Chapter 13. Memory, Learning, and Development
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Elizabeth Pennisi "What's for dinner?" The words roll off the tongue without even thinking about it—for adults, at least. But how do humans learn to speak as children? Now, a new study in mice shows how a gene, called FOXP2, implicated in a language disorder may have changed between humans and chimps to make learning to speak possible—or at least a little easier. As a uniquely human trait, language has long baffled evolutionary biologists. Not until FOXP2 was linked to a genetic disorder that caused problems in forming words could they even begin to study language’s roots in our genes. Soon after that discovery, a team at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, discovered that just two bases, the letters that make up DNA, distinguished the human and chimp versions of FOXP2. To try to determine how those changes influenced the gene's function, that group put the human version of the gene in mice. In 2009, they observed that these "humanized" mice produced more frequent and complex alarm calls, suggesting the human mutations may have been involved in the evolution of more complex speech. Another study showed that humanized mice have different activity in the part of the brain called the striatum, which is involved in learning, among other tasks. But the details of how the human FOXP2 mutations might affect real-world learning remained murky. To solve the mystery, the Max Planck researchers sent graduate student Christiane Schreiweis to work with Ann Graybiel, a neuroscientist at the Massachusetts Institute of Technology in Cambridge. She's an expert in testing mouse smarts by seeing how quickly they can learn to find rewards in mazes. © 2014 American Association for the Advancement of Science
By Linda Searing THE QUESTION Benzodiazepines such as Valium, Xanax and Ativan, widely prescribed to relieve anxiety and alleviate insomnia, are known to affect memory and cognition in the short term. Might they also have a more serious, longer-term effect on the brain? THIS STUDY analyzed data on 8,990 adults older than 66, including 1,796 with Alzheimer’s disease. In a five-to-10-year span before the start of the study, 3,767 of the participants (52 percent) had taken benzodiazepines. Overall, those who had taken the drugs were 51 percent more likely to have Alzheimer’s than were those who had never taken benzodiazepines. The longer people took the drugs, the greater their risk for Alzheimer’s. Those who took the drugs for less than 90 days had essentially the same risk as those who never took them. But risk nearly doubled for people who took them for longer than six months. Risk also was greater for longer-acting vs. shorter-acting benzodiazepines. WHO MAY BE AFFECTED? Adults, especially older people, who take benzodiazepines. The drugs have a calming effect on the body and work quickly, unlike antidepressants, which can take weeks to have an effect. The American Geriatrics Society lists benzodiazepines as inappropriate for treating older people for insomnia or agitation because of their negative effect on cognition seen in that age group and an increased likelihood of falls and accidents. However, some recent estimates note that roughly half of older adults take benzodiazepines. CAVEATS Some study participants may have been prescribed benzodiazepines to treat early symptoms of unrecognized dementia, which can include depression, anxiety and sleep disorders; the study authors noted that use of the drugs “might be an early marker of a condition associated with an increased risk of dementia and not the cause.”
By ANDREW POLLACK New York State’s attorney general filed an antitrust lawsuit on Monday seeking to stop a pharmaceutical company from forcing patients with Alzheimer’s disease to switch to a new version of a widely used drug. The lawsuit contends that the switch is designed to blunt competition from low-priced generic versions of the medication. Forest Laboratories, now owned by Actavis, announced in February that it would stop selling the existing tablet form of the drug, Namenda, in favor of new extended-release capsules called Namenda XR that can be taken once a day instead of twice. While the company said that patients preferred the newer drug, it has made little secret of its desire to switch all patients to the newer form, which has a longer patent life, before the old tablets face generic competition in July. The strategy would make it much harder for the generics to gain traction. The lawsuit, filed in Federal District Court in Manhattan, says the step is an illegal attempt by Forest to maintain its monopoly even after its patent expires. “A drug company manipulating vulnerable patients and forcing physicians to alter treatment plans unnecessarily, simply to protect corporate profits, is unethical and illegal,” the attorney general, Eric T. Schneiderman, said in a statement. A spokesman for Actavis said the company did not comment on pending litigation as a matter of policy. The company said that the once-a-day drug had “significant advantages” for patients and their caregivers. The lawsuit argues that the benefit of switching is not very great. It says the company decided to force the switch because it feared that not enough patients would switch voluntarily. © 2014 The New York Times Company
Link ID: 20078 - Posted: 09.16.2014
by Michael Slezak It's one of the biggest mysteries of Alzheimer's. The disease is associated with the formation of protein plaques in the brain, but why is it that some people with plaques seem not to have the disease? Research suggests that some people's brains are able to reorganise during the early stages of Alzheimer's, delaying the appearance of initial symptoms. The plaques in question are small mounds of a protein called beta-amyloid, and are found in the brains of people with Alzheimer's disease. Whether these plaques are a cause of the disease has been hotly debated. One reason for doubt is the appearance of plaques in many older people who have no symptoms Movie Cameraof dementia at all. Using fMRI to measure changes in blood flow around the brain, William Jagust from the University of California in Berkley and colleagues compared brain function in three groups of people without symptoms of dementia: 22 young people, 16 older people with beta-amyloid plaques and 33 older people without the plaques. He asked each of them to memorise a photographed scene while inside the machine. Jagust found that older people with plaques had increased blood flow – which means stronger activation of that brain area – in the regions of the brain that are usually activated during memory formation, compared with the older people who did not have plaques. The team then analysed whether this extra brain activation might be helping to compensate for the plaques. © Copyright Reed Business Information Ltd.
