Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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Scicurious Guest Writer, Nicole Baganz! 4:02 PM. It took every ounce of energy I had to drag myself to the bathroom. Arriving in the room that is located 2 feet from my bed felt like a victory. I rifled through the medicine cabinet, stuck the thermometer in my mouth and collapsed on the bathroom floor. 103.2° F. Yep, I’m sick. Sleepiness. Fatigue. Loss of appetite and motivation. Lethargy. Leave me alone. We all know what it feels like to be sick. Clinicians collectively describe this group of symptoms as “sickness behavior”. Evolutionarily speaking, the idea that the immune system would produce these symptoms makes sense. An organism infected with a pathogenic bug should retreat from its social group to protect others from the spread of infection. The organism essentially shuts down in order to send every ounce of energy to the immune system to battle the bug that has invaded the body’s cells. This sickness state would facilitate recovery of the organism and also protect the community from the spread of the infection by limiting the interaction of the infected party from its entire social group. All of the symptoms of sickness behavior are displayed not only by people who have an infection, but also by those who have been diagnosed with Major Depressive Disorder (MDD). Could sickness behavior and MDD be linked? What happens in the brain to produce sickness behaviors, and how might these relate to depression? Mice are good models for scientists to use to study the effect of immune system activation on brain function and behavior (research studies that subject people to infectious agents before probing their brains in the name of science draw few willing volunteers). Laboratory mice also display sickness behavior when their immune systems are turned on. Sick rodents sleep more, eat less, and lose interest in drinking sugary water (usually a scrumptious treat for mice). They also stop interacting socially – mice are, by nature, very social creatures that like to sniff, groom, lick and cuddle up to their roommates. © 2012 Scientific American
Link ID: 17551 - Posted: 11.29.2012
By David Levine People with depression or other mental illnesses often report trouble sleeping, daytime drowsiness and other sleep-related issues. Now a growing body of research is showing that treating sleep problems can dramatically improve psychiatric symptoms in many patients. Much of the latest work illustrates how sleep apnea, a common chronic condition in which a person repeatedly stops breathing during sleep, may cause or aggravate psychiatric symptoms. In past years sleep apnea has been linked to depression in small studies and limited populations. Now a study by the Centers for Disease Control and Prevention strengthens that connection. The CDC analyzed the medical records of nearly 10,000 American adults with sleep apnea. Men diagnosed with this disorder had twice the risk of depression—and women five times the risk—compared with those without sleep apnea. Writing in the April issue of Sleep, lead author Anne G. Wheaton and her colleagues speculate that in addition to interrupting sleep, the oxygen deprivation induced by sleep apnea could harm cells and disrupt normal brain functioning. Treating this disorder shows promise for reducing symptoms of depression, a recent study at the Cleveland Clinic suggests. In the experiment, patients went to bed wearing a mask hooked up to a machine that increases air pressure in their throat. The increased pressure prevents the airway from collapsing, which is what causes breathing to cease in most cases of this disorder. Using this machine, psychiatrist Charles Bae and his colleagues treated 779 patients who had been diagnosed with sleep apnea. After an average of 90 days of sleeping with the machine, all the patients scored lower on a common depression survey than before the treatment—regardless of whether they had a prior diagnosis of depression or were taking an antidepressant. The data were presented in June at the SLEEP 2012 conference in Boston. © 2012 Scientific American
By BENEDICT CAREY For years they have lived as orphans and outliers, a colony of misfit characters on their own island: the bizarre one and the needy one, the untrusting and the crooked, the grandiose and the cowardly. Their customs and rituals are as captivating as any tribe’s, and at least as mystifying. Every mental anthropologist who has visited their world seems to walk away with a different story, a new model to explain those strange behaviors. This weekend the Board of Trustees of the American Psychiatric Association will vote on whether to adopt a new diagnostic system for some of the most serious, and striking, syndromes in medicine: personality disorders. Personality disorders occupy a troublesome niche in psychiatry. The 10 recognized syndromes are fairly well represented on the self-help shelves of bookstores and include such well-known types as narcissistic personality disorder, avoidant personality disorder, as well as dependent and histrionic personalities. But when full-blown, the disorders are difficult to characterize and treat, and doctors seldom do careful evaluations, missing or downplaying behavior patterns that underlie problems like depression and anxiety in millions of people. The new proposal — part of the psychiatric association’s effort of many years to update its influential diagnostic manual — is intended to clarify these diagnoses and better integrate them into clinical practice, to extend and improve treatment. But the effort has run into so much opposition that it will probably be relegated to the back of the manual, if it’s allowed in at all. © 2012 The New York Times Company
