Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By Lenny Bernstein, Lena H. Sun and Sandhya Somashekhar Suicides are the 10th-leading cause of death in the United States and eighth among people in the 55- to 64-year-old age group. Comedian Robin Williams, who died Monday of an apparent suicide, was 63. In 2010, 38,364 people died this way. Many suicides are the result of undiagnosed or untreated depression, often masked by self-medicating behaviors such as alcohol and drug use. Though we don’t yet know the exact circumstances of Williams’s death, we do know that he long battled addictions to cocaine and alcohol and, according to his publicist, was struggling with “severe depression.” But unlike many people, Williams had the resources and the motivation to seek treatment, at least for his addictions. According to this report, he had undergone rehab at the famed Hazelden Addiction Treatment Center in Minnesota two months ago, and had sought treatment in 2006 when he began drinking again after 20 years of sobriety. How, then, do we explain the death of someone who appeared to recognize the danger he faced and was trying to address it? Here are some thoughts: • Suicides are often impulsive acts: People who kill themselves are not thinking clearly, have trouble solving problems and weigh risks differently from us, Jill Harkavy-Friedman, vice president of research for the American Foundation for Suicide Prevention, told To Your Health in March. If thwarted in their first attempt, they often do not try again immediately, she said.
|By Nathan Collins Time zips by when you're having fun and passes slowly when you're not—except when you are depressed, in which case your time-gauging abilities are pretty accurate. Reporting in PLOS ONE, researchers in England and Ireland asked 39 students—18 with mild depression—to estimate the duration of tones lasting between two and 65 seconds and to produce tones of specified lengths of time. Happier students overestimated intervals by 16 percent and produced tones that were short by 13 percent, compared with depressed students' 3 percent underestimation and 8 percent overproduction. The results suggest that depressive realism, a phenomenon in which depressed people perceive themselves more accurately (and less positively) than typical individuals, may extend to aspects of thought beyond self-perception—in this case, time. They speculate that mindfulness treatments may be effective for depression, partly because they help depressed people focus on the moment, rather than its passing. © 2014 Scientific American
Helen Shen Most people gradually recover from trauma, but a small fraction of individuals develop post-traumatic stress disorder (PTSD) — prompting scientists to look for the biological underpinnings of this extreme response to traumatic situations such as warfare, car accidents and natural disasters. Research published on 11 August in Proceedings of the National Academy of Sciences identifies up to 334 genes that may be involved in vulnerability to post-traumatic stress in rats1. Most animal studies of stress use intense stimuli such as electric shocks, designed to produce large, group differences between exposed and unexposed animals. But Nikolaos Daskalakis and his colleagues tried a subtler approach to elicit a wide range of individual responses in rats that had all experienced the same trauma — more closely mimicking the variability of human responses to disturbing events. "We wanted to capture the differences between a susceptible individual and one that is not susceptible to the same experience," says Daskalakis, a neuroendocrinologist at the Icahn School of Medicine at Mount Sinai in New York. The researchers exposed around 100 rats to soiled cat litter — which evokes a feared predator — and tested the animals one week later for lingering effects of the trauma. About one-quarter of the exposed animals were classified as 'extreme' responders, showing high levels of anxiety and startling easily on hearing loud noises. Another quarter of the animals were 'minimal' responders, and exhibited anxiety levels similar to those of non-exposed rats. © 2014 Nature Publishing Group
