Chapter 12. Psychopathology: The Biology of Behavioral Disorders
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By Victoria Sayo Turner Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Credit: ©iStock Around March, some of us take a kick at the snow mounded on the curb and wonder if spring is finally going to drop by. The sun sets before we go home, and the cold coops us up except for runs to the grocery store. All of this amounts to something known informally as the winter blues, because those wintry days and dead trees can put us in a glum mood. But in the 1980s, research at the National Institutes of Mental Health led to recognition of a form of depression known as seasonal affective disorder (shortened, of course, to SAD). Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Mention of SAD in research and books peaked in the 1990s, and today SAD is considered a diagnosable (and insurable) disorder. Treatment ranges from psychotherapy to antidepressants to light therapy — large boxes filled with lightbulbs that look like tanning beds for your face. However, a recent study questions the existence of seasonal depression entirely. Each year, the Centers for Disease Control conducts a large cross-sectional study of the US population. A group of researchers realized they could use the CDC results independently to investigate how much depression changes by season. The 2006 version of the CDC study included a set of questions typically used to screen for depression. By analyzing the answers gathered from 34,000 adults over the course of the year, the researchers might detect flareups of seasonal affective disorder. They might see wintertime surges in depression. “To be honest, we initially did not question the [SAD] diagnosis,” writes investigator Dr. Steven LoBello, the goal being “to determine the actual extent to which depression changes with the seasons.” © 2016 Scientific American
Deborah Orr The psychologist Oliver James has for many years been a part of the cultural landscape, writing best-selling books, making television programmes, contributing articles to newspapers and generally offering his views. As a practicing psychotherapist of many years’ standing, he has good reason to believe that he has important insights to offer. James is particularly exercised by the damage caused by casual emotional abuse – the explosive parent who shouts and swears at their kids, displays resentment against them or tries to coerce them into doing things instead of employing reason. No sensible person disagrees with him on this, and only a harsh critic would deny that James has played a strong and positive part in popularising these simple, important wisdoms. That’s why it’s so very odd that James has chosen now to perpetrate casual emotional abuse on a grand scale. His latest book, Not in Your Genes: The Real Reason Parents Are Like Their Children, expands on an argument he’s been making for years: that there is no scientific basis for belief in the idea that there is any genetic element to any psychological trait. Even illnesses such as schizophrenia and bipolar disorder are completely down to the environment in which you grew up, not the complex interplay between nature and nurture that mainstream science espouses. Even if James had conclusive evidence to back up his absolutist claim – which he does not – I would suggest that such news should be broken gently. © 2016 Guardian News and Media Limited
Shefali Luthra Depression prompts people to make about 8 million doctors' appointments a year, and more than half are with primary care physicians. A study suggests those doctors often fall short in treating depression because of insurance issues, time constraints and other factors. More often than not, primary care doctors fail to teach patients how to manage their care and don't follow up to see how they're doing, according to the study, which was published Monday in Health Affairs. Those are considered effective tactics for treating chronic illnesses. "The approach to depression should be like that of other chronic diseases," said Dr. Harold Pincus, vice chair of psychiatry at Columbia University's College of Physicians and Surgeons and one of the study's co-authors. But "by and large, primary care practices don't have the infrastructure or haven't chosen to implement those practices for depression." Most people with depression seek help from their primary care doctors, the study notes. That can be because patients often face shortages and limitations of access to specialty mental health care, including lack of insurance coverage, the authors write. Plus there's stigma: Patients sometimes feel nervous or ashamed to see a mental health specialist, according to the authors. Meanwhile, physicians and researchers have increasingly been calling for mental health conditions such as depression and anxiety to be treated like physical illnesses. Historically, those have been handled separately and not always with the same attention and care as things like high blood pressure and heart disease. © 2016 npr
Link ID: 21964 - Posted: 03.08.2016
Story by Amy Ellis Nutt She relaxed in the recliner, her eyes closed, her hands resting lightly in her lap. The psychiatrist’s assistant made small talk while pushing the woman’s hair this way and that, dabbing her head with spots of paste before attaching the 19 electrodes to her scalp. In the struggle over the future of psychiatry, researchers are looking deep within the brain to understand mental illness and find new therapeutic tools. As the test started, her anxiety ticked up. And that’s when it began: the sensation of being locked in a vise. First, she couldn’t move. Then she was shrinking, collapsing in on herself like some human black hole. It was a classic panic attack — captured in vivid color on the computer screen that psychiatrist Hasan Asif was watching. “It’s going to be okay,” he said, his voice quiet and soothing. “Just stay with it.” The images playing out in front of him were entirely unexpected; this clearly wasn’t a resting state for his patient. With each surge of anxiety, a splotch of red bloomed on the computer screen. Excessive activity of high-energy brain waves near the top of her head indicated hyper-arousal and stress. Decreased activity in the front of her brain, where emotions are managed, showed she couldn’t summon the resources to keep calm.
