Most Recent Links
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
Sara Reardon Every time something poked its foot, the mouse jumped in pain. Researchers at Circuit Therapeutics, a start-up company in Menlo Park, California, had made the animal hypersensitive to touch by tying off a nerve in its leg. But when they shone a yellow light on its foot while poking it, the mouse did not react. The treatment is one of several nearing clinical use that draw on optogenetics — a technique in which light is used to control genes and neuron firing. In March, RetroSense Therapeutics of Ann Arbor, Michigan, began the first clinical-safety trial of an optogenetic therapy to treat the vision disorder retinitis pigmentosa. Many scientists are waiting to see how the trial turns out before they decide how to move forward with their own research on a number of different applications. “I think it will embolden people if there’s good news,” says Robert Gereau, a pain researcher at Washington University in St Louis, Missouri. “It opens up a whole new range of possiblilities for how to treat neurological diseases.” Retinitis pigmentosa destroys photoreceptors in the eye. RetroSense’s treatment seeks to compensate for this loss by conferring light sensitivity to retinal ganglion cells, which normally help to pass visual signals from photoreceptors to the brain. The therapy involves injecting patients who are blind or mostly blind with viruses carrying genes that encode light-sensitive proteins called opsins. The cells fire when stimulated with blue light, passing the visual information to the brain. Chief executive Sean Ainsworth says that the company has injected several individuals in the United States with the treatment, and plans to enroll a total of 15 blind patients in its trial. RetroSense will follow them for two years, but may release some preliminary data later this year. © 2016 Nature Publishing Group
Link ID: 22235 - Posted: 05.21.2016
By Diana Kwon A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being Credit: Thomas Koehler/Getty Images Life in the city can be taxing. City dwellers often face higher rates of crime, pollution, social isolation and other environmental stressors than those living in rural areas. For years studies have consistently linked the risk of developing schizophrenia to urban environments—but researchers are only beginning to understand why this association exists. Addressing the link is increasingly urgent: According to a recent U.N. report, the proportion of people living in cities will rise from 54 percent of the world’s population in 2014 to 66 percent by 2050. Researchers first suggested in the 1930s that urban living might increase schizophrenia risk. Since then many large epidemiological studies have reported an association between the two, primarily in European countries such as Sweden and Denmark. Converging evidence has revealed that growing up in the city doubles the risk of developing psychosis later in life. Studies have also begun to find that urban environments may heighten the risk of other mental health issues such as depression and anxiety. A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being. Conversely, people predisposed to mental illness may simply be more likely to move into urban environments. Two studies published this month shed new light on these effects and suggest both scenarios could be involved. © 2016 Scientific American, a Division
Bret Stetka We've all been caught in that hazy tug of war between wakefulness and sleep. But the biology behind how our brains drive us to sleep when we're sleep-deprived hasn't been entirely clear. For the first time scientists have identified the neurons in the brain that appear to control sleep drive, or the growing pressure we feel to sleep after being up for an extended period of time. The findings, published online Thursday by the journal Cell, could lead to better understanding of sleep disorders in humans. And perhaps, one day, if the work all pans out, better treatments for chronic insomnia could be developed. To explore which brain areas might be involved in sleep drive, Johns Hopkins neuroscientist Dr. Mark Wu and his colleagues turned to fruit flies, that long tinkered-with subject of scientific inquiry. Despite our rather obvious physical distinctions, humans and fruit flies – or Drosophila – have a good deal in common when it comes to genes, brain architecture and even behaviors. Included in the study were over 500 strains of fly, each with unique brain activation profiles (meaning certain circuits are more active in certain flies). By employing a genetic engineering technique in which specific groups of neurons can be activated with heat, the researchers were able to monitor the firing of nearly all the major circuits in the fruit fly brain and monitor the resulting effects on sleep. Moreover, the neurons of interest were engineered to glow green when activated allowing specific cells to be identified with fluorescent microscopy. Wu found that activating a group of cells called R2 neurons, which are found in a brain region known as the ellipsoid body, put fruit flies to sleep, even for hours after the neurons were "turned off." © 2016 npr