Link ID: 17542 - Posted: 11.27.2012
The long-held view that a full moon or even a new moon triggers psychological problems has been debunked by a study from Montreal. Researchers at the University of Laval's School of Psychology evaluated patients visiting Montreal's Sacré-Coeur Hospital and Hôtel-Dieu de Lévis between March 2005 and April 2008 and found no correlation between anxiety disorders and the phases of the moon — despite, it seems, what 80 per cent of nurses and 64 per cent of doctors surveyed believe. These researchers analyzed 771 individuals who had shown up at the emergency room with chest pains for which no medical cause could be determined. Psychological evaluations indicated many were suffering anxiety, panic attacks, mood disorders or suicidal thoughts. The time of their visit was then correlated with the phase of the moon at that moment. "We observed no full-moon or new-moon effect on psychological problems," said lead researcher Genevieve Belleville whose study is published in General Hospital Psychiatry. The study went on to suggest that health professionals may think there are more mental problems during a full-moon phase due to "self-fulfilling prophecies." © CBC 2012
The search for genes predisposing people to depression has taken an unexpected twist, according to Canadian researchers who found a clue in an obesity gene. Studies on families and twins suggest depression has a genetic component, but for 15 years, scientists haven't been able to find genes associated with the illness. Researchers at McMaster University in Hamilton, Ont., took a different approach by testing how obesity genes may be linked with depression. "We found the first gene predisposing to depression with consistent results," said David Meyre, an associate professor in clinical epidemiology and biostatistics at McMaster and a Canada Research Chair in genetic epidemiology. In Monday's issue of the journal Molecular Psychiatry, Meyre and his co-authors reported that a variant of the FTO gene may be associated with a lower risk of depression independent of the gene's effect on obesity. The common perception is that obese people become depressed because of their appearance and poor self-esteem or discrimination. Another common thought is that those who are depressed are less likely to be physically active or follow healthy eating habits. Taking antidepressants can also lead to weight gain. But the genetic findings challenge that thinking, Meyre said, since those with the genetic mutation predisposing to obesity were protected from depression. "This suggests that the FTO gene may have a broader role than initially thought with an effect on depression and other common psychiatric disorders," the researchers wrote. © CBC 2012
Richard A. Lovett Scientists have known for years that human medications, from anti-inflammatories to the hormones in birth-control pills, are ending up in waterways and affecting fish and other aquatic organisms. But researchers are only beginning to compile the many effects that those drugs seem to be having. And it isn't good news for the fish. One such drug, fluoxetine, is the active ingredient in the antidepressant Prozac. Like some other pharmaceuticals, fluoxetine is excreted in the urine of people taking it, and reaches lakes and waterways through sewage-treatment plants that are unequipped to remove it. To investigate the effects of fluoxetine, researchers have turned to a common US freshwater fish species called the fathead minnow (Pimephales promelas). Normally, fathead minnows show a complex mating behaviour, with males building the nests that females visit to lay their eggs. Once the eggs are laid and fertilized, the males tend to them by cleaning away any fungus or dead eggs. But when fluoxetine is added to the water, all of this changes, said Rebecca Klaper, an ecologist at the University of Wisconsin-Milwaukee's Great Lakes Water Institute. Klaper presented her results this week at the 2012 meeting of the North American division of the Society of Environmental Toxicology and Chemistry in Long Beach, California. © 2012 Nature Publishing Group,