By Emily Underwood The early signs of Creutzfeldt-Jakob disease (CJD)—a rare, incurable brain disorder caused by infectious, misshapen proteins called prions—are difficult to interpret. At first, people may simply feel depressed and can undergo personality changes or bouts of psychosis. By the time memory failure, blindness, and coma set in, typically within a year of infection, death is usually imminent. Now, researchers report that a simple nasal swab may help physicians detect the disease far more accurately and earlier than current methods. Finding simple, noninvasive diagnostic tests is “one of the holy grails” for CJD and other prion diseases, says biochemist Byron Caughey of the National Institute of Allergy and Infectious Diseases’ Rocky Mountain Laboratories in Hamilton, Montana, who helped lead the new work. Although there’s no cure for CJD, early diagnosis is important because it can help rule out other, treatable disorders, and it allows medical personnel to take precautions that prevent the disease from spreading to others through exposure to brain tissue or spinal fluid, he says. Researchers made a major stride toward better diagnostic methods in 2010, when Caughey and other researchers first described a new technique called the RT-QuIC test. The test requires removing cerebrospinal fluid (CSF) from patients by means of a spinal tap, putting samples into a bath of normally shaped prion proteins, and agitating the solution to encourage any abnormal prion “seeds” in the tissue to latch onto the regular proteins. If even trace amounts of pathogenic protein are present, they rapidly use the normal proteins to create millions of insoluble, fibrous amyloid strands. Researchers believe that these amyloid aggregates, also seen in other neurodegenerative diseases such as Alzheimer’s disease, ultimately cause CJD by interfering with or killing off neurons en masse. After death, the brains of people affected by CJD are so badly damaged that they often resemble Swiss cheese or sponges. © 2014 American Association for the Advancement of Science.
Link ID: 19926 - Posted: 08.07.2014
By Sandhya Somashekhar The first time Jeremy Clark met his 18-year-old client, the teenager was sitting in his vice principal’s office, the drawstrings of his black hoodie pulled tight. Jacob had recently disclosed to his friends on Facebook that he was hearing voices, and their reaction had been less than sympathetic. So Clark was relieved when a beaming Jacob showed up on time for their next meeting, at a comic book shop. As the pair bantered about “Star Wars” and a recent Captain America movie, however, Clark picked up troubling signs: Jacob said he was “detaching” from his family, often huddling alone in his room. As the visit ended, Clark gave the teen a bear hug and made a plan. “Let’s get together again next week,” he said. The visit was part of a new approach being used nationwide to find and treat teenagers and young adults with early signs of schizophrenia. The goal is to bombard them with help even before they have had a psychotic episode — a dramatic and often devastating break with reality that is a telltale sign of the disease. The program involves an intensive two-year course of socialization, family therapy, job and school assistance, and, in some cases, antipsychotic medication. What makes the treatment unique is that it focuses deeply on family relationships, and occurs early in the disease, often before a diagnosis. So far, the results have been striking: In Portland, Maine, where the treatment was pioneered, the rate of hospitalizations for first psychotic episodes fell by 34 percent over a six-year period, according to a March study. And just last month, a peer-reviewed study published in the journal Schizophrenia Bulletin found that young people undergoing the treatment at six sites around the country were more likely to be in school or working than adolescents who were not in the program. The research was funded by a $17 million grant from the Robert Wood Johnson Foundation.
