Telephobia – when someone has the fear of talking on the phone.
For more information click here

Cognitive-Behavioral Treatment for Phobias

The hallmarks of a phobia are persistent, irrational fears and avoidance of the specific things (for example, animals, heights, or closed spaces) or activities that induce these fears. The diagnosis of a phobic disorder is made only when the phobia significantly impairs the individual’s social or occupational functioning.

 

Although people can exhibit exaggerated or inappropriate fear toward almost any object or situation, certain phobias are more common than others. Common phobias include fear of dogs, spiders, snakes, open spaces, closed spaces, dental treatment, flying, heights, blood, injections, and social situations. Fortunately, many people with specific phobias experience much less fear and avoidance (often none at all) after receiving treatment for their condition.

Seeking Treatment for a Phobia
Experts recommend seeking treatment for a phobia if it interferes significantly with your social life or ability to perform your job. A good example of a candidate for phobia therapy is a person whose fear of flying limits his or her ability to visit family or leads to turning down a job that involves air travel.

Therapy begins with describing your phobia to a therapist. You then may be asked to create a list of 10 situations related to your phobia and to rank the situations in terms of how much fear and avoidance they each provoke. For example, a fearful flier may place driving to the airport and checking baggage low on the list, while being on a turbulent flight during a thunderstorm may rank the highest. This list will help the therapist gain a clearer idea of what exactly your phobia entails and help direct your treatment.

Some phobias—such as social phobia or fear of flying—inherently involve other people, and therapy is frequently conducted in group settings. However, a phobia-like fear of snakes can be addressed in one-on-one sessions with a therapist. Many people prefer one-on-one therapy because they are self-conscious about their phobia.

Cognitive Treatment for a Phobia
Once the therapist understands your phobia, you will work together to recognize and alter the thought patterns that lead to your fear and avoidance. People with phobias often feel that encountering the feared object or situation will have catastrophic results or cause a panic attack. For example, people with a phobia of snakes may fear being bitten and killed, even if the snake is far away or behind glass. The cognitive aspect of phobia treatment shows patients that their worst fears are usually unfounded.

Together, the therapist and patient work to replace the negative thinking with more realistic and accurate thoughts. Patients may also learn relaxation techniques to help them control their fear responses.

Behavioral Treatment for a Phobia
The main component of treatment for phobias is behavioral and entails exposure to the feared object or situation. Patients with a phobia are asked to confront the situation gradually, according to the hierarchy of fear and avoidance that they originally constructed. Often, therapists ask patients to confront these fears first using an imaginary setting (a process called systematic desensitization) and then in real life (in vivo desensitization).

Thus, a person who fears injections will, with the help of the therapist, first imagine preparing to go to the doctor’s office to receive a shot. After the patient is able to relax and be comfortable with that situation, the next steps might be to imagine arriving at the office, being seated in the examination room, seeing the needle, and so on, until the person is able to relax while imagining receiving an injection.

In addition, the therapist will usually ask the person to confront the phobia gradually in real life. People with a fear of spiders may begin by looking at a picture of a spider. Once they are comfortable with the picture, they may be asked to stand for a few seconds across the room from a spider in a tank. They gradually stay in the room longer, and their distance from the spider is shortened. Eventually, the patients may be asked to touch the spider and let the spider crawl across their arm. In some instances, the therapist may use systematic desensitization in therapy sessions and give the patients homework assignments that put them in real-life phobic situations.

Exposure training may be more important than cognitive therapy for phobias because successful treatment with exposure alone may bring about changes in thinking patterns. The number of exposure sessions varies (up to 14 may be necessary) and is dictated by the intensity of the person’s phobia. In some cases, cognitive-behavioral therapy may be combined with drug treatment (for example, antianxiety medication). Training in social skills may also help people with social phobia.

Source: Johns Hopkins Health Alerts Depression and Anxiety Treating Phobia with Cognitive-Behavioral Therapy 

Arachnophobia – Fear of Spiders

In moderation, fear is actually a good thing. It’s a survival instinct that helps us avoid activities and creatures that can harm us. But sometimes that fear increases out of proportion to the actual danger. While most of us eventually get past our fears — or at least learn to live with them — people with phobias are held prisoner by an irrational sense of panic.

Some experts estimate that nearly 80% of people with phobias don’t seek treatment because the thought of facing their fear is too overwhelming. But the benefit of treatment for a phobia is well worth it: a life without limitations imposed by fear.

Exposure therapy is the most common method of treatment for phobias. It’s a form of cognitive-behavioral therapy and involves putting yourself into increasingly stressful scenarios involving your particular phobia and overcoming your fear with new learning.

Although direct exposure therapy is usually the best way to treat specific phobias, it’s not always the most convenient. For example, if you want to confront your fear of flying by going to the airport and sitting at the gate, most airports today will not let you pass through security without a plane ticket.

 

Likewise, if you have a driving phobia, having a therapist take you on the road can be unsafe, as you may panic when driving through a tunnel or merging onto the highway. In these kinds of situations, virtual reality exposure therapy may be preferable to the real thing.

Virtual treatments for phobia. Virtual reality treatments involve computer programs that simulate, for example, sitting on a plane or driving a car. You wear a head-mounted display equipped with video cameras and earphones so that you can receive both visual and audio cues. To increase the sense of realism, some clinics may treat aviophobia (the fear of flying) by having you sit in an airplane seat on top of vibrating platforms to simulate the plane’s engines running beneath you.

