Most Recent Links

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 5361 - 5380 of 29488

Clayton Dalton When patients arrive in the emergency room, nearly all but those with the most minor complaints get an IV. To draw blood, give medications, or administer fluids — the IV is the way doctors and nurses gain access to the body. Putting one in is quick and simple, and it's no more painful than a mild bee sting. Yet for some patients this routine procedure becomes excruciating. On my shifts as an emergency physician, I began to notice a strange pattern. These hypersensitive patients often had a history of using opioids. Shouldn't these patients be less susceptible to pain, instead of more so? As I looked into it, I found that I was far from the first to notice the paradox of heightened pain sensitivity with opioid use. An English physician in 1870 reported on morphine's tendency to "encourage the very pain it pretends to relieve." In 1880, a German doctor named Rossbach described a similar hypersensitivity to pain with opioid dependence. A century passed before the phenomenon received serious scientific attention. That's when American scientists showed that rats exhibited increased sensitivity to pain after exposure to morphine, a phenomenon that became known as opioid-induced hyperalgesia. By the 1990s the evidence for this unusual reaction in animals was strong, but whether it occurred in humans wasn't clear. © 2018 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 24719 - Posted: 03.05.2018

By Simon Makin Ketamine has been called the biggest thing to happen to psychiatry in 50 years, due to its uniquely rapid and sustained antidepressant effects. It improves symptoms in as little as 30 minutes, compared with weeks or even months for existing antidepressants, and is effective even for the roughly one third of patients with so-called treatment-resistant depression Although there are multiple theories, researchers do not quite know how ketamine combats depression. Now, new research has uncovered a mechanism that may, in part, explain ketamine's antidepressant properties. Two studies, recently published in Nature, describe a distinctive pattern of neural activity that may drive depression in a region called the lateral habenula (LHb); Ketamine, in turn, blocks this activity in depression-prone rats. Originally licensed as an anesthetic in 1970, ketamine has since gained fame as a party drug for causing out-of-body experiences, hallucinations and other psychosislike effects. Its antidepressant properties in humans were discovered almost 20 years ago. Ketamine does not directly influence the same chemical messengers as standard antidepressants such as serotonin but rather works via interaction with another chemical, glutamate—not usually associated with mood but rather with brain plasticity. One prominent idea about how it alleviates depression is by promoting the growth of new neural connections. “We provide a new angle for people to think about how this drug works,” says neuroscientist Hailan Hu of Zhejiang University in China, leader of the team that conducted both studies. If she is right, her group may have identified multiple new lines of attack for treating a condition the World Health Organization calls the leading cause of disability worldwide. © 2018 Scientific American

Keyword: Depression; Drug Abuse
Link ID: 24718 - Posted: 03.02.2018

By Katarina Zimmer Jermaine Jones’s first memory of being a “bit of a scientist” was discovering that toilet water is actually pretty clean. While conducting a science fair pro-ject during his junior year of high school in Virginia, he learned that “you get much more varied bacteria from the toilet seat as opposed to the water,” he explains. With encouragement from his aunt, who was a biologist, Jones chose to pursue a degree in science at the University of Virginia. Over the course of several undergraduate internships, he got a taste of different fields of research, from probing decision making in mice to examining the analgesic effects of rainforest plant extracts in Brazil. By the time Jones had earned his master’s degree from Old Dominion University, he was certain that investigating drug abuse would be a good fit for his two main interests, pharmacology and psychology. For his PhD, Jones moved to Washington, D.C., where he worked on elucidating the neurobiological mechanisms of cocaine’s aversive effects in rodent models with Anthony Riley, a behavioral pharmacologist at American University. At the same time, Jones examined the effects of knocking out genes encoding the neurotransmitter transporters that the drug acts upon in mice with neuroscientists George Uhl and Scott Hall at the National Institute on Drug Abuse. For his dissertation, “he was able to show, pretty unequivocally, the role of neuro-transmitter systems in the aversive effects of cocaine in these mice,” Riley recalls.1 © 1986-2018 The Scientist

