Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By Erin Blakemore Despite all that neurotic clucking and scratching, domestic chickens are pretty unflappable. After all, we’ve bred them to be that way, preferring chill chicks to freaked-out fowl. But the behaviors of more anxious chickens could do more than ruffle a bunch of feathers: New research suggests that studying the genome of flustered birds could shed light on human mental disorders. In a new study published in the journal Genetics, evolutionary biologist Dominic Wright and his team looked at whether there’s a genetic connection between anxious behavior in chickens, mice and humans. Despite the compact size of the chicken genome — it’s just a third of the size of a human’s — the birds’ genes share surprising similarity to those of people. There's another reason why chickens are so great for genetic research. Because there are both wild and domesticated chickens, researchers can observe their contrasting behaviors and easily pin them to genetic differences. Wright bred wild red junglefowl chickens with their calmer cousins, white leghorn chickens, for the experiment. After eight generations, his team was able to run open field tests — experiments during which the birds were put in a brightly-lit arena and assessed for how much time they spent cowering on the periphery instead of strutting through the room. These behavioral tests helped the team identify brave and anxious birds, then narrow down areas of the genome related to variations in anxiety. They identified 10 candidate genes in the hypothalamus, an area of the brain which helps regulate anxiety.
By Elizabeth Pennisi Whether foraging for food, caring for young, or defending the nest, the worker castes of carpenter ants toil selflessly for their queen and colony. Now, biologists have figured out how to make some of those worker ants labor even harder, or change their very jobs in ant society, all by making small chemical modifications to their DNA. The finding calls attention to a new source of behavioral flexibility, and drives home the idea that so-called epigenetic modifications can connect genes to the environment, linking nature to nurture. The work is “a pioneering study establishing a causal link between epigenetics and complex social behavior,” says Ehab Abouheif, an evolutionary developmental biologist at McGill University, Montreal, in Canada. “These mechanisms may extend far beyond ants to other organisms with social behavior.” Insect biologists have long debated whether the division of labor in these sophisticated species with castes is driven by colony needs or is innate. Evidence in honey bees had pointed toward a genetic difference between queens and workers. In the past several years, however, work in both honey bees and ants had indicated that epigenetic modifications—changes to DNA other than to its sequence of bases (or DNA “letters”)—influence caste choices, indicating environmental factors can be pivotal. But subsequent research about one type of change, methylation, led to contradictory conclusions. © 2016 American Association for the Advancement of Science.
Link ID: 21744 - Posted: 01.02.2016
Bruce Bower Craig Bryan treats military personnel who struggle with thoughts of ending their own lives, as well as those who’ve survived an actual suicide attempt. But these days he’s fighting an uphill battle. Suicide rates in the United States have been rising, especially among veterans and members of the armed forces. Traditional assumptions about why people kill themselves have not led to effective strategies for suicide prevention, Bryan says. So in recent years psychologists and others have been reconsidering basic beliefs about why people carry out the ultimate act of self-destruction. “There has been an explosion of new thinking about suicide in the past decade,” says Bryan, a clinical psychologist at the University of Utah in Salt Lake City. This shift in focus was inspired by psychologist Thomas Joiner’s introduction in 2005 of the interpersonal theory of suicide. Unlike previous theorists, Joiner, of Florida State University in Tallahassee, treated thinking about suicide and attempting suicide as separate experiences, each with its own explanations and risk factors. Joiner’s approach has inspired much new suicide research by Bryan and others. One line of work suggests that three factors render individuals especially prone to moving from suicidal thoughts to actions: a partly inborn ability to withstand pain, self-hate triggered by extremely distressing experiences and, finally, access to guns or other lethal means. © Society for Science & the Public 2000 - 2015.
