Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

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

Links 1 - 20 of 2779

By Emily Underwood Alert! “Cats Can Literally Make You Crazy.” Wait! “Cats Don't Cause Mental Illness.” The news headlines are as alarming as they are contradictory. All refer to Toxoplasma gondii, a brain parasite carried by our feline companions that infects roughly one in three people. Scientists have long hypothesized that T. gondii plays a role in mental illness, including schizophrenia. But though more than 100 studies have found a correlation, none has shown that the parasite actually causes mental illness. So what’s really going on? Here’s what you need to know: T. gondii is not a bacterium or a virus, but a single-celled microscopic organism distantly related to the parasite that causes malaria. Cats get T. gondii and the disease it causes, toxoplasmosis, by eating infected rodents, birds, and other animals. Estimates suggest about 40% of cats in the United States are infected; most don’t show any symptoms, but they can develop jaundice or blindness and experience personality changes if the parasite spreads to the liver or nervous system. In the first few weeks after infection, a cat can shed millions of hardy egg pods called oocysts into its litterbox each day. Although some people get toxoplasmosis from direct contact with domestic cats and cat feces, many more are infected when oocysts shed by cats make it into the soil and water, where they can survive for a year or longer. © 2019 American Association for the Advancement of Science.

Keyword: Schizophrenia; Neuroimmunology
Link ID: 25968 - Posted: 02.15.2019

Sara Reardon A form of the hallucinogenic party drug ketamine has cleared one of the final hurdles toward clinical use as an antidepressant. At a 12 February meeting at the US Food and Drug Administration (FDA) in Silver Spring, Maryland, an independent advisory panel voted 14-2 in favour of recommending a compound known as esketamine for use in treating depression. If the FDA approves the drug, it could buoy the chances of other ketamine-inspired treatments currently under development. But questions remain about esketamine’s overall effectiveness at lifting mood and its potential to be abused. Mental health researchers rejoiced at the news. “I’m still a little bit in shock,” says James Murrough, a psychiatrist at Mount Sinai Hospital in New York City.If approved, esketamine would be the first truly novel antidepressant to enter the market in several decades. “If this comes to pass, we’ll have done what people have been quick to point out hasn’t been done since the original discovery of antidepressants.” The FDA is expected to make a decision on esketamine by 4 March. Researchers discovered ketamine’s antidepressant properties in the early 2000s. It’s unclear how ketamine, which is a mixture of two molecules that are mirror images of each other, works in the brain. But scientists do know that it acts extremely quickly to alleviate symptoms of depression — in a matter of hours as opposed to weeks — and in a very different way than other drugs approved to treat depression. © 2019 Springer Nature Publishing AG

Keyword: Depression
Link ID: 25960 - Posted: 02.13.2019

By Pam Belluck For the first time, a national health panel has recommended a way to prevent depression during and after pregnancy. This condition, known as perinatal depression, affects up to one in seven women and is considered the most common complication of pregnancy. The panel, the United States Preventive Services Task Force, said two types of counseling can help keep symptoms at bay. Its recommendation means that under the Affordable Care Act, such counseling must be covered by insurance with no co-payment. Here’s a guide to what to look for and how to get help. What is perinatal depression and what are the signs that you or a loved one might be experiencing it? Perinatal depression can occur during pregnancy or any time within a year after childbirth. As defined by the panel, it can involve major or minor depressive symptoms that last for at least two weeks, including loss of energy or concentration, changes in sleeping and eating patterns, feelings of worthlessness or suicidal thoughts. It’s not the same as the “baby blues,” which is less severe and doesn’t last as long. The panel said “baby blues” can occur right after childbirth and can include crying, irritability, fatigue and anxiety, symptoms that usually disappear within 10 days. Many things can raise a woman’s risk of depression during and after pregnancy. Having a personal or family history of depression is a significant risk factor. Others include a range of experiences that can generate stress: recent divorce or relationship strain; being a victim of abuse or domestic violence; being a single mother or a teenager; having an unplanned or unwanted pregnancy. Economic burdens increase the risk — about one in three low-income women develops depression during or after pregnancy. © 2019 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 25959 - Posted: 02.13.2019

