Carl Zimmer's Blog, page 29

What To Expect When You’re Expecting, By Charles Darwin

A few years back, a team of scientists combed through the records for a million births in New York City. They noted women who had developed gestational diabetes during their pregnancy, and they also noted the women’s ethnic backgrounds. Women of European descent, the scientists found, had the lowest risk for gestational diabetes, with only 3.6% of them developing the disorder. African Americans had a somewhat higher risk of 4.3%. South Asian women, by contrast, face a far higher risk of 14.3%, with Bangladeshis running the highest risk of all: one out of every five Bangladeshi mothers in New York developed gestational diabetes.

Another risk that pregnant women run is giving birth to babies with deformed spinal columns.  The pattern of these so called neural-tube defects is quite different from that of gestational diabetes. Dark-skinned women–in Africa, as well as Asia and Australia–are at low risk, while European women are the ones more likely to encounter this trouble.

A team of three Harvard biologists–Elizabeth Brown, Maryellen Ruvolo, and Pardis Sabeti–think that there’s a coherent explanation for these patterns, and many of the other puzzling features about pregnancy. They are the result of evolution.

In a paper to be published in Trends in Genetics, the researchers argue that pregnancy has been one of the most important targets of natural selection in all of human biology. Mutations that raise the success rate of pregnancies let women have more offspring, who can spread their genes throughout a population. Pregnancy has also posed huge risks to women that could threaten their own survival. A woman’s reproductive success depends not just on her newborn child surviving, but on her own survival as well.

Evolution was shaping pregnancy long before our species walked the Earth, but it continued to do so even in the past few thousand years. And the traits that help women out the most in one part of the world don’t necessarily help in another.

Local adaptations may account for some of the differences in pregnancy-related troubles seen in women around the world. Take gestational diabetes. Bad genes can make women more vulnerable to diabetes. But the food they eat can also raise their risk–specifically, diets rich in carbohydrates. It turns out that the women with the lowest rates of gestational diabetes come from parts of the world where people traditionally have a diet that’s the highest risk for the disease.

This may be an evolutionary impact of the Agricultural Revolution. When Europeans shifted from hunting and gathering to farming, they boosted the sugar in their diet by eating wheat and drinking milk. We know that mutations that enabled them to digest milk efficiently as adults were strongly favored by natural selection. Digesting milk may have been especially important for successful pregnancies. The calcium could have helped build a strong pelvis to make childbirth easier. And pregnant women drinking milk could use its calorie-rich fat to nourish their fetuses.

Women nourish their fetuses by raising the level of sugar in their blood. That’s a dangerous game, because it threatens to throw off their own delicate balance between sugar and insulin. If that balance gets out of whack, women may suffer gestational diabetes. The Harvard researchers suggest that the shift to high-carb agriculture in Europe led to more women dying of gestational diabetes. Women with mutations that lowered their blood sugar level during pregnancy were favored by natural selection. And today, European women enjoy the benefits of that suffering: a low risk of gestational diabetes.

A woman in Bangladesh has a very different history behind her. Her ancestors ate fish, unprocessed rice, and other foods with modest levels of carbohydrates. In that environment, women with mutations that increased their blood sugar during pregnancy might have had healthier children than women without them.  Throw those genes into a modern Western city, and trouble looms. Women with low-sugar genes are now drinking soda and eating bread, ice cream, and lots of other food loaded in carbs. They don’t have the evolved defenses to keep them from developing gestational diabetes.

Another evolutionary process could explain neural tube defects. In order for a baby’s spine to form properly, it needs a nutrient called folate. That’s why doctors are constantly nagging pregnant women to eat folate-rich food or take supplements, so that they can then pass some of it on to their fetus.

It turns out that the body stores folate in the blood vessels in the skin, from where it can then be dispensed to a fetus. Close to the surface of the body, the folate is vulnerable to ultraviolet rays, which can destroy it. Dark-skinned women can shield their folate with their pigment. Lighter-skinned women have fewer defenses.

