Chapter 13. Memory, Learning, and Development
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By Perri Klass, M.D. In the 1990s, in my first month in practice as a pediatrician, I asked the mother of a 4-year-old about discipline and she told me that her son was often out of line and wild, and spanking was the only thing that worked, though she was sure I was going to tell her not to, just as her previous pediatrician had done. Around the same time, my colleague in the same clinic walked into an exam room to find a cranky toddler who was acting out, and a frustrated father who was taking off his belt and threatening punishment. In each case, and in many others, we had to decide how to talk to the parents, and whether to bring up the issue of child abuse — which is definitely an issue when a child is being struck, or threatened, with a belt. Corporal punishment, also known as “physical discipline,” has become illegal in recent decades in many countries, starting with Sweden in 1979. The United States is not one of those countries, and pediatricians regularly find ourselves talking with parents about why hitting children is a bad idea. The American Academy of Pediatrics officially recommends against physical discipline, saying that evidence shows it is ineffective and puts children at risk for abuse; pediatricians are mandated reporters, responsible for notifying the authorities if we think there is a possibility of abuse, though the boundaries are not clearly defined by law. But many parents continue to spank, even when they don’t think it does much good. In a recent report by the nonprofit organization Zero to Three of a national sample of 2,200 parents of children birth to age 5, parents were asked which discipline strategies they used a few times a week or more. Twenty-six percent said they “pop or swat” their child, 21 percent spank, and 17 percent reported hitting with an object like a belt or a wooden spoon. (Parents could respond that they used more than one strategy.) Zero to Three reported that even those who used these strategies frequently did not rate them as effective, and 30 percent agreed with the statement, “I spank even though I don’t feel O.K. about it.” © 2016 The New York Times Company
By Elizabeth Pennisi Cave fish have long fascinated biologists because of their missing eyes and pale skin. Now, one researcher is studying them for another reason: Their behavior may provide clues to the genetic basis of some human psychiatric disorders. Last week at the 23rd International Conference on Subterranean Biology in Fayetteville, Arkansas, he demonstrated how drugs that help people with schizophrenia and autism similarly affect the fish. “I think there is a lot of potential” for these fish to teach us about mental disorders, says David Culver, an evolutionary biologist at American University in Washington, D.C., who was not involved in the study. Culver adds that—like other work on the cause of cave fish blindness—the new research may also have implications for human disease. A decade ago, the lead author on the new study, Masato Yoshizawa, wanted to understand brain evolution by investigating the effects of natural selection on behavior. The Mexican tetra (Astyanax mexicanus), a cave fish with very close surface relatives, seemed an excellent prospect for that work. Because the two populations can interbreed, it’s easier to pin down genes that might be related to the neural defects underlying behavioral differences. Such breeding studies are not possible in humans. The blind cave fish differ from their surface relatives in several notable ways. They don’t have a social structure and they don’t school. Instead, they lead solitary lives—a behavior that makes sense given their lack of natural predators. They also almost never sleep. They are hyperactive, and—unlike other fish—they are attracted to certain vibrations in the water. Finally, they tend to do the same behavior over and over again and seem to have higher anxiety than their surface relatives. © 2016 American Association for the Advancement of Science.