A study published in Behavior Therapy compared virtual reality exposure therapy with standard exposure therapy in people afraid to fly and found that both treatments resulted in a 76% success rate. The majority of participants in both groups also maintained their success at the 12-month follow-up.

 

Ophidiophobia – Fear of Snakes

How The Brain Stores Memories Of Specific Fears

The brain is capable of holding and retrieving memories for specific fears, revealing a more sophisticated storage and recall capacity than previously thought, neuroscientists have found. The study, which appears in the journal Nature Neuroscience, may have implications for treating post-traumatic stress syndrome – as scientists begin to understand how different fears are stored in the brain, they can move toward addressing specific fear memories.

The research was conducted by researchers at New York University’s Center for Neural Science, the Department of Psychiatry at NYU School of Medicine-Bellevue Hospital Center, the Copernicus Center for Interdisciplinary Studies in Krakow, Poland, Université Paris-Sud, and the Emotional Brain Institute at the Nathan S. Kline Institute for Psychiatric Research.

The research focused on the brain’s amygdala, which has previously been shown to store fear memories. However, prior studies have indicated that the amygdala does not discriminate among the different threats it holds and processes. In other words, whether you are afraid of dogs because you were once bitten by a dog or you are afraid of pizza because you once nearly choked to death eating it, all the amygdala remembers is that both of these experiences were scary. By contrast, other brain areas, such as cortex, ensures that all other aspects of these fearful events in your life are remembered.

The scientists on the Nature Neuroscience study sought to determine if there were differences in how the amygdala processes and remembers fears. To do so, they focused on a process called memory consolidation in which an experience is captured, or encoded, then stored. Once consolidation occurs, memories may be long lasting – one experience may create memories that last a lifetime. However, whenever recalled, memories become labile – that is, susceptible to changes. This process is called reconsolidation. In life, reconsolidation allows updating existing memories. But this process also serves as a valuable methodological tool as it lets researchers control the modification of memories.

When it comes to developing fear memories, one model posits that during a fear experience, a neutral stimulus (e.g., a musical passage) becomes associated with a negative encounter (e.g., a dog bite). Therefore, future occurrences of this neutral stimulus, or conditioned stimulus (CS), forewarns the onset of the negative encounter, or unconditioned stimulus (US). Previous research shows that the association between a CS and a US is processed and stored in the amygdala.

To replicate this process, the researchers devised an experiment using laboratory rats. In it, they paired two distinct audio tones, which served as the neutral stimulus, or conditioned stimulus (CS), with mild electric shocks to different parts of the rats’ bodies. As a result, the rats linked a mild shock to a certain part of their bodies with a certain tone.

Under the memory reconsolidation model, exposing an organism to any aspect of the learned experience brings this memory back to mind and makes it susceptible to changes. Thus, if two distinct tones were each paired with two distinct electric shocks and if the amygdala does not discriminate among different threats, then re-exposing a rat to any of these shocks should cause lability of all fear memories stored in the amygdala.

However, the Nature Neuroscience study yielded quite different results. The researchers found that re-exposing a rat to a particular shock (that is, one applied to a certain part of the body), followed by an injection of an antibiotic known to disrupt reconsolidation processes, impaired only these associations that were linked to this particular shock. Despite the disruption of one type of fear memory, rats were still able to express fear behavior to the tone which had been paired with a shock applied to another part of the body.

The finding demonstrates that the amygdala makes distinctions among the fear memories it holds and retrieves.

Source:
James Devitt
New York University

http://www.medicalnewstoday.com/articles/184391.php

 

Liv Casben reported this story on Tuesday, April 6, 2010 18:50:00

MARK COLVIN: It’s no coincidence that autistic people are often called savants. Many people with autism and Asperger’s have remarkable abilities with numbers, or technology, or even art. Some can perform extraordinary feats of memory. But their talents often go unnoticed or are wasted because they find it hard to get and keep full-time jobs.

Now three advocacy groups in Victoria have got together to try to change that.

Liv Casben has this report.

LIV CASBEN: Around 1 in 160 people live with autism in Australia. But advocacy groups say many of them are underemployed.

TRACEL DEVEREUX: Most people with Asperger’s and autism do not work full time, do not access, work at their particular skills level and many of them do not access or do not operate in the workforce at all.

LIV CASBEN: Tracel Devereux is the CEO of Alpha Autism. The not-for-profit organisation supports adults with autism and tries to find jobs for them. With 80 people on its books looking for work, it places an average of two people in a job every month. But it’s now hoping that number will increase with its sights firmly set on the IT market.

TRACEL DEVEREUX: People with Asperger’s tend to have a very strong logical framework, a capacity to think in a linear way and to focus on data and detail that leads them to be very, very good at picking up faults or aberrations in a system.

LIV CASBEN: Alpha Autism is one of three groups that have signed an agreement to get more people with autism into the workforce. The idea comes from Denmark where entrepreneur, Throkil Sonne, whose son has autism, set up a company which specialises in software testing – 90 per cent of its employees have autism and its clients include Computer Sciences Corporation and Cisco Systems.

