Chapter 12. Psychopathology: The Biology of Behavioral Disorders
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Amy Maxmen Before his 33-year-old son became bedridden with chronic fatigue syndrome, biochemist Ronald Davis created technologies to analyse genes and proteins faster, better and more cheaply. Now he aims his inventions at a different target: the elusive inner workings of his son’s malady. In his office at the Stanford Genome Technology Center in Palo Alto, California, Davis holds a nanofabricated cube the size of a gaming die. It contains 2,500 electrodes that measure electrical resistance to evaluate the properties of human cells. When Davis exposed immune cells from six people with chronic fatigue syndrome to a stressor — a splash of common salt — the cube revealed that they couldn’t recover as well as cells from healthy people could. Now his team is fabricating 100 more devices to repeat the experiment, and testing a cheaper alternative — a paper-thin nanoparticle circuit that costs less than a penny to make on an inkjet printer. Davis’s findings, although preliminary, are helping to propel research on chronic fatigue syndrome, also called myalgic encephalomyelitis (ME/CFS), into the scientific mainstream. Physicians used to dismiss the disease as psychosomatic, but studies now suggest that it involves problems in the chemical reactions, or pathways, within cells. “We now have a great deal of evidence to support that this is not only real, but a complex set of disorders,” says Ian Lipkin, an epidemiologist at Columbia University in New York City. “We are gathering clues that will lead to controlled clinical trials.” © 2017 Macmillan Publishers Limited,
By Melissa Banigan Twenty years ago, I started experiencing what turned into a long list of seemingly unrelated health issues. Headaches, depression, insomnia, peripheral neuropathy, fatigue, joint pain, chest pain, shortness of breath, a lesion on my spine and a variety of uncomfortable gastrointestinal ailments. Over the past five years, things went from bad to worse as I also became lactose-intolerant, developed mild vitiligo (a condition that leads to loss of skin pigmentation) and major vertigo, experienced a series of low-grade fevers and started to have some memory loss that I referred to as brain fogs. Doctors told me that as an overworked single mother of 40, I might just need to figure out ways to get more sleep and relax. Some of what was happening, they said, might be attributed to the normal processes of aging. What was happening, however, didn’t feel normal. Always a voracious reader and a writer by profession, I could no longer focus on work, read even a page of a book or grip a pen long enough to write a grocery list. I often felt too exhausted to keep plans with friends. When I did pull myself off my couch to see them, I couldn’t concentrate on conversations, so I sequestered myself in my apartment and let my friendships fade. I had been a runner, a swimmer and a hiker, but just walking up a flight of stairs made me lose my breath so completely that I succumbed to inactivity. I did everything the doctors asked me to do. I changed my diet and sleep schedule, went to a physical therapist and saw specialists in neurology and rheumatology and even a mental-health therapist. I then also turned to massage therapists, herbalists and an acupuncturist. © 1996-2017 The Washington Post
By Anil Ananthaswamy People who have chronic pain are more likely to experience mood disorders, but it’s not clear how this happens. Now a study in mice has found that chronic pain can induce genetic changes in brain regions that are linked to depression and anxiety, a finding that may lead to new treatments for pain. “At least 40 per cent of patients who suffer from severe forms of chronic pain also develop depression at some point, along with other cognitive problems,” says Venetia Zachariou of the Icahn School of Medicine at Mount Sinai in New York. To see if there might be a genetic link between these conditions, Zachariou and her team studied mice with damage to their peripheral nervous system. These mice show symptoms similar to chronic pain in people – they become hypersensitive to harmless touch, and avoid other situations that might also cause them pain. Until now, pain behaviour in mice had only been studied for at most a week at a time, says Zachariou, whose team monitored their mice for 10 weeks. “At the beginning, we saw only sensory deficits and pain-like symptoms. But several weeks later, the animals developed anxiety and depression-like behaviours.” The team then examined gene activity in three regions in the mouse brains we know are associated with depression and anxiety. Analysing the nucleus accumbens, medial prefrontal cortex, and periaqueductal gray, they found nearly 40 genes where activity was significantly higher or lower than in mice without the nervous system damage. © Copyright Reed Business Information Ltd.
