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January 2011



Recent Posts


Rising Above the Ebb & Flow

Adolescent anxiety, depression two distinct disorders


Adolescent depression and anxiety disorders are two distinct psychiatric disorders, according to Dr William W. Hale III (a researcher of the Langeveld Institute for the Study of Education and Development in Childhood and Adolescence at Utrecht University) in a recent publication in the Journal of Child Psychology and Psychiatry.

Hale and his colleagues conducted a five-year, longitudinal study of secondary school adolescents. Every year their depressive and anxiety disorder symptoms were measured. Hale and his colleagues concluded that while adolescent anxiety and depression were strongly related to one another, adolescent depression and anxiety disorder symptoms are in fact best classified as two distinct disorders with parallel, but unique growth processes.

These conclusions are of importance for the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) that is planned for publication in 2012. Adolescent depression and anxiety disorders are presently classified in the revised fourth edition of the DSM (DSM-IV-TR) as disctinct disorders, however it has been suggested that these two disorders be given a join classification in the DSM-V. Hale argues that the present-day classification of adolescent depression and anxiety disorders should be preserved in the DSM-V.

Hale 3rd WW, Raaijmakers QA, Muris P, van Hoof A, Meeus WH. One factor or two parallel processes? Comorbidity and development of adolescent anxiety and depressive disorder symptoms. J Child Psychol Psychiatry. 2009 Oct;50(10):1218-26   [Abstract]

Abstract: Diversity of effective treatments of panic attacks: what do they have in common?

Diversity of effective treatments of panic attacks: what do they have in common?

Roth WT.

Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, California; Department of Veterans Affairs Health Care System, Palo Alto, California

Funded by:

National Institutes of Health; Grant Number: MH066953-01

Department of Veterans Affairs; Grant Number: ROT0042825

By comparing efficacious psychological therapies of different kinds, inferences about common effective treatment mechanisms can be made.

We selected six therapies for review on the basis of the diversity of their theoretical rationales and evidence for superior efficacy: psychoanalytic psychotherapy, hypercapnic breathing training, hypocapnic breathing training, reprocessing with and without eye-movement desensitization, muscle relaxation, and cognitive behavior therapy.

The likely common element of all these therapies is that they reduce the immediate expectancy of a panic attack, disrupting the vicious circle of fearing fear.

Modifying expectation is usually regarded as a placebo mechanism in psychotherapy, but may be a specific treatment mechanism for panic. The fact that this is seldom the rationale communicated to the patient creates a moral dilemma: Is it ethical for therapists to mislead patients to help them? Pragmatic justification of a successful practice is a way out of this dilemma.

Therapies should be evaluated that deal with expectations directly by promoting positive thinking or by fostering non-expectancy.


Copyright © 2009 Wiley-Liss, Inc., A Wiley Company

CBT helps prevent panic attacks in COPD patients

By Mark Cowen

MedWire News: A brief, targeted cognitive behavior therapy (CBT) intervention is effective for the prevention and treatment of panic attacks and associated symptoms in patients with chronic obstructive pulmonary disease (COPD), researchers report.


© 2009 Current Medicine Group Ltd, a part of Springer Science+Business Media

Abstract: Increased risk of acute myocardial infarction for patients with panic disorder

Increased Risk of Acute Myocardial Infarction for Patients With Panic Disorder: A Nationwide Population-Based Study

Chen YH, Tsai SY, Lee HC, Lin HC.

From the School of Public Health (Y.-H.C.), Taipei Medical University, Taipei, Taiwan; School of Medicine (S.-Y.T., H.-C.L.), Department of Psychiatry, Taipei Medical University Hospital, Taipei, Taiwan; AND School of Health Care Administration (H.-C.L.), Taipei Medical University, Taipei, Taiwan.

Objective: To examine prospectively the relationship between a diagnosis of panic disorder and the risk of acute myocardial infarction within 1 year of follow-up. Panic disorder is associated prospectively with coronary artery disease, but the risk of acute myocardial infarction associated with panic disorder has not been specifically investigated.

Method: This nationwide population-based study used data from the Taiwan National Health Insurance Research Database covering the years 2000 to 2005. A total of 9641 patients diagnosed with panic disorder in 2004 were included, together with 28,923 matched nonpanic disorder enrollees as a comparison cohort. Cox proportional hazard regressions were conducted to compute hazard ratios, after adjustment for comorbid medical disorders and sociodemographic characteristics.