CAROLINE CROSSE: Throkil had identified that his son was very competent in very specific fields and one of these specific fields was software testing and the skills required for that. So on the basis of that, he set up specialist firm in Denmark and now has a very successful social enterprise.

LIV CASBEN: Caroline Crosse heads up Social Firms Australia which aims to create accessible employment for those people with a disability or mental illness. Her group will work with Alpha Autism to introduce the scheme here.

CAROLINE CROSSE: There’s a high unemployment rate for people with a mental illness and disability and people with autism spectrum disorders are no exception. It’s very difficult for people who have a range of barriers to employment to be able to advocate for themselves.

LIV CASBEN: The project’s already won plenty of support from autism advocacy groups. Nicole Rogerson is the CEO of Autism Awareness which is Australia’s largest advocacy group of parents who have children with autism.

NICOLE ROGERSON: A lot of employers would look with people with autism and they wouldn’t necessarily be able to look through what they see on the surface through to the skill set that might actually be there.

So, it’s difficult, so people with autism spectrum disorder often aren’t great team players, they may not be fabulous with social communication, they might seem to be a little off putting or they might ignore you or they might not give you great eye contacts. All those sorts of things in a corporate environment are a little bit difficult to be without.

LIV CASBEN: Nicole Rogerson is also hoping it works for a more personal reason. She has a 14-year-old son with autism and says she, like other parents, is worried what opportunities will be available for him once his formal schooling ends.

NICOLE ROGERSON: There is an army out there of young adults and that are unemployed and who really have above-average IQs and who could contribute a lot to this country but they aren’t.

MARK COLVIN: Nicole Rogerson from Autism Awareness finishing that report from Liv Casben. 

Source:  http://www.abc.net.au/pm/content/2010/s2865546.htm

 

 

In what may provide the most compelling evidence to date, researchers at Columbia University Medical Center have illuminated how a genetic variant may lead to schizophrenia by causing a disruption in communication between the hippocampus and prefrontal cortex regions of the brain, areas believed to be responsible for carrying out working memory. Findings are published in the current online edition of Nature.

This discovery coincides with the 15th anniversary of the first identification of the link between schizophrenia and a genetic mutation – a microdeletion on human chromosome 22 – known as 22q11 deletion, by Columbia Psychiatry researcher Maria Karayiorgou, M.D., a coauthor on the research. Previous studies have shown that approximately 30 percent of patients with this deletion will go on to develop schizophrenia.

“We know that this genetic deficit predisposes us to schizophrenia, and now we have identified a clear pathophysiological mechanism of how this deletion confers this risk for schizophrenia,” said Dr. Karayiorgou. Dr. Karayiorgou discovered the link between the 22q11 mutation and schizophrenia in 1995. Since then, Dr. Karayiorgou and Joseph A. Gogos, M.D., Ph.D, a senior author on the research, have established and pursued research focusing on the neurobiology of this mutation.

Though schizophrenia is best known for its delusions and hallucinations, it is the disease’s impact on such cognitive abilities like working memory – a key element of executive functioning – that best predict how well a person will function in society.

Using a mouse model with the 22q11 deletion, senior authors Joshua Gordon, M.D., Ph.D., and Joseph A. Gogos, M.D., Ph.D., and their teams, recorded the neural activity of the mice while they performed a cognitive task of working memory, and found that their performance was either completely disrupted, or was impaired, compared to that of the healthy mice.

(Dr. Karayiorgou is professor of psychiatry, Dr. Gogos is associate professor of physiology and neuroscience, and Dr. Gordon is assistant professor of psychiatry at Columbia University Medical Center).

In healthy mice, the hippocampus sends spatial information to the prefrontal cortex, but in the mouse model of the 22q11 mutation there is a breakdown in the connection and this communication is either weakened or fails completely.

As part of the cognitive trial, the mice were tested as they navigated a t-shaped maze. In order to successfully complete the task, the mice had to recall the direction in which they traveled, and then choose to go in the opposite direction to receive their next reward. While the healthy mice easily learned the task, mice carrying the schizophrenia mutation took longer to master it, demonstrating a behavioral deficit of the task in the mouse model of schizophrenia.

“We found that successful completion of the task in our healthy mice required the two regions of the brain – the hippocampus and the prefrontal cortex – to work together, and in our mouse model, the information transfer was less efficient, or was unable to take place at all,” said Dr. Gordon.

In addition, the researchers reported that they were able to show the extent of the deficit in individual mice.

“There was a variation in how much of a deficit they showed, and that correlated with the degree of the behavioral deficit, so that for individual mice that have less communication between these structures, there was more of a behavioral deficit,” said Torfi Sigurdsson, Ph.D., a postdoctoral research scientist in Dr. Gordon’s laboratory at Columbia Psychiatry and a coauthor on the paper.

Recent human imaging studies have suggested the possibility that there may be abnormalities in the functional connectivity between the hippocampus and prefrontal cortex in schizophrenia, however, it remained unclear how such findings related to a cause of the disease, like that of a genetic risk variant, or if they were the result of the disease itself or medications used.

“Here we are really at the level of the individual cells, so our findings extend beyond patient studies by showing how disrupted connectivity can arise at the level of single neurons, as a result of a genetic risk variant,” said Dr. Sigurdsson.

Another strength of the study, according to the researchers, is that the communication can be measured directly between the two regions.