Jon Hamilton Researchers have identified a substance in muscles that helps explain the connection between a fit body and a sharp mind. When muscles work, they release a protein that appears to generate new cells and connections in a part of the brain that is critical to memory, a team reports Thursday in the journal Cell Metabolism. The finding "provides another piece to the puzzle," says Henriette van Praag, an author of the study and an investigator in brain science at the National Institute on Aging. Previous research, she says, had revealed factors in the brain itself that responded to exercise. The discovery came after van Praag and a team of researchers decided to "cast a wide net" in searching for factors that could explain the well-known link between fitness and memory. They began by looking for substances produced by muscle cells in response to exercise. That search turned up cathepsin B, a protein best known for its association with cell death and some diseases. Experiments showed that blood levels of cathepsin B rose in mice that spent a lot of time on their exercise wheels. What's more, as levels of the protein rose, the mice did better on a memory test in which they had to swim to a platform hidden just beneath the surface of a small pool. The team also found evidence that, in mice, cathepsin B was causing the growth of new cells and connections in the hippocampus, an area of the brain that is central to memory. But the researchers needed to know whether the substance worked the same way in other species. So they tested monkeys, and found that exercise did, indeed, raise circulating levels of cathepsin in the blood. © 2016 npr
by Helen Thompson Young zebra finches (Taeniopygia guttata) learn to sing from a teacher, usually dad. Remembering dad’s tunes may even be hardwired into the birds’ brains. Researchers at the Okinawa Institute of Science and Technology in Japan measured activity in the brains of male juvenile birds listening to recordings of singing adult males, including their fathers. The team focused its efforts on neurons in a part of the brain called the caudomedial nidopallium that’s thought to influence song learning and memory. A subset of neurons in the caudomedial nidopallium lit up in response to songs performed by dad but not those of strangers, the team reports June 21 in Nature Communications. The more baby birds heard songs, the more their neurons responded and the clearer their own songs became. Sleep and a neurotransmitter called GABA influenced this selectivity. The researchers suggest that this particular region of the brain stores song memories as finches learn to sing, and GABA may drive the storage of dad’s songs over others. Researchers played a variety of sounds for young zebra finches: their own song, dad’s song and songs and calls from other adult finches. Over time, their songs became more and more similar to that of their father. |© Society for Science & the Public 2000 - 2016
By Nancy Stearns Bercaw In her memoir “Aliceheimer’s: Alzheimer’s Through the Looking Glass,” Dana Walrath uses drawings and stories to chronicle three years of caregiving for her mother, Alice, who was in the middle stages of Alzheimer’s disease. The experience turned out to be a magical trip down the rabbit hole of memory loss, an outcome that inspired Dr. Walrath, a medical anthropologist who taught at the University of Vermont College of Medicine and who also studied art and writing, to share their tale. Refusing to accept the dominant narrative of Alzheimer’s disease as a horror story, Dr. Walrath used the techniques of graphic medicine to create “Aliceheimer’s,” an 80-page, 35-picture tribute to her mother’s animated mind. Graphic medicine uses text and graphics to, as she writes in the book’s introduction, “let us better understand those who are hurting, feel their stories, and redraw and renegotiate those social boundaries.” We spoke with Dr. Walrath to learn more about graphic medicine, how the book came into being, and what it can teach others about caring for someone with Alzheimer’s disease. Here’s an edited excerpt of our conversation. Q. You say that “Aliceheimer’s” found you, not the other way around. What’s the backstory of your story? A. After a lifetime of mutually abrasive interaction, my mother moved into my home when a lock-down memory-care unit was her only other option. The years of living together not only brought us closure, but it also integrated my disparate career threads. Medical anthropology, creative writing, visual art — who knew they were connected? I sure didn’t. But Alice must have. During dementia, she said to me, “You should quit your job and make art full time.” © 2016 The New York Times Company
Link ID: 22350 - Posted: 06.23.2016