Tina Hesman Saey Sonia Vallabh knows what will probably kill her. In 2011, the Boston-area law school graduate learned she carries the same genetic mutation that caused her mother’s death from a rare brain-wasting prion disease. Prions are twisted forms of normal brain proteins that clump together and destroy nerves. About 10 to 15 percent of prion diseases are caused by a mutation in the PRNP gene, leading to such deadly diseases as Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome and fatal familial insomnia, the disease that killed Vallabh’s mother. Grief, shared with family and friends, came first. Eventually, Vallabh realized, “We can’t get around this prognosis.… We’ve got to go through it.” So began her and husband Eric Minikel’s odyssey to learn about the disease that had turned their lives upside down. A scientist friend came by with a flash drive loaded with research papers about prion diseases. “We didn’t have the vocabulary” to understand the information, Vallabh says. So she took a sabbatical from her job to take biology and chemistry classes. Minikel kept writing transportation software, but attended night classes with his wife. Vallabh’s first foray into brain research was as a technician in a lab studying Huntington’s disease. During “science nights” at the couple’s home, scientist pals team-taught biology and biochemistry. The couple took the biggest step when Minikel left his consulting job and both enrolled in graduate school to study prion diseases. Prion proteins, some of which clump together or form fibrils, as in this E. coli bacteria, are often used to model how proteins misfold in some neurodegenerative disorders. © Society for Science & the Public 2000 - 2016
By DONALD G. McNEIL Jr. A baby with a shrunken, misshapen head is surely a heartbreaking sight. But reproductive health experts are warning that microcephaly may be only the most obvious consequence of the spread of the Zika virus. Even infants who appear normal at birth may be at higher risk for mental illnesses later in life if their mothers were infected during pregnancy, many researchers fear. The Zika virus, they say, closely resembles some infectious agents that have been linked to the development of autism, bipolar disorder and schizophrenia. Schizophrenia and other debilitating mental illnesses have no single cause, experts emphasized in interviews. The conditions are thought to arise from a combination of factors, including genetic predisposition and traumas later in life, such as sexual or physical abuse, abandonment or heavy drug use. But illnesses in utero, including viral infections, are thought to be a trigger. “The consequences of this go way beyond microcephaly,” said Dr. W. Ian Lipkin, who directs The Center for Infection and Immunity at Columbia University. Here is a look at the most prominent rumors and theories about Zika virus, along with responses from scientists. Among children in Latin America and the Caribbean, “I wouldn’t be surprised if we saw a big upswing in A.D.H.D., autism, epilepsy and schizophrenia,” he added. “We’re looking at a large group of individuals who may not be able to function in the world.” © 2016 The New York Times Company
By Nancy Szokan It’s well known that physical activity is a mood elevator. But writing in “The Athlete’s Way” blog on Psychology Today’s website, endurance athlete Christopher Bergland discusses a study indicating that combining movement with the attention-focusing benefits of meditation can be an extra-effective tool in fighting depression. The small study, conducted at Rutgers University in New Jersey, was based on a set of assumptions: Healthy brains are constantly producing neurons. Brains of people under stress or suffering depression produce fewer neurons. Physical activity increases neuron production, as do antidepressant medications. (Meanwhile, a certain number of newborn neurons die off.) Mental exercise — “effortful learning,” which requires focus — reduces those deaths. People with depression often have problems with focus. The researchers tested a novel intervention — it’s called MAP because it involves mental and physical training — aimed at both increasing neuron production and keeping those neurons alive. Fifty-two people completed the study — 22 with major depressive disorder, or MDD, and 30 who were not depressed. Twice a week, they performed 30 minutes of meditation during which they were directed to constantly focus on their breathing; they began each session seated, but for the last 10 minutes they meditated while walking slowly. Then they performed 30 minutes of moderate physical activity on a treadmill or stationary cycle. After eight weeks, the researchers found that the MDD patients’ depressive symptoms had been reduced by 40 percent. (The non-depressed participants also said they felt happier.)