“It unequivocally establishes a deficit in that communication in a way that the early studies could not – not only because we can isolate the genetics of the disease, but we can also measure the connectivity between these structures directly,” said Dr. Gordon.

“The 22q11 deletion mouse model allows us to explore how these mutations alter brain function and the abnormal behavior that we see in schizophrenia patients. This is exactly what our study and our research program on 22q11, in general, has accomplished,” said Dr. Gogos.

“We now know that one of the consequences of that deletion is to disrupt functional communication between these two brain regions, and we have evidence from the study that the disruption actually has an impact on a cognitive behavior that is disrupted in patients, so it gives us a really strong indication of how the deletion can contribute to the development of schizophrenia,” he added. “It is possible that similar abnormalities in functional connectivity may also account for other symptoms of the disease, and can be used to better assess treatment response, and, most importantly, to develop new medications.”

Next, the researchers plan to test the structural links between the hippocampus and prefrontal cortex, since it appears likely that synchrony between these two regions is mediated through anatomical connections. The researchers will examine how the anatomical and synaptic properties of these connections change in this mouse model and will aim to identify the genes that account for this change.

Authors of the Nature study are Torfi Sigurdsson, Kimberly L. Stark, Maria Karayiorgou, Joseph A. Gogos and Joshua A. Gordon.

This study was supported in part by the Simons Foundation, the National Institute of Mental Health (NIMH), and the Lieber Center of Schizophrenia Research and Treatment.

Contrary to popular belief, schizophrenia is not a split personality; it is a chronic, severe, and disabling brain disorder that affects just over one percent of the adult population and is characterized by loss of contact with reality (psychosis), hallucinations (usually, hearing voices), firmly held false beliefs (delusions), abnormal thinking, a restricted range of emotions (flattened affect) or inappropriate and disorganized behavior, social withdrawal, and diminished motivation.

The disease often strikes in the early adult years, and although many individuals experience some recovery, many others experience substantial and lifelong disability. People with schizophrenia often have problems functioning in society and in relationships and are over-represented on disability rolls and among the homeless and imprisoned.

What precisely causes schizophrenia is not known, but current research suggests a combination of hereditary and environmental factors. Fundamentally, however, it is a biologic problem (involving changes in the brain), not one caused by poor parenting or a mentally unhealthy environment.

Source
Columbia University Medical Center

http://www.medicalnewstoday.com/articles/184131.php

 

 By Rick Nauert PhD Senior News Editor
Reviewed by John M. Grohol, Psy.D. on April 7, 2010

A new extensive review of scientific studies on the use of drugs to treat anxiety has found no evidence supporting the use of so-called “natural” treatments in combating the effects of anxiety.

St. John’s wort, kava extract and valerian, herbal remedies touted on the Internet, have not been proven to be effective in treating anxiety, according to Kimberly Zoberi, M.D., Saint Louis University School of Medicine.

Additionally, she raised concerns about the safety of valerian, particularly because long-term studies of the herb are lacking.

“Patients should be extremely cautious about garnering medical advice from the Internet,” says Zoberi.

“There is no evidence that those medications are effective. If a patient wishes to avoid drug therapy, her doctor can suggest alternatives such as cognitive behavioral therapy.”

In addition to the findings regarding “natural” treatments, Zoberi compared the differing prescription drug regimens available on the market for patients suffering from anxiety.

According to Zoberi, most physicians recommend selective serotonin reuptake inhibitors (SSRIs) as a first-line treatment because they are considered safe, effective and less expensive. However, some patients suffer sexual or gastrointestinal side effects.

Zoberi found that medications from the anticonvulsant class of drugs are among the quickest and most effective ways to provide relief to patients in distress without the side effects of other first-line treatments.

The downside is that these prescriptions are fairly expensive compared to other treatments.

Ultimately, Zoberi strongly recommends consulting with a health care professional before beginning any drug regimen for anxiety.

The review article was published in last month’s issue of the Journal of Family Practice.

Source: St. Louis University

http://psychcentral.com/news/2010/04/07/natural-remedies-ineffective-for-anxiety/12656.html

 

Genetic Link for Stress-Induced Depression?

Experts acknowledge that some mental health conditions can be triggered by environmental stimuli and often occur in response to stressful life events.

New research, using an animal model, hopes to discover why some people are at risk.

Well-known examples of stress-induced mental illness include depression and schizophrenia. Researchers are aware that some people have a genetic predisposition for stress-induced disorders.

They have learned that a high number of depressed people have a genetic change that alters a protein cells use to talk to each other in the brain. Also, brain imaging of people with depression also shows that they have greater activity in some areas of their brain.

Unfortunately, the techniques that are currently available have not been able to determine why stress induces pathological changes for some people and how their genetics contribute to disease.

A new mouse model may provide some clues about what makes some people more likely to develop depression after experiencing stress. A collaborative group of European researchers created a mouse that carries a genetic change associated with depression in people.

“This model has good validity for understanding depression in the human, in particularly in cases of stress-induced depression, which is a fairly widespread phenomenon,” says Dr. Alessandro Bartolomucci, the first author of the research published in the journal, Disease Models and Mechanisms (DMM).

The scientists made genetic changes in the transporter that moves a signaling protein, serotonin, out of the communication space between neurons in the brain. The changes they made are reminiscent of the genetic changes found in people who have a high risk of developing depression.