Alison Abbott It isn’t a scam, as neuroscientist Elena Cattaneo had first assumed. A total stranger really has left the prominent Italian, who is also a senator and a relentless campaigner against the misuse of science, his entire fortune to distribute for research. The sum is likely to be upwards of €1.5 million (US$1.7 million). The short, handwritten will of Franco Fiorini, an accountant from the small town of Molinella near Bologna, was officially made public on 21 June. “I’ll never know for sure why he decided to do this,” says Cattaneo, who adds that she has wept with regret that she cannot thank Fiorini. “But it gives a hopeful message that there are some people like Franco who are able to work out on their own the importance of science and research for Italy’s future.” She intends to make the money available for fellowships for young scientists in Italy, where funds for research are notoriously scarce. Cattaneo, who is based at the University of Milan, is no ordinary researcher. In 2013, then-president Giorgio Napolitano appointed her a senator-for-life in recognition of her activities in promoting science. One of her most famous achievements, made with a handful of colleagues, was a successful two-year battle to stop the Stamina Foundation in Brescia from administering unproven stem-cell therapies. Fiorini died on 21 May at the age of 64. A wheelchair user since a bout of childhood polio left him partially paralysed, he had been director of a construction company in Molinella before taking early retirement 15 years ago. © 2016 Macmillan Publishers Limited,
Keyword: Stem Cells
Link ID: 22349 - Posted: 06.23.2016
Laura Sanders Busy nerve cells in the brain are hungry and beckon oxygen-rich blood to replenish themselves. But active nerve cells in newborn mouse brains can’t yet make this request, and their silence leaves them hungry, scientists report June 22 in the Journal of Neuroscience. Instead of being a dismal starvation diet, this lean time may actually spur the brain to develop properly. The new results, though, muddy the interpretation of the brain imaging technique called functional MRI when it is used on infants. Most people assume that all busy nerve cells, or neurons, signal nearby blood vessels to replenish themselves. But there were hints from fMRI studies of young children that their brains don’t always follow this rule. “The newborn brain is doing something weird,” says study coauthor Elizabeth Hillman of Columbia University. That weirdness, she suspected, might be explained by an immature communication system in young brains. To find out, she and her colleagues looked for neuron-blood connections in mice as they grew. “What we’re trying to do is create a road map for what we think you actually should see,” Hillman says. When 7-day-old mice were touched on their hind paws, a small group of neurons in the brain responded instantly, firing off messages in a flurry of activity. Despite this action, no fresh blood arrived, the team found. By 13 days, the nerve cell reaction got bigger, spreading across a wider stretch of the brain. Still the blood didn’t come. But by the time the mice reached adulthood, neural activity prompted an influx of blood. The results show that young mouse brains lack the ability to send blood to busy neurons, a skill that influences how the brain operates (SN: 11/14/15, p. 22). © Society for Science & the Public 2000 - 2016.
Bentley Yoder was born with his brain outside his skull. Doctors said he didn’t have a chance, but he not only survived—he thrived. Now, some seven months later, Bentley has undergone reconstructive surgery to move his brain back into his skull. Bentley’s parents, Sierra and Dustin, both 25, found out something was wrong when they went in for a routine ultrasound at 22 weeks. Still in the womb, he was diagnosed with a rare condition called encephalocele, or cranium bifidum, in which parts of the brain protrude outside of gaps that have formed in the developing skull. The parents were told that their baby likely wouldn’t survive very long after birth, or that if he did he wouldn’t have any brain function; he was simply “incompatible with life.” As Sierra told the Washington Post, “We had no hope whatsoever.” The parents were unwilling to terminate the pregnancy, saying they wanted at least one chance to meet him before saying goodbye. To virtually everyone’s surprise, Bentley came out on his due date, October 31, 2015, kicking and screaming. After the first 36 hours, Sierra and Dustin had to take him home wearing the only onesie they bothered to purchase. Over the course of the next few weeks and months, Bentley continued to march on, save for a staph infection in his lungs. Aside from the large sac containing critical parts of his brain atop his head, Bentley developed normally. He continued to grow, and cried when he was hungry. The doctors were incredulous, and insisted that the growth above his head was just “damaged tissue,” and that “there’s no way it could be functioning,” but Bentley’s behaviors and normal developmental trajectory suggested otherwise.