Link ID: 21899 - Posted: 02.16.2016
By Dominic Howell BBC News A new therapy which involves a patient embodying themselves in a virtual reality avatar of a crying child could help with depression, research has suggested. Patients wear a headset that projects a life-sized image, firstly of an adult and then of a child. The new research tested the technology for the first time on patients with a mental health problem. The project is part of a continuing study at University College London. The university, which is working in collaboration with ICREA-University of Barcelona, has suspected for several years that virtual therapy could help with mental health conditions. This latest research - which has been published in the British Journal of Psychiatry Open and was funded by the Medical Research Council - lays the basis for a large-scale clinical trial to be carried out in the future. The study took 15 people who were all being treated by the NHS for depression and put them through the avatar experience. Firstly, the patients - 10 of whom were female and the rest male - put on a headset which projected an adult version of themselves into a virtual reality mirror. The patient was asked to mentally identify with the adult avatar, which exactly replicated the patient's body movements, in a process known as "embodiment". They then noticed a separate avatar of a small crying child, who was also in the mirror. They were told to say compassionate phrases to the child to try and comfort and console it. Patients asked the child to think of a time when it was happy, and to think of someone who loved them. At this stage of the experiment the roles were then reversed. © 2016 BBC
Link ID: 21897 - Posted: 02.15.2016
By Ann Gibbons Depressed? Your inner Neandertal may be to blame. Modern humans met and mated with these archaic people in Europe or Asia about 50,000 years ago, and researchers have long suspected that genes picked up in these trysts might be shaping health and well-being today. Now, a study in the current issue of Science details their impact. It uses a powerful new method for scanning the electronic health records of 28,000 Americans to show that some Neandertal gene variants today can raise the risk of depression, skin lesions, blood clots, and other disorders. Neandertal genes aren’t all bad. “These variants sometimes protect against a disease, sometimes make people more susceptible to disease,” says paleogeneticist Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. Two other new studies identified three archaic genes that boost immune response. And most archaic genes that persist in humans were likely beneficial in prehistoric times. But some now cause disease because modern lifestyles and environments are so different. Living people carry only trace amounts of Neandertal DNA, which makes its impact on health more striking. “The Neandertal genetic contribution to present-day people seems to have larger physiological effects than I would have naïvely thought,” says Pääbo, who helped launch this avenue of research by sequencing the first ancient genomes but was not involved in these studies. On average, Europeans and Asians have inherited about 1.5% of their genomes from Neandertals. Island Melanesians carry an additional 2% to 3% of DNA inherited from another extinct group, the Denisovans. Most Africans lack this archaic DNA because the interbreeding happened after modern humans left Africa. © 2016 American Association for the Advancement of Science
Bruce Bower Winter doesn’t deserve its dour reputation as the season of depression, scientists say. Rates of major depression, a psychiatric condition marked by intense sadness, hopelessness, insomnia and a general loss of interest or pleasure, don’t markedly change from one season to another among U.S. adults, says a team led by psychologist Steven LoBello of Auburn University at Montgomery in Alabama. Neither do symptoms intensify or become more numerous during winter among those already suffering from depression, the researchers report online January 19 in Clinical Psychological Science. A small number of people with regular fall or winter depression may have gone undetected in the new study, which surveyed more than 30,000 U.S. adults. Still, it’s becoming harder to justify the current psychiatric diagnosis of major depression “with seasonal pattern,” LoBello and Auburn colleagues Megan Traffanstedt and Sheila Mehta conclude. Because it’s a recurring disorder, depression can strike in two consecutive winters by chance, the researchers say. Depression in three or more consecutive winters could be due to personal and social factors unrelated to shorter days, they add. “Being depressed during winter is not evidence that one is depressed because of winter,” LoBello says. © Society for Science & the Public 2000 - 2016