“There is a clear relationship between a short form of the serotonin transporter and a very high vulnerability to develop clinical depression when people are exposed to increasing levels of stressful life events,” says Dr. Bartolomucci.

“This is one of the first studies performed in mice that only have about 50 percent of the normal activity of the transporter relative to normal mice, which is exactly the situation that is present in humans with high vulnerability to depression.”

Mice with the genetic change were more likely to develop characteristics of depression and social anxiety, which researchers measure by their degree of activity and their response to meeting new mice.

The work from this study now allows researchers to link the genetic changes that are present in humans with decreased serotonin turnover in the brain. It suggests that the genetic mutation impedes the removal of signaling protein from communication areas in the brain, which may result in an exaggerated response to stress.

Dr. Bartolomucci points out that many of the chemical changes they measured occurred in the areas of the brain that regulate memory formation, emotional responses to stimuli and social interactions, which might be expected.

“What we were surprised by was the magnitude of vulnerability that we observed in mice with the genetic mutation and the selectivity of its effects”.

Source: The Company of Biologists

http://psychcentral.com/news/2010/04/07/genetic-link-for-stress-induced-depression/12658.html

Related News Articles

• Genetic Link for Migraines and Depression
• Genetic Link for Teen Anxiety, Depres sion and Insomnia

FAA Still Stigmatizes Depression, Mental Illness

By John M Grohol PsyD

If You’re Depressed, Fearful, It Might Help To Worry, Too

A new study of brain activity in depressed and anxious people indicates that some of the ill effects of depression are modified – for better or for worse – by anxiety.

The study, in the journal Cognitive, Affective & Behavioral Neuroscience, looked at depression and two types of anxiety: anxious arousal, the fearful vigilance that sometimes turns into panic; and anxious apprehension, better known as worry.

The researchers used functional Magnetic Resonance Imaging (fMRI) at the Beckman Institute’s Biomedical Imaging Center to look at brain activity in subjects who were depressed and not anxious, anxious but not depressed, or who exhibited varying degrees of depression and one or both types of anxiety.

“Although we think of depression and anxiety as separate things, they often co-occur,” said University of Illinois psychology professor Gregory A. Miller, who led the research with Illinois psychology professor Wendy Heller. “In a national study of the prevalence of psychiatric disorders, three-quarters of those diagnosed with major depression had at least one other diagnosis. In many cases, those with depression also had anxiety, and vice versa.”

Previous studies have generally focused on people who were depressed or anxious, Miller said. Or they looked at both depression and anxiety, but lumped all types of anxiety together.

Miller and Heller have long argued that the anxiety of chronic worriers is distinct from the panic or fearful vigilance that characterizes anxious arousal.

In an earlier fMRI study, they found that the two types of anxiety produce very different patterns of activity in the brain. Anxious arousal lights up a region of the right inferior temporal lobe (just behind the ear). Worry, on the other hand, activates a region in the left frontal lobe that is linked to speech production.

(Other research has found that depression, by itself, activates a region in the right frontal lobe.)

In the new study, brain scans were done while participants performed a task that involved naming the colors of words that had negative, positive, or neutral meanings. This allowed the researchers to observe which brain regions were activated in response to emotional words.

The researchers found that the fMRI signature of the brain of a worried and depressed person doing the emotional word task was very different from that of a vigilant or panicky depressed person.

“The combination of depression and anxiety, and which type of anxiety, give you different brain results,” Miller said.

Perhaps most surprisingly, anxious arousal (vigilance, fear, panic) enhanced activity in that part of the right frontal lobe that is also active in depression, but only when a person’s level of anxious apprehension, or worry, was low. Neural activity in a region of the left frontal lobe, an area known to be involved in speech production, was higher in the depressed and worried-but-not-fearful subjects.

Despite their depression, the worriers also did better on the emotional word task than those depressives who were fearful or vigilant. The worriers were better able to ignore the meaning of negative words and focus on the task, which was to identify the color – not the emotional content – of the words.

These results suggest that fearful vigilance sometimes heightens the brain activity associated with depression, whereas worry may actually counter it, thus reducing some of the negative effects of depression and fear, Miller said.

“It could be that having a particular type of anxiety will help processing in one part of the brain while at the same time hurting processing in another part of the brain,” he said. “Sometimes worry is a good thing to do. Maybe it will get you to plan better. Maybe it will help you to focus better. There could be an up-side to these things.”

Researchers from the University of Illinois, Pennsylvania State University and the University of Colorado collaborated on the study. The National Institute of Mental Health and the National Institute of Drug Abuse at the National Institutes of Health; the Beckman Institute and Intercampus Research Initiative in Biotechnology supported the research.

Miller is affiliated with the U. of I. department of psychology, the Beckman Institute, the Neuroscience Program in the College of Liberal Arts and Sciences, and the department of psychiatry in the College of Medicine.

Article,: “Co-occurring Anxiety Influences Patterns of Brain Activity in Depression”

Source:
Diana Yates
University of Illinois at Urbana-Champaign

http://www.medicalnewstoday.com/articles/184310.php

It’s a dreadful place.

Relapse.

Maybe you had hoped you’d never go there. Or maybe you stay awake fearing you will. It doesn’t matter. You don’t have to stay there for long. You’ll be on your way shortly.