Keyword: Development of the Brain
Link ID: 22347 - Posted: 06.22.2016
Agata Blaszczak-Boxe, People with higher levels of education may be more likely to develop certain types of brain tumors, a new study from Sweden suggests. Researchers found that women who completed at least three years of university courses were 23 percent more likely to develop a type of cancerous brain tumor called glioma, compared with women who only completed up to nine years of mandatory education and did not go to a university. And men who completed at least three years of university courses were 19 percent more likely to develop the same type of tumor, compared with men who did not go to a university. Though the reasons behind the link are not clear, "one possible explanation is that highly educated people may be more aware of symptoms and seek medical care earlier," and therefore are more likely to be diagnosed, said Amal Khanolkar, a research associate at the Institute of Child Health at the University College Londonand a co-author of the study. [Top 10 Cancer-Fighting Foods] In the study, the researchers looked at data on more than 4.3 million people in Sweden who were a part of the Swedish Total Population Register. The researchers tracked the people for 17 years, beginning in 1993, to see if they developed brain tumors during that time. They also collected information about the people's education levels, income, marital status and occupation. During the 17-year study, 5,735 men and 7,101 women developed brain tumors, according to the findings, published today (June 20) in the Journal of Epidemiology & Community Health. Copyright 2016 LiveScience,
Laura Sanders If you want to lock new information into your brain, try working up a sweat four hours after first encountering it. This precisely timed trick, described June 16 in Current Biology, comes courtesy of 72 people who learned the location of 90 objects on a computer screen. Some of these people then watched relaxing nature videos, while others worked up a sweat on stationary bikes, alternating between hard and easy pedaling for 35 minutes. This workout came either soon after the cram session or four hours later. Compared with both the couch potatoes and the immediate exercisers, the people who worked out four hours after their learning session better remembered the objects’ locations two days later. The delayed exercisers also had more consistent activity in the brain’s hippocampus, an area important for memory, when they remembered correctly. That consistency indicates that the memories were stronger, Eelco van Dongen of the Donders Institute in the Netherlands and colleagues propose. The researchers don’t yet know how exercise works its memory magic, but they have a guess. Molecules sparked by aerobic exercise, including the neural messenger dopamine and the protein BDNF, may help solidify memories by reorganizing brain cell connections. Citations E. van Dongen et al. Physical exercise performed four hours after learning improves memory retention and increases hippocampal pattern similarity during retrieval. Current Biology. Published online June 16, 2016. doi: 10.1016/j.cub.2016.04.071. © Society for Science & the Public 2000 - 2016
Keyword: Learning & Memory
Link ID: 22330 - Posted: 06.18.2016
Ian Sample Science editor Brain scans have highlighted “striking” differences between the brains of young men with antisocial behavioural problems and those of their better-behaved peers. The structural changes, seen as variations in the thickness of the brain’s cortex or outer layer of neural tissue, may result from abnormal development in early life, scientists at Cambridge University claim. But while the images show how the two groups of brains differ on average, the scans cannot be used to identify individuals with behavioural issues, nor pinpoint specific developmental glitches that underpin antisocial behaviour. Led by Luca Passamonti, a neurologist at Cambridge, the researchers scanned the brains of 58 young men aged 16 to 21 who had been diagnosed with conduct disorder, defined by persistent problems that ranged from aggressive and destructive behaviour, to lying and stealing, carrying weapons or staying out all night. When compared with brain scans from 25 healthy men of the same age, the scientists noticed clear differences. Those diagnosed with conduct disorder before the age of 10 had similar variations in the thickness of the brain’s cortex. “It may be that problems they experience in childhood affect and delay the way the cortex is developing,” said Passamonti. But the brains of men diagnosed with behavioural problems in adolescence differed in another way. Scans on them showed fewer similarities in cortical thickness than were seen in the healthy men. That, Passamonti speculates, may arise when normal brain maturation, such as the “pruning” of neurons and the connections between them, goes awry. © 2016 Guardian News and Media Limited