In 2009, Susannah Cahalan was a healthy 24-year-old reporter for the New York Post, when she began to experience numbness, paranoia, sensitivity to light and erratic behavior. Grasping for an answer, Cahalan asked herself as it was happening, "Am I just bad at my job — is that why? Is the pressure of it getting to me? Is it a new relationship?" But Cahalan only got worse — she began to experience seizures, hallucinations, increasingly psychotic behavior and even catatonia. Her symptoms frightened family members and baffled a series of doctors. After a monthlong hospital stay and $1 million worth of blood tests and brain scans that proved inconclusive, Cahalan was seen by Dr. Souhel Najjar, who asked her to draw a clock on a piece of paper. "I drew a circle, and I drew the numbers 1 to 12 all on the right-hand side of the clock, so the left-hand side was blank, completely blank," she tells Fresh Air's Dave Davies, "which showed him that I was experiencing left-side spatial neglect and, likely, the right side of my brain responsible for the left field of vision was inflamed." As Najjar put it to her parents, "her brain was on fire." This discovery led to her eventual diagnosis and treatment for anti-NMDA receptor encephalitis, a rare autoimmune disease that can attack the brain. Cahalan says that doctors think the illness may account for cases of "demonic possession" throughout history. Cahalan's new memoir is called Brain on Fire: My Month of Madness. ©2012 NPR
By Charles Q. Choi People with schizophrenia often experience the unnerving feeling that outside forces are controlling them. Other times they feel an illusory sense of power over uncontrollable events. Now scientists find these symptoms may arise from disabilities in predicting or recognizing their own actions. The findings suggest new therapies for treating schizophrenia, which afflicts an estimated 1 percent of the world population. To see where this confusion might stem from, researchers tested two ways people are known to link actions and their outcomes. We either predict the effects of our movements or retrospectively deduce a causal connection. Healthy participants and schizophrenic patients were asked to look at a clock and occasionally push a button. Most of the time the button push was followed by a tone. The participants then told researchers what time they had pushed the button and when the tone had occurred. Healthy volunteers reported later times for each button push if it was followed by a tone. This result suggests that awareness of a link between the two events causes people to perceive less time between them. Participants also tended to estimate later button pushes even in the few cases when no tone was emitted, revealing that the subjects were predicting they would hear the sound, says psychiatrist and cognitive neuroscientist Martin Voss of Charité University Hospital and St. Hedwig Hospital in Berlin. © 2012 Scientific American
Danish researchers Krogh and colleagues randomly 115 assigned depressed people to one of two exercise programs. One was a strenuous aerobic workout - cycling for 30 minutes, 3 times per week, for 3 months. The other was various stretching exercises. The idea was that stretching was a kind of placebo control group on the grounds that, while it is an intervention, it's not the kind of exercise that gets you fit. It doesn't burn many calories, it doesn't improve your cardiovascular system, etc. Aerobic exercise is the kind that's most commonly been proposed as having an antidepressant effect. So what happened? Not much. Both groups got less depressed but there was zero difference between the two conditions. The cyclists did get physically fitter than the stretchers, losing more weight and improving on other measures. But they didn't feel any better. If this is true, it might mean that the antidepressant effects of aerobic exercise are psychological rather than physical - it's about the idea of 'exercising', not the process of becoming fitter. While many trials have found modest beneficial effects of exercise vs a "control condition", the control condition was often just doing nothing much - such as being put on a waiting-list. So the placebo effect or the motivational benefits of 'doing something', rather than the effects of exercise per se, could be behind it. In the current study though the stretching avoided that problem.
Link ID: 17463 - Posted: 11.07.2012
By Stephanie Pappas, An over-excited immune system may explain why some people are susceptible to depression, according to new research on mice. Mice whose immune systems responded to stress by overproducing an inflammatory compound called Interleukin-6 were more likely to become the mousy versions of depressed than mice with non-overactive immune systems, the research found. This same compound is elevated in depressed humans, said study researcher Georgia Hodes, suggesting hope for new depression treatments. "There's probably a subset of people with depression who have this over-sensitive inflammatory response to stress and that this is leading to the symptoms of depression," Hodes, a postdoctoral researcher at the Mount Sinai Medical Center in New York, told LiveScience. Hodes added that stress could be thought of as an allergen, like pet dander, with the over-reactive immune system making you depressed rather than giving you runny nose. "In some ways, it is an analogy to an allergy," Hodes said. "You have something that is not really dangerous, but your body thinks it is, so you have this massive immune response. In this case, the stressor is what they're having this massive immune response to." Some of the symptoms of depression — lack of energy, loss of appetite — mirror the body's response to physical illness, Hodes noted. © 2012 Yahoo! Inc.
