than he knows, and for the rest of my eccentric but lovable blogging family.
• I am thankful for cheese. Yes, cheese. Cheese, bacon, sushi, curry, pasta and Dippin’ Dots. My six basic food groups.
• I’m thankful to the natural world for providing beautiful, intricate and complex puzzles that I, as a scientist, am lucky enough to study.
• I am thankful for my liver, for without its championship team of Alcohol Dehydrogenase and Aldehyde Dehydrogenase, I never could have become the marine scientist I am today. (#drunksci)
• I am thankful for the people and things that inspire me to do what I love.
• I am thankful for my wonderful roommate, who always knows whether a situation requires a bottle of wine, a hug, or a patient ear.
• I am thankful to her cat, Yoshi, for finally forgiving me for making him do the cat dance.
• I am thankful to the people who remind me that the greatest thing you can do for yourself is to love someone else fully.
• I am thankful for little surprises.
• And last but not least, thank you, for it is you, my readers, that make blogging worthwhile.

Enjoy your day of thanks, and don’t forget to express to the people you love just how thankful you are to have them. Happy Thanksgiving!

Image c/o holidays.kaboose.com

It seems you are upset at the torrent of outrage your Futures piece has caused. You’re “dumbfounded” that anyone could read so much into your frivolous little tale, and honestly didn’t mean for your short story to harm or offend anyone. After all, it was just supposed to be a joke.

That is totally understandable – I mean, come on, haven’t we all been there? You’re having this fun, friendly conversation with a colleague/friend/family member/whomever and you make some comment or joke. You giggle a little – because hey! It was a funny! – only to see that your companion clearly feels otherwise. You didn’t mean to offend, but by the awkward silence and sudden look of confusion, anger, or even hurt on their face, you realize that you did. It was completely by accident.

Most people’s instantaneous reaction to the above scenario is two simple words. Those words might be followed by an explanation of the joke to see if it changes the response (“See, it’s funny because I said XYZ when, really, we all know ABC…”). Or, even, when that clearly doesn’t improve things, defensive statements like “Wait – that didn’t come off right” or “That’s not what I meant” or even “What I meant to say was…”, but the first thing, the first thing that comes out of their mouth, is this:

“I’m sorry.”

Ed, you say that you totally didn’t mean to offend anyone, and with the benefit of the doubt, I’ll believe you. But you did offend people. A lot of people, especially women in science.

You say that the image painted by others of you isn’t accurate, that Womanspace isn’t a reflection of your views of women and gender, and that it was supposed to come off as a joke that, if anything, says women are superhuman while men are bumbling idiots.

But for what seems to be a large percentage of its readers, it didn’t. And while you seem to be able to go on and on about how really good a person you are, and how you didn’t mean any harm, and it was just a joke, you have to realize by now that to many people, it was offensive and anything but funny.

If Womanspace doesn’t reflect your views of gender and women, it should bother you that so many of your colleagues and other scientists were offended. When someone points out that your story reinforces negative stereotypes and promotes the kind of environment that discourages women from STEM careers, you should feel badly that your joke came off so poorly. That is, like when you accidentally step on someone’s toes, you should feel remorse that you caused harm to another when you really didn’t mean to.

Yes, you’re allowed to defend yourself. It’s understandable that you wanted to make sure that people know you didn’t mean to alienate women, or reinforce the notion that women should cook and clean while men ponder the intricacies of the universe. No one will fault you for quickly saying “Wait! I didn’t mean for it to sound like that!”

There was just one problem: your response lacked the two little words that should have been your knee-jerk reaction to making so many people feel badly. You should have felt compelled to apologize for the unintentional harm you may have caused.

In short, you should have said you’re sorry.

The fact that you didn’t reveals more about you as a person than any terribly-written, stereotypical science fiction story ever could.