Here again, evolution can explain the difference between women from different parts of the world. The skin needs sunlight to generate vitamin D. When humans moved to northern regions of the world, the sun was so low in the sky that there was an advantage to losing some of their pigmentation, allowing more sunlight in. Unfortunately, the ability to make vitamin D in low sunlight came at a price–a price that women today still pay.

Sunlight isn’t the only factor that’s different for women around the world. The altitude is as well. And for women living in mountains, pregnancy poses a risk that lowland women don’t have to worry about: low oxygen. Without enough oxygen to meet the demands of rearing a fetus, pregnant women face a risk of premature labor, bleeding, and other potentially devastating consequences.

People who have lived for centuries at high altitudes–in Tibet, the Ethiopian highlands, and the Andes–have genes that show signs of natural selection as an adaptation to high elevation. The Harvard researchers argue that pregnancy may have created a particularly strong pressure for such genes. A gene called BCL11A, for example, helps produce a special form of hemoglobin only found in fetuses. In Ethiopia, a variant of that gene has spread rapidly in the past few thousand years. Another potentially telling clue is the fact that Tibetan and Andean women don’t suffer many cases of low birth weight and other harm caused by high altitude. When women from nearby lowlands give birth at those high elevations, they have a higher risk of these problems.

At any elevation, pregnancy creates a quandary for a woman’s immune system.  Her fetus is not a perfect match to her own tissues, and so by all rights her immune system should attack it like a transplanted organ. A woman’s body avoids this devastating mistake with a number of strategies. For example, it suppresses its own immune system, so that it doesn’t unleash devastating inflammation.

While this may be good for the well-being of a woman’s baby, it’s dangerous to her own health because she’s left vulnerable to infection. In sub-Saharan Africa, for example, pregnant woman die two to three times more often from malaria than other people. During the flu pandemic of 1918, half of all infected pregnant women went on to develop pneumonia, which was 50% fatal. And in a sad irony, a disease acquired during pregnancy may lead to a spontaneous abortion or to low birth weight. In the spring of 1919, the birth rate dropped between 5 and 15% due to the deaths of pregnant women and their spontaneous abortions.

Sabeti and other scientists have identified a number of genes that show signs of having undergone strong natural selection for defenses against malaria and other diseases in the past few thousand years. One of those genes, called FLT1, turns out to be especially important for pregnant women. In Tanzania, where malaria is common, natural selection has favored a variant of FLT1 that lowers the rate of spontaneous abortion from the disease. Sabeti and her co-authors predict that more genes will show this special focus on pregnancy.

When evolutionary biologists seek to explain any pattern in nature, it’s always important to think about alternative explanations. And pregnancy is no exception. The high risk of gestational diabetes among South Asians in New York could conceivably not be the result of natural selection acting on a traditionally low-sugar diet. It could just be the shock of shifting from the diet of a poor country to an affluent one.

Fortunately, we don’t just have to juggle these alternative in a post-modern circus. Scientists can test them. They can pinpoint the genes that put women at risk of gestational diabetes (we don’t know them yet), and then look for signs that they’ve undergone natural selection in the past. Likewise, scientists can track immigrant families from different ethnic backgrounds over several generations to see if their risk of gestational diabetes drops or stays the same. This research may do more than reveal the fingerprints of evolution on our species. It may lead to better ideas for keeping babies and their mothers healthy during the troubled passage that is pregnancy.

Reference: Brown, Elizabeth A., Maryellen Ruvolo, and Pardis C. Sabeti. “Many ways to die, one way to arrive: how selection acts through pregnancy.” Trends in Genetics (2013)

The Perfect Blood-Sucker: My New Profile of the Tick

I’ve written about a lot of parasites over the years, but for some reason I haven’t gotten around to one that’s intensely familiar to suburbanties: the tick. Recently, Outside asked me to write a feature about these blood-sucking creatures–exploring their chilling sophistication as blood-suckers and their disturbing ability to spread pathogens. Fortunately (if that’s how you want to think about it) I live in Tick Central, otherwise known as Connecticut. To report on Lyme Disease, I can drive up the road to Lyme. My story is in the June issue of Outside. Check it out.

