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Article 1: Why we worry
Authors: Stern, Victoria
Source: Scientific American Mind. Nov/Dec2009, Vol.20 Issue 6, p40-47. 8p. 4 Color Photographs.
Document Type: Article
Subject Terms: *Worry
                            *Problem solving
                            *Nervous system
                           *Emotions (Psychology)
People: Brokovec, Thomas
Abstract: The article focuses on the problem of chronic worrying and over thinking. Psychologists believe that worry, defined as a person's negative thoughts about a future event, has evolved as a problem-solving behaviour, The psychologist, Thomas Borkovec, defined the components of worry which include over thinking, avoidance of negative outcomes and inhibition of emotions. Several studies have confirmed that excess fretting reduces activity in the sympathetic nervous system in response to a threat.
Full Text Word Count: 2201
Contents : Craving Control
                   Stunted Emotions
                   Seeking Solutions
                   FAST FACTS
                  Spiralling Out of Control
                  (Further Reading)
Why we worry
Chronic worrying stems from a craving for control. But the more we fret, the less our bodies are able to cope with stress
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 The young girl wanted to unburden herself about her problem. She told her doctor that she worried excessively and that she felt overwhelmed by these thoughts. One memory that she described to Douglas Mennin, director of the Yale Anxiety and Mood Services at Yale University, was particularly telling. Her grandmother had shared intense feelings about the recent passing of a good friend. As the young girl listened, her mind wandered to thoughts of her grandmother dying. The worry soon spiraled into concerns about the girl's own death. She became so disturbed, she cut short her visit to her grandmother and ran home.
Psychologists believe that worry, defined as a person's negative thoughts about a future event, evolved as a constructive problem-solving behavior [see box on page 47]. But excessive fretting — as happened with the girl — does more harm than good. Chronic worriers operate under the misperception that their overthinking and attempts at controlling every situation allow them to problem-solve and plan for the future. Instead their thought pattern hinders cognitive processing and also causes overstimulation of emotion- and fear processing areas in the brain. The hypervigilance that is the result can lead to cardiovascular problems, ultimately rendering the body unable to cope properly with stress.
An improved understanding of how excessive worry (the thought-driven aspect), which is linked with anxiety (the emotional element), affects our mental and physical functions can help us cope with this often self-induced foible.
Worry began to draw the attention of researchers about 25 years ago, when they started to fine-tune their understanding of the spectrum of anxiety-related pathologies. In the early 1980s psychologist Thomas Borkovec of Pennsylvania State University, a pioneer in this field, became interested in the trait while investigating sleep disorders. He found that intrusive cognitive activity at bedtime — worrying — was a factor in insomnia.
By 1990 Borkovec and his colleagues developed the Penn State Worry Questionnaire, a diagnostic tool that helped researchers show excessive fretting to be a feature of all anxiety disorders, especially generalized anxiety disorder (GAD). Psychologists revised the official psychiatric guidelines (then the Diagnostic and Statistical Manual of Mental Disorders III) to reflect this understanding, calling worry the cardinal feature of GAD and making chronic worry a recognized mental health problem. It is now known to affect 2 to 3 percent of the U.S. population, according to the National Institute of Mental Health.
Borkovec defined three main components of garden-variety worry: overthinking, avoidance of negative outcomes and inhibition of emotions. Mennin explains that worry piggybacks on humans' innate tendency to think about the future: "they crave control." He says "chronic worriers see the world as an unsafe place and want to fight this sense of unrest." Overworriers feel that fretting gives them this control, and they tend to avoid situations they can't have power over. In a 1995 study Borkovec found that people agonized about matters that rarely occurred. The participants, nonetheless, often reported that they believed the overthinking about a possible negative event had prevented it from taking place.
Unsurprisingly, worriers show increased activity in areas of the brain associated with executive functions, such as planning, reasoning and impulse control. In 2005 psychologist Stefan Hofmann of Boston University used an electroencephalogram (EEG) to measure activity in the prefrontal cortex, before and after 27 undergraduates were told to give a speech in public. He confirmed previous evidence that activity in the left frontal cortex increases for people who worry compared with those who do not, suggesting that the left frontal cortex plays a prominent role in worrying.
Trying too hard to be in command of a given situation or their own thoughts may backfire when worriers are instead overrun with repetitive apprehensions. Research shows that the more we dwell on negative thoughts, the more those threats feel real and the more they will repeat in our skulls, sometimes uncontrollably.
In 1987 Daniel M. Wegner, a psychologist at Harvard University, found that when people were told not to think about a white bear, they tended to mention it about once a minute. In the experiment, Wegner left a participant in a room with a microphone and a bell and asked the volunteer to talk freely about any topic. At one point, he interrupted the person's monologue and told him to continue talking — but this time, not to think of a white bear. If the subject did think of a white bear, he had to ring the bell. On average, people rang the bell more than six times in the next five minutes and even said "white bear" out loud several times.