Results: Results indicated that 4.77% of patients with panic disorder (approximately one in 21) experienced an acute myocardial infarction episode within a year, compared with 2.73% of patients in the comparison cohort. The adjusted hazard of acute myocardial infarction was significantly higher (1.75 times, 95% Confidence Interval = 1.55-1.97) for patients with panic disorder, relative to the comparison cohort. The association persisted in further analyses stratified by hypertension, coronary heart diseases, and age.

Conclusion: Panic disorder was identified as an independent risk factor for subsequent acute myocardial infarction. Comprehensive multidisciplinary approaches are needed to optimize primary and secondary prevention of acute myocardial infarction among patients with panic disorder.

© 2009 American Psychosomatic Society

Abstract: The fear circuitry in panic disorder and its modulation by CBT interventions

de Carvalho MR, Rozenthal M, Nardi AE.

Laboratory of Panic & Respiration, Institute of Psychiatry, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro (RJ), Brazil, INCT Translational Medicine (CNPq), Brazil; Escola de Medicina e Cirurgia/Centro Multidisciplinar de Pesquisa e Extenso sobre Envelhecimento (CEMPE) (School of Medicine and Surgery/Multi-disciplinary Center for Research and Longevity), Universidade Federal do Estado do Rio de Janeiro (UNIRIO), Rio de Janeiro (RJ), Brazil

Panic disorder (PD) is a multidimensional anxiety disorder that involves the activation of a complex brain fear-network. The goals of this systematic review are to pinpoint some working functions of the most important neuroanatomical structures of fear and panic neurocircuitry and to raise hypotheses about how cognitive-behaviour therapy (CBT) may work on modulating the neurocircuitry of fear.

The bibliographical search was carried out using mainly the PubMed database. Fifty-six articles were selected. A number of studies regarding several brain sites that participate in fear and anxiety circuitry were found and each region was described with its functionalities within the circuitry. Among the structures chosen were: the amygdala, the hippocampus and the prefrontal cortex, which play a special role.

Study hypotheses showed that CBT may operate upstream from the amygdala and exert inhibitory effects on a variety of learned responses. It may work by strengthening the medial prefrontal cortex ability to inhibit firing of amygdala neurons, under the modulation of the hippocampus. Only two studies examined the modulation of fear neurocircuitry with CBT in PD.

The results indicate that CBT has the potential to modify the dysfunctional neural circuitry associated with PD, but there is insufficient evidence to support the preliminary hypothesis.

© 2009 Informa plc

Stop worrying, help is on the way: York study

Written by By Raymond Kwan, Contributor

Thanks to a new study done by York University, help might be on the way for those who suffer from severe anxiety.

The study found that people with severe anxiety who receive motivational interviews prior to treatment respond better to their treatment.


Tips to Stop Emotional Eating
(Because Food Doesn’t Fix Stress)

ROCHESTER, Minn. — For emotional eaters, food is a best friend, there to boost sprits, calm stress and alleviate boredom.

But according to the August issue of Mayo Clinic Women’s HealthSource, emotional eating often leads to eating too much, especially high-calorie, sweet, salty and fatty foods. Women are especially prone to emotional eating — and then feel guiltier and less healthy than men do after snacking on “forbidden” foods.

The connection between stress and eating likely has roots in brain chemistry. Faced with a real threat, the fight-or-flight reaction kicks in and suppresses appetite temporarily. But when faced with persistent stress — health problems, difficult relationships or too much work — many people turn to high-fat, high-calorie foods for comfort. Using food as a coping strategy doesn’t alleviate stress and will likely cause weight gain.

Mayo Clinic Women’s HealthSource offers these suggestions to understand and overcome emotional eating:

Learn to recognize true hunger: A craving for chips or cookies soon after a meal is likely an emotional hunger, not real hunger.

Identify the food triggers: Keeping a journal can help identify patterns in emotional eating, including emotions and feelings when eating; what and how much was eaten; and feelings after eating.

Read in Full:  http://www.mayoclinic.org/news2009-mchi/5380.html?rss-feedid=4

Pregabalin facilitates successful switch from benzodiazepine therapy in patients with generalised anxiety disorder: Presented at ECNP

By Jenny Powers

ISTANBUL, Turkey — September 18, 2009 — Patients with generalised anxiety disorder (GAD) can be switched off benzodiazepines with the assistance of pregabalin treatment, according to a study presented here at the 22nd European College of Neuropsychopharmacology (ECNP) Congress.