By Jordana Cepelewicz As the Panthers and Broncos faced off in the third quarter of last night’s Super Bowl, wide receiver Philly Brown suffered a possible concussion—and to the disappointment of Panthers fans, he never returned to the game. But for good reason: concussions are now known to be much more serious injuries than once thought. And the danger may not be limited to the immediate repercussions. Researchers have already linked more severe traumatic brain injury to later suicide—particularly in military veterans and professional athletes—and have more recently explored the connection between concussion and depression. Now, new research published in the Canadian Medical Association Journal shows that even mild concussions sustained in ordinary community settings might be more detrimental than anyone anticipated; the long-term risk of suicide increases threefold in adults if they have experienced even one concussion. That risk increases by a third if the concussion is sustained on a weekend instead of a weekday—suggesting recreational concussions are riskier long-term than those sustained on the job. “The typical patient I see is a middle-aged adult, not an elite athlete,” says Donald Redelmeier, a senior scientist at the University of Toronto and one of the study’s lead authors. “And the usual circumstances for acquiring a concussion are not while playing football; it is when driving in traffic and getting into a crash, when missing a step and falling down a staircase, when getting overly ambitious about home repairs—the everyday activities of life.” Redelmeier and his team wanted to examine the risks of the concussions acquired under those circumstances. © 2016 Scientific American
By Steven Petrow I have slogged through a number of difficult situations in recent months, among them the ongoing crises of my elderly parents’ illnesses and the suicide of a friend. I never lost my appetite nor burst into tears, and I didn’t suffer from any of the other typical symptoms of depression. Maybe I was more irritable than usual, a bit more prone to snap. And yes, I buried myself in my work. But I didn’t think I’d tripped down into the rabbit hole of depression. You would think I would have been more self-aware, both personally and professionally. As a health journalist, I have often used my own stories to write about difficult-to-discuss medical conditions, including learning I had testicular cancer at age 26 and my misdiagnosis with H.I.V./AIDS — back when it was a death sentence. But I had never written about suffering from depression, even though it’s plagued me since I first put pen to paper, at age 11, when I started keeping a diary. Still, I’m far from alone. At least six million men in the United States suffer from depression, according to the National Institute of Mental Health. The true number is likely to be even higher, said Dr. Matthew Rudorfer, the institute’s associate director for treatment research, since men are less likely than women to report classic symptoms like low mood, sadness or crying, so they often go undiagnosed. Men, he told me, more often demonstrate “externalizing” symptoms like irritability, anger and aggressiveness, substance and alcohol abuse, risk-taking behaviors and “workaholism.” Oh, that macho thing: Men don’t get depressed; they just work, drink and compete harder. Andrew Solomon, author of the pathbreaking memoir about depression, “Noonday Demon,” told me that ridiculous attitude is part of the mind-set that guys should “cover up our moods with militarism or athleticism.” © 2016 The New York Times Company
Link ID: 21874 - Posted: 02.09.2016
It’s well known that some people report that their mood is influenced by the seasons. But can the time of year affect other cognitive functions? To find out, Gilles Vandewalle and colleagues at the University of Liege in Belgium scanned the brains of 28 volunteers while they performed attention and working memory tests at different times of the year. To ensure the results were influenced by the seasons rather than the environmental conditions on the test day, the participants were confined to a lab for 4.5 days prior to the test, exposed to a constant light level and temperature. Although their test scores didn’t change with the seasons, activity in some brain areas showed a consistent seasonal pattern among the volunteers: brain activity peaked in the summer on the attention task and in the autumn on the memory task. Many seasonally changing factors could regulate such a pattern, including day length (known as photoperiod), temperature, humidity, social interaction and physical activity. Since these weren’t all controlled for in the study, it’s impossible to say what is responsible for the seasonal changes seen. “In our data it seems that photoperiod, or the rate of change of photoperiod, was more likely to explain what we were seeing. But we can’t exclude all the others,” says Vandewalle. The results suggest that over the course of a year, the brain might work in different ways to compensate for seasonal factors that could affect its function, enabling it to maintain a stable performance. Vandewalle speculates that these mechanisms might not work as well in some people, for example, those vulnerable to the winter blues. © Copyright Reed Business Information Ltd.