by Simon Makin Talking in your sleep might be annoying, but listening may yet prove useful. Researchers have shown that sleeping brains not only recognise words, but can also categorise them and respond in a previously defined way. This could one day help us learn more efficiently. Sleep appears to render most of us dead to the world, our senses temporarily suspended, but sleep researchers know this is a misleading impression. For instance, a study published in 2012 showed that sleeping people can learn to associate specific sounds and smells. Other work has demonstrated that presenting sounds or smells during sleep boosts performance on memory tasks – providing the sensory cues were also present during the initial learning. Now it seems the capabilities of sleeping brains stretch even further. A team led by Sid Kouider from the Ecole Normale Supérieur in Paris trained 18 volunteers to classify spoken words as either animal or object by pressing buttons with their right or left hand. Brain activity was recorded using EEG, allowing the researchers to measure the telltale spikes in activity that indicate the volunteers were preparing to move one of their hands. Since each hand is controlled by the motor cortex on the opposite side of the brain, these brainwaves can be matched to the intended hand just by looking at which side of the motor cortex is active. © Copyright Reed Business Information Ltd.
David Cyranoski A Japanese patient with a debilitating eye disease is about to become the first person to be treated with induced pluripotent stem cells, which have generated enthusiastic expectations and earned their inventor a Nobel Prize. A health-ministry committee has vetted researchers' safety tests and cleared the team to begin the experimental procedure. Masayo Takahashi, an ophthalmologist at the RIKEN Center for Developmental Biology (CDB) in Kobe, has been using induced pluripotent stem (iPS) cells to prepare a treatment for age-related macular degeneration. Unlike embryonic stem cells, iPS cells are produced from adult cells, so they can be genetically tailored to each recipient. They are capable of becoming any cell type in the body, and have the potential to treat a wide range of diseases. The CDB trial will be the first opportunity for the technology to prove its clinical value. In age-related macular degeneration, extra blood vessels form in the eye, destabilizing a supportive base layer of the retina known as the retinal pigment epithelium. This results in the loss of the light-sensitive photoreceptors that are anchored in the epithelium, and often leads to blindness. Takahashi took skin cells from people with the disease and converted them to iPS cells. She then coaxed these cells to become retinal pigment epithelium cells, and then to grow into thin sheets that can be transplanted to the damaged retina. Takahashi and her collaborators have shown in monkey studies1 that iPS cells generated from the recipients' own cells do not provoke an immune reaction that causes them to be rejected. There have been concerns that iPS cells could cause tumours, but Takahashi's team has found that to be unlikely in mice2 and monkeys1. © 2014 Nature Publishing Group
By Helen Briggs Health editor, BBC News website There may be a link between a rare blood type and memory loss in later life, American research suggests. People with AB blood, found in 4% of the population, appear more likely to develop thinking and memory problems than those with other blood groups. The study, published in Neurology, builds on previous research showing blood type may influence heart risk. A charity said the best way to keep the brain healthy was a balanced diet, regular exercise and not smoking. A US team led by Dr Mary Cushman, of the University of Vermont College of Medicine, Burlington, analysed data from about 30,000 US citizens aged 45 and above. It identified 495 participants who had developed thinking and memory problems, or cognitive impairment, during the three-year study. They were compared to 587 people with no cognitive problems. People with AB blood type made up 6% of the group who developed cognitive impairment, which is higher than the 4% found in the general population. They were 82% more likely to have difficulties with day-to-day memory, language and attention, which can signal the onset of dementia. However, the study did not look at the risk of dementia. The study supported the idea that having a certain blood group, such as O, may give a lower risk for cardiovascular disease, which in turn protected the brain, the researchers said. "Our study looks at blood type and risk of cognitive impairment, but several studies have shown that factors such as high blood pressure, high cholesterol and diabetes increase the risk of cognitive impairment and dementia," said Dr Cushman. BBC © 2014