By Gretchen Reynolds Jogging for 15 minutes a day, or walking or gardening for somewhat longer, could help protect people against developing depression, according to an innovative new study published last month in JAMA Psychiatry. The study involved hundreds of thousands of people and used a type of statistical analysis to establish, for the first time, that physical activity may help prevent depression, a finding with considerable relevance for any of us interested in maintaining or bolstering our mental health. Plenty of past studies have examined the connections between exercise, moods and psychological well-being, of course. And most have concluded that physically active people tend to be happier and less prone to anxiety and severe depression than people who seldom move much. But those past studies showed only that exercise and depression are linked, not that exercise actually causes a drop in depression risk. Most were longitudinal or cross-sectional, looking at people’s exercise habits over a certain period or at a single point of time and then determining whether there might be statistical relationships between the two. In other words, active people might be less likely to become depressed than inactive people. But it’s also possible that people who aren’t prone to depression may be more likely to exercise. Those types of studies may be tantalizing, but they can’t prove anything about cause and effect. To show causation, scientists rely on randomized experiments, during which they assign people to, for instance, exercise or not and then monitor the outcomes. Researchers have been using randomized trials to look at whether exercise can treat depression after people already have developed the condition, and the results have been encouraging. © 2019 The New York Times Company

Keyword: Depression
Link ID: 25956 - Posted: 02.13.2019

By Ricardo Muñoz More than 300 million individuals worldwide suffer from major depression. About 16 million of them are in the U.S., where 90 percent report difficulties with work, home or social activities related to their symptoms. While there are many effective treatments for depression, including medications and psychological therapies, the rate of depression is not going down, and treatment is not enough to reduce the burden. Recently, research has emerged indicating that about half of all cases of depression are preventable. Yet we’re not doing much to prevent it. In much the same way we vaccinate against other debilitating diseases, it is our moral obligation to begin concerted prevention efforts to reduce the number of new cases of depression in our communities. Depression is the number one cause of disability worldwide. It produces substantial suffering not only for the depressed individual, but also for those around them—when it leads to suicide, the impact on surviving loved ones is devastating. Depression is also related to a number of other health problems. Take smoking, for example, which is the leading cause of preventable death in the world, and how it is affected by depression. People who suffer from depression are more likely to start smoking, less likely to quit, and, if they quit, more likely to start again. This is the case with the use of alcohol and other drugs as well. Adolescent girls who have suffered at least one episode of major depression have a greater probability of having sexual relations as teenagers, having more than one sexual partner and having unintended pregnancies. © 2019 Scientific American

Keyword: Depression
Link ID: 25953 - Posted: 02.12.2019

Adrian Woolfson Globally, the burden of depression and other mental-health conditions is on the rise. In North America and Europe alone, mental illness accounts for up to 40% of all years lost to disability. And molecular medicine, which has seen huge success in treating diseases such as cancer, has failed to stem the tide. Into that alarming context enters the thought-provoking Good Reasons for Bad Feelings, in which evolutionary psychiatrist Randolph Nesse offers insights that radically reframe psychiatric conditions. In his view, the roots of mental illnesses, such as anxiety and depression, lie in essential functions that evolved as building blocks of adaptive behavioural and cognitive function. Furthermore, like the legs of thoroughbred racehorses — selected for length, but tending towards weakness — some dysfunctional aspects of mental function might have originated with selection for unrelated traits, such as cognitive capacity. Intrinsic vulnerabilities in the human mind could be a trade-off for optimizing unrelated features. Similar ideas have surfaced before, in different contexts. Evolutionary biologists Stephen Jay Gould and Richard Lewontin, for example, critically examined the blind faith of ‘adaptationist’ evolutionary theorizing. Their classic 1979 paper ‘The spandrels of San Marco and the Panglossian paradigm’ challenged the idea that every aspect of an organism has been perfected by natural selection (S. J. Gould et al. Proc. R. Soc. Lond. B 205, 581–598; 1979). Instead, like the curved triangles of masonry between arches supporting domes in medieval and Renaissance architecture, some parts are contingent structural by-products. These might have no discernible adaptive advantage, or might even be maladaptive. Gould and Lewontin’s intuition has, to some extent, been vindicated by molecular genetics. Certain versions of the primitive immune-system protein complement 4A, for instance, evolved for reasons unrelated to mental function, and yet are associated with an increased risk of schizophrenia. © 2019 Springer Nature Publishing AG