|By Tori Rodriguez and Victoria Stern A growing number of people are seeking alternatives to antidepressant medications, and new research suggests that acupuncture could be a promising option. One new study found the traditional Chinese practice to be as effective as antidepressants, and a different study found that acupuncture may help treat the medications' side effects. In acupuncture, a practitioner inserts needles into the skin at points of the body thought to correspond with specific organs (right). Western research suggests the needles may activate natural painkillers in the brain; in traditional Chinese medicine, the process is believed to improve functioning by correcting energy blocks or imbalances in the organs. A study published last fall in the Journal of Alternative and Complementary Medicine found that electroacupuncture—in which a mild electric current is transmitted through the needles—was just as effective as fluoxetine (the generic name of Prozac) in reducing symptoms of depression. For six weeks, patients underwent either electroacupuncture five times weekly or a standard daily dose of fluoxetine. The researchers, the majority of whom specialize in traditional Chinese medicine, assessed participants' symptoms every two weeks and tracked their levels of glial cell line–derived neurotrophic factor (GDNF), a neuroprotective protein. Previous studies have found lower amounts of GDNF among patients with major depressive disorder, and in other research levels of the protein rose after treatment with antidepressant medication. © 2014 Scientific American,
Link ID: 19920 - Posted: 08.06.2014
By Caelainn Hogan A simple blood test could determine a person’s risk of suicide and provide a future tool of prevention to stem suicide rates. In a study published online Wednesday in the American Journal of Psychiatry, researchers say they have discovered a genetic indicator of a person’s vulnerability to the effects of stress and anxiety and, therefore, the risk of suicidal thoughts or attempts. The Johns Hopkins researchers looked at how a group of chemicals known as methyls affect the gene SKA2, which modifies how the brain reacts to stress hormones. If the gene’s function is impaired by a chemical change, someone who is stressed won’t be able to shut down the effect of the stress hormone, which would be like having a faulty brake pad in a car for the fear center of the brain, worsening the impact of even everyday stresses. Researchers studied about 150 postmortem brain samples of healthy people and those with mental illness, including some who had committed suicide. They found that those who died by suicide had significantly higher levels of the chemical that altered the SKA2 gene. As a result of the gene’s modification, it was not able to “switch off” the effect of the stress hormone. The researchers then tested sets of blood samples from more than 325 participants in the Johns Hopkins Center for Prevention Research study to see whether they could determine those who were at greater risk of suicide by the same biomarker. They were able to guess with 80 to 90 percent accuracy whether a person had thoughts of suicide or made an attempt by looking at the single gene, while accounting for age, gender and levels of stress or anxiety.
By ANNA NORTH What does it mean to be lonely? It’s tempting to equate the feeling with a dearth of social interaction, but some people are now saying that it’s more complicated than that — and that true loneliness might be dangerous. In a story at Medium, Robin Marantz Henig busts some common loneliness myths. Lonely people aren’t necessarily weird or uncool: Ms. Henig cites a study of Ohio State undergrads showing that “those who called themselves lonely had just as much ‘social capital’ — defined by physical attractiveness, height, weight, socioeconomic status, and academic achievement — as their non-lonely peers.” And they may not be actually alone: “The students at Ohio State who were lonely belonged to as many clubs and had as many roommates as those who were ‘socially embedded.’ And while some studies indicate that living alone puts people at greater risk for loneliness, living with a spouse is not necessarily any protection.” Rather, loneliness may be psychological. The lonely, writes Ms. Henig, are more likely than others “to feel put upon and misunderstood” in social situations, to see “social danger even where none might exist.” She writes: “People grow lonely because of the gloomy stories they tell themselves. And, in a cruel twist, the loneliness itself can further distort their thinking, making them misread other people’s good intentions, which in turn causes them to withdraw to protect themselves from further rejection — and causes other people to keep them at arm’s length.” This distancing can have a physical impact; Ms. Henig argues that loneliness deserves further study, in part because it may increase the risk of high blood pressure, sleep problems and Alzheimer’s disease. © 2014 The New York Times Company
|By Fikri Birey What’s the difference between you and a rat? The list is unsurprisingly long but now, we can cross a universal human experience — feelings of regret — off of it. A new study shows for the first time that rats regret bad decisions and learn from them. In addition to existentialist suggestions of a rat’s regret — and what that takes away from, or adds to, being “human” — the study is highly relevant to basic brain research. Researchers demonstrated that we can tap into complex internal states of rodents if we hone in on the right behavior and the right neurons. There is a significant literature on what brain regions are representative of certain states, like reward predictions and value calculations, but the study, powered by a novel behavioral test, is able to put together such discrete behavioral correlates into a “rat” definition of regret. Finding better animal models of human behavior constitute a long-standing challenge in neuroscience: It has been difficult