By Karen Weintraub There are case reports of people with no previously known risks having a heart attack after a nightmare, though they appear to be quite rare. No studies have been done to determine just how rare nightmare-induced heart attacks might be, and experts do not know whether they may result from the pulse-racing effects of the frightening dream itself. Nightmares are more commonly seen in the rapid eye movement, or REM, phase of sleep, which gets longer as the night progresses. Therefore, nightmares are more likely to occur in the early morning hours. Heart attacks, too, are most common in the early morning hours, when internal body clocks start secreting stress hormones and blood pressure tends to rise, said Dr. Mary Ann McLaughlin, a cardiologist at the Icahn School of Medicine at Mount Sinai in New York. If someone is at risk for a heart attack — because of high blood pressure, diabetes, sleep apnea, smoking or other factors — that attack is more likely to occur in the early morning. But “it’s rare for an otherwise healthy person to have a nightmare that causes a heart attack,” said Dr. McLaughlin. Nightmares can be triggered by alcohol, lack of sleep and medications, including some antidepressants and blood pressure medications, she said. Anxiety and depression have also been linked to increased risk of nightmares. On the flip side, patients with heart disease often have sleep apnea, a form of disordered breathing that can lead to fragmented sleep, and potentially more nightmares, said Dr. Neomi Shah, a sleep specialist, also at Mount Sinai. One 2013 study found that apnea patients with regular nightmares woke up more often than those who didn’t. Nightmares disappeared in more than 90 percent of the patients who used a continuous positive airway pressure, or CPAP, machine to treat their apnea. © 2016 The New York Times Company
Link ID: 22232 - Posted: 05.21.2016
Laura Sanders In mice, a long course of antibiotics that wiped out gut bacteria slowed the birth of new brain cells and impaired memory, scientists write May 19 in Cell Reports. The results reinforce evidence for a powerful connection between bacteria in the gut and the brain (SN: 4/2/16, p. 23). After seven weeks of drinking water spiked with a cocktail of antibiotics, mice had fewer newborn nerve cells in a part of the hippocampus, a brain structure important for memory. The mice’s ability to remember previously seen objects also suffered. Further experiments revealed one way bacteria can influence brain cell growth and memory. Injections of immune cells called Ly6Chi monocytes boosted the number of new nerve cells. Themonocytes appear to carry messages from gut to brain, Susanne Wolf of the Max Delbrück Center for Molecular Medicine in Berlin and colleagues found. Exercise and probiotic treatment with eight types of live bacteria also increased the number of newborn nerve cells and improved memory in mice treated with antibiotics. The results help clarify the toll of prolonged antibiotic treatment, and hint at ways to fight back, the authors write. L. Möhle et al. Ly6Chi monocytes provide a link between antibiotic-induced changes in gut microbiota and adult hippocampal neurogenesis. Cell Reports. Vol. 15, May 31, 2016. doi: 10.1016/j.celrep.2016.04.074. © Society for Science & the Public 2000 - 2016
By D. T. Max When a spinal cord is damaged, location is destiny: the higher the injury, the more severe the effects. The spine has thirty-three vertebrae, which are divided into five regions—the coccygeal, the sacral, the lumbar, the thoracic, and the cervical. The nerve-rich cord traverses nearly the entire length of the spine. The nerves at the bottom of the cord are well buried, and sometimes you can walk away from damage to these areas. In between are insults to the long middle region of the spine, which begins at the shoulders and ends at the midriff. These are the thoracic injuries. Although they don’t affect the upper body, they can still take away the ability to walk or feel below the waist, including autonomic function (bowel, bladder, and sexual control). Injuries to the cord in the cervical area—what is called “breaking your neck”—can be lethal or leave you paralyzed and unable to breathe without a ventilator. Doctors who treat spinal-cord-injury patients use a letter-and-number combination to identify the site of the damage. They talk of C3s (the cord as it passes through the third cervical vertebra) or T8s (the eighth thoracic vertebra). These morbid bingo-like codes help doctors instantly gauge the severity of a patient’s injury. Darek Fidyka, who is forty-one years old, is a T9. He was born and raised in Pradzew, a small farming town in central Poland, not far from Lodz. ... Several of the wounds punctured his lungs, and one nearly cut his spinal cord in half. As Fidyka lay on the ground, he felt his body change. “I can remember very vividly losing feeling in my legs, bit by bit,” he says. “It started in the upper part of the spine and was moving down slowly while I lay waiting for the ambulance to arrive.”