Link ID: 21738 - Posted: 12.30.2015
Carl Zimmer Throughout the day, a clock ticks inside our bodies. It rouses us in the morning and makes us sleepy at night. It raises and lowers our body temperature and at the right times, and regulates the production of insulin and other hormones. From Our Advertisers The body’s circadian clock even influences our thoughts and feelings. Psychologists have measured some of its effects on the brain by having people take cognitive tests at different times of day. As it turns out, late morning turns out to be the best time to try doing tasks such as mental arithmetic that demand that we hold several pieces of information in mind at once. Later in the afternoon is the time to attempt simpler tasks, like searching for a particular letter in a page of gibberish. Another clue about the clock in our brains comes from people with conditions such as depression and bipolar disorder. People with these disorders often have trouble sleeping at night, or feel groggy during the day. Some people with dementia experience “sundowning,” becoming confused or aggressive at the end of the day. “Sleep and activity cycles are a very big part of psychiatric illnesses,” said Huda Akil, a neuroscientist at the University of Michigan. Yet neuroscientists have struggled to understand exactly how the circadian clock affects our minds. After all, researchers can’t simply pop open a subject’s skull and monitor his brain cells over the course of each day. A few years ago, Dr. Akil and her colleagues came up with an idea for the next best thing. © 2015 The New York Times Company
By BENEDICT CAREY SAN FRANCISCO — The idea was to go out in an emotional swan dive, a lunge for the afterlife that would stretch his 17-year-old imagination. He settled on a plan and shared the details with a Facebook friend: He would drop DMT, a powerful psychedelic, and then cut his throat. “Everyone was telling me what I could and couldn’t do — doctors, my parents,” said Frank, now a 19-year-old college student. “I was going to hurt myself, to show people, ‘Look, I am still in control of my life.’” And so, in time, he was. Frank, who eight months earlier had received a diagnosis of psychosis, the signature symptom of schizophrenia, and had been in and out of the hospital, gradually learned to take charge of his own recovery, in a new approach to treatment for people experiencing a first psychotic “break” with reality. At a time when lawmakers in Washington are debating large-scale reforms to the mental health care system, analysts are carefully watching a handful of new first-break programs like the one that treated Frank in New York as a way to potentially ease the cycle of hospitalization and lifetime disability that afflict so many mentally ill people. More than two million people in the United States have received a diagnosis of schizophrenia. Most are consigned to whatever treatment is available amid a hodgepodge of programs that often focus on antipsychotic drugs to blunt delusions and paranoia — medicines that can come with side effects so debilitating that many patients go off them and end up in a loop of hospitalization and despair. But over the past several years, a number of states have set up programs with a different approach, emphasizing supportive services, like sustained one-on-one therapy, school and work assistance, and family education, as well as medication. The therapists work to engage each patient as an equal partner in decisions — including about medication dosage, to make it as tolerable as possible. © 2015 The New York Times Company
Link ID: 21731 - Posted: 12.29.2015
By BENEDICT CAREY Dr. Robert L. Spitzer, who gave psychiatry its first set of rigorous standards to describe mental disorders, providing a framework for diagnosis, research and legal judgments, as well as a lingua franca for the endless social debate over where to draw the line between normal and abnormal behavior, died on Friday. He was 83. From Our Advertisers Dr. Spitzer died from complications of heart disease at the assisted living facility where he lived in Seattle, his wife, Janet Williams, said. The couple had moved to Seattle from Princeton, N.J., this year. Dr. Spitzer’s remaking of psychiatry began with an early interest in one of the least glamorous and, historically, most ignored corners of the field: measurement. In the early 1960s, the field was fighting to sustain its credibility, in large part because diagnoses varied widely from doctor to doctor. For instance, a patient told he was depressed by one doctor might be called anxious or neurotic by another. The field’s diagnostic manual, at the time a pamphlet-like document rooted in Freudian ideas, left wide latitude for the therapist’s judgment. Dr. Spitzer, a rising star at Columbia University, was himself looking for direction, increasingly frustrated with Freudian analysis. A chance meeting with a colleague working on a new edition of the manual — the Diagnostic and Statistical Manual of Mental Disorders, or the D.S.M. for short — led to a job taking notes for the committee debating revisions. There, he became fascinated with reliable means for measuring symptoms and behavior — i.e., assessment. “At the time, there was zero interest in assessment,” said Dr. Michael First, a professor of clinical psychiatry at Columbia. “He saw how important it was, and his whole career led to assessment being taken seriously.” © 2015 The New York Times Company
