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The Relationship of Stress to the Expression and Treatment of Bipolar Disorder – Part III

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The Relationship of Stress to the Expression and Treatment of Bipolar Disorder – Part III

 by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego, California

Etiology

 The strong relationship between stress and BD generates speculation about the etiology of the disorder.  The exact nature of the relationship between the two is unclear (Simon, et al., 2004).  Anxiety in early life may represent a prodromal symptom, or they may both share the same biological or genetic origin.   Heritability rates of BD are between 40 (a narrow definition) and 97% (a broad-spectrum definition) (Correll, et al., 2007).

 Preston and colleagues (2002) summarize the etiological theories that have been proposed for BD.  Several of these relate directly to the role that stress may play in the treatment of the disorder.  The Deregulation Theory revolves around the homeostatic regulation of mood.  Over activity outside of the bounds of homeostasis leads to associated behavioral manifestations.  The Chaotic Attractor Theory hypothesizes that there is a biochemical deficit that leads to deregulation of the synthesis of neurotransmitters.  The mood state depends on the physiological or environmental conditions present.  It predicts a chaotic course of the illness.  The HPA Axis Theory associates the overactivation of the HPA axis in mixed state and depressive states.   The Kindling Theory hypothesizes that the buildup of subclinical biochemical changes in the limbic system.  Eventually there is a build-up of neuronal excitability until symptoms appear.  This theory explains the progressive nature of the disorder, resulting in more frequent and severe symptoms.  It is the Kindling Theory that is the most relevant to the interaction of stress disorders and BD.

 The Kindling hypothesis asserts that the first episode of a mood disorder “… is more likely to be associated with major psychosocial stressors than are episodes occurring later in the course of the illness” (Post, 1992, pp. 999-1000).  Post further hypothesized that sensitization to stressors and episodes became encoded at the level of gene expression.

There is confusion in the literature about the Kindling Hypothesis, which may be generated primarily from the ambiguities surrounding poorly described ideas and terminology in early studies.  Specifically “do recurrent episodes become autonomous of stress, such that stress is no longer an etiological mechanism in the precipitation of recurrence? Or, do individuals become sensitized to stress, such that ever more minor forms of adversity are capable of precipitating recurrence? Most generally, if minor events increase in their frequency and impact in precipitating onsets of depression across recurrence, then this would support  sensitization. By contrast, if all forms of stress (major and minor) decrease in their frequency and impact in precipitating recurrences, then this would support autonomy and suggest that some other mechanism “ (Monroe & Harkness, 2005, p. 442). The disruptions of the social rhythms that cause bipolar episodes gives credence to the psychobiological hypothesis of the etiology of BD (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000).

With either interpretation, studies have shown that stress in early life predicts earlier onset of the disorder.  They also agree on stress as being a precipitator to episodes in early life.  Childhood abuse, for example, was reported in nearly half of one study of veterans with BD (Brown, McBride, Bauer, & Willifor, 2005).  Abuse may cause a change in brain physiology, making  BD more difficult to treat, with more rapid cycling, anxiety, and panic disorder (Post, 1992) and  (Brown, McBride, Bauer, & Willifor, 2005).  But the confusion in interpretation lies in what occurs after the initial onset.

In the first interpretation, the person with BD experience life stressors, which may be severe.  These stressors precipitate a manic or depressive episode.  Although the person has reacted to the stressor, it has desensitized him/her to further episodes of stress.  In other words, it is not that the person no longer has bipolar episodes, but that these episodes are endogenous  in nature and come independent (or at least less dependent) of the stressors.  McPherson, Hervison, and Romans (1994) found life events precipitate bipolar episodes only for earlier episodes. In another study, stress levels predict relapse, although the number of previous levels did not affect the stress response, which showed that BD episodes were not increasingly independent of stressors.  However, it did show that personality traits, such as introversion and obsessionality, did affect the patient’s reactivity to stress (Swendsen, Hammen, Heller, & Gitlin, 1995).  There are a certain number of episodes that cannot be explained be stress events (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000)

In the second interpretation of the Kindling Theory, earlier stressors actually sensitize the person with BD to stress events.  That is, once someone has had experienced stress preceding a bipolar episode, they become more sensitive to any future stress.  In this case, even minor stressors may precipitate an episode.  Hammen and Gitlin (1997), for example, found that stressors may precipitate BD episodes and more quickly, especially in those with more prior episodes.  This, they say, is “inconsistent” with the Kindling Hypothesis.  They confirmed the importance of stressful life events as a contributor to BD and showed that patients with prior history of episodes were more likely to have had a several stressors in the previous months.