Keyword: Depression; Schizophrenia
Link ID: 25946 - Posted: 02.11.2019

Sujata Gupta The task was designed to scare the kids. One by one, adults guided children, ranging in age from 3 to 7, into a dimly lit room containing a mysterious covered mound. To build anticipation, the adults intoned, “I have something in here to show you,” or “Let’s be quiet so it doesn’t wake up.” The adult then uncovered the mound — revealed to be a terrarium — and pulled out a realistic looking plastic snake. Throughout the 90-second setup, each child wore a small motion sensor affixed to his or her belt. Those sensors measured the child’s movements, such as when they sped up or twisted around, at 100 times per second. Researchers wanted to see if the movements during a scary situation differed between children diagnosed with depression or anxiety and children without such a diagnosis. It turns out they did. Children with a diagnosis turned further away from the perceived threat — the covered terrarium — than those without a diagnosis. In fact, the sensors could identify very young children who have depression or anxiety about 80 percent of the time, researchers report January 16 in PLOS One. Such a tool could be useful because, even as it’s become widely accepted that children as young as age 3 can suffer from mental health disorders, diagnosis remains difficult. Such children often escape notice because they hold their emotions inside. It’s increasingly clear, though, that these children are at risk of mental and physical health problems later in life, says Lisabeth DiLalla, a developmental psychologist at Southern Illinois University School of Medicine in Carbondale. “The question is: ‘Can we turn that around?’” |© Society for Science & the Public 2000 - 2019

Keyword: Development of the Brain; Depression
Link ID: 25936 - Posted: 02.06.2019

By Elizabeth Pennisi Of all the many ways the teeming ecosystem of microbes in a person’s gut and other tissues might affect health, its potential influences on the brain may be the most provocative. Now, a study of two large groups of Europeans has found several species of gut bacteria are missing in people with depression. The researchers can’t say whether the absence is a cause or an effect of the illness, but they showed that many gut bacteria could make substances that affect nerve cell function—and maybe mood. “It’s the first real stab at tracking how” a microbe’s chemicals might affect mood in humans, says John Cryan, a neuroscientist at University College Cork in Ireland who has been one of the most vocal proponents of a microbiome-brain connection. The study “really pushes the field from where it’s been” with small studies of depressed people or animal experiments. Interventions based on the gut microbiome are now under investigation: The University of Basel in Switzerland, for example, is planning a trial of fecal transplants, which can restore or alter the gut microbiome, in depressed people. Several studies in mice had indicated that gut microbes can affect behavior, and small studies of people suggested this microbial repertoire is altered in depression. To test the link in a larger group, Jeroen Raes, a microbiologist at the Catholic University of Leuven in Belgium, and his colleagues took a closer look at 1054 Belgians they had recruited to assess a “normal” microbiome. Some in the group—173 in total—had been diagnosed with depression or had done poorly on a quality of life survey, and the team compared their microbiomes with those other participants. Two kinds of microbes, Coprococcus and Dialister, were missing from the microbiomes of the depressed subjects, but not from those with a high quality of life. The finding held up when the researchers allowed for factors such as age, sex, or antidepressant use, all of which influence the microbiome, the team reports today in Nature Microbiology. They also found the depressed people had an increase in bacteria implicated in Crohn disease, suggesting inflammation may be at fault. © 2018 American Association for the Advancement of Science