Keyword: Drug Abuse; Genes & Behavior
Link ID: 24717 - Posted: 03.02.2018

Russell Bonduriansky Wouldn’t it be wonderful if we could bring back a deceased loved one? Such ideas used to be pure science fiction, but recent advances in biotechnology seem to have brought this possibility within reach (at least for the wealthy). When American singer-actress Barbra Streisand lost her beloved dog Sammie last year, she decided to have her cloned. She’s now raising Miss Scarlet and Miss Violet, both of whom are exact genetic replicas of Sammie. (You’ll be glad to know that any pet owner can do the same: for a mere US$100,000 or so, you too could have a genetic replica of your favourite cat or dog.) But Miss Scarlett and Miss Violet almost certainly won’t turn out to be identical, mini versions of Sammie. Research on cloning started in the 1960s, when British biologist John Gurdon showed that a frog egg’s nucleus (which contains the DNA) could be swapped for another nucleus extracted from an intestinal cell, and that such eggs could develop into tadpoles. This technique makes it possible to create individuals that share every single one of the thousands of genes in the original genome. By comparison, you share only about 50% of your genes with your mother. The same nucleus-swapping technique can be used with mammals. In 1996, Dolly the sheep became the first cloned mammal, and today the technology is available to clone a human being – if we wanted to. © 2010–2018, The Conversation US, Inc.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 24716 - Posted: 03.02.2018

By VERONIQUE GREENWOOD If you think about being thirsty at all, it seems like a fairly simple thought process: Find water. Drink it. Move on. But in fact there is something rather profound going on as you take that long, refreshing drink after a run or a hot day in the garden. As you become dehydrated, there is less water in your blood, and neurons in your brain send out the word that it’s time to look for water. Then, once you take a drink, you feel almost instantly satisfied. But if that is obvious, it is also mysterious. You aren’t pouring water directly into your bloodstream, after all. It will take at least 10 or 15 minutes, maybe longer, for the water in your stomach to make its way into the blood. And yet somehow, the brain knows. Sometimes that process isn’t as straightforward as it should be: People with a syndrome called polydipsia feel excessive thirst and drink enormous quantities of water. That can be dangerous, because if the blood is diluted too much, a person can die — a victim of water intoxication. As neuroscientists ponder how and why we thirst, a group of researchers at the California Institute of Technology has shed light on one small corner of the problem. Interested in how the brain keeps track of what the body is drinking, they have identified a set of neurons that receive messages as thirsty mice gulp down water. Passed around in the brain’s thirst centers, these messages seem to be behind the sensation of swift satisfaction that comes after a drink, and also suggest that it’s not just what is drunk, but how it is slurped down, that affects the brain. If the circuits work the same way in people, it may be key to understanding the neuroscience of what happens as we feel thirsty. In the last few years, biologists have been mapping the neurons within an area in the brain that regulates thirst, said Yuki Oka, a professor at Caltech and senior author of the new paper, which was published Wednesday in Nature. Cells in this region had been observed going quiet after an animal had water, but it was not clear exactly why. © 2018 The New York Times Company

Keyword: Miscellaneous
Link ID: 24715 - Posted: 03.01.2018

Terry Gross Antidepressants and medications for bipolar disorder can be life-changing and even lifesaving, but journalist Lauren Slater warns that the long-term side effects of these drugs are "cloaked in mystery." "As a nation, we're consuming them; we're gobbling them down," she says. "And we don't really know what we're taking into our bodies." Slater, who suffers from depression and bipolar disorder, has firsthand experience with psychotropic drugs; she has been taking medication for 35 years. Her new book, Blue Dreams, dedicates separate chapters to drugs such as Thorazine, lithium and psilocybin. Slater says she wanted to "unveil" the drugs by explaining their history, as well as how they work and the benefits and consequences for people who take them: "My goal was to almost try to make the drug into a character in and of itself. ... I wanted to bring these drugs alive." On how Thorazine changed the way mental illness was treated [Long] before Thorazine, people thought that mental illness was the result of what are called "humors" — blood, phlegm, bodily fluids that went out of whack. ... [Later, they] believed that it could be the result of hereditary genes gone wrong. But then Thorazine was invented, and that sort of was the kick-start to a whole bunch of other drugs being invented and to doctors and later the public at large thinking that mental illness was biochemical in nature. ... © 2018 npr