The Evolution of the Country Mouse and the City Mouse

Cities may not seem like hotbeds of evolution. Tropical rain forests, maybe. The Galapagos Islands, certainly. But Central Park?

Yes, even Central Park. Wherever there is life, there is evolution. Organisms reproduce, passing down their genes to their offspring. Some variants of those genes may become more common over the generations thanks to lucky rolls of the genetic dice. But they can also become more common thanks to natural selection–because they make individuals better able to survive and reproduce than others. That advantage depends in large part on their particular environment. If the environment changes dramatically–if, for example, people cut down forests and put up skyscrapers–then a new set of mutations may give organisms an evolutionary advantage.

Urban evolution is probably one of the most common forms of evolution on Earth today. After all, cities are spreading over so much of the terrestrial surface of the planet. Yet the city is still a lonely frontier for evolutionary biologists. They’ve traditionally searched out “natural” habitats in order to document the workings of evolution. Only recently have some evolutionary biologists made the city into a field site.

Jason Munshi-South, a scientist at Baruch College, is doing some of the most interesting research on urban evolution these days, working in the green spaces of New York City. New York has been growing for over three centuries, but twenty percent of it remains wooded today, and it’s still home to a variety of wild animals, plants, and other organisms. New Yorkers may think that their wildlife consists solely of cockroaches, but the streets and parks and rivers of the city are full of other species too. Some, like coyotes in the Bronx, are newcomers, while others never left. New York’s native biodiversity has many surprises left for urban biologists to discover–consider, for example, that a new species of frog turned up in Staten Island just last year. (See this 2011 article I wrote for the New York Times for more on evolution in New York.)

One of the animals Munshi-South studies most closely is the white-footed mouse, Permoyscus leucopus. This is not the house mouse that rummages around in the kitchen cabinets of New York apartments. It’s the white-footed mouse, which was living in the forests of New York before Europeans arrived and which stayed in those forests as they shrank into islands of parkland. While house mice will happily dart across Broadway in search of food, white-footed mice are far less bold. As New York’s forested land has become isolated, so have its populations of mice.

White-footed mouse. Phto by J.N. Stuart via Creative Commons http://www.flickr.com/photos/stuartwi...

Munshi-South wondered if these rodents have veered off on their own evolutionary trajectory, separate from the white-footed mice that live in the forests outside of New York City. As new mutations arise in a New York population of mice, they may become widespread–but only on their urban island. Compared to their rural counterparts, New York mice may face different challenges for survival. The air they breathe and the soil through which they burrow is more polluted. They may encounter more pathogens because New York is a hub for travelers. New York mice also live in denser populations, which may mean they have to compete more for food or mates. Munshi-South hypothesized that over the past couple centuries, the city mice have adapted to these challenges in ways that their rural cousins have not.

To test his hypothesis, Munshi-South and his students trapped mice in various spots around the city including Central Park. They also headed out of town to grab some mice living in forests where they don’t face the pressures of urban life. They then took a look at the genes of the mice. The genes bear the scars of the isolation in which the city mice live. Mice living in two New York parks may be more genetically distinct than rural mice living in different states.

Munshi-South and his colleagues then searched for genetic differences between city mice and country mice that might be the result of natural selection. Like other organisms, white-footed mice make copies of their genes out of a molecule called RNA, which they then use as a guide to building proteins. The scientists pulled out all the RNA from liver and brain tissue from their mice, a couple hundred animals all told. They then sequenced the RNA fragments and used a computer to reconstruct the sequence of the mouse genes.

Once they could look at the sequence of the mouse genes, they then hunted for mutations that showed signs of having spread thanks to natural selection. They found a handful of genes in the city mice that appear to have evolved due to natural selection. The functions of these genes are, in many cases, exactly the sort that you’d expect to evolve in a city mouse. Some of them are known to be involved in recognizing pathogens, and others help launch an immune system attack against them. Others help to detoxify pollutants. These genes not only evolved relatively quickly–in just the past couple centuries at most–but also repeatedly. In park after park, the same adaptations were favored by natural selection.