Keyword: Depression
Link ID: 25932 - Posted: 02.05.2019

by Esmé Weijun Wang "Schizophrenia terrifies." Those are the first two words of The Collected Schizophrenias, Esmé Weijun Wang's new book — part memoir, part scientific chronicle of her journey towards a diagnosis of schizoaffective disorder. She first noticed that her brain worked differently than others, she says, when she was just five or six years old. And then, she says, "severe depression started when I was about 11, depression that was diagnosed by a doctor probably happened when I was 15 or 16. Bipolar disorder was diagnosed when I was about 17 or 18, and then the schizoaffective disorder, bipolar type, was diagnosed when I was in my late 20s." Interview Highlights On her experience of schizoaffective disorder I like to kind of jokingly say that it's like a marriage between schizophrenia and bipolar disorder. So my first hallucination that I ever had was actually when I was in the shower in college, and I heard a voice very clearly say to me, "I hate you." And it was so clear to me, and this is why I say that hallucinations really effectively kidnap the senses, because it's exactly like someone is standing next to you and saying this thing to you. And I started thinking, oh, is there something going on with the pipes, where I can hear maybe something on the floor below me, or maybe the floor above me, but it didn't really make sense to me physically, so I started thinking, maybe this is a hallucination, and it kind of went off from there ... and then later I started having delusions in which I was believing that my loved ones were replaced by doubles, or replaced by robots — so it's been an interesting journey. © 2019 npr

Keyword: Schizophrenia
Link ID: 25929 - Posted: 02.04.2019

By Benedict Carey The world’s most common digital habit is not easy to break, even in a fit of moral outrage over the privacy risks and political divisions Facebook has created, or amid concerns about how the habit might affect emotional health. Although four in 10 Facebook users say they have taken long breaks from it, the digital platform keeps growing. A recent study found that the average user would have to be paid $1,000 to $2,000 to be pried away for a year. So what happens if you actually do quit? A new study, the most comprehensive to date, offers a preview. Expect the consequences to be fairly immediate: More in-person time with friends and family. Less political knowledge, but also less partisan fever. A small bump in one’s daily moods and life satisfaction. And, for the average Facebook user, an extra hour a day of downtime. The study, by researchers at Stanford University and New York University, helps clarify the ceaseless debate over Facebook’s influence on the behavior, thinking and politics of its active monthly users, who number some 2.3 billion worldwide. The study was posted recently on the Social Science Research Network, an open access site. “For me, Facebook is one of those compulsive things,” said Aaron Kelly, 23, a college student in Madison, Wis. “It’s really useful, but I always felt like I was wasting time on it, distracting myself from study, using it whenever I got bored.” Mr. Kelly, who estimated that he spent about an hour a day on the platform, took part in the study “because it was kind of nice to have an excuse to deactivate and see what happened,” he said. Well before news broke that Facebook had shared users’ data without consent, scientists and habitual users debated how the platform had changed the experience of daily life. A cadre of psychologists has argued for years that the use of Facebook and other social media is linked to mental distress, especially in adolescents. Others have likened habitual Facebook use to a mental disorder, comparing it to drug addiction and even publishing magnetic-resonance images of what Facebook addiction “looks like in the brain.” © 2019 The New York Times Company

Keyword: Attention; Depression
Link ID: 25919 - Posted: 01.31.2019

By Carl Zimmer In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body. Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease. The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled. A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions. For some neuroscientists, new studies have changed the way they think about the brain. One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test. “It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.” He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia. Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too. © 2019 The New York Times Company