Link ID: 22230 - Posted: 05.19.2016
By Christie Aschwanden When concussions make the news, it’s usually about football. But head injuries happen in other sports too, and not just to men. During a congressional hearing on concussions in youth sports on Friday, Dawn Comstock, an epidemiologist who studies sports injuries, told a House Energy and Commerce subcommittee that in sports like soccer and basketball in which girls and boys play by the same rules, with the same equipment and the same facilities, “girls have higher concussion rates than boys.” Comstock, a researcher at the Colorado School of Public Health, is the first author of a 2015 study published in JAMA Pediatrics that quantified concussions in high school soccer and found that they were about one and a half times more common in girls than in boys. When U.S. Rep. Diana DeGette, D-Colo., asked whether more data was needed to show that girls have higher concussion rates, Comstock replied, “We already have the data that’s consistently shown this gender difference.” What we don’t have, she said, is a proven explanation for the discrepancy. Some researchers have wondered whether women and girls are simply more likely to report their symptoms than men and boys are. “It’s a sexist way to say that they’re not as tough,” said Katherine Price Snedaker, executive director of Pink Concussions,1 an organization that is seeking answers to how concussions affect women and girls. The group recently held a summit on female concussion and traumatic brain injuries at Georgetown University, and one of the speakers was Shannon Bauman, a sports physician who presented data from 207 athletes — both male and female — who’d been evaluated at her specialty concussion clinic in Barrie, Ontario, between September 2014 and January 2016.
Stephen Cave For centuries, philosophers and theologians have almost unanimously held that civilization as we know it depends on a widespread belief in free will—and that losing this belief could be calamitous. Our codes of ethics, for example, assume that we can freely choose between right and wrong. In the Christian tradition, this is known as “moral liberty”—the capacity to discern and pursue the good, instead of merely being compelled by appetites and desires. The great Enlightenment philosopher Immanuel Kant reaffirmed this link between freedom and goodness. If we are not free to choose, he argued, then it would make no sense to say we ought to choose the path of righteousness. Today, the assumption of free will runs through every aspect of American politics, from welfare provision to criminal law. It permeates the popular culture and underpins the American dream—the belief that anyone can make something of themselves no matter what their start in life. As Barack Obama wrote in The Audacity of Hope, American “values are rooted in a basic optimism about life and a faith in free will.” So what happens if this faith erodes? The sciences have grown steadily bolder in their claim that all human behavior can be explained through the clockwork laws of cause and effect. This shift in perception is the continuation of an intellectual revolution that began about 150 years ago, when Charles Darwin first published On the Origin of Species. Shortly after Darwin put forth his theory of evolution, his cousin Sir Francis Galton began to draw out the implications: If we have evolved, then mental faculties like intelligence must be hereditary. But we use those faculties—which some people have to a greater degree than others—to make decisions. So our ability to choose our fate is not free, but depends on our biological inheritance. © 2016 by The Atlantic Monthly Group.