/ By Katie Rose Quandt One afternoon in 2013, after swimming and playing outside, 9-year-old Taylor Johnson, from outside Atlanta, began sneezing incessantly. The fit lasted days before stopping abruptly, only to return months later. For a year, her violent sneezing fits came and went, to the bewilderment of a series of doctors. For families, the diagnosis can seem like an answer to their prayers. But there’s a catch: Most doctors won’t treat the diseases — and many don’t believe they even exist. “She was making this noise with her mouth at times 140 to 150 times a minute,” said her mother, Lori Johnson. “She was frantic, she couldn’t eat, she couldn’t sleep.” And “when she wasn’t sneezing, she was very depressed… She lost all interest in anything. Her whole personality just dissolved into nothing.” Then an otolaryngologist (an ear, nose, and throat doctor) realized Taylor wasn’t sneezing at all — the behavior was a repetitive, sneeze-like tic. That prompted a round of visits to neurologists, psychologists, and other specialists, until an allergist finally suggested a set of diagnoses unfamiliar to the Johnsons: PANS and PANDAS. These disorders, a specialist told them, can arise in certain predisposed children when the immune system responds to an infection like strep throat by attacking the brain. The resulting inflammation can lead to violent body tics and OCD-like symptoms. Copyright 2017 Undark
By Daisy Yuhas, Spectrum on March 22, 2017 In children with a deletion on chromosome 22, having autism does not boost the risk of developing schizophrenia later in life, according to a new study1. The children in the study have 22q11.2 deletion syndrome, which is linked to a 25-fold increase in the risk of developing a psychotic condition such as schizophrenia. A deletion in the region is also associated with an increased risk of autism. Some researchers have suggested that the relatively high autism prevalence in this population is the result of misdiagnoses of early signs of schizophrenia. The new findings, published 21 January in Schizophrenia Research, support an alternate theory: Autism and schizophrenia are independent outcomes of the same genetic syndrome. If there is a relationship between the two conditions, “that can only be a very small, probably negligible effect,” says lead investigator Jacob Vorstman, assistant professor of child psychiatry and genetics at the University Medical Center Utrecht in the Netherlands. The new findings could help guide clinical care, says Opal Ousley, assistant professor of psychiatry at the Emory Autism Center in Atlanta. If prenatal testing picks up the 22q11.2 deletion, for instance, clinicians could discuss the risk of both autism and schizophrenia with parents. © 2017 Scientific American
As the father of two sons with schizophrenia, author Ron Powers is familiar with the pain and frustration of dealing with a chronic, incurable disease of the brain. Powers' younger son, Kevin, was a talented musician whose struggles with schizophrenia began at age 17. Just before his 21st birthday, in 2005, Kevin took his own life. A few years later, Powers' older son, Dean, started experiencing symptoms of schizophrenia and had a psychotic break. "There is no greater ... feeling of helplessness than to watch two beloved sons deteriorate before [your] eyes, not knowing what to do to bring them back," Powers tells Fresh Air's Terry Gross. Powers' new book, No One Cares About Crazy People, is both a memoir about his sons and a history of how the mentally ill have been treated medically, legally and socially. Although Dean is now medicated and doing well, Powers notes that many people with schizophrenia don't receive the treatment they need — in part because they often don't believe they are ill. "This unwillingness to believe that one is afflicted has led to tremendous problems," Powers says. "To force that person into being helped is a violation of his or her civil rights ... and the law may penalize the care workers who give [people with schizophrenia] medications or admit them to a hospital against their will. ... That is the great reigning Catch-22 of the way our society deals — or fails to deal — with schizophrenia." © 2017 npr
Link ID: 23383 - Posted: 03.21.2017
Jon Hamilton Gerard Sanacora, a professor of psychiatry at Yale University, has treated hundreds of severely depressed patients with low doses of ketamine, an anesthetic and popular club drug that isn't approved for depression. This sort of "off-label" prescribing is legal. But Sanacora says other doctors sometimes ask him, "How can you be offering this to patients based on the limited amount of information that's out there and not knowing the potential long-term risk?" Sanacora has a simple answer. "If you have patients that are likely to seriously injure themselves or kill themselves within a short period of time, and they've tried the standard treatments, how do you not offer this treatment?" he says. Dozens of clinics now offer ketamine to patients with depression. And a survey of providers in the U.S. and Canada showed that "well over 3,000" patients have been treated so far, Sanacora says. A number of small studies have found that ketamine can do something no other drug can: it often relieves even suicidal depression in a matter of hours in patients who have not responded to other treatments. Ketamine's potential as an antidepressant was recognized more than a decade ago. And studies done since then provide "compelling evidence that the antidepressant effects of ketamine infusion are both rapid and robust, albeit transient," according to a consensus statement from a task force of the American Psychiatric Association. Sanacora is one of the task force members. © 2017 npr