Keyword: Obesity; Depression
Link ID: 25915 - Posted: 01.29.2019

/ By Dave Levitan Scientific research on the effects of marijuana is rife with holes, thanks in large part to it still being categorized at the federal level alongside drugs such as heroin and LSD. Unfortunately, when research is scarce, it becomes easier to mislead people through cherry-picked data, sneaky word choice, and misinterpreted conclusions. On virtually every issue in his 272-page book, Adam Berenson commits one of the most common logical errors: He mixes up correlation and causation. Which brings us to Alex Berenson and Malcolm Gladwell, and what happens when tidy narratives outrun the science. Two weeks ago, Berenson, a former New York Times reporter and subsequent spy novelist, published a book with the ominous title “Tell Your Children: The Truth about Marijuana, Mental Illness, and Violence.” Gladwell, meanwhile, published a feature in the New Yorker, where he is a staff writer, drawing largely on Berenson’s book and questioning the supposed consensus that weed is among the safest drugs. Combined, these two works offer a master class in statistical malfeasance and a smorgasbord of logical fallacies and data-free fear-mongering that serve only to muddle an issue that, as experts point out, needs far more good-faith research. Berenson’s main argument is relatively simple. In his book, he claims, essentially, that the existing evidence really does contain solid answers, painting a truly alarming picture about marijuana: That it can and does cause psychosis and schizophrenia. He then makes the leap that since psychosis and schizophrenia can lead to violence, marijuana itself is causing violence to increase in the United States and elsewhere. Copyright 2019 Undark

Keyword: Drug Abuse; Schizophrenia
Link ID: 25892 - Posted: 01.22.2019

Alison Abbott Neuroscientists have for the first time discovered differences between the ‘software’ of humans and monkey brains, using a technique that tracks single neurons. They found that human brains trade off ‘robustness’ — a measure of how synchronized neuron signals are — for greater efficiency in information processing. The researchers hypothesize that the results might help to explain humans’ unique intelligence, as well as their susceptibility to psychiatric disorders. The findings were published in Cell1 on 17 January. Scientists say that this type of unusual study could help them to better translate research in animal models of psychiatric diseases into the clinic. The research exploited a rare set of data on the activity of single neurons collected deep in the brains of people with epilepsy who were undergoing neurosurgery to identify the origin of their condition. The technique is so difficult that only a handful of clinics around the world can participate in this type of research. The study also used similar, existing data from three monkeys and collected neuron information from two more. Over the decades, neuroscientists have discovered many subtle and significant differences in the anatomy — the hardware — of the brains of humans and other primates. But the latest study looked instead at differences in brain signals. © 2019 Springer Nature Publishing AG

Keyword: Schizophrenia; Epilepsy
Link ID: 25889 - Posted: 01.21.2019

By Benedict Carey Nearly a century after the film “Reefer Madness” alarmed the nation, some policymakers and doctors are again becoming concerned about the dangers of marijuana, although the reefers are long gone. Experts now distinguish between the “new cannabis” — legal, highly potent, available in tabs, edibles and vapes — and the old version, a far milder weed passed around in joints. Levels of T.H.C., the chemical that produces marijuana’s high, have been rising for at least three decades, and it’s now possible in some states to buy vape cartridges containing little but the active ingredient. The concern is focused largely on the link between heavy usage and psychosis in young people. Doctors first suspected a link some 70 years ago, and the evidence has only accumulated since then. In a forthcoming book, “Tell Your Children,” Alex Berenson, a former Times reporter, argues that legalization is putting a generation at higher risk of schizophrenia and other psychotic syndromes. Critics, including leading researchers, have called the argument overblown, and unfaithful to the science. Can cannabis use cause psychosis? Yes, but so can overuse of caffeine, nicotine, alcohol, stimulants and hallucinogens. Psychosis is a symptom: a temporary disorientation that resembles a waking dream, with odd, imagined sights and sounds, often accompanied by paranoia or an ominous sensation. The vast majority of people who have this kind of psychotic experience do not go on to develop a persistent condition such as schizophrenia, which is characterized by episodes of psychosis that recur for years, as well as cognitive problems and social withdrawal. © 2019 The New York Times Company