Link ID: 22228 - Posted: 05.18.2016
George Johnson At the Science of Consciousness conference last month in Tucson, I was faced with a quandary: Which of eight simultaneous sessions should I attend? In one room, scientists and philosophers were discussing the physiology of brain cells and how they might generate the thinking mind. In another, the subject was free will — real or an illusion? Next door was a session on panpsychism, the controversial (to say the least) idea that everything — animal, vegetable and mineral — is imbued at its subatomic roots with mindlike qualities. Running on parallel tracks were sessions titled “Phenomenal Consciousness,” the “Neural Correlates of Consciousness” and the “Extended Mind.” For much of the 20th century, the science of consciousness was widely dismissed as an impenetrable mystery, a morass of a problem that could be safely pursued only by older professors as they thought deep thoughts in their endowed chairs. Beginning in the 1990s, the field slowly became more respectable. There is, after all, a gaping hole in science. The human mind has plumbed the universe, concluding that it is precisely 13.8 billion years old. With particle accelerators like the Large Hadron Collider at CERN, scientists have discovered the vanishingly tiny particles, like the Higgs boson, that underpin reality. But there is no scientific explanation for consciousness — without which none of these discoveries could have been made. © 2016 The New York Times Company
Link ID: 22227 - Posted: 05.18.2016
Andrea Hsu Scientists and doctors say the case is clear: The best way to tackle the country's opioid epidemic is to get more people on medications that have been proven in studies to reduce relapses and, ultimately, overdoses. Yet, only a fraction of the more than 4 million people believed to abuse prescription painkillers or heroin in the U.S. are being given what's called medication-assisted treatment. One reason is the limited availability of the treatment. But it's also the case that stigma around the addiction drugs has inhibited their use. Methadone and buprenorphine, two of the drugs used for treatment, are themselves opioids. A phrase you often hear about medication-assisted treatment is that it's merely replacing one drug with another. While doctors and scientists strongly disagree with that characterization, it's a view that's widespread in recovery circles. Now, the White House is pushing to change the landscape for people seeking help. In his 2017 budget, President Obama has asked Congress for $1.1 billion in new funding to address the opioid epidemic, with almost all of it geared toward expanding access to medication-assisted treatment. The White House is also highlighting success stories. At the National Prescription Drug Abuse and Heroin Summit held in Atlanta in March, President Obama appeared on stage with Crystal Oertle, a 35-year-old mother of two from Ohio. Oertle spoke of her spiral into addiction, which began with prescription painkillers and progressed to heroin. She tried unsuccessfully to quit on her own several times, before being prescribed buprenorphine a year ago. © 2016 npr
Keyword: Drug Abuse
Link ID: 22226 - Posted: 05.18.2016
By Sarah Kaplan You probably wouldn't be surprised if a scientist told you that your genes influence when you hit puberty, how tall you are, what your BMI will be and whether you're likely to develop male pattern baldness. But what if he said that the same gene could hold sway over all four things? That finding comes from a study published Monday in the journal Nature Genetics. Using data from dozens of genome-wide association studies (big scans of complete sets of DNA from many thousands of people), researchers at the New York Genome Center and the genetic analysis company 23andMe found examples of single "multitasking" genes that influence diverse and sometimes seemingly disparate traits. The scientists say that the links they uncovered could help researchers understand how certain genes work, and figure out better ways of treating some of the health problems they might control. "Most studies tend to go one disease at a time," said Joseph Pickrell, a professor at Columbia University and the New York Genome Center's lead investigator on the project. "But if we can try to make these sorts of connections between what you might think of as unrelated traits ... that gives us another angle of attack to understand the connections between these different diseases." To start, Pickrell and his team sought out genome-wide association studies (GWAS) identifying particular genetic variants associated with 42 different traits. Many had to do with diseases (for example, studies that linked certain genes to the risk of developing Alzheimer's or type 2 diabetes) and other personal health traits (body mass index, blood type, cholesterol levels).