By OLIVER SACKS HALLUCINATIONS are very startling and frightening: you suddenly see, or hear or smell something — something that is not there. Your immediate, bewildered feeling is, what is going on? Where is this coming from? The hallucination is convincingly real, produced by the same neural pathways as actual perception, and yet no one else seems to see it. And then you are forced to the conclusion that something — something unprecedented — is happening in your own brain or mind. Are you going insane, getting dementia, having a stroke? In other cultures, hallucinations have been regarded as gifts from the gods or the Muses, but in modern times they seem to carry an ominous significance in the public (and also the medical) mind, as portents of severe mental or neurological disorders. Having hallucinations is a fearful secret for many people — millions of people — never to be mentioned, hardly to be acknowledged to oneself, and yet far from uncommon. The vast majority are benign — and, indeed, in many circumstances, perfectly normal. Most of us have experienced them from time to time, during a fever or with the sensory monotony of a desert or empty road, or sometimes, seemingly, out of the blue. Many of us, as we lie in bed with closed eyes, awaiting sleep, have so-called hypnagogic hallucinations — geometric patterns, or faces, sometimes landscapes. Such patterns or scenes may be almost too faint to notice, or they may be very elaborate, brilliantly colored and rapidly changing — people used to compare them to slide shows. At the other end of sleep are hypnopompic hallucinations, seen with open eyes, upon first waking. These may be ordinary (an intensification of color perhaps, or someone calling your name) or terrifying (especially if combined with sleep paralysis) — a vast spider, a pterodactyl above the bed, poised to strike. © 2012 The New York Times Company
By WILLIAM C. RHODEN We’ve seen it hundreds of times. An athlete is injured and within seconds is surrounded by an armada of medical personnel: trainers, assistant trainers, team doctors. The athlete is helped off the field, given a diagnosis, treated and sent to physical therapy, often to return miraculously in a week or two. But when that same athlete has a mental disorder, there is no armada of trainers, no team doctors. That athlete is often abandoned. For all of the current focus on traumatic brain injury as a result of concussions, mental illness, often overlooked, exists at every level of sports. Sports too often is a masking agent that hides deeply rooted mental health issues. The better the athlete, the more desperate to reach the next level, the less likely he or she will reach out for help. The gladiator mentality remains a primary barrier. “Mental health has a stigma that is tied into weakness and is absolutely the antithesis of what athletes want to portray,” said Dr. Thelma Dye Holmes, the executive director of the Northside Center for Child Development, one of New York’s oldest mental health agencies, serving more than 1,500 children and their families. “Mental health is not something that you can easily know,” Holmes said. “You feel a pain in your side, you have discomfort. Mental illness is vague and makes us uneasy. Especially when it comes to athletes, there tends to be a stigma around coming forward.” © 2012 The New York Times Company
Link ID: 17436 - Posted: 10.30.2012
by Anil Ananthaswamy For the first time, one of the tics that bedevil people with Tourette's has been induced in volunteers who don't themselves have the disorder, an experiment that might help us to understand and even treat the condition. Jennifer Finis of Heinrich Heine University in Düsseldorf, Germany, and her colleagues suspected that a type of Tourette's tic called echophenomena, which involves mimicking other's movements, may be caused by over-excitation of the supplementary motor area (SMA) – a brain region involved in the initiation of movement. To investigate further, her team used a non-invasive technique called repetitive transcranial magnetic stimulation (rTMS), which involves delivering brief but strong magnetic pulses to the scalp. By changing the frequency of rTMS, the stimulation could either inhibit or excite the SMA. Thirty seconds before and after rTMS, 30 volunteers were shown video clips of someone making a spontaneous movement. Those who'd had their SMA excited were three times as likely to imitate the kind of behaviour they saw in the clips than those who'd had it suppressed. "We suspect that this is a mechanism that might underlie tics more generally than just echophenomena in people with Tourette's syndrome," says Peter Enticott of Monash University in Melbourne, Australia, who worked on the study. © Copyright Reed Business Information Ltd.
Link ID: 17434 - Posted: 10.30.2012
By Neil Swidey IMAGINE THAT ONE NIGHT you put your bright, athletic, well-adjusted 8-year-old son to bed, a kid who loves playing baseball and cracking jokes and scarfing down chocolate chip cookies. The next morning, he wakes up as someone entirely different, and in subsequent days turns into someone unrecognizable. He’s manic, spending hours doing sit-ups or running laps on the driveway — unwilling to sit down even for a minute. He alternates between tears of soul-crushing sadness and tantrums of rage directed at you and your spouse. He’s obsessed with the unhealthiness of food, refusing to eat or drink much of anything. More than anything, though, all the comforting touchstones of his life — home, school, even sleep — have suddenly been transformed into dangers. He seems trapped in a horror movie, his fear unmistakable in the way his pupils have overtaken the irises of both his eyes. As this bizarre behavior continues, you find yourself staring at your formerly normal, healthy son and you can’t help but wonder, Where did my boy go? You ask yourself: Is this what children of Alzheimer’s patients mean when they talk about looking at a loved one who’s no longer there? You take your son to your pediatrician, a sympathetic and smart woman who is nonetheless flummoxed. Because some of your son’s symptoms appear to be compulsions, she refers you to a psychologist. Actually, because the need for pediatric mental health treatment dwarfs the supply of mental health professionals, your pediatrician turns to a state referral service called MCPAP, or Massachusetts Child Psychiatry Access Project. © 2012 NY Times Co.