Although the debate about the interpretation of the hypothesis has not been resolved, I believe that both interpretations may be valid. I have seen bipolar episodes that appear to be independent of life events or stressors and those triggered by very minor stressors.  A bipolar client may switch into hypomania quite rapidly, without noticeable triggers, as if it is just “time to switch.”  What most people, even the patient, would not discern as a stress may be enough to trigger an event.  The bipolar event may thus look as if it was spontaneous.  This would give credence to the idea that prior stress might serve as a sensitizers, such that even minor stresses create a bipolar event.  Reactivity may actually be a complex interaction between age, stress, onset, and new episodes (Hlastala, et al., 2000).

(to be continued)

– Julie Myers, PsyD

http://www.DrJulieMyers.com

 

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Written by Julie Myers, PsyD, MSCP

June 27, 2011 at 5:09 pm

The SMART Recovery® Activities Scale (SRAS)

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The SMART Recovery® Activities Scale (SRAS)

by Julie Myers, PsyD and Donald Meichenbaum, PhD

The SMART Recovery® Activities Scale (SRAS) is a new tool to help those engaged with SMART Recovery®.   The SRAS was developed by Julie Myers, Psy.D.1 and Donald Meichenbaum, Ph.D.2   

The SRAS can be used by participants to assess how far they have come in their own recovery, by facilitators, and by professional therapists/counselors with their clients.  Professionals may wish to use the SRAS in order to:

  1. Assess what SMART Recovery® activities clients have already engaged in and what SMART Recovery® beliefs they have embraced.
  2. Assess the reasons why clients have or have not engaged in these activities (possible barriers, lack of motivation, confidence, or skills) and how these obstacles can be addressed.
  3. Engage would-be participants to join SMART Recovery® and treatment, highlighting what new members may get out of some form of treatment

The SRAS for participants is available on-line in an easy-to-use PDF format, which can be filled-out on-line or can be saved and printed.  (http://www.smartrecovery.org/resources/library/Tools_and_Homework/Quick_Reference/SRAS_for_participants.pdf

 The SRAS for therapists/facilitators containing additional instructions is available at http://www.smartrecovery.org/resources/library/Tools_and_Homework/Quick_Reference/SRAS_for_therapists.pdf

Dr. Meichenbaum and Dr. Myers are seeking feedback about your experience with the SRAS.  Your feedback is greatly appreciated, as it will help to refine the scale and  help develop other SMART Recovery® materials that will have wide distribution throughout the world.  Please direct your e-mail to Julie.Myers100@gmail.com.
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1 Dr. Myers is a Licensed Clinical Psychologist in San Diego, California

2 Dr Meichenbaum is one of the founders of Cogntivie Behavior Therapy and is presently Research Director of the Melissa Institute for Violence Prevention in Miami ( www.melissainstitute.org)


The Relationship of Stress to the Expression and Treatment of Bipolar Disorder – Part II

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The Relationship of Stress to the Expression and Treatment of Bipolar Disorder  (Part II)

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

The Comorbidity of Bipolar Disorder and Stress disorders

 Comorbidity is common in BD, further complicating the diagnosis.  In one study, a comorbid disorder was found in all of the samples, and in 59% the condition preceded the onset of BD symptoms (Kessler, Rubinow, Holmes, Abelson, & Ahao, 1997).  Common among the comorbid disorders are anxiety, substance abuse, ADHD, Oppositional-Defiant Disorder, Bulimia, Social Phobia, Panic Disorder, and Obsessive Compulsive Disorder  (Correll, et al., 2007) and (Perugi, Ghaemi, & Akiskal, 2006), many of which are stress related.  Personality disorders also occur at a higher rate than the general public, which may actually be an expression of phenotypic expression of a bipolar diathesis (Correll, et al., 2007).  BD has the highest prevalence of any psychiatric disorder for alcohol and other substance use disorders, with a lifetime comorbidity estimated from 17 – 61% (Vizzarri, et al., 2007).  In one large study of 500 bipolar patients, a lifetime substance use disorders was found in the entire sample (Simon, et al., 2004).     In many cases, it is unclear whether these co-occurring disorders are truly biologically distinct, or simply risk markers, prodromal states, overlapping  characteristics, or subtypes (Correll, et al., 2007).