Keyword: Drug Abuse; Schizophrenia
Link ID: 25875 - Posted: 01.18.2019

By Alex Berenson Marijuana seems to be on an unstoppable march to legalization in the United States. New York and New Jersey are racing to join the 10 states that already allow recreational use of cannabis. Some 65 percent of Americans favor legalization, and several potential Democratic candidates for president support ending federal prohibitions on marijuana. This huge shift in public attitudes comes even though most Americans do not use the drug. Only 15 percent of people over 12 used it even once in 2017, according to a large federal survey. That year, only three million people tried it for the first time. Instead, the change has been largely driven by decadeslong lobbying by marijuana legalization advocates and for-profit cannabis companies. Those groups have shrewdly recast marijuana as a medicine rather than an intoxicant. Some have even claimed that marijuana can help slow the opioid epidemic, though studies show that people who use cannabis are more likely to start using opioids later. Meanwhile, legalization advocates have squelched discussion of the serious mental health risks of marijuana and THC, the chemical responsible for the drug’s psychoactive effects. As I have seen firsthand in writing a book about cannabis, anyone who raises those concerns may be mocked as a modern-day believer in “Reefer Madness,” the notorious 1936 movie that portrays young people descending into insanity and violence after smoking marijuana. A strange disconnect has resulted. With large studies in peer-reviewed journals showing that marijuana increases the risk of psychosis and schizophrenia, the scientific literature around the drug is far more negative than it was 20 years ago. Comparing two major reports from the National Academy of Medicine, the nonprofit group that advises the federal government on health and medicine, makes the difference clear. © 2019 The New York Times Company

Keyword: Drug Abuse; Schizophrenia
Link ID: 25843 - Posted: 01.07.2019

By Jocelyn Kaiser, Ann Gibbons In early 2017, epidemiologist Rory Collins at the University of Oxford in the United Kingdom and his team faced a test of their principles. They run the UK Biobank (UKB), a huge research project probing the health and genetics of 500,000 British people. They were planning their most sought-after data release yet: genetic profiles for all half-million participants. Three hundred research groups had signed up to download 8 terabytes of data—the equivalent of more than 5000 streamed movies. That's enough to tie up a home computer for weeks, threatening a key goal of the UKB: to give equal access to any qualified researcher in the world. "We wanted to create a level playing field" so that someone at a big center with a supercomputer was at no more of an advantage than a postdoc in Scotland with a smaller computer and slower internet link, says Oxford's Naomi Allen, the project's chief epidemiologist. They came up with a plan: They gave researchers 3 weeks to download the encrypted files. Then, on 19 July 2017, they released a final encryption key, firing the starting gun for a scientific race. Within a couple of days, one U.S. group had done quick analyses linking more than 120,000 genetic markers to more than 2000 diseases and traits, data it eventually put up on a blog. Only 60,000 markers had previously been tied to disease, says human geneticist Eric Lander, president and director of the Broad Institute in Cambridge, Massachusetts. "[They] doubled that in a week." © 2018 American Association for the Advancement of Science

Keyword: Genes & Behavior; Depression
Link ID: 25841 - Posted: 01.05.2019

By Consumer Reports s has no financial relationship with any advertisers on this site. All medications have the potential to cause unwanted side effects, and depression is among them. One-third of Americans are now taking meds that can cause this mood disorder, according to a study published in the Journal of the American Medical Association in June. Other research has had similar findings, but this is the largest review on the topic to date. The study authors found that about 200 prescription drugs, including some often used by older adults — such as proton-pump inhibitors (PPIs) to treat acid reflux and beta blockers for hypertension — can lead to depression. But doctors may not know this. “Many physicians may not be aware that several commonly prescribed medications are associated with an increased risk of this disorder,” says study author Mark Olfson, professor of psychiatry and epidemiology at the Columbia University Irving Medical Center in New York. In the study, the more drugs people took, the higher their depression risk. About 7 percent of those taking one such drug were depressed compared with 15.3 percent of those taking at least three. This is concerning for older adults, who may take multiple medications and are more vulnerable to drug side effects, says Michael Hochman, an associate professor of clinical medicine at Keck Medicine at the University of Southern California in Los Angeles. © 1996-2018 The Washington Post