Ian Sample, science editor Heartbreak can impair the immune system of older people and make them more prone to infections, researchers have found. Scientists said older people who had suffered a recent bereavement had poorer defences against bacteria, which could leave them more vulnerable to killer infections, such as pneumonia. Blood tests showed that the same group had imbalances in their stress hormones, which are known to have a direct impact on the body's ability to fight off bugs. Anna Phillips, a reader in behavioural medicine at Birmingham University, said the damaging effects of bereavement on the immune system were not seen in younger people, whose defences seemed more resilient. The finding suggests that in the weeks and months after the loss of a loved one, older people should keep in touch with their friends and family, and exercise and eat well, to reduce stress levels and boost their immune systems. "Bereavement is a really key stressor that happens to all of us at some point so it's worth being aware of the negative impact it can have on your health," Phillips said. "It's a key time to look after yourself in terms of your psychological and physical wellbeing. Don't try and cope by staying in, drinking more and exercising less. Try to cope by having social interactions, looking after yourself by keeping a certain level of fitness and eating well," she added. For her study, Phillips recruited people who had lost a loved one, either a spouse or family member, in the past two months. She then looked at how well bacteria-killing immune cells called neutrophils performed. © 2014 Guardian News and Media Limited
By Helen Briggs Health editor, BBC News website Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer's, research suggests. A study of older Canadian adults found that past benzodiazepine use for three months or more was linked to an increased risk (up to 51%) of dementia. NHS guidelines say the drugs should be used for eight to 12 weeks at most. The French-Canadian team says while the link is not definitive, it is another warning that treatments should not exceed three months. "Benzodiazepine use is associated with an increased risk of Alzheimer's disease," lead researcher, Sophie Billioti de Gage of the University of Bordeaux, France, and colleagues wrote in the BMJ. "Unwarranted long-term use of these drugs should be considered as a public health concern." The study involved about 2,000 cases of Alzheimer's disease in adults aged over 66 living in Quebec. All had been prescribed benzodiazepines. They were compared with about 7,000 healthy people of the same age living in the same community. While an increased risk was found in those on benzodiazepines, the nature of the link was unclear. Dr Eric Karran, director of research at Alzheimer's Research UK, said: "This study shows an apparent link between the use of benzodiazepines and Alzheimer's disease although it's hard to know the underlying reason behind the link. BBC © 2014
Ewen Callaway Researchers found 69 genes that correlate with higher educational attainment — and three of those also also appear to have a direct link to slightly better cognitive abilities. Scientists looking for the genes underlying intelligence are in for a slog. One of the largest, most rigorous genetic study of human cognition1 has turned up inconclusive findings, and experts concede that they will probably need to scour the genomes of more than 1 million people to confidently identify even a small genetic influence on intelligence and other behavioural traits. Studies of twins have repeatedly confirmed a genetic basis for intelligence, personality and other aspects of behaviour. But efforts to link IQ to specific variations in DNA have led to a slew of irreproducible results. Critics have alleged that some of these studies' methods were marred by wishful thinking and shoddy statistics. A sobering editorial in the January 2012 issue of Behavior Genetics2 declared that “it now seems likely that many of the published findings of the last decade are wrong or misleading and have not contributed to real advances in knowledge”. In 2011, an international collaboration of researchers launched an effort to bring more rigour to studies of how genes contribute to behaviour. The group, called the Social Sciences Genetic Association Consortium, aimed to do studies using practices borrowed from the medical genetics community, which emphasizes large numbers of participants, rigorous statistics and reproducibility. In a 2013 study3 comparing the genomes of more than 126,000 people, the group identified three gene variants associated with with how many years of schooling a person had gone through or whether they had attended university. But the effect of these variants was small — each variant correlated with roughly one additional month of schooling in people who had it compared with people who did not. © 2014 Nature Publishing Group
By C. CLAIBORNE RAY Q. Is there a difference between alcoholic dementia and “regular” dementia in the elderly? A. Dementia refers to the general category of diseases that cause acquired cognitive loss, usually in later life, said Dr. Mark S. Lachs, director of geriatrics for the NewYork-Presbyterian Healthcare System. Such loss has scores of possible causes, he said, but Alzheimer’s disease is the culprit in a vast majority of cases in the developed world. Alzheimer’s and what doctors call alcohol-related dementia affect parts of the brain cortex that control memory, language and the ability to follow motor commands. Because Alzheimer’s and excessive drinking are relatively common in the older population and can occur at the same time, and because many of their clinical features overlap and affect similar parts of the brain, “it is more accurate to say that each condition potentially exacerbates the other,” Dr. Lachs said. Abstinence is the treatment of choice in alcohol-related dementia, with or without concurrent Alzheimer’s disease or another form of dementia. Even in patients with “pure” Alzheimer’s disease or another kind of dementia, Dr. Lachs said, most experts recommend greatly moderating alcohol consumption or eliminating it, as even occasional drinking “can serve as a brain stress test for a patient with impaired cognition from any cause.” © 2014 The New York Times Company