"By trying to put a worry or a thought out of our mind, it only makes the worry worse," Wegner says. "Just like when a song gets stuck in your head, you think you ought to be able to get rid of it, but you only end up making it stick more by trying to push it away." Two mental processes may be at play here, according to Wegner. First, by consciously looking for distractions from the white bear (or your nagging worry), you remain somewhat aware of the undesired thought. The second reason suppression fails is that often you are making an unconscious effort to catch yourself thinking of the forbidden thought, ultimately sensitizing your brain to it.
Two emotion-processing areas of the brain are also involved in worry: the anterior insula and the amygdala. A 2008 Psychological Science study that used functional MRI found that when participants anticipated losing a significant amount of money in the future, activity increased in their anterior insula. That area not only becomes more active in response to worry, but the inclination to worry is also reinforced, because people believe that the act helps them avoid potential losses. The researchers concluded that sometimes, when it comes to making daring monetary decisions, overthinking may turn out to be a good thing.
In 2009 Jack Nitschke, a clinical psychologist at the University of Wisconsin-Madison School of Medicine and Public Health, reported using fMRI to measure activity in the amygdala while GAD patients and healthy subjects viewed pictures of items that were negative (for instance, mutilated bodies) or neutral (say, a fire hydrant). A few seconds before seeing the images, patients received a cue to let them know whether to expect a negative or neutral photograph. Although GAD and healthy subjects experienced no difference in amygdala activation when shown either type of picture, GAD patients displayed unusually high levels of amygdala activity to both negative and neutral cues — suggesting that merely anticipating the possibility of something negative in the future recruits specific neural circuitry, Nitschke says.
Although worry hijacks aspects of our emotional circuitry, chronic worriers seek to control their emotions — and their fretting does tend to numb emotional responses. For instance, it is fairly well established that damage to the frontal lobe — which, as the Boston University study showed, has been demonstrated to be more active in worriers who are thinking about the future — is associated with blunted, or an absence of, emotions.
In another emotion-damping mechanism, several studies have confirmed that excess fretting reduces activity in the sympathetic nervous system in response to a threat. This branch of the nervous system normally allows the body to react quickly to impending danger by accelerating breathing and also increasing heart rate to oxygenate muscles to fight or flee.
In one classic study from 1990 Borkovec showed by observing heart rates how worry can dull emotional reactions. He found that people with anxiety about public speaking did not experience variations in their heart rate when relaxing, remaining neutral (that is, neither worrying nor relaxing) or engaging in worry before viewing scary images. After seeing the images, however, subjects in the worry group displayed significantly less variation in heart rate than those in the neutral or relaxed condition, despite reporting feeling more fearful.
At the same time, worry hinders a person's physical reaction to a threat by amplifying activity in the parasympathetic nervous system. When working properly, this part of the nervous system quiets the body as it recovers from a stressful experience. I experienced this system in operation when I participated in a study in Mennin's laboratory at Yale.
The scene was a lone arm suspended in midair. A hand carrying a razor started slicing it. Blood seeped out of the wound as the razor dug deeper, exposing a mass of blood and cartilage. I wanted nothing more than to look away.
Amelia Aldao, the Ph.D. student conducting the experiment, wanted to measure my physiological reaction to various film segments, each one meant to elicit a distinct emotion (for instance, disgust in the case of the mutilated arm). Aldao recorded with electrocardiography how I dealt with a variety of emotions (this Yale study was the first to expand beyond fear), removed the electrodes from my body and led me into the adjacent room. She did some quick calculations on her computer and out popped a few of my stats. Good news. My heart rate variability was high, and my average heart rate measured about 58 beats per minute. These values indicated that my heart could cope well with intense emotions.
In contrast, by consciously trying to be ready for the worst, worriers are actually compromising their body's ability to react to a truly traumatic event. In 2006 researchers at Columbia University, the National Institute on Aging and Leiden University in the Netherlands reviewed more than two dozen studies and found that over-worrying can tax the body and promote cardiovascular problems.
Overall, increased worry was associated with an elevated resting heart rate but low heart rate variability. Excessive worriers and GAD patients experienced lower heart rate variability during periods of worry; in other words, their hearts returned to a resting rate more slowly than those of healthy worriers did.
Prolonged periods of stress even weakened participants' endocrine and immune function. Some studies reported that excess worry is linked to elevated levels of the stress hormone Cortisol, which slows immune responses and may make chronic worriers more susceptible to disease.
Everybody worries now and again [see box on page 43], but if it becomes a pathology, assistance is available. First-line treatments for generalized anxiety disorder currently include drugs and a form of psychotherapy called cognitive-behavior therapy (CBT).