By Jonathan Leo Last week, according to many media accounts, scientists from Harvard Medical School, Boston Children’s Hospital, and the Broad Institute discovered the genetic basis of schizophrenia. The researchers reported in Nature that people with schizophrenia were more likely to have the overactive forms of a gene called complement component 4, or C4, which is involved in pruning synapses during adolescence. However, suggesting a biologic mechanism for a small subset of those diagnosed with schizophrenia is not the same as confirming the genetic theory of schizophrenia. Benedict Carey, science reporter for the New York Times, delved into the details and reported the all-important fact that having the C4 variant would increase a person’s risk by about 25 percent over the 1-percent base rate of schizophrenia—that is, to 1.25 percent. Genes for schizophrenia and depression have been discovered before, and in those cases, the subsequent enthusiastic headlines were shortly followed by retractions and more sober thinking. There are so many open questions (for instance, why do many people with the problematic variant not develop schizophrenia, and why do many people who don’t have the variant develop schizophrenia?) that the same may occur with the C4 discovery. The idea that mental illness is the result of a genetic predisposition is the foundation for modern-day psychiatry and has been the driving force for how research money is allocated, how patients are treated, and how society views people diagnosed with conditions identified in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Schizophrenia holds a unique spot in the annals of mental health research because of its perceived anatomical underpinnings and is often cited as evidence in favor of a genetic predisposition to other conditions.
By Diana Kwon Antidepressants are some of the most commonly prescribed medications out there. More than one out of 10 Americans over age 12—roughly 11 percent—take these drugs, according to a 2011 report by the National Center for Health Statistics. And yet, recent reports have revealed that important data about the safety of these drugs—especially their risks for children and adolescents—has been withheld from the medical community and the public. In the latest and most comprehensive analysis, published last week in BMJ (the British Medical Journal),a group of researchers at the Nordic Cochrane Center in Copenhagen showed that pharmaceutical companies were not presenting the full extent of serious harm in clinical study reports, which are detailed documents sent to regulatory authorities such as the U.S. Food and Drug Administration and the European Medicines Agency (EMA) when applying for approval of a new drug. The researchers examined documents from 70 double-blind, placebo-controlled trials of two common types of antidepressants—selective serotonin reuptake inhibitors (SSRI) and serotonin and norepinephrine reuptake inhibitors (SNRI)—and found that the occurrence of suicidal thoughts and aggressive behavior doubled in children and adolescents who used these medications. This paper comes on the heels of disturbing charges about conflicts of interest in reports on antidepressant trials. Last September a study published in the Journal of Clinical Epidemiology revealed that a third of meta-analyses of antidepressant studies were written by pharma employees and that these were 22 times less likely than other meta-studies to include negative statements about the drug. © 2016 Scientific American
Link ID: 21860 - Posted: 02.04.2016
Heidi Ledford Difficulty with concentration, memory and other cognitive tasks is often associated with depression. In the past quarter of a century, a wave of drugs has transformed the treatment of depression. But the advances have struggled to come to grips with symptoms that often linger long after people start to feel better: cognitive problems such as memory loss and trouble concentrating. On 3 February, the US Food and Drug Administration (FDA) will convene a meeting of its scientific advisers to discuss whether such cognitive impairments are components of the disorder that drugs might be able to target — or just a result of depressed mood. The discussion will help the agency to decide whether two companies that sell the antidepressant vortioxetine should be allowed to label it as a treatment for the cognitive effects. A ‘yes’ could spur drug developers to invest in ways to test cognitive function during their antidepressant trials. Psychiatrists have long noted that some people with depression also struggle to concentrate and to make decisions. The question has been whether such difficulties are merely an offshoot of altered mood and would thus clear up without specific treatment, says Diego Pizzagalli, a neuroscientist at McLean Hospital, an affiliate of Harvard Medical School in Belmont, Massachusetts. But some patients who report improved mood after treatment still struggle with cognitive deficits — so psychiatrists sometimes prescribe concentration-enhancing drugs that are approved to treat attention deficit hyperactivity disorder to people with depression. © 2016 Nature Publishing Group
By Sara Solovitch It was November 2012 when Dennis Hartman, a Seattle business executive, managed to pull himself out of bed, force himself to shower for the first time in days and board a plane that would carry him across the country to a clinical trial at the National Institute of Mental Health (NIMH) in Bethesda. After a lifetime of profound depression, 25 years of therapy and cycling through 18 antidepressants and mood stabilizers, Hartman, then 46, had settled on a date and a plan to end it all. This clinical trial would be his last stab at salvation. For 40 minutes, he sat in a hospital room as an IV drip delivered ketamine through his system. Several more hours passed before it occurred to him that all his thoughts of suicide had evaporated. “My life will always be divided into the time before that first infusion and the time after,” Hartman says today. “That sense of suffering and pain draining away. I was bewildered by the absence of pain.” Ketamine, popularly known as the psychedelic club drug Special K, has been around since the early 1960s. It is a staple anesthetic in emergency rooms, regularly used for children when they come in with broken bones and dislocated shoulders. It’s an important tool in burn centers and veterinary medicine, as well as a notorious date-rape drug, known for its power to quickly numb and render someone immobile.