By Maggie Fox, Erika Edwards and Judy Silverman Here’s how you might be able to turn autism around in a baby: Carefully watch her cues, and push just a little harder with that game of peek-a-boo or “This little piggy.” But don’t push too hard — kids with autism are super-sensitive. That’s what Sally Rogers of the University of California, Davis has found in an intense experiment with the parents of infants who showed clear signs of autism. It’s one of the most hopeful signs yet that if you diagnose autism very early, you can help children rewire their brains and reverse the symptoms. It was a small study, and it’s very hard to find infants who are likely to have autism, which is usually diagnosed in the toddler years. But the findings, published in the Journal of Autism and Developmental Disorders, offer some hope to parents worried about their babies. “With only seven infants in the treatment group, no conclusions can be drawn,” they wrote. However, the effects were striking. Six out of the seven children in the study had normal learning and language skills by the time they were 2 to 3. Isobel was one of them. “She is 3 years old now and she is a 100 percent typical, normally developing child,” her mother, Megan, told NBC News. The family doesn’t want their last name used for privacy reasons. “We don’t have to do the therapy any more. It literally rewired her brain.” Autism is a very common diagnosis for children in the U.S. The latest survey by the Centers for Disease Control and Prevention shows a startling 30 percent jump among 8-year-olds diagnosed with the disorder in a two-year period, to one in every 68 children.
Link ID: 20047 - Posted: 09.09.2014
By BENEDICT CAREY Imagine that on Day 1 of a difficult course, before you studied a single thing, you got hold of the final exam. The motherlode itself, full text, right there in your email inbox — attached mistakenly by the teacher, perhaps, or poached by a campus hacker. No answer key, no notes or guidelines. Just the questions. Would that help you study more effectively? Of course it would. You would read the questions carefully. You would know exactly what to focus on in your notes. Your ears would perk up anytime the teacher mentioned something relevant to a specific question. You would search the textbook for its discussion of each question. If you were thorough, you would have memorized the answer to every item before the course ended. On the day of that final, you would be the first to finish, sauntering out with an A+ in your pocket. And you would be cheating. But what if, instead, you took a test on Day 1 that was just as comprehensive as the final but not a replica? You would bomb the thing, for sure. You might not understand a single question. And yet as disorienting as that experience might feel, it would alter how you subsequently tuned into the course itself — and could sharply improve your overall performance. This is the idea behind pretesting, one of the most exciting developments in learning-science. Across a variety of experiments, psychologists have found that, in some circumstances, wrong answers on a pretest aren’t merely useless guesses. Rather, the attempts themselves change how we think about and store the information contained in the questions. On some kinds of tests, particularly multiple-choice, we benefit from answering incorrectly by, in effect, priming our brain for what’s coming later. That is: The (bombed) pretest drives home the information in a way that studying as usual does not. We fail, but we fail forward. © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 20043 - Posted: 09.08.2014
by Sandrine Ceurstemont Screening an instructional monkey movie in a forest reveals that marmosets do not only learn from family members: they also copy on-screen strangers. It is the first time such a video has been used for investigations in the wild. Tina Gunhold at the University of Vienna, Austria, and her colleagues filmed a common marmoset retrieving a treat from a plastic device. They then took the device to the Atlantic Forest near Aldeia in Pernambuco, Brazil, and showed the movie to wild marmosets there. Although monkeys are known to learn from others in their social group, especially when they are youngMovie Camera, little is known about their ability to learn from monkeys that do not belong to the same group. Marmosets are territorial, so the presence of an outsider – even a virtual one on a screen – could provoke an attack. "We didn't know if wild marmosets would be frightened of the video box but actually they were all attracted to it," says Gunhold. Compared to monkeys shown a static image of the stranger, video-watching marmosets were more likely to manipulate the device, typically copying the technique shown (see video). Young monkeys spent more time near the video box than older family members, suggesting that they found the movie more engaging – although as soon as one monkey mastered the task, it was impossible to tell whether the others were learning from the video or from their relative. "We think it's a combination of both," says Gunhold. © Copyright Reed Business Information Ltd.