Keyword: Depression; Schizophrenia
Link ID: 24714 - Posted: 03.01.2018

Alice M. Gregory, Erin Leichman, Jodi Mindell Pairing the words “baby” and “sleep” can evoke strong emotions. Those who have had limited contact with little ones might interpret this word-combination as implying deep and prolonged slumber. For others, this union of words may elicit memories of prolonged periods of chaotic sleep (or what can feel like no sleep at all). Coping with the way babies sleep can be difficult. It’s not that babies don’t sleep. In fact, they sleep more than at any other stage of life. It’s more an issue of when they sleep. Newborns start by sleeping and waking around the clock. This is not always easy for parents. There is even research suggesting that in adults waking repeatedly at night can feel as bad as getting hardly any sleep in terms of attentional skills, fatigue levels and symptoms of depression. As to why infants wake at night, this is best explained by thinking about the two things that govern our sleep: the homeostatic and circadian processes. The crux of the homeostatic process is the straightforward idea that the longer we have been awake the greater our sleep drive (and the more sleepy we feel). It may take an adult an entire day to build up enough sleep drive to fall asleep at bedtime, but an infant may only need an hour or two of wakefulness before being able to drift off to sleep. The second process is circadian, which works like a clock. Adults typically feel more awake during the morning hours and sleepy at night, regardless of when we last slept. In very young babies this process is not yet developed. This means that sleep is more likely to occur at different points across the 24-hour day. © 2018 Guardian News and Media Limited

Keyword: Sleep; Development of the Brain
Link ID: 24713 - Posted: 03.01.2018

By NICHOLAS BAKALAR Some experts have suggested that there is an “obesity paradox,” the idea that obese people live longer than those of normal weight. But a new study found that obesity was associated with an increased risk for cardiovascular disease and a two- to three-year shorter life span. The study, in JAMA Cardiology, pooled data from 10 studies of 190,672 people followed from 1964 to 2015. Compared with those of normal weight, overweight men (body mass index of 25 to 29.9) had a 21 percent higher lifetime risk of cardiovascular disease and women a 32 percent higher risk. Among the obese (B.M.I. of 30 to 39.9), the risk was 67 percent higher for men and 85 percent higher for women, with even higher risk for those with a B.M.I. over 40. Longevity in men who were overweight but not obese was similar to that of men of normal weight. But they had an increased risk of cardiovascular disease at a younger age. “We were able to measure how much time is spent in healthy life years rather than just life span,” said the study’s senior author, Dr. Sadiya S. Khan, an assistant professor of medicine at Northwestern. “Maintaining a healthy B.M.I. is associated with a longer, healthier life, with less risk for cardiovascular disease.” © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24712 - Posted: 03.01.2018

By NICHOLAS BAKALAR Overweight mothers are more likely to have overweight babies, and the gut bacteria the babies inherit may in part be to blame. Researchers report that overweight mothers are more likely to have a cesarean section, and that babies born by cesarean to those mothers have species of gut bacteria different from those in babies born to normal weight women. And that difference in the gut microbiome — specifically an abundance of bacteria of the family Lachnospiraceae in infants of overweight mothers — may contribute to an increased risk for obesity. The study included 935 mother-infant pairs. Compared to children born to normal weight mothers, those born vaginally to overweight women were more than three times as likely to be overweight by age 3. But C-section babies born to overweight mothers were more than five times as likely to be overweight. For normal weight mothers, vaginal or C-section delivery made no difference in the risk for overweight babies. The study, in JAMA Pediatrics, controlled for breast-feeding, antibiotic exposure and other factors. The senior author, Anita L. Kozyrskyj, a professor of pediatrics at the University of Alberta, said that there is no probiotic that would lead to a positive change in gut bacteria. “If a cesarean is unavoidable, there is no easy answer,” she added, “but breast-feeding is effective in helping to prevent infants from becoming overweight.” © 2018 The New York Times Company