 Comorbidity of BD with anxiety disorders is particularly high.  In one large study of 500 BD patients, the lifetime comorbidity with anxiety disorder occurred in over half the sample (Simon, et al., 2004); approximately 11-63% had panic disorder, 8-47% social anxiety disorder, 3-35% obsessive compulsive disorder, 7-39% posttraumatic stress disorder and 7-32% generalized anxiety disorder.   Overall anxiety comorbidity was higher in Bipolar I disorder than Bipolar II disorder. The presence of anxiety predicted a lower age of onset (about 16 as opposed 20 years old) and a shorter time in the euthymic state.  Presence of anxiety disorder also was associated with impaired function, poorer quality of life, decreased likelihood of recovery, greater prevalence of substance abuse, and greater likelihood of suicide attempt.    In my experience, those in hypomanic states have a high reactivity to stress, often engaging in activities to relieve stress, such as compulsive shopping, sexual activity, or risk-taking.  Substances are often used to “self-medicate.”

When chronic stress in family, romantic, and peer relationships is present, there is less improvement in mood symptoms in adolescents.  “The association between chronic stress in peer relationships and mania symptoms is likely a recursive one in which the most impaired youths generate the highest levels of peer-related stress, which further exacerbates their mood symptomatology”  (Kim, Miklowitz, Biuckians, & Mullen, 2007, p. 37).  Possibly, this may create a pattern of dysfunctional reactivity to stress.

In one case example, Bob is an 18 year old male, who expressed BD at the age of 5 after a family stress.  Although he did not receive a diagnosis of BD until the age of 12, his symptoms where characteristic of juvenile BD.   He had symptoms of obsessive compulsive disorder, social anxiety disorder, separation anxiety, and generalized anxiety disorder.  His mind was often occupied with ruminative “bad” thoughts.  He developed many compensatory behaviors to relieve his stress including a shut-down depressive state, psychomotor agitation and tics.  Bob manifested psychotic symptoms and suicidal ideation during times of heightened stress.  School, for example, was a continual source of stress from teachers and peers, resulting in poor performance and exacerbation of bipolar switching.  This further resulted in a deterioration of peer relationships, recursively leading to a greater number of bipolar episodes.

Copyright (2011):  Julie Myers, PsyD:   All rights reserved.

Written by Julie Myers, PsyD, MSCP

June 25, 2011 at 6:48 pm

The Relationship of Stress to the Expression and Treatment of Bipolar Disorder – Part I

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The Relationship of Stress to the Expression and Treatment of Bipolar Disorder – Part I

 

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

It is generally agreed in the literature that stress affects the course and severity of Bipolar Disorder (BD.)  Stress, particularly in early life, appears to have lasting effect and marks for early onset, although the exact mechanism of this effect is poorly understood.  The relationship of stress to the onset of the disorder and its course has implications for the treatment and management of the disorder, and perhaps even its onset.  In this paper, I discuss the characteristics of BD and its co-occurrence with anxiety disorders, and the etiology and the treatment of BD in relationship to stress management techniques.  Case examples are presented.

 

The Nature of Bipolar Disorder

 Bipolar Disorder is a mood disorder, characterized by shifting states between mania or hypomania and depression.   The length of time that a person spends in either the up or the down phases are not fixed in length nor in severity, although those with Bipolar I Disorder have periods of mania, while those with Bipolar II Disorder only reach hypomania.  Periods may last from years to hours in rapid or ultra-rapid cycling BD.  In most cases, it is a progressive disorder, with the length of time spent in the depressive stage increasing with time.  Those with BD have other characteristics, such as delayed-sleep cycle and neurocognitive deficits (Correll, et al., 2007).

The DSM-IV (APA, 1994) characterizes those with mania as having pronounced and persistent moods of euphoria, grandiosity or elevated self-esteem, decreased need for sleep, rapid pressure speech, racing thoughts, distractibility, increased activity or psychomotor agitation, behavior that reflects expansiveness, and poor judgment.  Hypomania is the occurrence of a persistent elevated, irritable or expansive mood for at least four days, with the presence of three additional symptoms including “inflated self-esteem or grandiosity, decreased need for sleep, pressure of speech, flight of ideas, distractibility, increased involvement in goal-directed activities or psychomotor agitation, and excessive involvement in pleasurable activities that have a high potential for painful consequences (p. 335.)

The depressive state of BD is much like that of Major Depressive Disorder, although there is usually an increased need for sleep and psychomotor retardation rather than agitation.  Other signs include depressed mood, anhedonia, fatigue, feelings of worthless, guilt, thoughts of suicide, and executive functioning difficulties such as trouble concentrating.  Periods of mixed states or dysphoric mania also occur with BD. Symptoms of dysphoric mania include, marked irritability, severe agitation or anxiety, pessimism and unrelenting worry and despair, marked insomnia, and decreased need for sleep (APA, 1994).   In my experience, it is these mixed states that are the most troublesome, and they appear to be marked by severe stress reactivity.