By Fredrick Kunkle Years ago, many scientists assumed that a woman’s heart worked pretty much the same as a man’s. But as more women entered the male-dominated field of cardiology, many such assumptions vanished, opening the way for new approaches to research and treatment. A similar shift is underway in the study of Alzheimer’s disease. It has long been known that more women than men get the deadly neurodegenerative disease, and an emerging body of research is challenging the common wisdom as to why. Although the question is by no means settled, recent findings suggest that biological, genetic and even cultural influences may play heavy roles. Of the more than 5 million people in the United States who have been diagnosed with Alzheimer’s, the leading cause of dementia, two-thirds are women. Because advancing age is considered the biggest risk factor for the disease, researchers largely have attributed that disparity to women’s longer life spans. The average life expectancy for women is 81 years, compared with 76 for men. Yet “even after taking age into account, women are more at risk,” said Richard Lipton, a physician who heads the Einstein Aging Study at Albert Einstein College of Medicine in New York. With the number of Alzheimer’s cases in the United States expected to more than triple by 2050, some researchers are urging a greater focus on understanding the underlying reasons women are more prone to the disease and on developing gender-specific treatments. The area of inquiry has been growing in part because of a push by female Alzheimer’s researchers, who have formed a group to advocate for a larger leadership role in the field and more gender-specific research.
By Kate Wong In 1871 Charles Darwin surmised that humans were evolutionarily closer to the African apes than to any other species alive. The recent sequencing of the gorilla, chimpanzee and bonobo genomes confirms that supposition and provides a clearer view of how we are connected: chimps and bonobos in particular take pride of place as our nearest living relatives, sharing approximately 99 percent of our DNA, with gorillas trailing at 98 percent. Yet that tiny portion of unshared DNA makes a world of difference: it gives us, for instance, our bipedal stance and the ability to plan missions to Mars. Scientists do not yet know how most of the DNA that is uniquely ours affects gene function. But they can conduct whole-genome analyses—with intriguing results. For example, comparing the 33 percent of our genome that codes for proteins with our relatives' genomes reveals that although the sum total of our genetic differences is small, the individual differences pervade the genome, affecting each of our chromosomes in numerous ways. © 2014 Scientific American
By Virginia Morell Figaro, a Goffin’s cockatoo (Cacatua goffini) housed at a research lab in Austria, stunned scientists a few years ago when he began spontaneously making stick tools from the wooden beams of his aviary. The Indonesian parrots are not known to use tools in the wild, yet Figaro confidently employed his sticks to rake in nuts outside his wire enclosure. Wondering if Figaro’s fellow cockatoos could learn by watching his methods, scientists set up experiments for a dozen of them. One group watched as Figaro used a stick to reach a nut placed inside an acrylic box with a wire-mesh front panel; others saw “ghost demonstrators”—magnets that were hidden beneath a table and that the researchers controlled—displace the treats. Each bird was then placed in front of the box, with a stick just like Figaro’s lying nearby. The group of three males and three females that had watched Figaro also picked up the sticks, and made some efforts reminiscent of his actions. But only those three males, such as the one in the photo above, became proficient with the tool and successfully retrieved the nuts, the scientists report online today in the Proceedings of the Royal Society B. None of the females did so; nor did any of the birds, male or female, in the ghost demonstrator group. Because the latter group failed entirely, the study shows that the birds need living teachers, the scientists say. Intriguingly, the clever observers developed a better technique than Figaro’s for getting the treat. Thus, the cockatoos weren’t copying his exact actions, but emulating them—a distinction that implies some degree of creativity. Two of the successful cockatoos were later given a chance to make a tool of their own. One did so immediately (as in the video above), and the other succeeded after watching Figaro. It may be that by learning to use a tool, the birds are stimulated to make tools of their own, the scientists say. © 2014 American Association for the Advancement of Science.