Keyword: Obesity
Link ID: 24711 - Posted: 03.01.2018

Helen Thomson In March 2015, Li-Huei Tsai set up a tiny disco for some of the mice in her laboratory. For an hour each day, she placed them in a box lit only by a flickering strobe. The mice — which had been engineered to produce plaques of the peptide amyloid-β in the brain, a hallmark of Alzheimer’s disease — crawled about curiously. When Tsai later dissected them, those that had been to the mini dance parties had significantly lower levels of plaque than mice that had spent the same time in the dark1. Tsai, a neuroscientist at Massachusetts Institute of Technology (MIT) in Cambridge, says she checked the result; then checked it again. “For the longest time, I didn’t believe it,” she says. Her team had managed to clear amyloid from part of the brain with a flickering light. The strobe was tuned to 40 hertz and was designed to manipulate the rodents’ brainwaves, triggering a host of biological effects that eliminated the plaque-forming proteins. Although promising findings in mouse models of Alzheimer’s disease have been notoriously difficult to replicate in humans, the experiment offered some tantalizing possibilities. “The result was so mind-boggling and so robust, it took a while for the idea to sink in, but we knew we needed to work out a way of trying out the same thing in humans,” Tsai says. “There’s been an explosion in brain wave research…pick your area and different people are trying to apply extra cranial stimulation.” The neuroscience that’s making waves for a wide range of conditions. © 2018 Macmillan Publishers Limited,

Keyword: Alzheimers; Learning & Memory
Link ID: 24710 - Posted: 02.28.2018

By Virginia Morell Want to say “Hello,” but don’t know the local language? Try waving your hand. Such gestures, common among humans, are also surprisingly similar among chimpanzees and bonobos, our closest great ape relatives. Now, a new study has identified numerous gestures that mean the same thing to both species. That suggests these signals have biological underpinnings and could be inherited from our last common ancestor. Gestures, signals often used to get someone’s attention or ask for or stop something, are not technically languages. They don’t have specific linguistic and grammatical rules or accepted vocabularies. But gestures still have meaning: Among chimpanzees, for example, scientists have documented that many of their movements—from mouth stroking to request food or arm raising to request grooming—are used to elicit specific responses from other chimpanzees. Researchers have now found something similar in bonobos, great apes closely related to chimpanzees but with longer legs, pink lips, and long hair that’s parted in the middle on their heads. Scientists started by shooting and analyzing videos of wild bonobos in the Democratic Republic of the Congo. When a bonobo made a common gesture that brought a consistent, satisfying response from others, it was added to the list. For example, when one bonobo looked at another while loudly scratching one arm, the second often responded by grooming the first. Because the first bonobo was almost always satisfied by this response, the researchers concluded that a “big, loud scratch” is a request for grooming. The scientists next compared the bonobo gestures to those of chimpanzees, and found that their repertoires overlapped by about 90%, significantly more than “would be expected by chance,” says lead author Kirsty Graham, a comparative psychologist at the University of York in the United Kingdom. © 2018 American Association for the Advancement of Science

Keyword: Animal Communication; Evolution
Link ID: 24709 - Posted: 02.28.2018

by Amy Ellis Nutt In the first broad demographic study of trends in gender-affirming surgeries in the United States, researchers found that the number of operations increased fourfold from 2000 to 2014. Some of the dramatic rise, according to a study published Wednesday in the journal JAMA Surgery, may be related to an increase in insurance coverage for the procedures. “Early on we recognized there’s been a lot of work on health disparities having to do with age, race and so on that get collected in health-care settings,” said Brandyn Lau, an assistant professor of surgery and health sciences informatics at Johns Hopkins University School of Medicine. “One of the things we need to know is whether [lesbian, gay and transgender] patients are getting the same care.” Lau and other researchers from Johns Hopkins Medicine and Harvard University analyzed 15 years of data from the National Inpatient Sample, a collection of hospital inpatient information from across the country, and found a total of 4,118 gender-affirming surgeries. The surgeries took place as LGBTQ people are finding increasing acceptance, especially among younger generations. The majority of the surgeries that occurred between 2000 and 2011 involved patients not covered by health insurance. About half of the transgender patients in the study paid out of pocket between 2000 and 2005. That number rose to 65 percent between 2006 and 2011. However, the trend reversed between 2012 and 2014, with the number plummeting to 39 percent. Much of that decrease, say the study's authors, is due to Medicare and Medicaid. In May 2014, Medicare ended its 33-year ban on transgender surgeries. Loren Schechter, who specializes in transgender surgeries, says he does about 300 procedures a year, whereas it was only about 50 in 2000. The plastic surgeon also accepts Medicare, which others do not. © 1996-2018 The Washington Post