By Aleszu Bajak Can the various puzzles and quizzes associated with commercial brain-training games really improve cognitive function — or better yet, stave off cognitive decline? To date, the scientific evidence is murky, but that hasn’t kept companies from trying to cash-in on consumers’ native desire for quick fixes to complex health problems. The most famous among such companies is probably Lumosity, a product of San Francisco-based Lumos Labs, which once marketed its suite of web-based games and mobile apps as being “built on proven neuroscience,” and by encouraging users to “harness your brain’s neuroplasticity and train your way to a brighter life.” Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Those claims were among several that attracted the attention of the Federal Trade Commission, which earlier this year filed a complaint against the company. Lumosity was ultimately slapped with $50 million in fines for deceiving consumers — although $48 million of that was reportedly suspended by a district court, because the company was financially unable to pay the full amount. “Lumosity preyed on consumers’ fears about age-related cognitive decline, suggesting their games could stave off memory loss, dementia, and even Alzheimer’s disease,” said Jessica Rich, Director of the FTC’s Bureau of Consumer Protection, in a statement accompanying the settlement. “But Lumosity simply did not have the science to back up its ads.” Copyright 2016 Undark
By Gretchen Reynolds Physical activity is good for our brains. A wealth of science supports that idea. But precisely how exercise alters and improves the brain remains somewhat mysterious. A new study with mice fills in one piece of that puzzle. It shows that, in rodents at least, strenuous exercise seems to beneficially change how certain genes work inside the brain. Though the study was in mice, and not people, there are encouraging hints that similar things may be going on inside our own skulls. For years, scientists have known that the brains of animals and people who regularly exercise are different than the brains of those who are sedentary. Experiments in animals show that, for instance, exercise induces the creation of many new cells in the hippocampus, which is a part of the brain essential for memory and learning, and also improves the survival of those fragile, newborn neurons. Researchers believe that exercise performs these feats at least in part by goosing the body’s production of a substance called brain-derived neurotropic factor, or B.D.N.F., which is a protein that scientists sometimes refer to as “Miracle-Gro” for the brain. B.D.N.F. helps neurons to grow and remain vigorous and also strengthens the synapses that connect neurons, allowing the brain to function better. Low levels of B.D.N.F. have been associated with cognitive decline in both people and animals. Exercise increases levels of B.D.N.F. in brain tissue. But scientists have not understood just what it is about exercise that prompts the brain to start pumping out additional B.D.N.F. So for the new study, which was published this month in the journal eLIFE, researchers with New York University’s Langone Medical Center and other institutions decided to microscopically examine and reverse engineer the steps that lead to a surge in B.D.N.F. after exercise. They began by gathering healthy mice. Half of the animals were put into cages that contained running wheels. The others were housed without wheels. For a month, all of the animals were allowed to get on with their lives. Those living with wheels ran often, generally covering several miles a day, since mice like to run. The others remained sedentary. © 2016 The New York Times Company
Megan Scudellari Shinya Yamanaka looked up in surprise at the postdoc who had spoken. “We have colonies,” Kazutoshi Takahashi said again. Yamanaka jumped from his desk and followed Takahashi to their tissue-culture room, at Kyoto University in Japan. Under a microscope, they saw tiny clusters of cells — the culmination of five years of work and an achievement that Yamanaka hadn't even been sure was possible. Two weeks earlier, Takahashi had taken skin cells from adult mice and infected them with a virus designed to introduce 24 carefully chosen genes. Now, the cells had been transformed. They looked and behaved like embryonic stem (ES) cells — 'pluripotent' cells, with the ability to develop into skin, nerve, muscle or practically any other cell type. Yamanaka gazed at the cellular alchemy before him. “At that moment, I thought, 'This must be some kind of mistake',” he recalls. He asked Takahashi to perform the experiment again — and again. Each time, it worked. Over the next two months, Takahashi narrowed down the genes to just four that were needed to wind back the developmental clock. In June 2006, Yamanaka presented the results to a stunned room of scientists at the annual meeting of the International Society for Stem Cell Research in Toronto, Canada. He called the cells 'ES-like cells', but would later refer to them as induced pluripotent stem cells, or iPS cells. “Many people just didn't believe it,” says Rudolf Jaenisch, a biologist at the Massachusetts Institute of Technology in Cambridge, who was in the room. But Jaenisch knew and trusted Yamanaka's work, and thought it was “ingenious”. © 2016 Macmillan Publishers Limited,