For now, these genes are only promising candidates for targets of natural selection. Researchers will have to examine them more closely and see if their mutations do indeed alter the biology of the city mice in important ways. It will be fascinating to see them investigate this grand experiment in evolution that is New York. Urban evolution may turn out to transform species in unexpected ways. Among the genes that show hints of natural selection in the white-footed mice of New York are genes involved in sperm, for example. In the crowded populations of mice in New York’s parks, males may be competing more intensely to father the next generation. Perhaps there’s a sexual revolution underway in the big city.

(Munshi-South’s results are available as a preprint at PeerJ, a new scientific publisher.)

City Mouse and Country Mouse. By Arthur Rackham. Via Wikipedia http://commons.wikimedia.org/wiki/Fil...

Coelacanth hangout at 11 AM ET today!

We’re just about to start our hangout about the coelacanth. Details are here.

If you’d like to ask a question, go to the event page and post it there.

Big Dog Data

It used to be that many people who studied animal behavior thought dogs were too weird to bother with. We had bred them far away from the “natural” state of animals, so their brain had little insight to offer us.

That’s changed a lot in in the past couple decades. We have transformed wolves into some cognitively remarkable creatures, it turns out, and the diversity of breeds we’ve produced can serve as an unplanned experiment in the genetics of social behavior.

Of course, one of the biggest rules in all science is the more data the better. Which in this case means the more dogs that scientists can study, the more they may be able to discover about them.

All of which is introduction to an article I’ve written in today’s New York Times about a new push to gather Big Data about dogs–and to provide some insights from that data to dog-owners themselves. Check it out!

A most amazing fish: Join our Google Hangout about coelacanths on Thursday

If you want to know something about how our ancestors came out of the ocean and onto land, there are just two sorts of fish you should get to know really well. One is the lungfish, our closest aquatic relatives, and the other is the coelacanth, our next-closest. Trout, goldfish, salmon–they are all just distant ray-finned cousins. Lungfish and coelacanths, by contrast, have much in common with us, including a few of the bones that would give rise to our legs and arms. And coelacanths are especially fascinating because until the 1930s, scientists believed that they had gone extinct 65 million years ago. Now they turn out to live off the coasts of both Africa and Indonesia.

Which is why I hope you’ll join me Thursday at 11 am ET to participate in a Google Hangout with a panel of scientists to talk about the latest scientific discoveries about this amazing fish. The occasion is the publication of the coelacanth genome last week.

Now, if you read the Loom with any regularity, you know that the mere publication of a genome is not, in my opinion, automatically news. But the scientists who sequenced the coelacanth genome have analyzed it to explore some very interesting questions, and their work has provided some intriguing clues about the evolution of our limbs and many other aspects of our biology–as well as some puzzling features unique to coelacanths themselves. The genome paper has also inspired some criticism in the blogosphere.

All of which is great fodder for a conversation. The Google Hangout will last about an hour–I’ll kick it off by talking to the scientists about their study, and then we’ll be able to field questions from you–live! I’ve never done a full-blown Google Hangout before, so I’m particularly interested in seeing how this works as a way to talk about science online. I believe I’ll be able to embed it here on Thursday, and it will (I think) be archived on YouTube. Feel free to post any questions about how this will all work in the comments below. I’ll try to answer them (provided I know the answer!).

For more on coelacanths, here’s an excerpt from Samantha Weinberg’s book on the creatures. I also wrote about coelacanths in my first book, At the Water’s Edge.

Finally, here’s a nice diagram created by Raul Domingo a couple years ago for National Geographic. Click to embiggen!

 

“I Think I’ve Just Thought Up Something Important”–Francois Jacob (1920-2013)

Francois Jacob. Image from http://www.nobelprize.org

I just learned the sad news that the great biologist Francois Jacob has died. He won the Nobel Prize for his work in the 1950s that showed how cells switch genes off–the first crucial step to understanding how life can use the genome like a piano, to make a beautiful melody instead of a blaring cacophony.