to authentically recapitulate mental states in animal models of neuropsychiatric disorders: For example, an attempt to model depression in rodents can often go no further than relatively coarse approximations of the core symptoms like guilt or sadness, which often translates to behaviors like social avoidance or anhedonia in rodents. The inability to efficiently approach the questions of mental abnormalities is a major problem. Depression is currently ranked as the leading cause of disability globally, and it’s estimated that by 2020, depression will lead 1.5 million people to end their lives by suicide. Now, thanks to a simple yet well-conceived series of experiments by Steiner and Redish, a compound behavior like regret is fully open to investigation. The investigators use a spatial decision-making set-up called “Restaurant Row”: an arena with four zones where four different flavors of food (banana, cherry, chocolate or unflavored) are introduced in sequence. © 2014 Scientific American
By Smitha Mundasad Health reporter, BBC News Scientists say a part of the brain, smaller than a pea, triggers the instinctive feeling that something bad is about to happen. Writing in the journal PNAS, they suggest the habenula plays a key role in how humans predict, learn from and respond to nasty experiences. And they question whether hyperactivity in this area is responsible for the pessimism seen in depression. They are now investigating whether the structure is involved in the condition. Animal studies have shown that the habenula fires up when subjects expect or experience adverse events, But in humans this tiny structure (less than 3mm in diameter) has proved difficult to see on scans. Inventing a technique to pinpoint the area, scientists at University College London put 23 people though MRI scanners to monitor their brain activity. Participants were shown a range of abstract pictures. A few seconds later, the images were linked to either punishment (painful electric shocks), reward (money) or neutral responses. For some images, a punishment or reward followed each time but for others this varied - leaving people uncertain whether they were going to feel pain or not. And when people saw pictures associated with shocks the habenula lit up. And the more certain they were a picture was going to result in a punishment, the stronger and faster the activity in this area. Scientists suggests the habenula is involved in helping people learn when it is best to stay away from something and may also signal just how bad a nasty event is likely to be. BBC © 2014
By CATHERINE SAINT LOUIS “This has happened before,” she tells herself. “It’s nowhere near as bad as before, and it will pass.” Robbie Pinter’s 21-year-old son, Nicholas, is upset again. He yells. He obsesses about something that can’t be changed. Even good news may throw him off. So Dr. Pinter breathes deeply, as she was taught, focusing on each intake and release. She talks herself through the crisis, reminding herself that this is how Nicholas copes with his autism and bipolar disorder. With these simple techniques, Dr. Pinter, who teaches English at Belmont University in Nashville, blunts the stress of parenting a child with severe developmental disabilities. Dr. Pinter, who said she descends from “a long line of the most nervous women,” credits her mindfulness practice with giving her the tools to cope with whatever might come her way. “It is very powerful,” she said. All parents endure stress, but studies show that parents of children with developmental disabilities, like autism, experience depression and anxiety far more often. Struggling to obtain crucial support services, the financial strain of paying for various therapies, the relentless worry over everything from wandering to the future — all of it can be overwhelming. “The toll stress-wise is just enormous, and we know that we don’t do a really great job of helping parents cope with it,” said Dr. Fred R. Volkmar, the director of Child Study Center at Yale University School of Medicine. “Having a child that has a disability, it’s all-encompassing,” he added. “You could see how people would lose themselves.” But a study published last week in the journal Pediatrics offers hope. It found that just six weeks of training in simple techniques led to significant reductions in stress, depression and anxiety among these parents. © 2014 The New York Times Company
By Emily Underwood The Broad Institute, a collaborative biomedical research center in Cambridge, Massachusetts, has received a $650 million donation from philanthropist and businessman Ted Stanley to study the biological basis of diseases such as schizophrenia and bipolar disorder. The largest donation ever made to psychiatric research, the gift totals nearly six times the current $110 million annual budget for President Barack Obama’s Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative. Stanley has already given Broad $175 million, and the $650 million will be provided as an annual cash flow on the order of tens of millions each year, with the remainder to be given after Stanley’s death. The gift accompanies a paper published online today in Nature from researchers at Broad and worldwide, which identifies more than 100 areas of the human genome associated with schizophrenia, based on samples from almost 37,000 people with schizophrenia and about 113,000 without the disease. Researchers are likely to find hundreds of additional genetic variations associated with the disease as the number of patients sampled grows, says psychiatrist Kenneth Kendler of the Virginia Institute for Psychiatric and Behavioral Genetics in Richmond, a co-author on the study. Identifying the variants themselves is unlikely to lead directly to new drug targets, Kendler says. Instead, the hope is that researchers at Broad and elsewhere will be able to use those data to reveal clusters of genetic variation, like placing pins on a map, he says. © 2014 American Association for the Advancement of Science.