By Taylor Beck LSD, “magic” mushrooms and mescaline have been banned in the U.S. and many other countries since the 1970s, but psychedelic medicine is making a comeback as new therapies for depression, nicotine addiction and anxiety. The drugs have another scientific use, too: so-called psychotomimetics, or mimics of psychosis, may be useful tools for studying schizophrenia. By creating a brief bout of psychosis in a healthy brain, as indigenous healers have for millennia, scientists are seeking new ways to study—and perhaps treat—mental illness. “We think that schizophrenia is a group of psychoses, which may have different causes,” says Franz Vollenweider, a psychiatrist and neuroscientist at the University of Zurich. “The new approach is to try to understand specific symptoms: hearing voices, cognitive problems, or apathy and social disengagement. If you can identify the neural bases of these, you can tailor the pharmacology.” Vollenweider and his colleagues have found an existing drug for anxiety that blocks specific effects of psilocybin, the psychoactive ingredient in magic mushrooms. When healthy people were given the drug before tripping, they did not report visual hallucinations and other common effects, according to a study published in April 2016 in European Neuropsychopharmacology. The effort is part of a burgeoning movement in pharmacology that seeks to induce psychosis to learn how to treat it. And schizophrenia desperately needs new treatments. Seventy-five percent of afflicted patients have cognitive problems. And most commonly used drugs do not treat the disorder's “negative” symptoms—apathy, social withdrawal, negative thinking—nor the cognitive impairments, which best predict how well a patient will fare in the long term. © 2017 Scientific American
By JULIE REHMEYER and DAVID TULLER What are some of the treatment regimens that sufferers of chronic fatigue syndrome should follow? Many major medical organizations cite two: psychotherapy and a steady increase in exercise. There’s just one problem. The main study that has been cited as proof that patients can recover with those treatments overstated some of its results. In reality, the claim that patients can recover from these treatments is not justified by the data. That’s the finding of a peer-reviewed preliminary re-analysis of previously unpublished data from the clinical trial, the largest ever for chronic fatigue syndrome. Nicknamed the PACE trial, the core findings of the British study appeared in The Lancet in 2011 and Psychological Medicine in 2013. Patients battled for years to obtain the underlying data, and last spring, a legal tribunal in Britain, the General Regulatory Chamber, directed the release of some of the study’s information. The impact of the trial on treatment options for the estimated one million chronic fatigue patients in the United States has been profound. The Mayo Clinic, Kaiser Permanente, WebMD, the American Academy of Family Physicians and others recommend psychotherapy and a steady increase in exercise. But this approach can be harmful. According to a 2015 report from the Institute of Medicine, now the National Academy of Medicine, even minimal activity can cause patients prolonged exhaustion, muscle pain, cognitive problems and more. In severe cases, a short conversation or a trip to the bathroom can deplete patients for hours, days or more. In surveys, patients routinely report deterioration after a program of graded exercise. The psychotherapeutic intervention also encourages patients to increase their activity levels. Many patients (including one of us) have remained ill for years or decades with chronic fatigue syndrome, also known as myalgic encephalomyelitis, or ME/CFS. It can be triggered by a viral infection, resulting in continuing or recurring immunological and neurological dysfunction. The Institute of Medicine dismissed any notion that it is a psychiatric illness. © 2017 The New York Times Company
Richard A. Friedman Jet lag makes everyone miserable. But it makes some people mentally ill. There’s a psychiatric hospital not far from Heathrow Airport that is known for treating bipolar and schizophrenic travelers, some of whom are occasionally found wandering aimlessly through the terminals. A study from the 1980s of 186 of those patients found that those who’d traveled from the west had a higher incidence of mania, while those who’d traveled from the east had a higher incidence of depression. I saw the same thing in one of my patients who suffered from manic depression. When he got depressed after a vacation to Europe, we assumed he was just disappointed about returning to work. But then he had a fun trip out West and returned home in what’s called a hypomanic state: He was expansive, a fount of creative ideas. It was clear that his changes in mood weren’t caused by the vacation blues, but by something else. The problem turned out to be a disruption in his circadian rhythm. He didn’t need drugs; he needed the right doses of sleep and sunlight at the right time. It turns out that that prescription could treat much of what ails us. Clinicians have long known that there is a strong link between sleep, sunlight and mood. Problems sleeping are often a warning sign or a cause of impending depression, and can make people with bipolar disorder manic. Some 15 years ago, Dr. Francesco Benedetti, a psychiatrist in Milan, and colleagues noticed that hospitalized bipolar patients who were assigned to rooms with views of the east were discharged earlier than those with rooms facing the west — presumably because the early morning light had an antidepressant effect. The notion that we can manipulate sleep to treat mental illness has also been around for many years. Back in the late 1960s, a German psychiatrist heard about a woman in Tübingen who was hospitalized for depression and claimed that she normally kept her symptoms in check by taking all-night bike rides. He subsequently demonstrated in a group of depressed patients that a night of complete sleep deprivation produced an immediate, significant improvement in mood in about 60 percent of the group. © 2017 The New York Times Company