Jacob was also a wonderful writer, and so I had enormous pleasure mining his memoirs for my book Microcosm: E. coli and the New Science of Life. I hope this passage gives a sense of what he was like–

One day in July 1958, François Jacob squirmed in a Paris movie theater. His wife, Lise, could tell that an idea was struggling to come out. The two of them walked out of the theater and headed for home.

“I think I’ve just thought up something important,” François said to Lise.

“Tell!” she said.

Her husband believed, as he later wrote, that he had reached “the very essence of things.” He had gotten a glimpse of how genes work together to make life possible.

Jacob had been hoping for a moment like this for a long time. Originally trained as a surgeon, he had fled Paris when the Nazis swept across France. For the next four years he served in a medical company in the Allied campaigns, mostly in North Africa. Wounds from a bomb blast ended his plans of becoming a surgeon, and after the war he wandered Paris unsure of what to do with his life. Working in an antibiotics lab, Jacob became enchanted with scientific research. But he did not simply want to find a new drug. Jacob decided he would try to understand “the core of life.” In 1950, he joined a team of biologists at the Pasteur Institute who were toiling away on E. coli and other bacteria in the institute’s attic.

Jacob did not have a particular plan for his research when he ascended into the attic, but he ended up studying two examples of one major bio- logical puzzle: why genes sometimes make proteins and sometimes don’t. For several years, Jacob investigated prophages, the viruses that disappear into their E. coli host, only to reappear generations later. Working with Élie Wollman, Jacob demonstrated that prophages actually insert their genes into E. coli’s own DNA. They allowed prophage-infected bacteria to mate with uninfected ones and then spun them apart. If the microbes stopped mating too soon, they could not transfer the prophage. The experiments revealed that the prophage consistently inserts itself in one spot in E. coli’s chromosome. The virus’s genes are nestled in among those of its host, and yet they remain silent for generations.

E. coli offered Jacob another opportunity to study genes that some- times make proteins and sometimes don’t. To eat a particular kind of sugar, E. coli needs to make the right enzymes. In order to eat lactose, the sugar in milk, E. coli needs an enzyme called beta-galactosidase, which can cut lactose into pieces. Jacob’s colleague at the Pasteur Institute, Jacques Monod, found that if he fed E. coli glucose—a much better source of energy for E. coli than lactose—it made only a tiny amount of beta- galactosidase. If he added lactose to the bacteria, it still didn’t make much of the enzyme. Only after the bacteria had eaten all the glucose did it start to produce beta-galactosidase in earnest.

No one at the time had a good explanation for how genes in E. coli or its prophages could be quiet one moment and busy the next. Many scientists had assumed that cells simply churned out a steady supply of all their proteins all the time. To explain E. coli’s reaction to lactose, they suggested that the microbe actually made a steady stream of beta-galactosidase. Only when E. coli came into contact with lactose did the enzymes change their shape so that they could begin to break the sugar down.

Jacob, Monod, and their colleagues at the Pasteur Institute began a series of experiments to figure out the truth. They isolated mutant E. coli that failed to eat lactose in interesting ways. One mutant could not digest lactose, despite having a normal gene for beta-galactosidase. The scientists realized that E. coli used more than one gene to eat lactose. One of those genes encoded a channel in the microbe’s membranes that could suck in the sugar.

Strangest of all the mutants Jacob and Monod discovered were ones that produced beta-galactosidase and permease all the time, regardless of whether there was any lactose to digest. The scientists reasoned that E. coli carries some other molecule that normally prevents the genes for beta- galactosidase and permease from becoming active. It became known as the repressor. But Jacob and his colleagues had not been able say how the repressor keeps genes quiet.

In the darkness of the Paris movie theater, Jacob hit on an answer. The repressor is a protein that clamps on to E. coli’s DNA, blocking the production of proteins from the genes for beta-galactosidase and the other genes involved in feeding on lactose. A signal, like a switch on a circuit, causes the repressor to stop shutting down the genes.