By Ashley P. Taylor Sleep is known to aid memory and learning. For example, people who learn something, sleep on it, and are tested on the material after they wake up tend to perform better than those who remain awake in the interim. Within that general phenomenon, however, there’s a lot of unexplained variation. University of California, Riverside, sleep researcher Sara Mednick wondered “what else might be going during that sleep period that helps people’s memories,” she told The Scientist. As it turns out, activity of the autonomic nervous system (ANS) explains a large part of this variation, Mednick and colleagues show in a paper published today (June 13) in PNAS. The researchers measured not only the electrical activity of the brain during sleep, but also that of the heart, providing an indicator of ANS activity. They found that the beat-to-beat variation in heart rate accounted for much of the previously unexplained variation in how well people performed on memory and creativity tests following a nap. “There is a good possibility that this additional measure [heart-rate variability] may help account for discrepant findings in the sleep-dependent memory consolidation literature,” sleep and cognition researcher Rebecca Spencer of the University of Massachusetts, Amherst, who was not involved in the work, wrote in an email. “Perhaps we put too large of a focus on sleep physiology from the CNS [central nervous system] and ignore a significant role of the ANS.” © 1986-2016 The Scientist
By Brady Dennis In one city after another, the tests showed startling numbers of children with unsafe blood lead levels: Poughkeepsie and Syracuse and Buffalo. Erie and Reading. Cleveland and Cincinnati. In those cities and others around the country, 14 percent of kids — and in some cases more — have troubling amounts of the toxic metal in their blood, according to new research published Wednesday. The findings underscore how despite long-running public health efforts to reduce lead exposure, many U.S. children still live in environments where they're likely to encounter a substance that can lead to lasting behavioral, mental and physical problems. "We've been making progress for decades, but we have a ways to go," said Harvey Kaufman, senior medical director at Quest Diagnostics and a co-author of the study, which was published in the Journal of Pediatrics. "With blood [lead] levels in kids, there is no safe level." Kaufman and two colleagues at Quest, the nation's largest lab testing provider, examined more than 5.2 million blood tests for infants and children under age 6 that were taken between 2009 and 2015. The results spanned every state and the District of Columbia. The researchers found that while blood lead levels declined nationally overall during that period, roughly 3 percent of children across the country had levels that exceed five micrograms per deciliter — the threshold that the Centers for Disease Control and Prevention considers cause for concern. But in some places and among particular demographics, those figures are much higher.
By Julia Shaw Can you trust your memory? Picture this. You are in a room full of strangers and you are going around introducing yourself. You say your name to about a dozen people, and they say their names to you. How many of these names are you going to remember? More importantly, how many of these names are you going to misremember? Perhaps you call a person you just met John instead of Jack. This kind of thing happens all the time. Now magnify the situation. You are talking to a close friend, and you disclose something important to them, perhaps even something traumatic. You might, for example, say you witnessed the Paris attacks in 2015. But, how can you know for sure that your memory is accurate? Like most people, you probably feel that misremembering someone’s name is totally different from misremembering an important and emotional life event. That you could never forget #JeSuisParis, and will always have stable and reliable memories of such atrocities. I’m sure that is what those who witnessed 9/11, the 7/7 bombings in London or the assassination of JFK also thought. However, when experimenters conduct research on the accuracy of these so-called “flashbulb memories,” they find that many people make grave errors in their recollections of important historical and personal events. And these errors are more than just omissions. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22320 - Posted: 06.14.2016
By Linda Marsa| Helen Epstein felt deeply isolated and alone. Haunted by her parents’ harrowing experiences in Nazi concentration camps in World War II, she was troubled as a child by images of piles of skeletons and barbed wire, and, in her words, “a floating sense of danger and incipient harm.” But her Czech-born parents’ defense against the horrific memories was to detach. “Their survival strategy in the war was denial and dissociation, and that carried into their behavior afterward,” recalls Epstein, who was born shortly after the war and grew up in Manhattan. “They believed in action over reflection. Introspection was not encouraged, but a full schedule of activities was.” It was only when she was a student at Israel’s Hebrew University in the late 1960s that she realized she was part of a community that shared a cultural and historical legacy that included both pain and fear. “I met dozens of kids of survivors,” she says, “one after the other who shared certain characteristics: preoccupation with a family past and Israel, and who spoke several middle European languages — just like me.” Epstein’s 1979 book about her observations, Children of the Holocaust, gave voice to that sense of alienation and free-floating anxiety. In the years since, mental health professionals have largely attributed the second generation’s moodiness, hypervigilance and depression to learned behavior. It is only now, more than three decades later, that science has the tools to see that this legacy of trauma becomes etched in our DNA — a process known as epigenetics, in which environmental factors trigger genetic changes that may be passed on, just as surely as blue eyes and crooked smiles.