I prefer to use the term “set back” when I get sucked back into the Black Hole — bam! — stuck inside a brain that covets relief, any form of relief, and will do just about anything to get it. Because it’s certainly not the end of recovery. From depression or any addiction. A relapse merely gives you a new starting place.

Since I’ve been struggling with this recently in my own life, I’ve laid out seven strategies to get unstuck … to recover from a relapse.

1. Listen to the right people.

If you’re like me, you’re convinced that you are lazy, ugly, stupid, weak, pathetic, and self-absorbed when you are depressed or have given into an addiction. Unconsciously, you seek people, places, and things that will confirm those opinions. So, for example, when my self-esteem has plummeted to below-seawater status, I can’t stop thinking about the relative who asked me, after I had just returned from the psych ward and was doing everything I possibly could to recover from depression: “Do you WANT to feel better?” Indicating that I was somehow willing myself to stay sick in order to get attention or maybe because fantasizing about death is so much fun. I can’t get her and that question out of my mind when I’m pedaling backward. SO I draw a picture of her, with her question inside a bubble. Then I draw me with a bubble that says “HELL YES, DIMWIT!” Then I get out my self-esteem file and read a few of the affirmations of why I’m not lazy, ugly, stupid, weak, pathetic, and self-absorbed.

2. Make time to cry.

I’ve listed the healing faculties of tears in my piece “7 Good Reasons to Cry Your Eyes Out.” Your body essentially purges toxins when you weep. It’s as if all your emotions are bubbling to the surface, and when you cry, you release them, which is why it is so cathartic. Lately, I’ve been allowing myself 10 to 15 minutes in the morning to have a good cry, to say whatever I want without cognitive adjustments, to let it all out, and not to judge it.

3. Ditch the self-help.

As I wrote in my piece “Use Caution with Positive Thinking,” cognitive-behavioral adjustments can be extremely helpful for persons struggling with mild to moderate depression, or struggling with an addition that isn’t destroying them. With severe depression or a crippling addiction, though, positive thinking can sometimes make matters worse. I was so relieved the other day when my psychiatrist told me to put the self-help books away. Because I do think they were contributing to my self-battery.

Right now, when I start to think “I can’t take it anymore,” I try not to fret. I don’t worry about how I can adjust those thoughts. I simply consider the thoughts as symptoms of my bipolar disorder, and say to myself, “It’s okay. You won’t feel that way when you’re better. The thoughts are like a drop in insulin to a diabetic … a symptom of your illness, and a sign you need to be especially gentle with yourself.”

4. Distract yourself.

Instead of sitting down with some self-help books, you would be better off doing whatever you can to distract yourself. I remember this from my former therapist who told me, during the months of my severe breakdown, to do mindless things … like word puzzles and reading trashy novels. Recently, I’ve been going to Navy football games, which does take my mind off of my thoughts for a few hours on Saturdays. Not that I understand football … but there is a lot to watch besides the cheerleaders. Like my children trying to score all kinds of junk food.

5. Look for signs of hope.

The little, unexpected signs of hope kept me alive during my mega-breakdown, and they are the gas for my sorry-performing engine during a fragile time like this. Yesterday, a saw a rose bloom on our rose bush out front. In October! Since roses symbolize healing for me, I took it as a sign of hope … that I won’t plummet too far … there are things in this life that I’m meant to do.

6. Say yes anyway.

In her book Solace: Finding Your Way Through Grief and Learning to Live Again, author Roberta Temes suggests a policy whereby you always say yes to an invitation out. That keeps you from isolating, which is so easy to do when you’re grieving or stuck in a depression or off the wagon in a big way. I’ve been following this piece of advice. When a friend asks me to have coffee (and I really hope she doesn’t!), I have to say yes. It’s non-negotiable. Until I feel better and get back my brain.

7. Break your day into moments.

Most depressives and addicts would agree that “a day at a time” simply doesn’t cut it. That’s WAY too long. Especially first thing in the morning. I have to get to bedtime? Are you kidding me? So when rear-ended in the depression tunnel or fighting one of my many addictions, I break the day into about 850 moments. Each minute has a few moments. Right now it’s 11:00. I only have to worry about what I’m doing now, until, say 11:02.

For all 12 strategies on how to recover from a relapse, click here!

Source:  http://psychcentral.com/blog/archives/2010/04/03/7-strategies-to-help-you-recover-from-a-relapse/

Postpartum Depression in Adoptive Parents

By Rick Nauert PhD Senior News Editor
Reviewed by John M. Grohol, Psy.D. on April 1, 2010

New research suggests postpartum blues can occur even when a baby or child is adopted. The altered mood often follows unrealistic expectations that peak during the adoption process.

“People often hear about postpartum blues when having a baby, but the emotional well-being of adoptive parents once the child is placed in the home is not really talked about,” said Karen J. Foli, an assistant professor of nursing and an adoptive mother.

“In this study, the majority of the adoptive parents who self-reported having experienced depression after the child was placed in their home often described unmet or unrealistic expectations of him- or herself, the child, family and friends, or society.

“For example, some parents shared that they did not anticipate that bonding with their child would be a struggle or that family members or friends would not offer the same support that birthparents enjoy.”