Antidepressants such as Zoloft and Prozac may also help by boosting levels of serotonin, a brain-signaling chemical that enhances mood, sexual desire, memory and learning. Doctors may prescribe antianxiety drugs such as Valium and Xanax. These drugs inhibit a neurotransmitter called GABA, which can dull feelings of anxious arousal and thus a person's desire to worry.
Drugs do not remedy the underlying psychological problems, but CBT may bring relief. Therapists teach patients to detect early cues of unhealthy worry and integrate techniques into their daily life to revise these negative thought patterns. CBT also includes a relaxation component to soothe the muscle tension associated with excess worry.
Gaining deeper insight into how people manage their thoughts about the future will help even healthy worriers cope with the stresses and concerns they confront in everyday life [see box above]. The key for most of us is not letting our worries become problems themselves.
People agonize about matters that rarely occur. Worriers nonetheless often report that they believe overthinking about a possible negative event prevented it from taking place.
Fretting can tax the body and promote cardiovascular problems. Worry is associated with an elevated resting heart rate and low heart rate variability.
Worry hinders a person's reaction to a threat by amplifying activity in the parasympathetic nervous system, which quiets the body as it recovers from a stressful experience.
FAST FACTSÂ Spiraling Out of Control
1Â Worrying about the future is a natural tendency, but for some people it is a constant, unwelcome state of mind. These chronic worriers crave a sense of control they can never seem to find.
2Â Spending too much time fretting actually undermines the body's ability to react to stress, weakening the cardiovascular system and disrupting normal emotional functioning.
3Â When overworrying seriously threatens a person's health and happiness, drugs or psychotherapy can help.
·        The Effect of Worry on Cardiovascular Response to Phobic Imagery. Thomas Borkovec and Senqi Hu in Behaviour Research and Therapy, Vol. 28, No. 1, pages 69-73; January 1990.
·        The Worried Mind: Autonomic and Prefrontal Activation during Worrying. Stefan Hofmann et al. in Emotion, Vol. 5, No. 4, pages 464-475; December 2005.
·        The Worry Cure: Seven Steps to Stop Worry from Stopping You. Robert Leahy. Harmony, 2005.
·        The Perseverative Cognition Hypothesis: A Review of Worry, Prolonged Stress-Related Physiological Activation, and Health. Jos Brosschot, William Gerin and Julian Thayer in Journal of Psychosomatic Research, Vol. 60, No. 2, pages 113-124; February 2006.
·        Anticipatory Activation in the Amygdala and Anterior Cingulate in Generalized Anxiety Disorder and Prediction of Treatment Response. Jack Nitschke et al. in American Journal of Psychiatry, Vol. 166, No. 3, pages 302-310; March 2009.
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Article 2: Obsessions revisited
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Authors: Moyer, Melinda Wenner
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Source: Scientific American Mind. May/Jun 2011, Vol. 22 Issue 2, p36-41. 6p.
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Document Type: Article
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Subject Terms: *Obsessive-compulsive disorder-- Treatment
                        *Neuroses
                        *Neurons
                        *Serotonin
                        *Neurotransmitters
Abstract: The article offers information on the causes and therapies of obsessive-compulsive disorder (OCD). The researchers found that certain variations in the gene that increase the production of the protein are indeed more common in some OCD patients. The researchers looked at variation in a single gene, the one for the serotonin transporter between neurons. The researchers found that certain variations in the gene that increase the production of the protein are indeed more common in some OCD patients.
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Full Text Word Count: 3169
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Contents:Â *Repetition and Reward
                *Infectious Behavior?
                *Tweaking Treatments
                *Fast Facts
                *Compulsive Circuitry
                *(Further Reading)
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Obsessions revisited
Scientists are taking a fresh look at obsessive-compulsive disorder, identifying its likely causes -- and hints for new therapies
One day 12-year-old Elizabeth Mclngvale became obsessed with the number 42, which happened to be her mother's age at the time, 11 years ago. When she washed her hands, she had to turn the sink on and off 42 times, get 42 pumps of soap and rinse her hands 42 times. Sometimes she decided that she actually needed to do 42 sets of 42. When she dressed, she put her right leg in and out of her pant leg 42 times, then the left. Even getting up from a chair took 42 attempts. She was afraid that if she did not follow her self-prescribed ritual, something terrible would happen to her family -- they might die in a car accident, for instance. "Everything I did was completely exhausting and grueling," she recalls. "I was probably doing 12 to 13 hours a day of rituals."
Mclngvale was diagnosed with obsessive-compulsive disorder (OCD), a psychiatric illness that afflicts 2 to 3 percent of Americans, not all of them as severely as Mclngvale. Individuals with OCD experience debilitating recurrent and persistent thoughts, or obsessions, which they try to suppress or eliminate with rituals, known as compulsions. Compared with people who have other anxiety or mood disorders, adults with OCD are more likely to be single and unemployed. In fact, OCD is among the 10 most disabling medical and psychiatric conditions.