Jon Hamilton Taking antidepressants during the second or third trimester of pregnancy may increase the risk of having a child with autism spectrum disorder, according to a study of Canadian mothers and children published Monday in JAMA Pediatrics. But scientists not involved in the research say the results are hard to interpret and don't settle the long-running debate about whether expectant mothers with depression should take antidepressants. "This study doesn't answer the question," says Bryan King, program director of the autism center at Seattle Children's Hospital and a professor of psychiatry and behavioral sciences at the University of Washington. "My biggest concern is that it will be over-interpreted," says King, who wrote an editorial that accompanied the study. "It kind of leaves you more confused," says Alan Brown, a professor of psychiatry and epidemiology at Columbia University who studies risk factors for autism. "Mothers shouldn't get super worried about it," he says. One reason it's confusing is that there's strong evidence that mothers with depression are more likely than other women to have a child with autism, whether or not they take antidepressants during pregnancy. King and Brown say that makes it very hard to disentangle the effects of depression itself from those of the drugs used to treat it. © 2015 npr
By ALAN SCHWARZ Andrew Rios’s seizures began when he was 5 months old and only got worse. At 18 months, when an epilepsy medication resulted in violent behavior, he was prescribed the antipsychotic Risperdal, a drug typically used to treat schizophrenia and bipolar disorder in adults, and rarely used for children as young as 5 years. From Our Advertisers When Andrew screamed in his sleep and seemed to interact with people and objects that were not there, his frightened mother researched Risperdal and discovered that the drug was not approved, and had never even been studied, in children anywhere near as young as Andrew. “It was just ‘Take this, no big deal,’ like they were Tic Tacs,” said Genesis Rios, a mother of five in Rancho Dominguez, Calif. “He was just a baby.” Cases like that of Andrew Rios, in which children age 2 or younger are prescribed psychiatric medications to address alarmingly violent or withdrawn behavior, are rising rapidly, data shows. Many doctors worry that these drugs, designed for adults and only warily accepted for certain school-age youngsters, are being used to treat children still in cribs despite no published research into their effectiveness and potential health risks for children so young. Almost 20,000 prescriptions for risperidone (commonly known as Risperdal), quetiapine (Seroquel) and other antipsychotic medications were written in 2014 for children 2 and younger, a 50 percent jump from 13,000 just one year before, according to the prescription data company IMS Health. Prescriptions for the antidepressant fluoxetine (Prozac) rose 23 percent in one year for that age group, to about 83,000. The company’s data does not indicate how many children received these prescriptions (many children receive several prescriptions a year), but previous studies suggest that the number is at least 10,000. IMS Health researched the data at the request of The New York Times. © 2015 The New York Times Company
Call it the optimism fallacy. It’s widely thought that staying happy and stress-free helps keep you healthy. But a massive study on the link between mood and mortality suggests that happiness actually has no effect on death rates. Other research that has found the opposite must have been mixing up cause and effect, says epidemiologist Richard Peto of the University of Oxford. “It’s likely that being ill makes you unhappy, rather than the other way round.” The power of positive thinking has passed into folklore, helping to fuel a large self-help industry – not to mention people who like to post “inspirational” quotes on social media. Some cancer bloggers complain that common advice to “fight” their illness by staying cheerful can be unhelpful. “Forcing optimism may have its own negative consequences,” says Gayle Sulik, who writes the “Pink Ribbon Blues” blog. “The emotional work to display optimism when a person does not feel it may add to stress.” To find out if there is indeed a link, Peto’s team conducted surveys with more than 700,000 UK women. At the start, they were asked questions about their health and how happy and relaxed they felt. A year later, the questionnaire was resent to a random sample of the women. Their responses suggested that most still felt the same as they did the year before. Ten years later, after allowing for any initial disparities in health, there turned out to be no difference in death rates between those who saw their glass as half-full or half-empty. © Copyright Reed Business Information Ltd.