The signs and symptoms of depression include depressed mood, decreased interest or pleasure in activities, significant weight changes, difficulty sleeping or excessive sleeping, feeling agitated, fatigue, excessive guilt and shame, and indecisiveness.

“Postadoption depression not only affects the parents, but it also has an influence on the well-being of the child,” she said.

Foli, who is co-author of the book The Post-Adoption Blues: Overcoming the Unforeseen Challenges of Adoption, interviewed 21 adoptive parents about their adoption and depression experiences, as well as 11 adoption experts and professionals.

The adopted children’s range of age at placement was newborn to 12 years, and when the study was conducted the children’s ages ranged from 12 months to 24 years. Foli’s findings are published in this month’s Western Journal of Nursing Research.

“Many adoptive parents spend their time during the adoption process demonstrating they are not only going to be fit parents, but super parents, and then they struggle with trying to be the world’s best parent when the child is placed in the home,” Foli said.

“Adoptive parents also may experience feelings about their legitimacy as a parent, or even surprise if they don’t readily bond with the infant or child.”

Other factors that contribute to postadoption depression may include the expectations surrounding the child’s attachment to the parent, a lack of peers, the lack of boundaries with birthparents in open adoptive agreements, and society’s attitude toward adoptive families as a whole.

Adoptive parents also are tired by the time the child comes into the home, Foli said. They have endured a rigorous adoption process and much of their lives have been out of their control.

“Obtaining that next form or checking that next box while waiting for the child can shift the focus away from parenting and emphasize the process of adoption,” Foli said.

It’s estimated there are 2 million adoptive parents in the United States. Adoptions can take place through public agencies, international organizations, private organizations, kinship agreements or tribal adoptions.

“Even though adoption continues to grow in the United States and become more mainstream, there is conventional wisdom that implies adoption was ‘Plan B’ for the parents,” Foli said.

“New adoptive parents often realize they weren’t as prepared as they thought they were and the child’s needs may overwhelm them. Some family members may not be receptive to news about an adoption or they may even treat the adopted children differently.

“Some parents in the study reported that acquaintances or strangers felt entitled to ask probing questions about the adoption, such as, ‘How much did the child cost?”

The adoption professionals who participated in the study said parents were often reluctant to admit their struggles out of fear and shame.

Parents also echoed feelings of extreme guilt and confusion over how they were struggling, particularly after their intense longing and eagerness to bring a child home.

“We need to empower parents to share their feelings with adoption-smart professionals, online or face-to-face support groups, trusted significant others, and friends,” Foli said.

“Parents should realize they are not being disloyal to their children or families to feel the way they do. Health-care providers, especially nurses, can be instrumental in detecting issues related to depression or the mental well-being of the parents.

“Being more open about such concerns can lead to a healthier, happier family. By helping themselves, they are helping their children.”

Source: Purdue University

http://psychcentral.com/news/2010/04/01/postpartum-depression-in-adoptive-parents/12519.html

 

Sri Carmichael, Consumer Affairs Reporter

A Londoner who suddenly went blind has overcome his disability and built a £1 million catering business.

John Charles, 37, lost his sight over three weeks in 1996 after suffering severe headaches. Now he runs a firm based in Bermondsey that has won catering contracts for the Olympic Delivery Authority and employs other blind people.

Mr Charles experienced the traumatic deterioration in his vision shortly after graduating in business and finance from the University of East London. Despite a good degree, the only job he was offered was as a factory worker.

He said his friends and family avoided him as they struggled to come to terms with his disability but he was determined to set up his own company.

Mr Charles, who lives at Surrey Quays, applied to the main high street banks for backing but was turned down by all of them once they met him in person. Finally charity Action for Blind People helped him secure funding to set up Catering2Order.

The organisation now refers on clients to chief executive Mr Charles as potential staff members.

The businessman, who often works from 4am to 8pm, said: “Once we got the business off the ground I thought, I’m really fortunate and really lucky.’

“I’ve met some great people who have helped me along the way. A lot of people with disabilities are put off working in catering but there’s no reason they can’t do it.”

Action for Blind People hopes to help more visually-impaired people set up their own businesses through its self-employment project, Future Visions.

Source:  http://www.thisislondon.co.uk/standard/article-23820264-i-beat-trauma-of-blindness-to-build-pound-1m-firm.do

By Rick Nauert PhD Senior News Editor
Reviewed by John M. Grohol, Psy.D. on April 6, 2010

A new study has an old answer for mental health issues: Physical exercise is an underutilized method to reduce depression and anxiety.

According to researchers who analyzed the results of numerous published studies, exercise is a magic drug for many people with depression and anxiety disorders, and it should be more widely prescribed by mental health care providers.

“Exercise has been shown to have tremendous benefits for mental health,” says Jasper Smits, director of the Anxiety Research and Treatment Program at Southern Methodist University in Dallas.

“The more therapists who are trained in exercise therapy, the better off patients will be.”

Smits and Michael Otto, psychology professor at Boston University, based their finding on an analysis of dozens of population-based studies, clinical studies and meta-analytic reviews related to exercise and mental health, including the authors’ meta-analysis of exercise interventions for mental health and studies on reducing anxiety sensitivity with exercise.

The researchers’ review demonstrated the efficacy of exercise programs in reducing depression and anxiety.