Sara Reardon Broad population studies are shedding light on the genetic causes of mental disorders. Researchers seeking to unpick the complex genetic basis of mental disorders such as schizophrenia have taken a huge step towards their goal. A paper1 published in Nature this week ties 108 genetic locations to schizophrenia — most for the first time. The encouraging results come on the same day as a US$650-million donation to expand research into psychiatric conditions. Philanthropist Ted Stanley gave the money to the Stanley Center for Psychiatric Research at the Broad Institute in Cambridge, Massachusetts. The institute describes the gift as the largest-ever donation for psychiatric research. “The assurance of a very long life of the centre allows us to take on ambitious long-term projects and intellectual risks,” says its director, Steven Hyman. The centre will use the money to fund genetic studies as well as investigations into the biological pathways involved in conditions such as schizophrenia, autism and bipolar disorder. The research effort will also seek better animal and cell models for mental disorders, and will investigate chemicals that might be developed into drugs. The Nature paper1 was produced by the Psychiatric Genomics Consortium (PGC) — a collaboration of more than 80 institutions, including the Broad Institute. Hundreds of researchers from the PGC pooled samples from more than 150,000 people, of whom 36,989 had been diagnosed with schizophrenia. This enormous sample size enabled them to spot 108 genetic locations, or loci, where the DNA sequence in people with schizophrenia tends to differ from the sequence in people without the disease. “This paper is in some ways proof that genomics can succeed,” Hyman says. © 2014 Nature Publishing Group
Emily A. Holmes, Michelle G. Craske & Ann M. Graybiel How does one human talking to another, as occurs in psychological therapy, bring about changes in brain activity and cure or ease mental disorders? We don't really know. We need to. Mental-health conditions, such as post-traumatic stress disorder (PTSD), obsessive–compulsive disorder (OCD), eating disorders, schizophrenia and depression, affect one in four people worldwide. Depression is the third leading contributor to the global burden of disease, according to the World Health Organization. Psychological treatments have been subjected to hundreds of randomized clinical trials and hold the strongest evidence base for addressing many such conditions. These activities, techniques or strategies target behavioural, cognitive, social, emotional or environmental factors to improve mental or physical health or related functioning. Despite the time and effort involved, they are the treatment of choice for most people (see ‘Treating trauma with talk therapy’). For example, eating disorders were previously considered intractable within our life time. They can now be addressed with a specific form of cognitive behavioural therapy (CBT)1 that targets attitudes to body shape and disturbances in eating habits. For depression, CBT can be as effective as antidepressant medication and provide benefits that are longer lasting2. There is also evidence that interpersonal psychotherapy (IPT) is effective for treating depression. Ian was filling his car with petrol and was caught in the cross-fire of an armed robbery. His daughter was severely injured. For the following decade Ian suffered nightmares, intrusive memories, flashbacks of the trauma and was reluctant to drive — symptoms of post-traumatic stress disorder (PTSD). © 2014 Nature Publishing Group,
By Emily Anthes The women that come to see Deane Aikins, a clinical psychologist at Wayne State University, in Detroit, are searching for a way to leave their traumas behind them. Veterans in their late 20s and 30s, they served in Iraq and Afghanistan. Technically, they’d been in non-combat positions, but that didn’t eliminate the dangers of warfare. Mortars and rockets were an ever-present threat on their bases, and they learned to sleep lightly so as not to miss alarms signaling late-night attacks. Some of the women drove convoys of supplies across the desert. It was a job that involved worrying about whether a bump in the road was an improvised explosive device, or if civilians in their path were strategic human roadblocks. On top of all that, some of the women had been sexually assaulted by their military colleagues. After one woman was raped, she helped her drunk assailant sneak back into his barracks because she worried that if they were caught, she’d be disciplined or lose her job. These traumas followed the women home. Today, far from the battlefield, they find themselves struggling with vivid flashbacks and nightmares, tucking their guns under their pillows at night. Some have turned to alcohol to manage their symptoms; others have developed exhausting routines to avoid any people or places that might trigger painful memories and cause them to re-live their experiences in excruciating detail. © 2014 Nautilus,