Another similar repressor might keep the genes of prophages silent as well, Jacob thought. Perhaps these circuits are common in all living things. “I no longer feel mediocre or even mortal,” he wrote.

But when François tried to sketch out his ideas for his wife, he was disappointed.

“You’ve already told me that,” Lise said. “It’s been known for a long time, hasn’t it?”

Jacob’s idea was so elegantly simple that it seemed obvious to anyone other than a biologist.

Why Menopause?

Last fall, a 96-year-old man named Ramajit Raghav became a father. No woman could become a mother at 96, or even 76. That’s because women typically lose the capacity to have children around the age 50–not because they become decrepit, not because civilization has poisoned them, but because they undergo a distinct biological transition, known as menopause.

Scientists have debated for years about why menopause exists. Some have argued that it’s a trait that evolved through natural selection in our ancestors. Women who stopped reproducing ended up with more descendants than women who didn’t. Some scientists proposed that older mothers were better off putting all their effort into caring for their children who were already born, rather than having new ones. As their limited supply of eggs deteriorated, they faced a higher risk of miscarriages and even death during childbirth. (In terms of reproduction, men have it easy by comparison: they can make new sperm through their whole life and don’t have to suffer any of the risks of pregnancy.)

But some studies raise questions about this hypothesis. The risks that childbirth poses to women later in life may not be big enough to make menopause much of an evolutionary benefit. Some scientists have come up with a different explanation: they argue that menopause provides the opportunity for women to help raise their grandchildren. Researchers who studied population records from Finland before the Industrial Revolution found that children were more likely to survive till adulthood if their grandmothers were still alive. Menopause might therefore be a winning evolutionary strategy because it leads to more grandchildren who can carry on Grandma’s genes.

But is it even necessary to think of menopause as a special adaptation in humans? Some scientists don’t think so. They argue that what happens to women as they get older is not terribly different from what happens to females of other species. In many species, females are born with a supply of eggs that then gradually deteriorate over their lifetime. They can invest energy into repairing the eggs, but if they invest too much, they have less energy for other tasks. This evolutionary balance leads females to eventually run out of viable eggs. Whether a female survives beyond that point or not simply has to do with how well her body is equipped to resist aging. There’s nothing special, then, about the fact that females in many species, including rats and elephants, can live past their reproductive years.

In the latest issue of Evolutionary Anthropology, three scientists take a closer look at the nature of human menopause. Daniel Levitis of the University of Southern Denmark, Oskar Burger of the Max Planck Institute for Demographic Research, and Laurie Bingaman Lackey of the International Species Information System started by comparing human biology to that of our primate relatives. Reviewing records from 66 species of primates, they found that in every case females could lived well beyond their last birth. Their post-reproductive life ranged between 25% and 95% of their breeding years.

Taken on its own, this result might suggest that human menopause isn’t anything special. But Levitis and his colleagues caution their readers to take it with a gorilla-sized grain of salt. Most of the records of longevity and births come from zoos, not surprisingly, where primates are well-fed, enjoy the attention of vets, and don’t face a daily threat from predators. Data on wild primates are a lot more sparse, understandably, but the picture that emerges from them is pretty brutal: only a tiny fraction of female primates survive to post-reproductive years.

Humans are different. A substantial portion of the women in any population are post-menopausal. This pattern is not limited to affluent societies. Take the Hadza, a group of people in Tanzania who survive by gathering fruit and killing game. A typical Hadza woman can expect to spend almost half her adult life in a post-fertile state. The slaves of Trinidad experienced some of the most brutal conditions ever recorded–so brutal, in fact, that their population was continually shrinking due to early deaths. And yet even among Trinidad’s slaves, a third of a woman’s adult life, on average, came after her last child.

It seems, then, that there really is something remarkable about the lives of human females compared to other primates. But is menopause what makes them remarkable, or is it just the side effect of something else that evolved in our ancestors? Humans have big brains, for example, and the bigger a primate’s brains, the longer its lifespan tends to be. This link may be due to the fact that big-brained babies demand a huge amount of energy and effort, both during pregnancy and afterwards. Those demands impose a slower pace of life on big-brained primates. So this pattern naturally raises the possibility that big brains in humans led to menopause.