Keyword: Sexual Behavior
Link ID: 24708 - Posted: 02.28.2018

Rhiannon Lucy Cosslett In my first year of university, just after I had been prescribed fluoxetine for depression, I had an argument about it with a close friend. He told me that taking antidepressants would make my feelings false, my emotions manufactured. I wouldn’t be able to tell if what I was feeling was real – and that was wrong. At the time I did not know how to articulate that all of our feelings are linked to chemicals: that even eating a chocolate bar can give me a blood-sugar spike and alter my behaviour, that feeling the sunshine on my skin can give me hope and energy. Furthermore, that the contraceptive pills his girlfriends took were liable to make them angry, not to mention less horny. I did not know how to say that the antidepressant I took in order to cope with my life was not that different to the ketamine and cocaine he used to cope with his. In any case, it was a pretentious argument of the kind one has at university, and both of us lacked the scientific knowledge to really underpin our views. It was all posturing. Once I accepted that I needed help and began treatment, I felt calmer within a week I think of it now because antidepressants are in the news again: whether they work or don’t work, whether other treatments – therapy, mindfulness, exercise, volunteering, being a 96-year-old Italian with a diet of fish and olive oil – are more effective than that “magic” pill. The chemical imbalance theory is posited, then debunked, in a never-ending cycle, as we, the mentally ill and medicated, watch on with hope but also exasperation. Because for all the scientific advances, therapeutic studies and happiness indexes, the only thing an individual can say with any certainty is whether or not antidepressants worked for them.

Keyword: Depression
Link ID: 24707 - Posted: 02.28.2018

By Kimberly Hickok If you ever wanted to know what a moth was thinking, this might be as close as you’re going to get. In a new study published today in Cell Reports, researchers placed female hawkmoths (Manduca sexta) in a wind tunnel containing two pieces of filter paper—one covered in a test odor, and one with no odor. Perhaps not surprisingly, the insects were most attracted to odors containing aromatic chemicals, which are present in plants that are common nectar sources. Some odors consistently caused the moths to touch their feet to the paper while curving their abdomen, which is how they lay eggs, indicating that moths associate those odors with egg laying. With six different odors, the moths alternated touching their feet and their mouths to the same odor, suggesting that plants containing one or all of those chemicals, such as jimson weed, are important for both feeding and egg laying. By combining these data with imaging of nerve cells at the base of the moths’ antennae, the researchers identified four clusters of nerves specifically associated with feeding behavior and six specifically associated with egg laying, but none associated with both behaviors. This means moths use specific odors to direct their behavior. The scientists say more research is needed to see whether nerve clusters respond to odor the same way in other species of moths and pollinating insects, which can help identify important odors and the plants that make them. © 2018 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Sexual Behavior
Link ID: 24706 - Posted: 02.28.2018

By Ashley Yeager | Human neural stem cells transplanted into the injured spines of monkeys matured into nerve cells, spurring neuronal connections and giving the animals an improved ability to grasp an orange, researchers report today (February 26) in Nature Medicine. “This type of cellular therapy, though still in its infancy, may eventually be a reasonable approach to treating central nervous system injury and possibly even neurodegenerative disease in humans,” Jonathan Glass, a neurologist at Emory University School of Medicine, tells The Scientist by email. Glass, who was not involved in the study, notes that the differentiation of stem cells over time is “impressive,” as is their ability to make connections in the monkeys’ central nervous systems, but more work needs to be done to show if the cells can grow extremely long axons to connect motor and sensory neurons after spinal injury in humans. Up to this point, most of the work on transplanting neural stem cells had been done in rats. This is the first study to show the treatment can be successfully scaled up to primates. “We definitely have more confidence to do this type of treatment in humans,” study coauthor Mark Tuszynski, a neuroscientist at the University of California, San Diego, School of Medicine, tells The Scientist. In the study, Tuszynski and his colleagues cut into a section of the spinal cord of rhesus monkeys and then two weeks later inserted a graft of human neural progenitor cells into the injury site. In the first four monkeys, the grafts did not stay in position, a finding that forced the researchers to add to the transplants more fibrinogen–thrombin, a protein-enzyme mixture the makes the graft adhere more quickly to site. The team also had to tilt the operating table to drain cerebral spinal fluid, which would wash the graft away. © 1986-2018 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 24705 - Posted: 02.27.2018