Current psychotherapy techniques and drugs help reduce or extinguish obsessive thoughts, but only rarely do patients overcome the disorder. Part of the problem, scientists now believe, is that researchers have had little grasp of OCD's true nature. Now, however, they may be reaching a turning point in their understanding, a change they hope will lead to new therapies.
Identifying the neural circuits involved provides possible targets for medicines. With the help of genetic studies, researchers have learned that a brain-signaling chemical, or neurotransmitter, called glutamate plays a role, for example. Glutamate drives a brain circuit involved in making decisions that are associated with positive outcomes -- one that operates abnormally in individuals with OCD. Perturbations of the immune system can also affect the same neuronal wiring, predisposing some people to OCD and related conditions. "This circuitry, which we're defining, is important for lots of different things that cross diagnoses," says Benjamin Greenberg, a research psychiatrist at Brown University. The new data point away from the long-held notion that OCD results mainly from anxiety. Instead the disorder seems to spring from a drive to revisit thoughts and perform tasks over and over again.
For centuries scientists have sought the roots of the affliction we now know as OCD. In the 1600s people who suffered from repetitive obsessions and compulsions were assumed to be afflicted with "religious melancholy." By the mid-20th century psychiatrists in the tradition of Sigmund Freud described OCD symptoms as signs of "neuroses" that result from repressed instinctual or sexual drives. Vaguely echoing the Freudian view, the Diagnostic and Statistical Manual of Mental Disorders (DSM), the "bible" of mental health diagnoses, currently classifies OCD as an anxiety disorder based on the persistent nervousness that patients typically display.
That thinking has begun to change, however. In a 2007 international survey, 60 percent of 187 authors of OCD publications challenged this rationale, with many arguing that no data show that anxiety actually causes the disorder. They believe anxiety is more of a sidelight than a defining feature of OCD, and as a result, studying and treating anxiety may not be the best way forward. Instead, these experts contend, researchers should consider OCD as a problem based on urges that cause repetitive thoughts and behaviors. With that understanding, they think OCD should be officially grouped with illnesses such as body dysmorphic disorder (BDD), a preoccupation with an imagined defect in appearance [see "Imagined Ugliness," by Susanne Rytina; SCIENTIFIC AMERICAN MIND, April/May 2008]; Tourette's syndrome, which causes physical and vocal tics; and hypochondriasis, excessive fear about having a serious illness. After all, these three disorders often develop in concert: about one third of BDD patients and up to half of Tourette's sufferers also have OCD; meanwhile up to 15 percent of OCD patients are hypochondriacs.
This proposed new grouping -- which could be penned in the next iteration of the DSM due out in 2013 -- may even have an important biological basis. Relatives of people with OCD are more likely than average to have Tourette's and BDD, suggesting that these ailments may have common genetic roots. (OCD itself is known to run in families: relatives of people with OCD are eight times more likely than others to also have the disorder.) And genetic clues are beginning to reveal the biology of OCD.
Some of the new insights confirm what we already suspected. Psychiatrists know that serotonin reuptake inhibitors (SRIs), drugs that increase the amount of the neurotransmitter serotonin (a regulator of mood, appetite and sleep) outside of neurons, are among the most effective medications for OCD; that fact suggests that serotonin signaling could be malfunctioning in OCD. A statistical analysis in 2008 added weight to this idea. In that study, James Leckman and his colleagues at the Yale University Child Study Center analyzed data from 19 studies involving 1,797 individuals with OCD and 3,786 people who did not have the disorder.
The researchers looked at variation in a single gene -- the one for the serotonin transporter, a protein that mops up serotonin from between neurons. When too much of this protein is made, too little serotonin is left in the spaces between neurons, suppressing signaling. The researchers found that certain variations in the gene that increase the production of the protein are indeed more common in some OCD patients -- in particular, Caucasians and those with child-onset OCD. In a 2005 experiment radiologist Georg Berding and his colleagues at Hannover Medical School in Germany reported that the serotonin transporter also binds abnormally to serotonin in unmedicated Tourette's patients and that BDD is sometimes successfully treated with SRIs as well.
Although the effectiveness of SRI drugs suggested that serotonin (and dopamine, another brain chemical) played a role, researchers have long suspected that glutamate might be important, too, based on the fact that these neurotransmitter systems frequently work together. Glutamate is the brain's primary excitatory neurotransmitter: it tends to stimulate (rather than inhibit) neuronal signaling. As it turns out, glutamate facilitates neuronal communication in brain regions that have been implicated in OCD. Several family genetic studies, including one published in 2002 by psychiatrist Edwin Cook, Jr., and his colleagues at the University of Chicago and the University of Michigan at Ann Arbor, have associated OCD with variations in the gene for a protein that removes glutamate from outside neurons. And in 2007 neurobiologist Guoping Feng, now at the Massachusetts Institute of Technology, and his colleagues reported that turning off a structural protein in mice that regulates activity at the glutamate receptor led to compulsive grooming.