Keyword: Depression
Link ID: 25825 - Posted: 12.26.2018

Cheryl Platzman Weinstock Sometimes a psychiatric crisis can be triggered by something small. For Alexia Phillips, 21, it was a heated argument with a close family member in February 2017. She remembers the fight blew up before she left the house to go to classes at Queens College in Flushing, New York. By midday, Phillips, then a sophomore, says she began to cry loudly and uncontrollably. "It really triggered me. I just got really angry really fast...I was crying so much I couldn't breathe and couldn't talk. I didn't know how to handle it," she says. As she would come to understand later, Phillips was experiencing symptoms of her underlying borderline personality disorder, anxiety and depression. But at the time, all she knew was she felt too overwhelmed to go home, or to go to class. She also didn't want anyone to see her like that. Finally, she went to her college counseling center for the first time and asked for help. Minutes later, Phillips' counselor, a college public safety officer and a paramedic trained to deal with psychiatric crises, calmly and unobtrusively escorted her to the back of the college through a quiet hallway door that led out to a parked ambulance sent from Zucker Hillside Hospital. She was ferried — without the lights or sirens — to be assessed at the hospital's special program for college students. This kind of response to a student crisis is unusual. In a lot of colleges, if staff think the student who's having a crisis may be unsafe, they have little choice but to call 911. Many schools lack resources to address serious crises and students are left to navigate the health care system on their own. © 2018 npr

Keyword: Schizophrenia; Depression
Link ID: 25802 - Posted: 12.20.2018

Nicola Davis An overactive immune response appears to be a trigger for persistent fatigue, say researchers in a study that could shed light on the causes of chronic fatigue syndrome. Chronic fatigue syndrome (CFS) is a debilitating long-term condition in which individuals experience exhaustion that is not helped by rest, as well as pain, mental fogginess and trouble with memory and sleep. It is also known as myalgic encephalomyelitis (ME). Some studies into the condition have suggested the immune system could be involved, with viral infections one potential trigger for CFS. “The evidence is largely inconclusive – there are studies which have shown elevated levels of the inflammatory markers, but such abnormalities are quite inconsistent across studies,” said Alice Russell, first author of the research from King’s College London. Because it is not possible to predict who will get a virus, it is impossible to look at levels of biological molecules before, during and after a potential CFS “trigger” infection. Experts say they have used a group of people with a different condition as a model to explore how immune response might be linked to persistent fatigue. Writing in the journal Psychoneuroendocrinology, Russell and colleagues describe how they recruited 55 patients with a chronic hepatitis C infection. To treat the condition, all were given a six- to 12-month course of injections of interferon alpha, a protein that is produced naturally by the body and stimulates the white blood cells to provoke an immune response. The treatment has previously been linked to a side effect of ongoing fatigue in some patients. © 2018 Guardian News and Media Limited

Keyword: Neuroimmunology; Depression
Link ID: 25792 - Posted: 12.17.2018

By Benedict Carey For the past two decades, scientists have been exploring the genetics of schizophrenia, autism and other brain disorders, looking for a path toward causation. If the biological roots of such ailments could be identified, treatments might follow, or at least tests that could reveal a person’s risk level. In the 1990s, researchers focused on genes that might possibly be responsible for mental distress, but then hit a wall. Choosing so-called candidate genes up front proved to be fruitless. In the 2000s, using new techniques to sample the entire genome, scientists hit many walls: Hundreds of common gene variants seemed to contribute some risk, but no subset stood out. Even considered together, all of those potential contributing genes — some 360 have been identified for schizophrenia — offered nothing close to a test for added risk. The inherited predisposition was real; but the intricate mechanisms by which all those genes somehow led to symptoms such as psychosis or mania were a complete mystery. Now, using more advanced tools, brain scientists have begun to fill out the picture. In a series of 11 papers, published in Science and related journals, a consortium of researchers has produced the most richly detailed model of the brain’s genetic landscape to date, one that incorporates not only genes but also gene regulators, cellular data and developmental information across the human life span. The work is a testament to how far brain biology has come, and how much further it has to go, toward producing anything of practical value to doctors or patients, experts said. © 2018 The New York Times Company

Keyword: Schizophrenia; Genes & Behavior
Link ID: 25789 - Posted: 12.15.2018