By Agata Blaszczak-Boxe Recognizing when a friend or colleague feels sad, angry or surprised is key to getting along with others. But a new study suggests that a knack for eavesdropping on feelings may sometimes come with an extra dose of stress. This and other research challenge the prevailing view that emotional intelligence is uniformly beneficial to its bearer. In a study published in the September 2016 issue of Emotion, psychologists Myriam Bechtoldt and Vanessa Schneider of the Frankfurt School of Finance and Management in Germany asked 166 male university students a series of questions to measure their emotional smarts. For example, they showed the students photographs of people's faces and asked them to what extent feelings such as happiness or disgust were being expressed. The students then had to give job talks in front of judges displaying stern facial expressions. The scientists measured concentrations of the stress hormone cortisol in the students' saliva before and after the talk. In students who were rated more emotionally intelligent, the stress measures increased more during the experiment and took longer to go back to baseline. The findings suggest that some people may be too emotionally astute for their own good, says Hillary Anger Elfenbein, a professor of organizational behavior at Washington University in St. Louis, who was not involved in the study. “Sometimes you can be so good at something that it causes trouble,” she notes. Indeed, the study adds to previous research hinting at a dark side of emotional intelligence. A study published in 2002 in Personality and Individual Differences suggested that emotionally perceptive people might be particularly susceptible to feelings of depression and hopelessness. © 2017 Scientific American
By Clare Wilson The repeated thoughts and urges of obsessive compulsive disorder (OCD) may be caused by an inability to learn to distinguish between safe and risky situations. A brain-scanning study has found that the part of the brain that sends out safety signals seems to be less active in people with the condition. People with OCD feel they have to carry out certain actions, such as washing their hands again and again, checking the oven has been turned off, or repeatedly going over religious thoughts. Those worst affected may spend hours every day on these compulsive “rituals”. To find out more about why this happens, Naomi Fineberg of Hertfordshire Partnership University NHS Foundation Trust in the UK and her team trained 78 people to fear a picture of an angry face. The team did it by sometimes giving the volunteers an electric shock to the wrist when they saw the picture while they were lying in an fMRI brain scanner. About half the group had OCD. The team then tried to “detrain” the volunteers, by showing them the same picture many times, but without any shocks. Judging by how much the volunteers sweated in response to seeing the picture, the team found that people without OCD soon learned to stop associating the face with the shock, but people with the condition remained scared. © Copyright Reed Business Information Ltd.
by Laura Sanders Amid a flurry of cabinet appointments and immigration policies, the Trump administration has announced one thing it will not do: pursue policies that protect transgender children in public schools. The Feb. 22 announcement rescinds Obama administration guidelines that, among other protections, allow transgender kids to use bathrooms and participate in sports that correspond with their genders, and to be called by their preferred names and pronouns. In a Feb. 23 news briefing, White House press secretary Sean Spicer said that this is a states’ rights issue. “States should enact laws that reflect the values, principles, and will of the people in their particular state,” he said. “That's it, plain and simple.” But this “plain and simple” move could be quite dangerous, even deadly, science suggests. Transgender children, who are born one biological sex but identify as the other, already face enormous challenges as they move through a society that often doesn’t understand or accept them. Consider this: Nearly half (46.5 percent) of young transgender adults have attempted suicide at some point in their lives, a recent survey of over 2,000 people found. Nearly half. For comparison, the attempted suicide rate among the general U.S. population is estimated to be about 4.6 percent. What’s more, a 2015 study in the Journal of Adolescent Health found that transgender youth are two to three times as likely as their peers to suffer from depression and anxiety disorders, or to attempt suicide or harm themselves. These troublesome stats, based on a sample of 180 transgender children and young adults in Boston ages 12 to 29, applied equally to those who underwent male-to-female transitions and those who underwent female-to-male transitions. © Society for Science & the Public 2000 - 2017.