Laura Sanders With fevers, chills and aches, the flu can pound the body. Some influenza viruses may hammer the brain, too. Months after being infected with influenza, mice had signs of brain damage and memory trouble, researchers report online February 26 in the Journal of Neuroscience. It’s unclear if people’s memories are affected in the same way as those of mice. But the new research adds to evidence suggesting that some body-wracking infections could also harm the human brain, says epidemiologist and neurologist Mitchell Elkind of Columbia University, who was not involved in the study. Obvious to anyone who has been waylaid by the flu, brainpower can suffer at the infection’s peak. But not much is known about any potential lingering effects on thinking or memory. “It hasn’t occurred to people that it might be something to test,” says neurobiologist Martin Korte of Technische Universität Braunschweig in Germany. The new study examined the effects of three types of influenza A — H1N1, the strain behind 2009’s swine flu outbreak; H7N7, a dangerous strain that only rarely infects people; and H3N2, the strain behind much of the 2017–2018 flu season misery (SN: 1/19/18, p. 12). Korte and colleagues shot these viruses into mice’s noses, and then looked for memory problems 30, 60 and 120 days later. A month after infection, the mice all appeared to have recovered and gained back weight. But those that had received H3N2 and H7N7 had trouble remembering the location of a hidden platform in a pool of water, the researchers found. Mice that received no influenza or the milder H1N1 virus performed normally at the task. |© Society for Science & the Public 2000 - 2018

Keyword: Learning & Memory; Neuroimmunology
Link ID: 24704 - Posted: 02.27.2018

By Dina Fine Maron Millions of Americans who suffer from bipolar disorder depend on lithium. The medication has been prescribed for half a century to help stabilize patients’ moods and prevent manic or depressive episodes. Yet what it does in the brain—and why it does not work for some people—has remained largely mysterious. But last year San Diego–based researchers uncovered new details about how lithium may alter moods, thanks to an approach recently championed by a small number of scientists studying mental illness: The San Diego team used established lab techniques to reprogram patients’ skin cells into stem cells capable of becoming any other kind—and then chemically coaxed them into becoming brain cells. This process is now providing the first real stand-ins for brain cells from mentally ill humans, allowing for unprecedented direct experiments. Proponents hope studying these lab-grown neurons and related cells will eventually lead to more precise and effective treatment options for a variety of conditions. The San Diego team has already used this technique to show some bipolar cases may have more to do with protein regulation than genetic errors. And another lab discovered the activity of glial cells (a type of brain cell that supports neuron function) likely helps fuel schizophrenia—upending the theory that the disorder results mainly from faulty neurons. This new wave of research builds on Shinya Yamanaka’s Nobel-winning experiments on cellular reprogramming from a decade ago. His landmark findings about creating induced pluripotent stem cells (iPSCs) have only recently been applied to studying mental illness as the field has matured. “What’s really sparked that move now has been the ability to make patient-specific stem cells—and once you can do that, then all sorts of diseases become amenable to investigation,” says Steven Goldman, who specializes in cellular and gene therapy at the University of Rochester Medical Center. © 2018 Scientific American,