Levitis and his colleagues don’t think so. They analyzed primate females, humans included, comparing their brain size to the age at which they stopped reproducing and the age at which they died. Even taking into account our gigantic brains, women are still odd. Compared to other primates, women stop reproducing sooner than you’d predict, and then go on living much longer than you’d predict.

So Levitis and his colleagues are left with the fact that human females typically enjoy a vastly longer post-reproductive life than their fellow primates, a life that can’t be explained away by other factors such as the size of their brains. Through human history, it appears, at least a third of women were post-fertile at any moment–a percentage that’s ten times higher than among the most pampered zoo-dwelling primates. There seems to be something special, something worth explaining, about menopause.

To explain this remarkable turn of evolutionary events, the scientists offer up a hypothesis. Six million years ago, our early hominin female ancestors were like other female primates. They could potentially live beyond their last childbirth, but they almost never did because most were dead by then.

And then hominins took an unusual evolutionary course. They evolved big brains and acquired new capacities–for making more versatile tools, for example, and for communicating with language. These factors may have allowed hominins to live longer. As a result, more females lived beyond their reproductive years.

Now the benefits of life after menopause could emerge. Any genes that enabled women to live longer would be favored by natural selection, because older women could raise the odds of their descendants surviving. Over many generations, women evolved a life in which they spent a dramatically larger part of it not having children.

In this new hypothesis, human menopause becomes at once special and yet not unique. In many species, females have the capacity to live beyond reproduction, but they rarely do, depriving evolution of the opportunity to expand that stage of life. But if other animals get that chance–for whatever reason–they may evolve to be menopausal too. Even insects can benefit from menopause. In species known as the Japanese gall aphid, females stop reproducing midway through their lives. Now that their abdomens are no longer dedicated to growing eggs, they can use that space to manufacture a sticky chemical. When a predator attacks the aphid colony, the menopausal females rush forward and glue themselves to its body. The predator is swamped by the heroic females, which die in the process. The evolutionary forces behind menopause may differ between humans and aphids, but the outcome is the same.

Tributes to A Twin Brother, Old and New (Science Ink Sunday)

The ancient Greeks believed that the constellation Gemini represented the twin horsemen Castor and Pollux. According to one version of the story, Castor was an ordinary human, while Pollux, the son of Zeus, lived forever. Castor was mortally wounded during a battle, whereupon Zeus offered Pollux a choice: he could let Castor die or he could give his brother half his immortality. Pollux chose to save his brother, and forever afterwards they would spend a day Olympus followed by a day in Hades.

“My twin brother died from suicide in 2011,” writes Zach Poynter. He chose to memorialize his brother with two tattoos on his arm. One is of the constellation Gemini. The other is of DNA. “We were identical twins, thus sharing the same DNA (although not expressing it the same way!)” Poynter writes.

You can read about the science of that paradox here and here. And you can see the rest of the Science Tattoo Emporium here or in my book, Science Ink: Tattoos of the Science Obsessed.

The Centrifuge Brain Project

For the past few years I’ve been a judge for the Imagine Science Film Festival. One of my favorites from last year is called The Centrifuge Brain Project; I was so delighted by it that I went hunting for it online to share here. For whatever reason, it didn’t show up until recently. You can now watch it on Vimeo, and I’ve embedded it below.

The Centrifuge Brain Project from Till Nowak on Vimeo.

I have complicated feelings about movies about science. I don’t like movies that come after you with a pedagogical cudgel. To me, the best movies are the ones that take the most liberties with science. I guess I like The Centrifuge Brain Project so much because it toys with science in such a deadpan way–so deadpan that some commenters at Vimeo asked if the crazy amusement park rides were real or not. And yet, in the end, it’s not a simplistic joke, but a short meditation on how we humans try to fight gravity–and nature in general–both in the lab and at amusement parks.

(Mark your calendars–the next Imagine Science Film Festival will be coming to New York this October.)