By Daniel Barron On January 2, 1979, Dr. Rafael Osheroff was admitted to Chestnut Lodge, an inpatient psychiatric hospital in Maryland. Osheroff had a bustling nephrology practice. He was married with three children, two from a previous marriage. Everything had been going well except his mood. For the previous two years, Osheroff had suffered from bouts of anxiety and depression. Dr. Nathan Kline, a prominent psychopharmacologist in New York City, had begun Osheroff on a tricyclic antidepressant and, according to Kline’s notes—which were later revealed in court—he improved. But then Osheroff decided, against Kline’s advice, to change his dose. He got worse. So much worse that he was brought to Chestnut Lodge. For the next seven months, Osheroff was treated with intensive psychotherapy for narcissistic personality disorder and depression. It didn’t help. He lost 40 pounds, suffered from excruciating insomnia, and began pacing the floor so incessantly that his feet became swollen and blistered. Osheroff’s family, distressed by the progressive unraveling of his mind, hired a psychiatrist in Washington D.C. to intervene. In response, Chestnut Lodge held a clinical case conference yet decided to not change treatment. Importantly, they decided to not begin medications but to continue psychotherapy. They considered themselves “traditional psychiatrists”—practitioners of psychodynamic psychotherapy, the technique used by Sigmund Freud and other pioneers. © 2017 Scientific American
By James Gallagher Health and science reporter, Maps have revealed "hotspots" of schizophrenia and other psychotic illnesses in England, based on the amount of medication prescribed by GPs. The analysis by the University of East London showed North Kesteven, in Lincolnshire, had the highest rates. The lowest rate of schizophrenia prescriptions was in East Dorset. However, explaining the pattern across England is complicated and the research team says the maps pose a lot of questions. They were developed using anonymous prescription records that are collected from doctors' surgeries in England. They record only prescriptions given out by GPs - not the number of patients treated - so hospital treatment is missed in the analysis. Data between October 2015 and September 2016 showed the average number of schizophrenia prescriptions across England was 19 for every 1,000 people. Prof Allan Brimicombe, one of the researchers from UEL, said: "The pattern is not uniformly spread across the country." He suggests this could be due to "environmental effects" such as different rates of drink or drug abuse. Prof Brimicombe told the BBC: "The top one is in the Lincolnshire countryside and there are others in the countryside." © 2017 BBC
Link ID: 23281 - Posted: 02.25.2017
By Jennifer Couzin-Frankel At least two dozen junior and senior researchers are stuck in scientific limbo after being barred from publishing data collected over a 25-year period at a National Institutes of Health (NIH) lab. The unusual ban follows the firing last summer of veteran neurologist Allen Braun by the National Institute on Deafness and Other Communication Disorders (NIDCD) for what many scientists have told Science are relatively minor, if widespread, violations of his lab’s experimental protocol. Most of the violations, which were unearthed after Braun himself reported a problem, involve the prescreening or vetting of volunteers for brain imaging scans and other experiments on language processing. The fallout from the case was recently chronicled on a blog by one of Braun’s former postdocs, and it highlights a not-uncommon problem across science: the career harm to innocent junior investigators following lab misconduct or accidental violations on the part of senior scientists. But this case, say those familiar with it, is extreme. “We’re truly collateral damage,” says Nan Bernstein Ratner of the University of Maryland in College Park, who researches stuttering. She spent 5 years collaborating with Braun. Now, two of her graduate students have had to shift their master’s theses topics, and an undergraduate she mentored cannot publish a planned paper. “The process has been—you can use this term—surreal.” © 2017 American Association for the Advancement of Science
By Esther Landhuis For much of her life Anne Dalton battled depression. She seldom spoke with people. She stayed home a lot. The days dragged on with a sense of “why bother?” for the 61-year-old from New Jersey who used to work at a Wall Street investment firm. After trying more than a dozen combinations of antidepressant drugs to no avail, things got so bad two years ago that Dalton went in for electroconvulsive therapy—in which “basically they shock your brain,” as she puts it. Like Dalton, most of the estimated 16 million U.S. adults who have reported a major depressive episode in the past year find little relief even after several months on antidepressants—a problem that some researchers say may stem from the way mental illness is diagnosed. Objective lab tests can physically confirm heart disease or cancer, but psychiatric conditions are classified somewhat vaguely as clusters of reported symptoms. Doctors consider people clinically depressed if they say they have low mood and meet at least four additional criteria from an overall list of nine. Yet depression can manifest differently from person to person: One might be putting on pounds and sleeping much of the time whereas another might be losing weight, feeling anxious and finding it difficult to sit still, says Conor Liston, a neuroscientist and psychiatrist at Weill Cornell Medical College. “The fact that we lump people together like this has been a big obstacle in understanding the neurobiology of depression,” Liston explains. © 2017 Scientific American,