Angus Chen Loneliness has been linked to everything from heart disease to Alzheimer's disease. Depression is common among the lonely. Cancers tear through their bodies more rapidly, and viruses hit them harder and more frequently. In the short term, it feels like the loneliness will kill you. A study suggests that's because the pain of loneliness activates the immune pattern of a primordial response commonly known as fight or flight. For decades, researchers have been seeing signs that the immune systems of lonely people are working differently. Lonely people's white blood cells seem to be more active in a way that increases inflammation, a natural immune response to wounding and bacterial infection. On top of that, they seem to have lower levels of antiviral compounds known as interferons. That seemed to provide a link to a lot of the poor health outcomes associated with loneliness, since chronic inflammation has been linked to everything from cancer to depression. The human body isn't built to hold a high level of inflammation for years. "That explains very clearly why lonely people fall at increased risk for cancer, neurodegenerative disease and viral infections as well," says Steve Cole, a genomics researcher at the University of California, Los Angeles, and lead author on the study published in the Proceedings of the National Academy of Sciences on Monday But it still doesn't explain how or why loneliness could change our bodies. To find that out, Cole and his collaborators tracked 141 people over five years. Every year, the researchers measured how lonely the participants felt and took blood samples to track the activity of genes involved with immunity and inflammation. © 2015 npr
Sara Reardon Suicide is a puzzle. Fewer than 10% of people with depression attempt suicide, and about 10% of those who kill themselves were never diagnosed with any mental-health condition. Now, a study is trying to determine what happens in the brain when a person attempts suicide, and what sets such people apart. The results could help researchers to understand whether suicide is driven by certain brain biology — and is not just a symptom of a recognized mental disorder. The project, which launched this month, will recruit 50 people who have attempted suicide in the two weeks before enrolling in the study. Carlos Zarate, a psychiatrist at the US National Institute of Mental Health in Bethesda, Maryland, and his colleagues will compare these people's brain structure and function to that of 40 people who attempted suicide more than a year ago, 40 people with depression or anxiety who have never attempted suicide and a control group of 40 healthy people. In doing so, the researchers hope to elucidate the brain mechanisms associated with the impulse to kill oneself. Zarate's team will also give ketamine, a psychoactive ‘party drug’, to the group that has recently attempted suicide. Ketamine, which is sometimes used to treat depression, can quickly arrest suicidal thoughts and behaviour — even in cases when it does not affect other symptoms of depression1. The effect is known to last for about a week. © 2015 Nature Publishing Group,
By Nicholas Bakalar Bright light therapy has been used effectively for seasonal affective disorder, the kind of depression that comes on at a specific time every year, often the dark days of late fall and winter, and then lifts. Now a new study has found that it may work to treat nonseasonal depression as well. Researchers randomly assigned 122 patients, 19 to 60 years old, with major depression to receive one of four treatments: 30 minutes of daily exposure to fluorescent light; 20 milligrams of Prozac daily; both light and Prozac; and a control group that received a dummy pill and exposure to an electric air purifier. The study, in JAMA Psychiatry, lasted eight weeks. Using well-validated scales that quantify depression severity, the researchers found improvements in all four groups. The difference between Prozac alone and the placebo was not statistically significant, but light therapy alone was significantly better than placebo, and light therapy with medication was the most effective treatment of all. “This is the first study to show that light treatment is an option for people with nonseasonal depression, which is much more common than seasonal depression,” said the lead author, Dr. Raymond W. Lam, a professor of psychiatry at the University of British Columbia. “Light treatment can be combined with medicine and psychotherapy, and it’s a safe treatment without a lot of side effects.” © 2015 The New York Times Company
By Jonathan Webb Science reporter, BBC News A study of 153 brain scans has linked a particular furrow, near the front of each hemisphere, to hallucinations in schizophrenia. This fold tends to be shorter in those patients who hallucinate, compared with those who do not. It is an area of the brain that appears to have a role in distinguishing real perceptions from imagined ones. Researchers say the findings, published in Nature Communications, might eventually help with early diagnosis. The brain wrinkle, called the paracingulate sulcus or PCS, varies considerably in shape between individuals. It is one of the final folds to develop, appearing in the brain only just before birth. "The brain develops throughout life, but aspects such as whether the PCS is going to be a particularly prominent fold - or not -may be apparent in the brain at an early stage," said Jon Simons, a neuroscientist at the University of Cambridge, UK. "It might be that a reduction in this brain fold gives somebody a predisposition towards developing something like hallucinations later on in life." If further work shows that the difference can be detected before the onset of symptoms, for example, Dr Simons said it might be possible to offer extra support to people who face that elevated risk. But he stressed that schizophrenia is a complicated phenomenon. Hallucinations are one of the main symptoms, but some patients are diagnosed on the basis of other irregular thought processes. "We've known for some time that disorders like schizophrenia are not down to a single region of the brain. Changes are seen throughout various different areas. "To be able to pin such a key symptom to a relatively specific part of the brain is quite unusual." © 2015 BBC.