Among other functions, glutamate fuels a brain circuit involved in making decisions that will lead to positive, or rewarding, outcomes, particularly when the choice requires sifting through data and experience. The so-called cortical-basal ganglia circuit comprises the orbit-ofrontal cortex (OFC), a decision-making hub; the striatum, a section of the basal ganglia involved in learning and the experience of reward; the thalamus, a region that filters facts and other data; and the anterior cingulate cortex, which detects errors. Mutations in the glutamate transporter gene might impair the protein's ability to regulate activity in this circuit, leading to nonsensical decisions and behaviors. Although investigators are loath to propose a precise mechanism, glitches in this neural wiring could alter a person's ability to sift through information or make decisions based on experience, leading them to sometimes see danger when none is present -- and obsess over it. Other anomalies could in theory alter the experience of reward, such that repetitive behaviors trigger it.
In any event, these brain regions and their communications suffer a range of abnormalities in OCD. In a 2009 statistical analysis of 21 studies comparing the brains of mentally healthy people with those of OCD patients, psychiatrist Bruno Aouizerate and his colleagues at the University of Bordeaux in France reported that the OFC and part of the anterior cingulate cortex tend to be smaller in OCD patients. And in a 2008 study neuropsychologist Barbara Sahakian and her co-workers at the University of Cambridge used functional MRI scans to show that 14 OCD patients had reduced OFC activation, compared with control subjects, while performing a computer task that required them to update their behavioral responses based on new information.
Imaging studies hint that the repetitive thoughts and behaviors that characterize disorders such as Tourette's and BDD are similarly driven by problems with this brain circuit. In Tourette's patients, data published in 2008 point to abnormalities in the connections between different nodes in the circuit; these are formed by so-called white matter, which is made up of the long axons that link one neuron to another. And a 2010 study hints that an abnormally small OFC and anterior cingulate cortex may underlie some cases of BDD.
Recent work has implicated another possible culprit in OCD: the body's immune system. For instance, a 2002 study reported that mice missing a gene involved in immune function demonstrated OCD-like behaviors. Molecular geneticist Mario R. Capecchi and his colleagues at the University of Utah bred mice lacking a gene for a protein called Hoxb8 that was known to regulate the development of body shape in mice. Previous research had shown that the gene also helps to maintain myeloid progenitor cells, which mature into immune cells in the brain called microglia. The researchers were curious to see what happened to mice in the gene's absence. They found that the mice were surprisingly healthy -- but groomed themselves and one another twice as often as mice typically do.
In a follow-up study published in May 2010 Capecchi's team discovered that these Hoxb8-deficient mice had 15 percent fewer microglia in their brains than normal, confirming that Hoxb8 is important for microglia development. Then, when the scientists replaced the missing microglia by giving the mice bone marrow transplants, the rodents groomed themselves the ordinary amount, hinting that an adequate number of microglia are critical for staving off the repetitive actions characteristic of OCD. No one is yet sure of the connection between microglia and the disorder, but in addition to scavenging infectious material, microglia may also release immune chemicals called cytokines that control activity at neuronal junctions known as synapses [see "The Hidden Brain," by R. Douglas Fields, on page 52]. These immune cells are abundant in the cortical-basal ganglia circuit and make direct contact with synapses. Other studies reveal that microglia regulate neuronal cell death during development, and the absence of normal cellular pruning may create structural oddities that spawn behaviors characteristic of OCD.
Other types of abnormal immune responses seem to incite OCD as well. In 1998 pediatrician Susan Swedo of the National Institutes of Mental Health (NIMH) identified a group of children who had acquired OCD or related tic disorders immediately after suffering group A streptococcus infections, the cause of strep throat. Her work suggests that in the process of fighting the infection, the brain can accidentally develop antibodies against -- and begin attacking -- basal ganglia neurons, which are mistaken for the bacteria. These immune attacks may ultimately disrupt the cortical-basal ganglia circuit, leading to OCD symptoms. Swedo has found that severe tics characteristic of Tourette's disorder can also appear suddenly after strep throat infections.
The overactive immunity described in strep sufferers contrasts with the apparent underactive immunity Capecchi's group saw in their hyperhygienic rodents. Other studies that have assessed the levels of immune cells and proteins in patients with OCD have produced similarly conflicting results, suggesting that either overly vigorous or weakened immunity could put a person at risk. That said, most OCD cases are probably not caused by infection or immune system irregularities. "There are so many patients [with strep infections], and not all of them get obsessive," says Aye-Mu Myint, a neuroimmunologist at Ludwig Maximilian University in Munich.