By Nathaniel P. Morris Cardiovascular disease and mental illness are among the top contributors to death and disability in the United States. At first glance, these health conditions seem to lie at opposite ends of the medical spectrum: Treating the heart is often associated with lab draws, imaging and invasive procedures, whereas treating the mind conjures up notions of talk therapy and subjective checklists. Yet researchers are discovering some surprising ties between cardiac health and mental health. These connections have profound implications for patient care, and doctors are paying attention. Depression has become recognized as a major issue for people with heart disease. Studies have found that between 17 and 44 percent of patients with coronary artery disease also have major depression. According to the American Heart Association, people hospitalized for a heart attack are roughly three times as likely as the general population to experience depression. As many as 40 percent of patients undergoing coronary artery bypass surgery suffer from depression. Decades of research suggest these illnesses may actually cause one another. For example, patients with heart disease are often sick and under stressful circumstances, which can foster depressive symptoms. But depression itself is also a risk factor for developing heart disease. Researchers aren’t sure why, but something about being depressed — possibly a mix of factors including inflammatory changes and behavior changes — appears to increase risk of heart disease. © 1996-2017 The Washington Post
By Andy Coghlan It’s as if a switch has been flicked. Evidence is mounting that chronic fatigue syndrome (CFS) is caused by the body swapping to less efficient ways of generating energy. Also known as ME or myalgic encephalomyelitis, CFS affects some 250,000 people in the UK. The main symptom is persistent physical and mental exhaustion that doesn’t improve with sleep or rest. It often begins after a mild infection, but its causes are unknown. Some have argued that CFS is a psychological condition, and that it is best treated through strategies like cognitive behavioural therapy. But several lines of investigation are now suggesting that the profound and painful lack of energy seen in the condition could in many cases be due to people losing their ability to burn carbohydrate sugars in the normal way to generate cellular energy. Instead, the cells of people with CFS stop making as much energy from sugar as usual, and start relying more on lower-yielding fuels, such as amino acids and fats. This kind of metabolic switch produces lactate, which can cause pain when it accumulates in muscles. Together, this would explain both the shortness of energy, and why even mild exercise can be exhausting and painful. © Copyright Reed Business Information Ltd.
Link ID: 23226 - Posted: 02.14.2017
By BENEDICT CAREY The number of retirement-age Americans taking at least three psychiatric drugs more than doubled between 2004 and 2013, even though almost half of them had no mental health diagnosis on record, researchers reported on Monday. The new analysis, based on data from doctors’ office visits, suggests that inappropriate prescribing to older people is more common than previously thought. Office visits are a close, if not exact, estimate of underlying patient numbers. The paper appears in the journal JAMA Internal Medicine. Geriatric medical organizations have long warned against overprescribing to older people, who are more susceptible to common side effects of psychotropic drugs, such as dizziness and confusion. For more than 20 years, the American Geriatrics Society has published the so-called Beers Criteria for potentially inappropriate use, listing dozens of drugs and their mutual interactions. In that time, prescription rates of drugs like antidepressants, sleeping pills and painkillers nonetheless generally increased in older people, previous studies have found. The new report captures one important dimension, the rise in so-called polypharmacy — three drugs or more — in primary care, where most of the prescribing happens. Earlier research has found that elderly people are more likely to be on at least one psychiatric drug long term than younger adults, even though the incidence of most mental disorders declines later in life. “I was stunned to see this, that despite all the talk about how polypharmacy is bad for older people, this rate has doubled,” said Dr. Dilip Jeste, a professor of psychiatry and neurosciences at the University of California, San Diego, who was not involved in the new work. © 2017 The New York Times Company