Keyword: Genes & Behavior
Link ID: 22225 - Posted: 05.18.2016
Zoe Cormier A hallucinogenic drug derived from magic mushrooms could be useful in treating depression, the first safety study of this approach has concluded. Researchers from Imperial College London gave 12 people psilocybin, the active component in magic mushrooms. All had been clinically depressed for a significant amount of time — on average 17.8 years. None of the patients had responded to standard medications, such as selective serotonin re-uptake inhibitors (SSRIs), or had electroconvulsive therapy. One week after receiving an oral dose of psilocybin, all patients experienced a marked improvement in their symptoms. Three months on, five patients were in complete remission. “That is pretty remarkable in the context of currently available treatments,” says Robin Carhart-Harris, a neuropsychopharmacologist at Imperial College London and first author of the latest study, which is published in The Lancet Psychiatry1. The equivalent remission rate for SSRIs is around 20%. The study's authors are not suggesting that psilocybin should be a treatment of last resort for depressed patients. “Our conclusion is more sober than that — we are simply saying that this is doable,” says Carhart-Harris. “We can give psilocybin to depressed patients, they can tolerate it, and it is safe. This gives us an initial impression of the effectiveness of the treatment.” © 2016 Nature Publishing Group
By Simon Oxenham The “cuddle chemical”. The “moral molecule”. Oxytocin has quite a reputation – but much of what we thought about the so-called “love hormone” may be wrong. Oxytocin is made by the hypothalamus and acts on the brain, playing a role in bonding, sex and pregnancy. But findings that a sniff of the hormone is enough to make people trust each other more are being called into question after a string of studies failed to replicate classic experiments. Paul Zak at the Centre for Neuroeconomic Studies in Claremont, California, made his moral molecule hypothesis famous in 2011 when he memorably squirted a syringe of the hormone into the air while delivering a TED talk. When people sniff oxytocin before playing a money-lending game, it increases how much they trust each other, he explained. But several teams have been unable to replicate his finding. Last November, Gideon Nave at the California Institute of Technology in Pasadena and his colleagues reviewed studies of oxytocin, and concluded that the effect of nasal squirts of the hormone on trust are not reliably different from zero. Nave’s team aren’t the only ones calling the moral molecule hypothesis into question. In 2012, Moïra Mikolajczak at the Catholic University of Louvain (UCL) in Belgium and her colleagues published their own seminal findings backing a link between trust and oxytocin. They found that when people filled out an anonymous questionnaire about their sex lives and fantasies, they were less likely to seal the envelopes they returned them in if given a nasal dose of oxytocin beforehand. © Copyright Reed Business Information Ltd.
A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American
Link ID: 22222 - Posted: 05.17.2016
By JONATHAN BALCOMBE Washington — IN March, two marine biologists published a study of giant manta rays responding to their reflections in a large mirror installed in their aquarium in the Bahamas. The two captive rays circled in front of the mirror, blew bubbles and performed unusual body movements as if checking their reflection. They made no obvious attempt to interact socially with their reflections, suggesting that they did not mistake what they saw as other rays. The scientists concluded that the mantas seemed to be recognizing their reflections as themselves. Mirror self-recognition is a big deal. It indicates self-awareness, a mental attribute previously known only among creatures of noted intelligence like great apes, dolphins, elephants and magpies. We don’t usually think of fishes as smart, let alone self-aware. As a biologist who specializes in animal behavior and emotions, I’ve spent the past four years exploring the science on the inner lives of fishes. What I’ve uncovered indicates that we grossly underestimate these fabulously diverse marine vertebrates. The accumulating evidence leads to an inescapable conclusion: Fishes think and feel. Because fishes inhabit vast, obscure habitats, science has only begun to explore below the surface of their private lives. They are not instinct-driven or machinelike. Their minds respond flexibly to different situations. They are not just things; they are sentient beings with lives that matter to them. A fish has a biography, not just a biology. Those giant manta rays have the largest brains of any fish, and their relative brain-to-body size is comparable to that of some mammals. So, an exception? Then you haven’t met the frillfin goby. © 2016 The New York Times Company
Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o
By CLYDE HABERMAN At respected research centers in the United States and other countries, scientists have spent much of their professional lives in drug rehabilitation. It is not because they themselves struggle with addiction. What they are trying to rehabilitate are the drugs. Their focus is on mind-altering compounds that fell far from grace nearly half a century ago, LSD prominent among them. Along with other psychedelics, it was outlawed by the federal government, damned as bearing a high potential for abuse and offering no accepted medical benefit. But in recent years, researchers have sought to rescue hallucinogens from exile by examining their efficacy in treating certain disorders of the mind, and perhaps even in understanding the nature of consciousness and spirituality. The work of these scientists now draws the attention of Retro Report, a series of video documentaries that examine major news stories of the past and their enduring significance. Psychoactive substances, often derived from mushrooms, have been part of human cultures from Central and South America to the Sahara for thousands of years. But there is no need to look that far back; 1938 will do. That was when Albert Hofmann, a Swiss chemist searching for a drug to combat circulatory ailments, happened to synthesize lysergic acid diethylamide: LSD or, more familiarly, acid. Five years later, Dr. Hofmann, who died in 2008 at age 102, accidentally ingested a small dose of his creation and discovered its mind-blowing potential as he embarked on the first known acid trip. Many more such journeys would follow, for him and for countless others. © 2016 The New York Times Company
By Julia Shaw You see a crime take place. You are interviewed about it. You give a statement about what you saw. Do you think that at a later date you would be able to detect whether someone had tampered with your statement? Or re-written parts of it? This is currently a hot topic in the UK, where a very recently published inquiry into the so-called Hillsborough disaster, in which 96 people were crushed to death during a soccer match in 1989, found that testimonies had been deliberately altered by police. Research published earlier this year by the false memory dream team at the University of California, looked directly into the implications of such police (mis)conduct. They found that it is possible that changed statements can go unnoticed by the person who gave the original testimony, and may even develop into a false memory that accommodates the false account. To describe this effect, the researchers came up with the term "memory blindness"—the phenomenon of failing to recognize our own memories. The term was intended to mirror the ‘choice blindness’ literature. Choice blindness is forgetting choices that we have made. The researchers wanted to know “Can choice blindness have lasting effects on eyewitness memory?” To examine this, PhD Student Kevin Cochran and his colleagues conducted two experiments. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22218 - Posted: 05.16.2016
Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr
By John Horgan Speakers at the 2016 Tucson consciousness conference suggested that “temporal nonlocality” or other quantum effects in the brain could account for free will. But what happens when the brain is immersed in a hot tub? This is the second of four posts on “The Science of Consciousness” in Tucson, Arizona, which lasted from April 26 to April 30. (See Further Reading for links to other posts.) Once again, I’m trying to answer the question: What is it like to be a skeptical journalist at a consciousness conference? -- John Horgan DAY 2, THURSDAY, APRIL 28. HOT TUBS AND QUANTUM INCOHERENCE Breakfast on the patio with Stuart Kauffman, who has training in… almost everything. Philosophy, medicine, science. We’ve bumped heads in the past, but we’re friendly now. In his mid-70s, Stu is still obsessed with--and hacking away at--the biggest mysteries. We talk about… almost everything. Quantum mechanics, the origin of life, materialism, free will, God, the birth and death of his daughter, the death of his wife, his re-marriage, predictability versus possibility. As Stu speaks, his magnificent, weathered face looks happy/sad, arrogant/anxious. Superposition of emotions. He tells me about his brand-new book, Humanity in a Creative Universe, in which he outlines a perspective that can help lift us out of our spiritual crisis. Who saves the savior? I scoot to a morning session, “Consciousness and Free Will.” I hope it will supply me with ammo for my defenses of free will. I can do without God, but not free will. © 2016 Scientific American, a Division of Nature America, Inc.
Link ID: 22216 - Posted: 05.16.2016