Copyright (c) 1995-2009 Doctor’s Guide Publishing Limited. All rights reserved.

Abstract: Preliminary evidence of white matter abnormality in the uncinate fasciculus in generalized social anxiety disorder

Phan KL, Orlichenko A, Boyd E, Angstadt M, Coccaro EF, Liberzon I, Arfanakis K.

Department of Psychiatry, University of Michigan, VA Ann Arbor Healthcare System, Ann Arbor, Michigan; Mental Health Service, VA Ann Arbor Healthcare System, Ann Arbor, Michigan; Departments of Biomedical Engineering and Electrical and Computer Engineering, Illinois Institute of Technology, Chicago, Illinois; Department of Psychiatry, the University of Chicago, Chicago, Illinois

Background: Individuals with generalized social anxiety disorder (GSAD) exhibit exaggerated amygdala reactivity to aversive social stimuli. These findings could be explained by microstructural abnormalities in white matter (WM) tracts that connect the amygdala and prefrontal cortex, which is known to modulate the amygdala’s response to threat. The goal of this study was to investigate brain frontal WM abnormalities using diffusion tensor imaging (DTI) in patients with social anxiety disorder.

Methods: A Turboprop DTI sequence was used to acquire diffusion tensor images in 30 patients with GSAD and 30 matched healthy control subjects. Fractional anisotropy, an index of axonal organization, within WM was quantified in individual subjects, and an automated voxel-based, whole-brain method was used to analyze group differences.

Results: Compared with healthy control subjects, patients had significantly lower fractional anisotropy localized to the right uncinate fasciculus WM near the orbitofrontal cortex. There were no areas of higher fractional anisotropy in patients than controls.

Conclusions: These findings point to an abnormality in the uncinate fasciculus, the major WM tract connecting the frontal cortex to the amygdala and other limbic temporal regions, in GSAD, which could underlie the aberrant amygdala-prefrontal interactions resulting in dysfunctional social threat processing in this illness.

Copyright © 2009 Published by Elsevier Inc.

Blocking enzyme may repair stress induced brain damage

Bill Hathaway – Yale

Damage to the brain caused by chronic stress or lead poisoning can be repaired by blocking a key molecular pathway, Yale University researchers report in the Proceedings of the National Academy of Sciences.

Rats subjected to chronic stress develop damage to the prefrontal cortex, an area of the brain crucial to working memory, impulse control and the ability to stay focused on tasks. Long-term stress triggers excessive activity of a family of enzymes called protein kinase C, which in turn damages the cytoskeleton of neurons and hinders their ability transmit information. This loss of the brain’s grey matter due to stress has been linked to poor impulse control, a decline in working memory and inability to focus on tasks. These findings have direct relevance to our understanding of bipolar disorder, where genetic insults increase protein kinase C signaling which may be associated with a loss of prefrontal grey matter and behavioral control.

The Yale team led by senior author Amy Arnsten, professor of neurobiology at Yale, succeeded in protecting against the effects of stress by blocking the action of protein kinase C in rats. The researchers found that dendritic spines of neurons stayed intact and that the rats’ ability to perform a task requiring working memory and impulse control was improved.

When you inhibit protein kinase C, cells can talk to each other again and you rescue cognition,” Arnsten said.

Blocking protein kinase C has potential for treating bipolar disorder and post-traumatic stress disorder, Arnsten said. Medications such as lithium can inhibit protein kinase C and have been shown to restore normal levels of grey matter in patients with bipolar disorder. She also noted such a therapy might help reverse the effects of lead poisoning, which causes learning disabilities and behavioral problems in tens of thousands of children. Lead, like stress, can also increase protein kinase C activity and erode grey matter in the prefrontal cortex. These findings suggest that medications that inhibit protein kinase C may help restore prefrontal brain function in children with residual problems from lead poisoning.

The study was funded by the U.S. National Institutes of Health and the Yale Stress Center.