By ARTHUR A. STONE DESPITE the beating that Mondays have taken in pop songs — Fats Domino crooned “Blue Monday, how I hate blue Monday” — the day does not deserve its gloomy reputation. Two colleagues and I recently published an analysis of a remarkable yearlong survey by the Gallup Organization, which conducted 1,000 live interviews a day, asking people across the United States to recall their mood in the prior day. We scoured the data for evidence that Monday was bluer than Tuesday or Wednesday. We couldn’t find any. Mood was evaluated with several adjectives measuring positive or negative feelings. Spanish-only speakers were queried in Spanish. Interviewers spoke to people in every state on cellphones and land lines. The data unequivocally showed that Mondays are as pleasant to Americans as the three days that follow, and only a trifle less joyful than Fridays. Perhaps no surprise, people generally felt good on the weekend — though for retirees, the distinction between weekend and weekdays was only modest. Likewise, day-of-the-week mood was gender-blind. Over all, women assessed their daily moods more negatively than men did, but relative changes from day to day were similar for both sexes. And yet still, the belief in blue Mondays persists. Several years ago, in another study, I examined expectations about mood and day of the week: two-thirds of the sample nominated Monday as the “worst” day of the week. Other research has confirmed that this sentiment is widespread, despite the fact that, well, we don’t really feel any gloomier on that day. © 2012 The New York Times Company
Alison Abbott In 1965, health authorities in Camberwell, a bustling quarter of London's southward sprawl, began an unusual tally. They started to keep case records for every person in the area who was diagnosed with schizophrenia, depression, bipolar disorder or any other psychiatric condition. Decades later, when psychiatrists looked back across the data, they saw a surprising trend: the incidence of schizophrenia had more or less doubled, from around 11 per 100,000 inhabitants per year in 1965 to 23 per 100,000 in 1997 — a period when there was no such rise in the general population (J. Boydell et al. Br. J. Psychiatry 182, 45–49; 2003). The result raised a question in many researchers' minds: could the stress of city life be increasing the risk of schizophrenia and other mental-health disorders? The question is an urgent one. Back in 1950, less than one-third of the world's population lived in cities. Now, lured by the prospect of work and opportunity, more than half do. Mental illnesses already comprise the world's biggest disease burden after infectious diseases and, although global statistics do not yet show any major increase in incidence, the cost is rising. In Germany, the number of sick days taken for psychiatric ailments doubled between 2000 and 2010; in North America, up to 40% of disability claims for work absence are related to depression, according to some estimates. “It seems that cities may be making us sick,” says Jane Boydell at the Institute of Psychiatry in London, who led the Camberwell study. Anecdotally, the link between cities, stress and mental health makes sense. Psychiatrists know that stress can trigger mental disorders — and modern city life is widely perceived as stressful. City dwellers typically face more noise, more crime, more slums and more people jostling on the streets than do those outside urban areas. Those who have jobs complain of growing demands on them in the workplace, where they are expected to do much more in less time. © 2012 Nature Publishing Group
By RICHARD A. FRIEDMAN, M.D. Speed, instant gratification, accessibility — these are a few of the appealing hallmarks of digital technology. It’s no coincidence that we love our smart wireless devices: Humans are a notoriously impatient species, born with a preference for immediate rewards. But the virtues of the digital age are not always aligned with those of psychotherapy. It takes time to change behavior and alleviate emotional pain, and for many patients constant access is more harmful than helpful. These days, as never before, therapists are struggling to recalibrate their approach to patients living in a wired world. For some, the new technology is clearly a boon. Let’s say you have the common anxiety disorder social phobia. You avoid speaking up in class or at work, fearful you’ll embarrass yourself, and the prospect of going to a party inspires dread. You will do anything to avoid social interactions. You see a therapist who sensibly recommends cognitive-behavioral therapy, which will challenge your dysfunctional thoughts about how people see you and as a result lower your social anxiety. You find that this treatment involves a fair amount of homework: You typically have to keep a written log of your thoughts and feelings to examine them. And since you see your therapist weekly, most of the work is done solo. As it turns out, there is a smartphone app that will prompt you at various times during the day to record these social interactions and your emotional response to them. You can take the record to your therapist, and you are off and running. © 2012 The New York Times Company