Keyword: Schizophrenia; Stem Cells
Link ID: 24703 - Posted: 02.27.2018

Lauren Smith As a shark biologist, I enjoy nothing more than going scuba diving with sharks in the wild. However, I realise it’s an immense privilege to do this as part of my work – and that for the vast majority of people experiencing the underwater world in such a way is simply not possible. Nevertheless, even without the aid of an air tank humans interact with fish on many levels and in greater numbers than they do with mammals and birds. A review published by the journal Animal Cognition in 2014 by Culum Brown, an associate professor at Macquarie University, Sydney, explains that fish are one of the vertebrate taxa most highly utilised by humans. But despite the fact that they are harvested from wild stocks as part of global fishing industries, grown under intensive aquaculture conditions, are the most common pet and are widely used for scientific research, fish are seldom afforded the same level of compassion or welfare as warm-blooded vertebrates. As Brown highlights in his review, part of the problem is the large gap between people’s perception of fish intelligence and the scientific reality. This is an important issue because public perception guides government policy. The perception of an animal’s intelligence often drives our decision on whether or not to include them in our moral circle. From a welfare perspective, most researchers would suggest that if an animal is sentient, then it can most likely suffer and should therefore be offered some form of formal protection.

Keyword: Consciousness; Evolution
Link ID: 24702 - Posted: 02.27.2018

By Aaron E. Carroll I remember the first time my daughter discovered her hand. The look of amazement on her face was priceless. It wasn’t long before she was putting that discovery to use, trying to put everything she could find into her mouth. Babies want to feed themselves. It sometimes feels as if parents spend more time trying to stop them than encouraging them. Over the last few years, however, some people have begun to ask if we are doing the right thing. Baby-led weaning is an approach to feeding that encourages infants to take control of their eating. It’s based on the premise that infants might be better self-regulators of their food consumption. It has even been thought that baby-led weaning might lead to reductions in obesity. While babies have been spoon-fed for a long time, the explosion of commercial foods for them might be making it too easy to overfeed them, an idea that the results from a cohort study in 2015 seemed to hint at. Those weaned in a baby-led approach seemed to be more responsive to being sated and were less likely to be overweight. A case-control study from 2012 also argued that baby-led weaning was associated with a lower body mass index (B.M.I). Such trials cannot establish causality, however, and may be confounded in unmeasured ways. A recent randomized controlled trial accomplished what previous work could not. Pregnant women in New Zealand were recruited before they gave birth and randomly assigned to one of two groups. Both got standard midwifery and child care. But one group received eight more contacts, from pregnancy to the newborn’s ninth month. Five of these were with a lactation consultant, who encouraged the mothers to prolong breast-feeding and delay the introduction of solid foods until 6 months of age. The three other contacts were with research staffers who encouraged parents to read hunger and fullness cues from their infants and provide their babies (starting at 6 months) with foods that were high in energy and iron — easy to grab but hard to choke on. © 2018 The New York Times Company

Keyword: Obesity; Development of the Brain
Link ID: 24701 - Posted: 02.27.2018

Mike Shooter Sian was just 14, brought by her misery to the edge of self-harm, when I met her in a cafe at the top end of one of the old mining valleys. Neutral ground. She told me about her rugby-playing older brother and her bright little sister who had lots of pets and wanted to be a vet. She felt that her parents doted on them and that there could be no room in anyone’s heart for her. She told me about her only friend, who had been killed in a road accident just as they went up to big school. About the recent death of her grandmother, who had been the only person she could confide in. And about the GP who had said she was depressed and given her a course of pills. I thought about Sian again this week. The newspaper headlines across the world were welcoming a major study that confirmed the value of antidepressant medication in the treatment of depression in adults. And so did I. Depression was validated at long last as an illness every bit as serious as physical conditions, that could cause untold human suffering and economic devastation, but could be helped with a course of antidepressant pills. First things first, I heartily agree with what that survey was saying about adult treatment. After all, I have a recurrent depression myself that has needed frequent treatment over the years. I talked about it openly when I was president of the Royal College of Psychiatrists and have continued to do so from the public platform, in the media, and to anyone who will listen. I do this in the hope that it will help to dispel the stigma that surrounds mental illness and prevents people from seeking therapy until it is too late. The diagnosis made sense of what I was going through. It wasn’t my fault. And I was grateful for the medication.

Keyword: Depression; Development of the Brain
Link ID: 24700 - Posted: 02.27.2018