Hains AB, Vu MAT, Maciejewski PK, et al. Inhibition of protein kinase C signaling protects prefrontal cortex dendritic spines and cognition from the effects of chronic stress. Proc Natl Acad Sci U S A. 2009 Sep; doi:10.1073/pnas.0908563106 [Abstract | Full text (PDF)]

Myth exposed: Quitting smoking doesn’t worsen psychiatric disorders

Marla Paul – Northwestern University

People with mental illnesses such as depression and anxiety are the heaviest smokers in the country, but their doctors are afraid to ask them to quit. They assume that if their patients try to quit smoking, their mental disorders will get worse.

That is a myth, according to Brian Hitsman, a tobacco addiction specialist and assistant professor of preventive medicine at Northwestern University Feinberg School of Medicine and a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

This population’s tobacco use and dependence need to be treated, he said. Hitsman has designed and published the first comprehensive, evidence-based plan for psychiatrists, psychologists and other mental health providers to help their patients quit smoking. His paper appeared in a recent issue of the Canadian Journal of Psychiatry.

These doctors and mental health specialists focus on their patients’ psychiatric health and lose track of their physical health,” said Hitsman, who is a health psychologist. “Tobacco cessation gets a lot of attention, but we leave out a population that smokes the majority of all the cigarettes.

Between 40 to 80 percent of people with mental illness are daily smokers, depending on the disorder, compared to less than 20 percent of people who don’t have problems with mental illness, according to research. The mentally ill also smoke more cigarettes per day — often up to two packs. They have a disproportionately high rate of tobacco-related disease and mortality, such as cardiovascular disease or cancer, with a correspondingly heavy financial burden to the health-care system.

The mentally ill receive tobacco treatment on only 12 percent of their visits to a psychiatrist and 38 percent of their visits to a primary care physician, Hitsman said.

Doctors erroneously believe mental disorders will worsen if they take away a person’s tobacco. “Not a single study shows that symptoms get worse,” Hitsman said. He examined 13 randomized clinical trials that measured psychiatric symptoms during smoking cessation treatment. Seven studies showed that psychiatric symptoms actually improved during smoking cessation treatment, and six showed no changes.

Another problem is mental health professionals believe tobacco is not a real addiction compared to other drug addictions.

The perception is patients need tobacco because it’s their only source of pleasure and helps them feel better,” Hitsman said. “There is very little evidence, though, that smoking cigarettes serves to self-medicate emotional symptoms.

There is evidence from a few studies, however, that when mental health providers insert smoking cessation treatment into the mental health treatment plan, they can help their patients quit or cut down.

They find if you take advantage of the relationship with the counselor and insert smoking cessation counseling into treatment that you enhance quit rates,” Hitsman said.

His tobacco cessation plan combines cognitive behavior therapy, pharmacotherapy and motivational counseling to help the patient quit. Hitsman also has identified several treatment medications that may further facilitate quitting for this population.

People with mental disorders do have a harder time quitting than the general population, Hitsman acknowledged, but said newer studies show it is possible to enhance the chance of success with this approach. Even if patients simply reduce their smoking, they are much more likely to quit successfully at a later date.

To help motivate the patient, the counselor highlights the benefits of quitting, the personal costs of smoking and the barriers to cessation success. “It gets the person in a problem-solving mode, at the basis of which is a solid relationship with the counselor,” Hitsman said.

Tobacco dependence also needs to be treated as a chronic disease, Hitsman believes. “We know that treatment provided for a longer duration substantially increases the abstinence rates of people without mental disorders,” he noted. “Smokers with mental illness may be especially likely to benefit from extended or maintenance tobacco treatment.

Hitsman B, Moss TG, Montoya ID, George TP. Treatment of Tobacco Dependence in Mental Health and Addictive Disorders. Can J Psychiatry. 2009;54(6):368-78 [Full text (PDF)]


Another common myth is that smoking reduces stress levels. It does, but only of the additional stress produced by withdrawal symptoms as nicotine levels from the last ‘hit’ fall.

Naturopathic treatment significantly improves anxiety

A  Canadian study finds that naturopathic treatment including the herbal remedy ashwagandha, deep breathing exercises, dietary counseling, and a standard multi-vitamin supplement significantly reduced symptoms of anxiety. This was the first study to evaluate the potential of naturopathic treatment to treat anxiety.

Caution: Some Over-The-Counter (OTC) supplements may interact with prescription medications or be affected by them. Check with your doctor or pharmacist before taking any herbal or OTC supplement while on medication.

Most governments do not require dietary supplement makers to demonstrate the safety or effectiveness of their products. Ask your healthcare provider for advice on selecting a brand.

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