The traditional treatments of cognitive behavioral therapy and pharmacotherapy don’t reach everyone who needs them, says Smits, an associate professor of psychology.

“Exercise can fill the gap for people who can’t receive traditional therapies because of cost or lack of access, or who don’t want to because of the perceived social stigma associated with these treatments,” he says.

“Exercise also can supplement traditional treatments, helping patients become more focused and engaged.”

The researchers presented their findings at the annual conference of the Anxiety Disorder Association of America.

Their workshop was based on their therapist guide “Exercise for Mood and Anxiety Disorders,” with accompanying patient workbook (Oxford University Press, September 2009).

“Individuals who exercise report fewer symptoms of anxiety and depression, and lower levels of stress and anger,” Smits says.

“Exercise appears to affect, like an antidepressant, particular neurotransmitter systems in the brain, and it helps patients with depression re-establish positive behaviors. For patients with anxiety disorders, exercise reduces their fears of fear and related bodily sensations such as a racing heart and rapid breathing.”

After patients have passed a health assessment, Smits says, they should work up to the public health dose, which is 150 minutes a week of moderate-intensity activity or 75 minutes a week of vigorous-intensity activity.

At a time when 40 percent of Americans are sedentary, he says, mental health care providers can serve as their patients’ exercise guides and motivators.

“Rather than emphasize the long-term health benefits of an exercise program – which can be difficult to sustain – we urge providers to focus with their patients on the immediate benefits,” he says.

“After just 25 minutes, your mood improves, you are less stressed, you have more energy – and you’ll be motivated to exercise again tomorrow. A bad mood is no longer a barrier to exercise; it is the very reason to exercise.”

Smits says health care providers who prescribe exercise also must give their patients the tools they need to succeed, such as the daily schedules, problem-solving strategies and goal-setting featured in his guide for therapists.

“Therapists can help their patients take specific, achievable steps,” he says.

“This isn’t about working out five times a week for the next year. It’s about exercising for 20 or 30 minutes and feeling better today.”

Source: Southern Methodist University

http://psychcentral.com/news/2010/04/06/exercise-therapy-for-depression/12627.html

 

The Foundation for Art & Healing has released the proceedings from its groundbreaking Arts and the Heart Roundtable (AHR), a gathering of luminaries from the medical, arts and public health sectors regarding the connection between creative engagement and cardiac health. Held during the summer of 2009 in New York, the goal of the meeting was to draw on research and clinical expertise as well as the direct experiences of cardiac patients who have found creative endeavors to aid in their own personal healing processes. The Roundtable participants concurred with the findings of the research review (since published in the American Journal of Public Health, February 2010) as related to cardiac health, calling for a greater range of research both in establishing the connection between creative engagement and positive changes in cardiac health, as well further understanding the connection. The Foundation has responded to this call for action, planning multiple pilot programs that will not only directly connect individuals with the healing power of creative engagement, but provide populations among which to conduct further evaluation and research.

“We were quite pleased with the participation in and results of the AHR,” stated Jeremy Nobel, MD, MPH, Founder and President of the Foundation for Art & Healing. “The body of research connecting creative engagement to healing outcomes is compelling and it was wonderful to discuss what more could be done with such a fantastic group of minds.”

“Put simply, heart disease is affected by emotion and we know that art deals with emotion,” said Joshua Smyth, PhD, Professor of Psychology at Syracuse University. “Positive physiological and psychological changes occur in the individual who is creatively engaged. Although our current understanding of this relationship is in its infancy, millions of people can potentially be helped by combining creative engagement with more traditional biomedical treatments.”

As described a bit more poetically by Edward Hirsch, poet and President of the Guggenheim Memorial Foundation, “The activity of making something artistically is transformative but not entirely rational. Individuals take their obsession, grief, pain, and hope and try to turn it into something. This ‘making’ may not result in a cure, but it is ultimately healing.”

Harlan M. Krumholz, MD, SM, a leading cardiologist and Professor at the Yale University School of Medicine agreed by saying, “If we can demonstrate that emotion affects outcomes and art affects emotion, then a logical path to better outcomes would involve more attention to engaging people in artistic pursuits.”

The growing body of research referenced by Dr. Nobel and reviewed at the Roundtable was recently highlighted in an article published in the February 2010 edition of the American Journal of Public Health. Titled “The Connection Between Art, Healing & Public Health: A Review of Current Literature,” the article demonstrated that although there is evidence that art-based interventions are effective in reducing adverse physiological and psychological outcomes, the extent to which these interventions enhance health status is largely unknown.

In addition to reviewing the existing and potential research in this area, the AHR panel also discussed creating programmatic models for engagement of multiple populations that could provide immediate public benefit and serve as evaluation sites. Significant discussion focused on workplace-based programming opportunities, recognizing the current interest of employers in the health of their employees, and the potentially sizable populations available in which one could pilot programs and conduct evaluations of the impact.

For example, Roundtable participant Steven M. Safyer, MD, CEO of Montefiore Medical Center, said he could foresee an immediate benefit for his institution. “There are 17,000 employees working at Montefiore right now, who could probably benefit from this type of approach, not to mention the patients, families and communities we serve,” said Safyer. “There is no reason not to get started now!”

Source:
Dave Schemela
HealthStar PR

http://www.medicalnewstoday.com/articles/184294.php