By BENEDICT CAREY A new approach to treating early schizophrenia, which includes family counseling, results in improvements in quality of life that make it worth the added expense, researchers reported on Monday. The study, published by the journal Schizophrenia Bulletin, is the first rigorous cost analysis of a federally backed treatment program that more than a dozen states have begun trying. In contrast to traditional outpatient care, which generally provides only services covered by insurance, like drugs and some psychotherapy, the new program offers other forms of support, such as help with jobs and school, as well as family counseling. The program also tries to include the patients — people struggling with a first psychotic “break” from reality, most of them in their late teens and 20s — as equals in decisions about care, including drug dosage. In a widely anticipated study last fall, called the Raise trial, researchers reported that after two years, people who got this more comprehensive care did better on a variety of measures than those who received the standard care. But the study found no evidence of related cost savings or differences in hospitalization rates, a prime driver of expense. As lawmakers in Washington are considering broad changes in mental health care, cost issues loom especially large. Outside experts said this analysis — which was based on the Raise trial data — was an important test of the new care program’s value. “This is the way cost analysis should be done,” Sherry Glied, a professor of public service and the dean of New York University’s graduate school of public service, said. “One way to think about it is to ask, if this program were a drug, would we pay for it? And the answer is yes.” © 2016 The New York Times Company
Link ID: 21842 - Posted: 02.01.2016
By CHARLES SIEBERT Nearly 30 years ago, Lilly Love lost her way. She had just completed her five-year tour of duty as an Alaska-based Coast Guard helicopter rescue swimmer, one of an elite team of specialists who are lowered into rough, frigid seas to save foundering fishermen working in dangerous conditions. The day after she left active service, the helicopter she had flown in for the previous three years crashed in severe weather into the side of a mountain, killing six of her former crewmates. Devastated by the loss and overcome with guilt, Love chose as her penance to become one of the very fishermen she spent much of her time in the Coast Guard rescuing. In less than a year on the job, she nearly drowned twice after being dragged overboard in high seas by the hooks of heavy fishing lines. Love would not formally receive a diagnosis of severe post-traumatic stress disorder for another 15 years. In that time, she was married and divorced three times, came out as transgender and retreated periodically to Yelapa, Mexico, where she lived in an isolated cabin accessible only by water. She eventually ended up living on a boat in a Los Angeles marina, drinking heavily and taking an array of psychotropic drugs that doctors at the West Los Angeles Veterans Administration Medical Center began to prescribe with increasing frequency as Love proved resistant to traditional treatments like counseling and group therapy. One night, after her fifth stay in the center’s psych ward, she crashed her boat into a sea wall. Finally, in 2006, she was in the veterans’ garden and happened to catch sight of the parrots being housed in an unusual facility that opened a year earlier on the grounds of the center. ‘‘This place is why I’m still here,’’ Love, now 54, told me one day last summer as I watched her undergo one of her daily therapy sessions at the facility, known as Serenity Park, a name that would seem an utter anomaly to anyone who has ever been within 200 yards of the place. © 2016 The New York Times Company
Link ID: 21839 - Posted: 01.30.2016
By BENEDICT CAREY Scientists reported on Wednesday that they had taken a significant step toward understanding the cause of schizophrenia, in a landmark study that provides the first rigorously tested insight into the biology behind any common psychiatric disorder. More than two million Americans have a diagnosis of schizophrenia, which is characterized by delusional thinking and hallucinations. The drugs available to treat it blunt some of its symptoms but do not touch the underlying cause. The finding, published in the journal Nature, will not lead to new treatments soon, experts said, nor to widely available testing for individual risk. But the results provide researchers with their first biological handle on an ancient disorder whose cause has confounded modern science for generations. The finding also helps explain some other mysteries, including why the disorder often begins in adolescence or young adulthood. “They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University who has been critical of previous large-scale projects focused on the genetics of psychiatric disorders. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.” The researchers pieced together the steps by which genes can increase a person’s risk of developing schizophrenia. That risk, they found, is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant connections between neurons as it matures. During adolescence and early adulthood, this activity takes place primarily in the section of the brain where thinking and planning skills are centered, known as the prefrontal cortex. People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests. Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number of neural connections, compared with those of unaffected people. © 2016 The New York Times Company