Currently one of the most effective treatments for OCD is a therapy known as exposure and response prevention (ERP). The idea is simple: therapists repeatedly expose patients to the objects or other stimuli that trigger their repetitive behaviors -- by making them touch toilets, say -- without letting them perform their associated compulsions. Eventually the patients realize that nothing bad happens when they fail to perform their rituals, and "the stimulus is not linked to generating anxiety in the same way it was," says psychiatrist Helen Blair Simpson of Columbia University and also director of the New York State Psychiatric Institute's Anxiety Disorders Clinic. Simpson and her colleagues, along with researchers at the University of Pennsylvania, have studied the effects of ERP in clinical trials. In one collaborative study published in 2005, they found that about 60 percent of patients who started ERP treatment improved. The severity of their symptoms, as measured through tests, typically diminished by up to 55 percent, with improvements -- such as the reduced need to engage in rituals -- seen in as little as four weeks.
Adherence can be a problem, though. Eight of the 37 subjects withdrew from the trial after learning that they were assigned to ERP, and another eight dropped out in the middle of the therapy. "The side effect of the therapy is anxiety," Simpson says, even though the therapy reduces such distress in the long run.
The second-line therapies for OCD patients are SRIs. But the drugs typically take eight to 12 weeks to start working, if they ever do: on average, they reduce the severity of symptoms by only 20 to 40 percent. Combining SRIs with antipsychotic medications can, in some instances, boost response rates, as can using SRIs while undergoing ERP.
Individuals who do not respond well to SRIs might one day benefit from medications that calm glutamate activity in the brain. Several open-label trials and case reports have shown that drugs such as topiramate and riluzole -- which work, in part, by blocking specific glutamate receptors -- can improve symptoms when taken with SRIs. Scientists are now conducting placebo-controlled trials of these drugs to see how well they perform on their own. Another drug, D-cycloserine, which has been shown to help rats overcome conditioned fears by enhancing activity at receptors for the neurotransmitter N-methyl-D-aspartic acid, is now being tested in OCD patients in combination with ERP in hopes that it will help patients respond to therapy more quickly.
Greenberg and his colleagues are also studying whether deep brain stimulation (DBS) -- a proven treatment for Parkinson's disease that involves inserting electrodes into the brain -- could treat OCD. A handful of small trials suggest DBS reduces symptoms for some people with severe OCD, perhaps by normalizing the cortical-basal ganglia circuit. "We've found that DBS seems to actually restore rhythmic activity in these areas," says Anthony Grace, a neuroscientist at the University of Pittsburgh. In the ongoing trial, Greenberg is stimulating nerves that link to various parts of this circuit, pinpointing which components are the most important for regulating symptoms. "It gives us a tool to study the disease," says Suzanne Haber, a neuroscientist at the University of Rochester.
Researchers suspect that OCD may represent a cluster of different conditions rather than just a single disorder; after all, sufferers may exhibit disparate obsessions and compulsions with activities such as hoarding, cleaning, ordering and checking. "We're assuming that OCD is one thing, and it probably is not," says Gerald Nestadt, director of the Johns Hopkins University Obsessive-Compulsive Disorder Program. If a compulsion to order things, say, has a different biological cause than does obsessively collecting objects, researchers would like to identify those separate OCD conditions and tailor treatments to each one. To explore this approach, the NIMH is developing mental health research guidelines that will help scientists better identify relevant OCD subtypes and classify patients for research studies. As part of this program, Greenberg and his colleagues currently have a $10.5-million grant to identify the specific brain networks that affect treatment responses.
Some of these new and future approaches may ultimately benefit patients such as McIngvale. Thanks to ERP, Mc-Ingvale, now 23, is pursuing her Ph.D. in social work and is the spokesperson for the International OCD Foundation. She still contends with hand-washing compulsions, which she tries to hide from her colleagues, and struggles to stop herself from repeating fruitless tasks that consume her day. "There is no cure [for OCD]," she admits. But someday, McIngvale hopes, treatments stemming from a better understanding of OCD may make her life easier. She may even forget why she ever cared about the number 42.
MELINDA WENNER MOYER is a freelance science writer and frequent contributor to Scientific American Mind. She lives in Brooklyn, N.Y.
Relatives of people with OCD are more likely than average to have Tourette's syndrome and body dysmorphic disorder.
Studies suggest that either overly vigorous or weakened immunity could put a person at risk for obsessive behavior.
1 » Scientists are now challenging the long-held notion that anxiety is the defining feature of obsessive-compulsive disorder (OCD).