Fearful memories can be dampened by imagining past traumas in a safe setting. The "extinction" of fear is fragile, however, and surprising or unexpected events can cause fear memories to return. Inactivating brain areas that detect novelty prevents relapse of unwanted fear memories. Traumatic and emotional experiences often lead to debilitating mental health disorders, including post-traumatic stress disorder (PTSD). In the clinic, it is typical to use behavioral therapies such as exposure therapy to help reduce fear in patients suffering from traumatic memories. Using these approaches, patients are asked to remember the circumstances and stimuli surrounding their traumatic memory in a safe setting in order to "extinguish" their fear response to those events. While effective in many cases, the loss of fear and anxiety achieved by these therapies is often short-lived—fear returns or relapses under a variety of conditions. Many years ago, the famous Russian physiologist Ivan Pavlov noted that simply exposing animals to novel or unexpected events could cause extinguished responses (such as salivary responses to sounds) to return. Might exposure to novelty also cause extinguished fear responses to return? In a recent study (Maren, 2014), rats first learned that an innocuous tone predicted an aversive (but mild) electric shock to their feet. The subsequent fear response to the tone was then extinguished by presenting the stimulus to the animals many times without the shock. After the fear response to the tone was reduced with the extinction procedure, they were then presented with the tone in either a new location (a novel test box) or in a familiar location, but in the presence of an unexpected sound (a noise burst). In both cases, fear to the tone returned as Pavlov predicted: the unexpected places and sounds led to a disinhibition of fear—in other words, fear relapsed. © 2014 Publiscize
Some concussion symptoms that last three months after a head injury may be related to post-traumatic stress disorder, a new study suggests. Mild traumatic brain injury accounts for more than 90 per cent of brain injuries, according to an international review for the World Health Organization, but little is known about prognosis. TMR car accident Road crashes were the source of many of the head injuries suffered by patients in the study group. (Radio-Canada) In Wednesday’s issue of the journal JAMA Psychiatry, Emmanuel Lagarde of the University of Boredeaux, David Cassidy of Toronto Western Research Institute and their team focused on 534 patients with head injuries and 827 control patients with non-head injuries who went to an emergency department in France. Concussions or mild traumatic brain injury can lead to three different types of symptoms: During the three-month followup, 21 per cent of the patients with head injuries and 16 per cent of the patients with non-head injuries met the criteria for a diagnosis of post-concussion syndrome. Nearly nine per cent of patients with head injuries met the criteria for PTSD compared with two per cent of patients in the control group. In a statistical analysis, having a mild traumatic brain injury was a predicator of PTSD, but not post-concussion syndrome. "Available evidence does not support further use of post-concussion syndrome. Our results also stressed the importance of considering PTSD risk and treatment for patients with mild traumatic brain injury," the researchers concluded. Jane Topolovec-Vranic, a clinical researcher in mild traumatic brain injury and neuroscience at St. Michael’s Hospital in Toronto, said the study was well done with rigorous analyses and a control group that is often missing in such studies. © CBC 2014