Link ID: 21644 - Posted: 11.18.2015
By Elahe Izadi The days growing shorter and colder can be more than just a nuisance; the seasonal change can also trigger clinical depression. Those who suffer from seasonal affective disorder, or SAD, may turn to a light box to help make them feel better. But a new study suggests another form of therapy could be more powerful and enduring: talking. The benefits of cognitive behavioral therapy — a form of talk therapy — outlasted light therapy sessions for people suffering from SAD, according to a study published Thursday in the American Journal of Psychiatry. "Light therapy is a treatment that suppresses symptoms as long as you're using it," said lead author Kelly Rohan, a psychology professor at the University of Vermont. "So if you're not using it, there's no reason to expect the continued benefit for a treatment that works that way, whereas cognitive behavioral therapy teaches skills." And the people who learn those skills can use them long after their therapy sessions. For the study, researchers tracked 177 people who suffer from major depression that follows a recurring seasonal pattern. About half of the subjects received six weeks of daily light therapy; the others received 12 sessions of cognitive behavioral therapy over the same period of time.
By Nicholas Bakalar A person with depression is at higher risk for heart disease, and a person with heart disease is at higher risk for depression. The link between the two diseases is complex and not entirely understood. Many of the effects of depression — feeling unable to exercise or eat properly, for example — and the behaviors associated with depression, like smoking and abusing alcohol, are well established risk factors for heart disease. Some studies have suggested that insomnia, another symptom of depression, may also increase the risk for cardiovascular illness. Depression can also make heart disease worse. Heart patients with depression may find it more difficult to take medications and comply with the behavioral demands of living with heart disease. Depression may also have destructive physiological effects on heart rhythm, blood pressure, stress hormone levels and blood clotting, studies have shown. These may be among the reasons why depressed patients with stable cardiovascular disease, or those who have survived a heart attack or had coronary bypass surgery, are at two to three times higher risk of dying than similar patients without depression. Treating depressed heart patients with drugs like Prozac may help. These drugs, known as selective serotonin reuptake inhibitors, or S.S.R.I.’s, in addition to relieving depression, have blood-thinning effects that may be beneficial against heart disease. “It is clear that treatment with an S.S.R.I. reduces cardiac mortality in depressed patients post heart attack,” said Dr. Steven P. Roose, a professor of psychiatry at Columbia. “What is not clear is whether the reduction in mortality results from the antidepressant effect of the medication or the anti-platelet effect of the medication.” © 2015 The New York Times Company
By DAVE ITZKOFF and BENEDICT CAREY For the first time in more than a year, the widow of the actor Robin Williams is speaking publicly about the circumstances that preceded Mr. Williams’s death, and sharing details about a disease he had when he died. Stories from Our Advertisers In interviews with People magazine and with ABC News, the widow, Susan Schneider Williams, laid the blame for her husband’s suicide in 2014 not on depression but on diffuse Lewy body dementia. “It was not depression that killed Robin,” Mrs. Williams said in the People magazine interview. “Depression was one of let’s call it 50 symptoms and it was a small one.” She added: “This was a very unique case and I pray to God that it will shed some light on Lewy bodies for the millions of people and their loved ones who are suffering with it. Because we didn’t know. He didn’t know.” Parts of an interview with Mrs. Williams were shown Tuesday on ABC’s “Good Morning America,” with further segments scheduled for that evening on the network’s “World News Tonight” and “Nightline” programs, and Friday on its morning talk show “The View.” Robin Williams was one of the most explosively, exhaustingly, prodigiously verbal comedians who ever lived, says film critic A. O. Scott. And the only thing faster than Williams’s mouth was his mind. By Adam Freelander on Publish Date August 12, 2014. Photo by ABC, via Associated Press. Watch in Times Video » Mr. Williams, the stand-up comic and star of “Mork & Mindy,” “Good Morning, Vietnam,” “Good Will Hunting” (for which he won an Oscar) and “Dead Poets Society,” killed himself on Aug. 11, 2014, in the home he shared with Mrs. Williams in Tiburon, Calif. He was 63. © 2015 The New York Times Company