Keyword: Learning & Memory
Link ID: 20027 - Posted: 09.03.2014
by Chris Higgins Neuroscientists have pinpointed where imagination hides in the brain and found it to be functionally distinct from related processes such as memory. The team from Brigham Young University (BYU), Utah-- including research proposer, undergraduate student Stefania Ashby -- used functional Magnetic Resonance Imaging (fMRI) to observe brain activity when subjects were remembering specific experiences and putting themselves in novel ones. "I was thinking a lot about planning for my own future and imagining myself in the future, and I started wondering how memory and imagination work together," Ashby said. "I wondered if they were separate or if imagination is just taking past memories and combining them in different ways to form something I've never experienced before." The two processes of remembering and imagining have been previously proposed to be the same cognitive task, and so thought to be carried out by the same areas of the brain. However, the experiments derived by Ashby and her mentor (and coauthor) BYU professor Brock Kirwan have refuted these ideas. The studies -- published in the journal Cognitive Neuroscience -- required participants to submit 60 photographs of previous life events and use them to create prompts for the "remember" sections. They then carried out a questionnaire before putting the subject into the MRI scanner to determine what scenarios were the most novel to them and force them into imagination. Then, under fMRI testing, the subjects were prompted with various scenarios and the areas of their brain that became active during each scenario was correlated with each scene's familiarity -- pure memory, or imagination. © Condé Nast UK 2014
By JOHN ROGERS LOS ANGELES (AP) — The founder of a Los Angeles-based nonprofit that provides free music lessons to low-income students from gang-ridden neighborhoods began to notice several years ago a hopeful sign: Kids were graduating high school and heading off to UCLA, Tulane and other big universities. That’s when Margaret Martin asked how the children in the Harmony Project were beating the odds. Researchers at Northwestern University in Illinois believe that the students’ music training played a role in their educational achievement, helping as Martin noticed 90 percent of them graduate from high school while 50 percent or more didn’t from those same neighborhoods. A two-year study of 44 children in the program shows that the training changes the brain in ways that make it easier for youngsters to process sounds, according to results reported in Tuesday’s edition of The Journal of Neuroscience. That increased ability, the researchers say, is linked directly to improved skills in such subjects as reading and speech. But, there is one catch: People have to actually play an instrument to get smarter. They can’t just crank up the tunes on their iPod. Nina Kraus, the study’s lead researcher and director of Northwestern’s auditory neuroscience laboratory, compared the difference to that of building up one’s body through exercise. ‘‘I like to say to people: You’re not going to get physically fit just watching sports,’’ she said.
By RONI CARYN RABIN Pregnant women often go to great lengths to give their babies a healthy start in life. They quit smoking, skip the chardonnay, switch to decaf, forgo aspirin. They say no to swordfish and politely decline Brie. Yet they rarely wean themselves from popular selective serotonin reuptake inhibitor antidepressants like Prozac, Celexa and Zoloft despite an increasing number of studies linking prenatal exposure to birth defects, complications after birth and even developmental delays and autism. Up to 14 percent of pregnant women take antidepressants, and the Food and Drug Administration has issued strong warnings that one of them, paroxetine (Paxil), may cause birth defects. But the prevailing attitude among doctors has been that depression during pregnancy is more dangerous to mother and child than any drug could be. Now a growing number of critics are challenging that assumption. “If antidepressants made such a big difference, and women on them were eating better, sleeping better and taking better care of themselves, then one would expect to see better birth outcomes among the women who took medication than among similar women who did not,” said Barbara Mintzes, an associate professor at the University of British Columbia School of Population and Public Health. “What’s striking is that there’s no research evidence showing that.” On the contrary, she said, “when you look for it, all you find are harms.” S.S.R.I.s are believed to work in part by blocking reabsorption (or reuptake) of serotonin, altering levels of this important neurotransmitter in the brain and elsewhere in the body. Taken by a pregnant woman, the drugs cross the placental barrier, affecting the fetus. © 2014 The New York Times Company