Diagnosis is particularly difficult, because those with BD often do not recognize their hypomanic episodes as being abnormal and so do not report its presence; insight is state-dependent.  They may also loathe to give-up these hypomanic states. Patients usually present for help during the depressive stage (Perugi, Ghaemi, & Akiskal, 2006), and when in a depressive state, patients with BD have difficulty remembering their hypomanic states, feeling that they have always felt low. “Diagnosis may only be possible retrospectively utilizing histories from patients who have distorted recollections” (Stahl, 2005, p. 14.)     Because of these distorted recollections, it is important to have collaborating information from family members or close friends. The hypomania, which the client so often enjoys, is often more problematic to those close to the patient than to the patient themselves and may lead to dysfunctional family interactions and stress.  In my opinion, it is the client’s unwillingness to disclose these hypomanic states and the stressful events that trigger them that often leads to misdiagnosis.

(to be continued…….)

Copyright (2011) Julie Myers, PsyD:  All Rights Reserved

Making Changes in Recovery, Step-by-step

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Making Changes in Recovery, Step-by-Step

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

Have you ever wanted to make changes in your life, but felt so overwhelmed by the situation that you didn’t know where to start?  Sometimes it helps to break the change down, working through the situation step by step using pencil and paper.  (A useful worksheet can be found at http://www.smartrecovery.org/resources/library/Tools_and_Homework/Facilitators_Handout/Change_Plan_Worksheet.pdf).  First, think about why you want to make the change and then work through the steps you will need to get there. As you do this, you may find that the change you want to make really requires more than one significant change.

For example, let’s say you want to start exercising in the morning. As you work through the steps, you find that to do this, you will have to leave earlier in the morning, which means that you need to be more organized in the morning, which requires that you go to bed earlier, which means that you need to leave work earlier, which requires that you have lunch by noon.  Too many major changes means overwhelm!

Instead of becoming frustrated, break each of these steps into a different change plan, starting with the easiest change (such as having lunch earlier!)  By doing this, you will feel less overwhelmed, be more successful, and will feel better about your ability to make changes. With thoughtful forethought, you will be amazed at the changes you can make!

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com


Heart Rate Variability Biofeedback

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Heart Rate Variability Biofeedback

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

Biofeedback is a commonly used method to teach individuals voluntary control of physiological functions.   Specific biofeedback techniques include electromyography (measures muscle tension), galvanized skin response (measures sweat response), electroencephalographic (measures brain waves), skin temperature, and heart rate variability biofeedback (synchronizing heart rate and breathing).  Using biofeedback, an individual receives feedback about his/her own physiological state and learns methods to control these physiological states.

Heart rate variability biofeedback (HRVBF) teaches people how to regulate their own heart rhythm and rate to increase heart rate variability (HRV), which directly exercises the body’s physiological control mechanisms.  HRV is the measure of the rhythmicity of the heart, in its complexity and amplitude of the heart beat.  High HRV is recognized as a sign of healthy heart functioning and as a measure of autonomic activity.  Using HRVBF to sync breathing and heart patterns, an individual can learn how to breathe in a way that strengthens the parasympathetic response, thus creating a calmer mind-body state.

Decreased heart rate variability has been observed in those disorders related to autonomic dysregulation, substance use disorder, and some affective spectrum disorders, including fibromyalgia, depression, and anxiety.  HRVBF has been used for a variety of physiological and psychological disorders, particularly stress and stress related disorders, which are often directly or indirectly related to substance use disorders.  Learning how to regulate emotions that negatively affect heart rate variability, while learning how to regulate physiological signals through HRVBF, can be highly beneficial to those who experience problems with self-regulatory behaviors.

I use heart rate variability biofeedback in my practice to help patients learn a self-empowering way to calm themselves, particularly those recovering from addictive disorders and anxiety conditions, such as panic disorder.  I am Board Certified in Biofeedback.