By Esther Landhuis About 100 times rarer than Parkinson’s, and often mistaken for it, progressive supranuclear palsy afflicts fewer than 20,000 people in the U.S.—and two thirds do not even know they have it. Yet this little-known brain disorder that killed comic actor Dudley Moore in 2002 is quietly becoming a gateway for research that could lead to powerful therapies for a range of intractable neurodegenerative conditions including Alzheimer’s and chronic traumatic encephalopathy, a disorder linked to concussions and head trauma. All these diseases share a common feature: abnormal buildup of a protein called tau in the brains of patients. Progressive supranuclear palsy has no cure and is hard to diagnose. Although doctors may have heard of the disease, many know little about it. It was not described in medical literature until 1964 but some experts believe one of the earliest accounts of the debilitating illness appeared in an 1857 short story by Charles Dickens and his friend Wilke Collins: “A cadaverous man of measured speech. A man who seemed as unable to wink, as if his eyelids had been nailed to his forehead. A man whose eyes—two spots of fire—had no more motion than if they had been connected with the back of his skull by screws driven through them, and riveted and bolted outside among his gray hair. He had come in and shut the door, and he now sat down. He did not bend himself to sit as other people do, but seemed to sink bolt upright, as if in water, until the chair stopped him.” © 2016 Scientific American
Most available antidepressants do not help children and teenagers with serious mental health problems and some may be unsafe, experts have warned. A review of clinical trial evidence found that of 14 antidepressant drugs, only one, fluoxetine – marketed as Prozac – was better than a placebo at relieving the symptoms of young people with major depression. Another drug, venlafaxine, was associated with an increased risk of suicidal thoughts and suicide attempts. Blood test could identify people who will respond to antidepressants Read more But the authors stressed that the true effectiveness and safety of antidepressants taken by children and teenagers remained unclear because of the poor design and selective reporting of trials, which were mostly funded by drug companies. They recommended close monitoring of young people on antidepressants, regardless of what drugs they were prescribed, especially at the start of treatment. Professor Peng Xie, a member of the team from Chongqing Medical University in China, said: “The balance of risks and benefits of antidepressants for the treatment of major depression does not seem to offer a clear advantage in children and teenagers, with probably only the exception of fluoxetine.” Major depressive disorder affects around 3% of children aged six to 12 and 6% of teenagers aged 13 to 18. In 2004 the US Food and Drug Administration (FDA) issued a warning against the use of antidepressants in young people up to the age of 24 because of concerns about suicide risk. Yet the number of young people taking the drugs increased between 2005 and 2012, both in the US and UK, said the study authors writing in the Lancet medical journal. In the UK the proportion of children and teenagers aged 19 and under taking antidepressants rose from 0.7% to 1.1%. © 2016 Guardian News and Media Limited