·        2 » The neurotransmitter glutamate plays a role in OCD. It is critical to a brain circuit involved in making rewarding decisions that is abnormal in OCD patients.
·        3 » Immune system abnormalities could predispose some individuals to OCD by perturbing the same brain network.
• Recent Advances In the Genetics of Obsessive-Compulsive Disorder. Jack F. Samuels in Current Psychiatry Reports, Vol. 11, No. 4, pages 277-282; August 2009.
• Obsessive-Compulsive Disorder and Its Related Disorders: A Reappraisal of Obsessive-Compulsive Spectrum Concepts. D. L. Murphy et al. In Dialogues in Clinical Neuroscience, Vol. 12, No. 2, pages 131-148; 2010.
• OCD? Your Immune System Could Be to Blame. Mitch Leslie in ScienceNow; May 27, 2010. Available at http://news.sciencemag.org.ezproxy.langara.bc.ca/sclencenow
• Should an Obsessive-Compulsive Spectrum Grouping of Disorders Be Included In DSM-V? Katharine A. Phillips et al. in Depression and Anxiety, Vol. 27, No. 6, pages 528-555; 2010.
The essence of obsessive-compulsive disorder is now thought to be a repetitious stuttering of thoughts or actions, such as organizing and reorganizing a closet.
Obsessions and compulsions may stem from glitches in a brain circuit governing decision making and reward. The circuit includes the orbitofrontal cortex, a decision-making hub; part of the basal ganglia that mediates rewarding feelings; the fact-filtering thalamus; and the anterior cingulate cortex, which monitors mistakes.
The immune system may play a role In compulsions. Mice lacking one type of immune cell groomed themselves excessively.
Using exposure and response prevention, a therapist might ask a patient who repeatedly checks the stove before she leaves the house to practice checking the stove only once.
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By Melinda Wenner Moyer
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Article 3: Clutter, clutter everywhere
Authors: LILIENFELD, SCOTT O.
                ARKOWITZ, HAL
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Source: Scientific American Mind. Sep/Oct2013, Vol.24 Issue 4, p68-69. 2p.
Document Type: Article
Subject Terms: *Compulsive hoarding
                            *Anus (Psychology)
                           *Toilet training
People: Freud, Sigmund, 1856 - 1939
              Frost, Randy O.
Abstract: The article discusses hoarding, which was regarded by Sigmund Freud as a symptom of "anal character" that resulted from overly harsh toilet training. Hoarding was recognized as a serious clinical problem in the early and mid-1990s and psychologist Randy O. Frost of Smith College was one of the proponents of spreading information on pathological hoarding. The author says the limited treatment strategies to hoarding reflects the lack of understanding of the behavior.
Author Affiliations: Psychology professor, Emory University
                                   Associate professor of psychology, University of Arizona
Full Text Word Count: 1222
Contents
*If parting with possessions is a serious problem, you can now be officially diagnosed with hoarding disorder
*Distinct Pathology
*Deadly Business
*Help for Hoarders
*(Further Reading)
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Clutter, Clutter Everywhere
(facts & fictions in mental health)
STUFF, STUFF and more stuff. Many of us love to buy and keep things, even when the items are not useful. About 70 percent of children amass collections of favored objects, such as coins, dolls or baseball cards; many adults do the same. People often regard possessions as extensions of themselves and become attached to them accordingly.
Yet in rare cases, the habit of gathering and retaining things reaches unhealthy extremes, culminating in hoarding disorder, a condition that is poorly understood. Many laypeople believe that clinical hoarders are too lazy to discard their junk or that they enjoy living with it. Neither of those assumptions appears to be true. Moreover, most experts have long assumed that extreme hoarding is a variant of obsessive-compulsive disorder (OCD), even though most recent research suggests otherwise. Instead the ailment may stem from an exaggerated version of a basically adaptive tendency to accumulate materials that are important to us.
Nikolai Gogol's 1842 novel, Dead Souls, featured a character named Plyushkin, a landowner who saved almost everything he found. Sigmund Freud regarded hoarding as a symptom of what he termed the "anal character," purportedly stemming from overly harsh toilet training. (Few psychologists today share this view.) In the early and mid-1990s, however, hoarding increasingly came to be recognized as a serious clinical problem. Systematic research criteria for pathological hoarding, introduced in 1993 by psychologist Randy O. Frost of Smith College, spread awareness of the malady, as did a parade of television documentaries and reality shows, such as Hoarders, Clean House and Hoarding: Buried Alive.
Until recently, most mental health professionals regarded pathological hoarding as a subtype of OCD. Hoarding was considered a compulsion--a repeated, ritualized action intended to ward off anxiety, such as checking the stove repeatedly to make sure that it is turned off. According to a 2010 review by psychologist David Mataix-Cols of King's College London, however, 80 percent or more of people who engage in extreme hoarding do not meet criteria for OCD. For example, many do not experience the obsessions--recurrent or intrusive thoughts, images or impulses--that are widespread in OCD. Moreover, hoarders tend to be poorer, older, and more prone to mood and anxiety disorders than those with OCD; they are also less likely than OCD sufferers to be aware that they are disordered.