Link ID: 17345 - Posted: 10.09.2012
By RICHARD A. FRIEDMAN, M.D. You will never guess what the fifth and sixth best-selling prescription drugs are in the United States, so I’ll just tell you: Abilify and Seroquel, two powerful antipsychotics. In 2011 alone, they and other antipsychotic drugs were prescribed to 3.1 million Americans at a cost of $18.2 billion, a 13 percent increase over the previous year, according to the market research firm IMS Health. Those drugs are used to treat such serious psychiatric disorders as schizophrenia, bipolar disorder and severe major depression. But the rates of these disorders have been stable in the adult population for years. So how did these and other antipsychotics get to be so popular? Antipsychotic drugs have been around for a long time, but until recently they were not widely used. Thorazine, the first real antipsychotic, was synthesized in the 1950s; not just sedating, it also targeted the core symptoms of schizophrenia, like hallucinations and delusions. Later, it was discovered that antipsychotic drugs also had powerful mood-stabilizing effects, so they were used to treat bipolar disorder, too. Then, starting in 1993, came the so-called atypical antipsychotic drugs like Risperdal, Zyprexa, Seroquel, Geodon and Abilify. Today there are 10 of these drugs on the market, and they have generally fewer neurological side effects than the first-generation drugs. Originally experts believed the new drugs were more effective than the older antipsychotics against such symptoms of schizophrenia as apathy, social withdrawal and cognitive deficits. But several recent large randomized studies, like the landmark Catie trial, failed to show that the new antipsychotics were any more effective or better tolerated than the older drugs. © 2012 The New York Times Company
Link ID: 17297 - Posted: 09.25.2012
By Gary Stix Neuroscientists have devoted inordinate energy in recent years to publicize the need for, not only gene maps, but for a full wiring diagram of all brain circuits. The benefits of a connectome as it is known might yield new understanding that could eventually result in pharmaceuticals for intractable psychiatric disorders. This ultimate neural network might even divvy up intimations of the workings of consciousness. The futurist contingent, many of whom began careers hacking computers not neural circuity, has speculated that a whole brain blueprint of you or me might be copied to a hard drive so that we can live for a digital eternity like Max Headroom. Christof Koch, the chief scientist at the Allen Institute for Brain Science, the organization that produced the gene map, dismissed facile optimism about the prospects for these scenarios with a commentary in Science last month. In it, he calculated that it could take 2000 years to analyze all of the possible interactions among the 1,000 different proteins that populate a single synapse. Koch then went on to speculate about a way of reducing the complexity of such calculations. The question still remains of how we will know when we have actually started to make sense of the tangle of wiring that populates the deepest recesses inside our skulls. One plausible answer: when the FDA approves a new drug that fundamentally advances treatment of schizophrenia, the psychiatric illness that has aberrant effects on a multitude of neural pathways—an iconic example of the brain’s underlying complexity. © 2012 Scientific American
Link ID: 17289 - Posted: 09.22.2012
By DAVID TULLER Chronic fatigue syndrome is not caused by a mouse retrovirus, according to a study initiated by the National Institutes of Health to settle what had become a contentious scientific question. The long-awaited results, posted online Tuesday in the journal mBio, found no link between the illness, also called myalgic encephalomyelitis, and mouse leukemia retroviruses, including one called XMRV. Two earlier studies had identified higher levels of the viruses in patients with chronic fatigue syndrome. Later research did not confirm the finding, and scientists blamed laboratory contamination for the earlier results. The N.I.H. asked Dr. Ian Lipkin, a virologist at Columbia, to investigate. Dr. Lipkin recruited in the effort scientists who initially reported the link to mouse retroviruses, and they serve as authors on the mBio paper. In the study, none of the researchers reported finding mouse leukemia viruses in any of 293 blood samples, half from people with chronic fatigue syndrome and half from those without it. An estimated one million people in the United States have the condition; many are severely disabled and homebound. Dr. Lipkin said that he viewed chronic fatigue syndrome as a major illness and intended to use blood samples he had obtained to investigate the causes. Copyright 2012 The New York Times Company