Christian H. Cooper made his way from Appalachia to Wall Street, and from poverty to wealth. But is it because he worked harder than the family and friends still struggling in East Tennessee, or was it luck? In Nautilus, he digs into the emerging science of epigenetics to look at the way poverty actually changes our genetic expression, and therefore our physiology. If poverty has treatable physical aspects, what does that mean for economic policy, social policy, and politics? What does it mean for the American ideal of meritocracy?
Now, new evidence is emerging suggesting the changes can go even deeper—to how our bodies assemble themselves, shifting the types of cells that they are made from, and maybe even how our genetic code is expressed, playing with it like a Rubik’s cube thrown into a running washing machine. If this science holds up, it means that poverty is more than just a socioeconomic condition. It is a collection of related symptoms that are preventable, treatable—and even inheritable. In other words, the effects of poverty begin to look very much like the symptoms of a disease.
That word—disease—carries a stigma with it. By using it here, I don’t mean that the poor are (that I am) inferior or compromised. I mean that the poor are afflicted, and told by the rest of the world that their condition is a necessary, temporary, and even positive part of modern capitalism. We tell the poor that they have the chance to escape if they just work hard enough; that we are all equally invested in a system that doles out rewards and punishments in equal measure. We point at the rare rags-to-riches stories like my own, which seem to play into the standard meritocracy template.
Ross Andersen’s Atlantic profile of Nikita Zimov and his quest to re-create a Pleistocene ecosystem that will slow the thaw of Arctic permafrost, ultimately slowing global warming — it’s like Jurassic Park, but with a basis in science and no man-eating dinosaurs. Impressive and captivating, it’s a piece worth reading, not least for a fascinating explanation of how grasses went from being slimy ocean plants to covering huge swaths of the planet.
For the vast majority of the Earth’s 4.5 billion spins around the sun, its exposed, rocky surfaces lay barren. Plants changed that. Born in the seas like us, they knocked against the planet’s shores for eons. They army-crawled onto the continents, anchored themselves down, and began testing new body plans, performing, in the process, a series of vast experiments on the Earth’s surface. They pushed whole forests of woody stems into the sky to stretch their light-drinking leaves closer to the sun. They learned how to lure pollinators by unfurling perfumed blooms in every color of the rainbow. And nearly 70 million years ago, they began testing a new form that crept out from the shadowy edges of the forest and began spreading a green carpet of solar panel across the Earth.
For tens of millions of years, grasses waged a global land war against forests. According to some scientists, they succeeded by making themselves easy to eat. Unlike other plants, many grasses don’t expend energy on poisons, or thorns, or other herbivore-deterring technologies. By allowing themselves to be eaten, they partner with their own grazers to enhance their ecosystem’s nutrient flows.
I pause, perched on a rock inside the entrance, in order to consider this—people not so different from myself once sat here, facing the Mediterranean and Africa beyond. Before I arrived in Gibraltar, I used a commercial genome-testing service to analyse my ancestry. From the vial of saliva I sent them, they determined that 1 per cent of my DNA is Neanderthal. I don’t know what health advantages or risks these genes have given me—testing companies are no longer allowed to provide this level of detail—but it is an extraordinary experience to be so close to the intelligent, resourceful people who bequeathed me some of their genes. Sitting in this ancient home, knowing none of them survived to today, is a poignant reminder of how vulnerable we are—it could so easily have been a Neanderthal woman sitting here wondering about her extinct human cousins.
Maud Newton | Longreads | June 2015 | 24 minutes (5,889 words)
BBC America’s Orphan Black seems so immediate, so plausible, so unfuturistic, that Cosima Herter, the show’s science consultant, is used to being asked whether human reproductive cloning could be happening in a lab somewhere right now. If so, we wouldn’t know, she says. It’s illegal in so many countries, no one would want to talk about it. But one thing is clear, she told me, when we met to talk about her work on the show: in our era of synthetic biology — of Craig Venter’s biological printer and George Church’s standardized biological parts, of three-parent babies and of treatment for cancer that involves reengineered viruses— genetics as we have conceived of it is already dead. We don’t have the language for what is emerging. Read more…
A short piece published in BBC Magazine explored the science of whether murderers are born or made. A British neurocriminologist named Adrian Raine has made a career out of studying the brains of violent criminals. Raine was the first person to conduct a brain imaging study on murderers, and has since scanned the brains of numerous homicidal individuals, looking for similarities. Raine’s brain scanning studies found two similarities in the brains of nearly all his participants: 1) reduced activity in the pre-frontal cortex, which means less emotional impulse control, and 2) over activation of the part of the brain that controls our emotions, called the amygdala. According to the BBC, Raine’s study suggests that ” that murderers have brains that make them more prone to rage and anger, while at the same time making them less able to control themselves.” Childhood abuse could be a factor because of the damage it can cause to the brain, particularly to the pre-frontal cortex. But, as the BBC put it, “only a small proportion of those who have a terrible childhood grow up to become murderers,” which brings us to the next possibility: genetics. Are there genetic factors that predispose us to crime?
A breakthrough came in 1993 with a family in the Netherlands where all the men had a history of violence. Fifteen years of painstaking research revealed that they all lacked the same gene.
This gene produces an enzyme called MAOA, which regulates the levels of neurotransmitters involved in impulse control. It turns out that if you lack the MAOA gene or have the low-activity variant you are predisposed to violence. This variant became known as the warrior gene.
About 30% of men have this so-called warrior gene, but whether the gene is triggered or not depends crucially on what happens to you in childhood.
The research in question was conducted by Han Brunner, a Dutch geneticist working out of a teaching hospital in the Netherlands’ oldest city. Brunner’s research was first published in Science in October 1993, and that same month Sarah Richardson wrote about it for Discover magazine in an article entitled “Violence in the Blood.” Richardson’s piece is fascinating, especially in its explanation of how the geneticists used different clues to determine the origin of the aggressive behavior. This is how it begins:
One day in 1978 a woman walked into University Hospital in Nijmegen, the Netherlands, with a problem: the men in her family. Many of them–including several of her brothers and a son–seemed to have some sort of mental debility. Gradually, as the clinical geneticists who counseled the woman got to know her and her family, the details of the strange behavior of the woman’s male kin emerged. One had tried to rape his sister; another had tried to run his boss down with a car; a third had forced his sisters to undress at knife point. Furthermore, the violent streak had a long history. In 1962 the woman’s granduncle had prepared a family tree that identified nine other males with the same disorder, tracing it as far back as 1870. The granduncle, who was not violent himself–he worked in an institution for the learning disabled–had apparently come to suspect that something was terribly wrong with his family.
Three decades later, and 15 years after the woman’s first office visit, geneticist Han Brunner and his colleagues at the Nijmegen hospital think they’ve figured out what that something is. Some of the men in the woman’s family, they say, suffer from a genetic defect on the X chromosome- -a defect that cripples an enzyme that may help regulate aggressive behavior. If Brunner and his colleagues are right, it would be the first time a specific gene has been linked to aggression. That means their finding cannot fail to be controversial.