In recognition of these differences, the fifth edition of the American Psychiatric Association's diagnostic manual (DSM-5), published this past May, for the first time included pathological hoarding as a distinct condition. According to this volume, "hoarding disorder" is characterized by extreme and enduring difficulties parting with possessions, even if they have no tangible value. The afflicted have powerful urges to retain items or become very upset about tossing them out. Their home or workplace is filled with so much clutter that the space is unusable--and their problems seriously impair their everyday functioning or cause distress. Before diagnosing hoarding disorder, clinicians must rule out medical conditions that can lead to hoarding. For instance, in a 1998 study psychiatrist Jen-Ping Hwang of the Veterans Administration of Taipei and his colleagues found that 23 percent of patients with dementia displayed clinically significant hoarding behavior.
Hoarding disorder appears to be present in between 2 and 5 percent of the population, making it more prevalent than schizophrenia. It afflicts men and women in about equal numbers. People most often hoard books, magazines, newspapers and clothes; in some cases, they accrue scores of shirts, pants and dresses that have never been removed from their packaging. More rarely, individuals stockpile animals. In one case in 2010 authorities found more than 150 cats living in a home in Powell, Wyo. Animal hoarders tend to be more psychologically impaired than other hoarders and live in more squalid conditions, according to a 2011 article by Frost and his colleagues.
Hoarding can be a serious, even deadly, business. The clutter may reach such proportions that living spaces become essentially uninhabitable, and patients may need to construct narrow tunnels or "goat paths" to get from one location to another. In a 2008 study psychologist David Tolin of the Institute of Living in Hartford, Conn., and his co-workers reported that 2 percent of hoarders had been evicted because of their mess. In a 2009 investigation, psychology student Gregory Lucini and his colleagues at the Worcester Polytechnic Institute Project Center in Melbourne, Australia, revealed that hoarding contributed to 24 percent of preventable deaths in house fires. In other cases, hoarders have been smothered to death by their clutter; this past April a 68-year-old New Jersey woman was found dead underneath piles of rotting garbage, clothing, tote bags and other possessions.
No one knows for sure why hoarders hoard. One clue to the condition, however, is that they often report a powerful emotional attachment to objects; some may imbue them with humanlike qualities, such as feelings, while recognizing that doing so is irrational. In other cases, hoarders insist on maintaining old items, such as clothing, "just in case." Hoarding runs in families; in a 1993 study by Frost and psychology student Rachel C. Gross, now a professor at American University, 85 percent of pathological hoarders described one or more first-degree relatives (parents, children, siblings) as "pack rats"; this percentage significantly exceeded that of nonhoarders. In a 2009 study of more than 5,000 twin pairs, psychologist Alessandra C. Iervolino of King's College London and her collaborators found that this family pattern is genetically influenced; they estimated the heritability of severe hoarding at 50 percent.
Hoarding may have evolutionary origins. The behavior is present in a host of species, including honeybees, crows, rodents and monkeys, as psychologist Jennifer G. Andrews-McClymont, now at Morehouse College, and her colleagues pointed out in a 2013 review. This observation raises the possibility that the condition reflects a naturally selected urge to stockpile resources for times of scarcity.
Hoarding disorder is challenging to treat, but some types of cognitive-behavior therapy can reduce its severity, according to a 2007 literature review by Tolin and his colleagues. The treatment focuses on altering irrational beliefs about the value of objects and providing supervised practice with organizing and discarding things. This intervention is not a panacea, however, given that many people with hoarding disorder do not complete their "homework," which typically involves rearranging and tossing out clutter.
The limited treatment options for hoarders partly reflect our relatively poor understanding of this serious ailment. With the formal recognition of hoarding disorder in DSM-5, however, research into the causes of pathological hoarding will likely increase and, along with it, the promise of more effective therapies.
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♦ Hoarding Disorder: A New Diagnosis for DSM-V? David Mataix-Cols et al. in Depression and Anxiety, Vol. 27, No. 6, pages 556-572; June 2010.
♦ Stuff: Compulsive Hoarding and the Meaning of Things. Randy O. Frost and Gail Steketee. Houghton Mifflin Harcourt, 2010.
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By SCOTT O. LILIENFELD and HAL ARKOWITZ
SCOTT O. LILIENFELD and HAL ARKOWITZ serve on the board of advisers for Scientific American Mind. Lilienfeld is a psychology professor at Emory University, and Arkowitz is an associate professor of psychology at the University of Arizona.
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