By Lizzie Wade This week, a team from the National Institute on Drug Abuse (NIDA) reported that heavy marijuana use may damage the brain's pleasure center. Meanwhile, researchers in the United Kingdom say they’ve figured out why pot makes you paranoid. But does focusing research on cannabis’s “bad side” give the drug short shrift? Science talked to Ian Mitchell, an emergency physician at the University of British Columbia’s Southern Medical Program in Kamloops, Canada, and author of the blog Clinical Cannabis in Context, who says that politics influences research in this controversial field. As a doctor who recommends medical cannabis to patients, he follows research on the drug and often critiques studies he believes are based on outdated information or were performed with an anticannabis bias. This interview has been edited for clarity and brevity. Q: What do you think of the NIDA study? A: They said they gave marijuana abusers Ritalin and nothing happened. One of the ways you could interpret that is, OK, these pleasure centers are damaged. But you could also say, perhaps marijuana decreases the effects of [Ritalin] on people. That would be equally as right an interpretation. Q: Why do we hear more about studies that show negative effects of marijuana? A: NIDA is at the center of cannabis research in America. And their mandate, very plainly, is to study drug abuse. So they overwhelmingly fund studies that look at abuse. In America, if you wanted to run a study that showed a benefit of cannabis, you weren’t allowed to do that because NIDA couldn’t give you samples to use. So there were no trials [on potential medical benefits] being done. For example, there hasn’t been a good trial yet to study marijuana’s potential for treating posttraumatic stress disorder. They couldn’t get it done, due to all these political roadblocks. © 2014 American Association for the Advancement of Science
Claudia M. Gold At the recent gubernatorial candidates forum on mental health, Martha Coakley repeated the oft-heard phrase that depression is like diabetes. Her motivation was good, the idea being to reduce the stigma of mental illness, and to offer "parity" or equal insurance coverage, for mental and physical illness. However, I am concerned that this phrase, and its companion, "ADHD is like diabetes," will, in fact, have the exact opposite effect. A recent New York Times op ed, The Trouble with Brain Science, helped me to put my finger on what is troubling about these statements. Psychologist Gary Marcus identifies the need for a bridge between neuroscience and psychology that does not currently exist. Diabetes is a disorder of insulin metabolism. Insulin is produced in the pancreas. The above analogies disregard the intimate intertwining of brain and mind. For the pancreas, there is no corresponding "mind" that exists in the realm of feelings and relationships. While there is some emerging evidence of the brain structures involved in the collection of symptoms named by the DSM (Diagnostic and Statistical Manual of Mental Disorders,) there are no known biological processes corresponding to depression, ADHD or any other diagnosis in the DSM. There is, however, a wealth of new evidence showing how brain structure and function changes in relationships. ©2014 Boston Globe Media Partners, LLC
Link ID: 19836 - Posted: 07.16.2014
By Sharon Oosthoek, CBC News Mounting evidence that gut bacteria affect mood and behaviour has researchers investigating just how much power these tiny microbes wield over our mental health. "Many people with chronic intestinal conditions also have psychological disturbances and we never understood why," says McMaster University gastroenterologist Dr. Stephen Collins. Now, scientists such as Dr. Collins are starting to come up with answers. Our lower gastrointestinal tract is home to almost 100 trillion microorganisms, most of which are bacteria. They are, by and large, "good" bacteria that help us digest food and release the energy and nutrients we need. They also crowd out bacteria that can trigger disease. But when things go awry in our guts, they can also go awry in our brains. Up to 80 per cent of people with irritable bowel syndrome experience increased anxiety and depression. And those with autism — a syndrome associated with problems interacting with others — are more likely to have abnormal levels of gut bacteria. Dr. Collins and fellow McMaster gastroenterologist Premysl Bercik have done some of the seminal research into the bacteria-brain-behaviour connection. In a study published last year, they changed the behaviour of mice by giving them fecal transplants of intestinal bacteria. It involved giving adventurous mice bacteria from timid ones, thereby inducing timid behaviour. Before the transplant, adventurous mice placed in a dark, protected enclosure spent much of their time exploring an attached bright, wide-open area. After the transplant, they rarely ventured beyond their enclosure. © CBC 2014