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com
Copyright (2011):  Julie Myers, PsyD  All Rights Reserved

Assumptions About Substance Abuse: An Opinion

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Assumptions About Substance Abuse:  An Opinion

by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego;  http://www.DrJulieMyers.com

 

There are many different models of addiction, including moral, psychological (cognitive-behavioral, learning, psychodynamic, and personality), biological (genetic, biomedical, disease, medical) and socio-cultural (McNeese, 2005.)  Each of these different models operates under a different set of assumptions.  The disagreement between the models rests on the different political motivations, ideologies, personal interests, and professional training of the individual (McNeese, 2005.)  Substance abuse counselors, for example, have generally adopted the 12-step approach to the disease model, since it is what they themselves experienced.  Probably the most commonly held is the disease model. “The disease model of addiction rests on three primary assumptions: a predisposition to use a drug, loss of control over use, and progression” (Krivanek, 1988, p. 202.)  It has its roots in Alcoholics Anonymous (Yalisove, 1998.)

The World Health Organization has adopted the word drug dependence to describe the addiction process. “The general term (drug dependence) will help to indicate a relationship by drawing attention to a common feature associated with drug abuse and at the same time permit more exact description and differentiation of specific characteristics according to the nature of the agent involved.” (WHO, 1964.)

Perhaps the stress-diathesis model best describes substance abuse, dependence, and addiction.  This model describe a basis of genetic and neurological susceptibilities to addiction, either because of the genetic susceptibility to the substance (or behaviors) or because of the genetic susceptibility to certain mental disorders, which increases the likelihood of self-medication and the abuse of substances (or behaviors.)  For example, those with Bipolar
Disorder have a 50-80% increase in substance abuse, which is thought to be largely self-medication. Given a person’s susceptibility, the environmental factors then influence whether or not any one individual develops a problem with substances (or behaviors.)  Upbringing, peers, experiences, and culture all shape one’s use of substances.  How the individual responds and copes with environmental stressors in large part determines their use.  Addictions represent a maladaptive coping mechanism to these environmental stressors.

It may not be necessary to know the etiology of substance abuse to treat it.  Although such information is interesting scientifically, and it can perhaps lead to better identification of susceptible individuals, treatment should concentrate on identifying those individuals with addictive problems and implementing effective treatment.  The identification of addiction problems can be culturally influenced.  Although the scope of the problem throughout the world is massive, the definition of it as an “addiction”, “abuse” or “dependence” must be understood in light of cultural norms.

The DSM-IV (APA, 1994) defines substance abuse and dependence as:

  • Substance Abuse is a maladaptive pattern of substance use which results in clinically significant impairment, with one (or more) categories occurring within a 12 months:  failure to fulfill major obligations, use in hazardous situations, legal problems, or social problems.
  • Substance Dependence is a maladaptive pattern of substance use, which results in clinically significant impairment, with three (or more) categories occurring in the same 12 months: physical tolerance, withdrawal symptoms, a large amount consumed over a long period, a lot of time spent, negative consequences, and continued use despite recurrent problems.

Although the DSM criteria states that three criteria must be met, in my opinion, for any particularly individual, simply displaying one of these criteria could signify abuse/dependence.   For example, continued use, despite knowledge of significant problems may be enough to signify that there may be an addictive disorder.  Setting the criteria for dependence as three/five criteria may be necessary for those individuals for whom there is less clear evidence of maladaptive behaviors.

Julie Myers, PsyD, MSCP

Licensed Psychologist, MS Clinical Psychopharmacology, Master Addiction Counselor, Board Certified Biofeedbachttp://www.DrJulieMyers.com.  

Copyright (2011):  Julie Myers, PsyD.  All Rights Reserved

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APA.  (1994).  Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington DC: American Psychiatric Association.

Bergh, C., T. Eklund, P. Sodersten, & C. Nordin (1997).  Altered dopamine function in pathological gambling.  Psychological Medicine, 27: 473-475.

Doweiko, H. (2006). Concepts of chemical dependency. 6th ed. Belmont, CA: Thompson .

Goudriaan, A., J. Oosterlaan, E. de Beurs, & W. Van Den Brink (2004). Pathological gambling: a comprehensive review of biobehavioral findings.  Neuroscience & Biobehavioral Reviews.  28(2), pp.123-141.

Krivanek, (1988), p. 202., Addictions.  Sydney: Allen & Unwin.)

McNeese, C. & D. DiNitto (2005).  Chemical Dependency. United States: Pearson Education, Inc.

Sunderwirth, S., &H. Milkman (1991). Behavioral and neurochemical commonalities in addiction, Contemporary Family Therapy , 13(5 ) pp. 421-433

WHO (1964), Expert Committee on Addiction-producing Drugs: Thirteenth report, p. 53 -55.

Yalisove, A. (1998). The origins and evolution of the disease concept of treatment.  Journal of Studies on Alcohol, 59, 469-476.