By Simon Makin Most people have felt depressed or anxious, even if those feelings have never become debilitating. And how many times have you heard someone say, “I'm a little OCD”? Clearly, people intuitively think that most mental illnesses have a spectrum, ranging from mild to severe. Yet most people do not know what it feels like to hallucinate—to see or hear things that are not really there—or to have delusions, persistent notions that do not match reality. You're psychotic, or you're not, according to conventional wisdom. Evidence is growing, however, that there may be no clear dividing line. Psychiatrists have long debated whether psychosis exists on a spectrum, and researchers have been investigating the question for more than a decade now. A 2013 meta-analysis, combining much of the existing data, by Jim van Os of Maastricht University in the Netherlands and Richard Linscott of the University of Otago in New Zealand, found the prevalence of hallucinations and delusions in the general population was 7.2 percent—much higher than the 0.4 percent prevalence of schizophrenia diagnoses found in recent studies. Now the most comprehensive epidemiological study of psychotic experiences to date, published in July in JAMA Psychiatry, has given researchers the most detailed picture yet of how many people have these experiences and how frequently. The results strongly imply a spectrum—and suggest that the standard treatment for a psychotic episode might be due for an overhaul. After ruling out experiences caused by drugs or sleep, the researchers determined that 5.8 percent of the respondents had psychotic experiences. Two thirds of these people had had only one type of episode, with hallucinations being four times more common than delusions. © 2015 Scientific American
Link ID: 21591 - Posted: 11.02.2015
? Joanne Silberner Each year, nearly three times as many Americans die from suicide as from homicide. More Americans kill themselves than die from breast cancer. As Thomas Insel, longtime head of the National Institute of Mental Health, prepared to step down from his job in October, he cited the lack of progress in reducing the number of suicides as his biggest disappointment. While the homicide rate in the US has dropped 50 percent since the early 1990s, the suicide rate is higher than it was a decade ago. "That to me is unacceptable," Insel says. It hasn't been for lack of trying. The US has a national suicide hotline and there are suicide prevention programs in every state. There's screening, educational programs, and midnight walks to raise awareness. Yet over the last decade or so, the national suicide rate has increased. In 2003, the suicide rate was 10.8 per 100,000 people. In 2013, it was 12.6. An effort that began in Detroit in 2001 to treat depression, the most common cause of suicide, is offering hope. With a relentless focus on finding and treating people with depression, the Henry Ford Health System has cut the suicide rate among the people in its insurance plan dramatically. The story of the health system's success is a story of persistence, confidence, hope and a strict adherence to a very specific approach. © 2015 npr
Link ID: 21589 - Posted: 11.02.2015
By Diana Kwon | In the human form of mad cow disease, called Creutzfeldt-Jakob, a person's brain deteriorates—literally developing holes that cause rapidly progressing dementia. The condition is fatal within one year in 90 percent of cases. The culprits behind the disease are prions—misfolded proteins that can induce normal proteins around them to also misfold and accumulate. Scientists have known that these self-propagating, pathological proteins cause some rare brain disorders, such as kuru in Papua New Guinea. But growing evidence suggests that prions are at play in many, if not all, neurodegenerative disorders, including Alzheimer's, Huntington's and Parkinson's, also marked by aggregations of malformed proteins. Until recently, there was no evidence that the abnormal proteins found in people who suffer from these well-known diseases could be transmitted directly from person to person. The tenor of that discussion suddenly changed this September when newly published research in the journal Nature provided the first hint such human-to-human transmission may be possible. (Scientific American is part of Springer Nature.) For the study, John Collinge, a neurologist at University College London, and his colleagues conducted autopsies on eight patients who died between the ages of 36 and 51 from Creutzfeldt-Jakob. All the subjects had acquired the disease after treatment with growth hormone later found to be contaminated with prions. The surprise came when the researchers discovered that six of the brains also bore telltale signs of Alzheimer's—in the form of clumps of beta-amyloid proteins, diagnostic for the disease—even though the patients should have been too young to exhibit such symptoms. © 2015 Scientific American,
Bret Stetka Sometime around 1907, well before the modern randomized clinical trial was routine, American psychiatrist Henry Cotton began removing decaying teeth from his patients in hopes of curing their mental disorders. If that didn't work he moved on to more invasive excisions: tonsils, testicles, ovaries and, in some cases, colons. Cotton was the newly appointed director of the New Jersey State Hospital for the Insane and was acting on a theory proposed by influential Johns Hopkins psychiatrist Adolph Meyer, under whom Cotton had studied, that psychiatric illness is the result of chronic infection. Meyer's idea was based on observations that patients with high fevers sometimes experience delusions and hallucinations. In 1921 he published a well-received book on the theory called The Defective Delinquent and Insane: the Relation of Focal Infections to Their Causation, Treatment and Prevention. A few years later The New York Times wrote, "eminent physicians and surgeons testified that the New Jersey State Hospital for the Insane was the most progressive institution in the world for the care of the insane, and that the newer method of treating the insane by the removal of focal infection placed the institution in a unique position with respect to hospitals for the mentally ill." Eventually Cotton opened a hugely successful private practice, catering to the infected molars of Trenton, N.J., high society. © 2015 npr