Addiction and Mental Health

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What’s Your Caffeine IQ?

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What’s Your Caffeine IQ?

by Julie Myers, PsyD, MSCP

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

 

Caffeine Facts

For most people, moderate caffeine (200 – 300 mg, or about 2-3 cups of coffee a day) aren’t harmful.  But heavy caffeine use (more than 500 mg) can cause insomnia, nervousness, restlessness, irritability, nausea or other gastrointestinal problems, fast or irregular heartbeat, muscle tremors, headaches, and anxiety.

Some people are more sensitive to caffeine than are others.  Even one cup of tea may prompt unwanted anxiety, restlessness, irritability, and sleep problems. Research suggests that men may be more susceptible to caffeine than women.

Caffeine can interfere with sleep.  Sleep loss is cumulative, and even small nightly decreases can add up and disturb your daytime alertness and performance.  Caffeine keeps you from falling asleep at night, increases the number of times you wake during the night, and interfere with deep, restful sleep. Try to avoid caffeinated beverages eight hours before bedtime.

Reducing Your Intake

Too abrupt a decrease in caffeine can cause withdrawal symptoms that include headaches, fatigue, irritability and nervousness. Fortunately, these symptoms resolve after a few days. Try these simple tips:

  • Keep track of how much caffeine you use daily
  • Cut back gradually to lessen withdrawal effects.
  • Substitute decaffeinated beverages.  Try drinking half decaf.
  • Lower the caffeine content by brewing tea for less time or drinking weaker coffee
  • Read labels to check for caffeine content

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References

1       Mayo Clinic Staff, MayoClinic.com, Nutrition and healthy eating. “Caffeine: How much is too much?” http://www.mayoclinic.com/health/caffeine/NU00600, March 5, 2010

Therapeutic alliance as a predictor of outcome in treatment of cocaine dependence: A Review

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Therapeutic alliance as a predictor of outcome in treatment of cocaine dependence

by Barber, et al.

A Review by Julie Myers, PsyD, MSCP

Licensed Clinical Psychologist in San Diego

There has been an increasing interest in outcome measures in therapy.  Although there is a school of thought that technique is the primary predictor of outcome, some therapists believe that it is the therapeutic alliance that is the major predictor of outcome.  The study by Barber, et al. examines outcome measures in drug treatment.

Substance abusers are often difficult to engage in treatment, yet the therapeutic alliance has rarely been studied.  This study is the first to examine the self-reports of the therapeutic alliance as a means to predict the outcome of cocaine treatment.  Because there is a high drop-out rate for cocaine dependence (50-80 % dropout within 3 months), the research also attempts to distinguish between intent-to-treat and completer samples to see if the alliance early in treatment predicts treatment outcome.

The study used a sample size of 252; many co-occurring disorders were excluded.  Clients were randomly assigned to three different treatment techniques:  Cognitive therapy (based on Aaron Beck), dynamic therapy (support-expressive therapy), and 12-step drug counseling.  A fourth treatment group was added later in the study, which used 12-step group drug counseling only.  In addition to the targeted technique, all treatment groups were mandated to attend group drug counseling 2 times per week for initial two weeks, then once per week for four months.  Therapists in the different treatment groups were not similarly trained; drug counselors had the least training.

Both patient and therapists completed two alliance scales, the Helping Alliance (Haq-II) and the California Psychotherapy Alliance Scales (CALPAS).  In addition, patients were administered measures of functioning.  Statistical analysis of the results looked at a number of different relationships, including the prediction of outcome from alliance given symptom improvement, completer sample, and the number of sessions.

The results did not find a strong relationship between the outcome measures and the therapeutic alliance.  The alliance didn’t predict drug outcome at six months, although at one month there was stronger correlation; the therapeutic alliance was a better predictor of outcome for depression scales.  Results also showed that the therapist’s rating of alliance was less predictive than patients.  Measures were similar across completer and intent-to treat samples.  The only strongly conclusive results were that the shorter the lag time between assessment and outcome measures and the longer clients remain in treatment, the better the outcome associations.   These results do not seem to be particularly surprising to me.  The authors state that a “good therapeutic alliance with the therapist, as viewed by the patient early in treatment, is important in predicting outcome when it is embedded in a long term relationship with that therapist.”

The authors state that there are several possible reasons for the weak predictive results, including the choice of the outcome and alliance variables, the nature of the patient population and/or disorder, and the restriction of range in the measures of alliance.  Although these seem likely influences on the results of the study, I found there to be several other possible explanations.

If a study is not well designed, all of the statistical analysis in the world will be meaningless.  In my own graduate-level econometrics classes, I was taught that when designing a study, the researcher must be careful not to examine too many variables, otherwise it becomes a study that is “hunting for” statistical significance, which biases and invalidates the results.  In my opinion, this study threw too many variables into the mix, both in the design of the study and in the statistical analysis.  A far more rigorous study would have chosen one or two associations to measure, then designed the groups with stricter protocol.

In my opinion, the addition of the fourth group-counseling treatment group invalidated the results, not only because of the late introduction of the treatment, but because of the cross-over between the different treatment samples in this group counseling.  Although the researchers attempted to make the treatment samples significantly different from one another, using different therapy methods and different therapist qualifications, for therapists and counselors who do not use 12-step methods, the mandatory attendance in a 12-step group treatment adjunct to therapy may harm the therapeutic alliance.  Cognitive therapists, in particular, may have little or no belief in the 12-step method.  From my understanding, when therapists do not believe in the methods being used, outcome is compromised.

This study may be better used as a guide to setting up treatment protocols to assess therapeutic alliance than it is useful for the results of the study.  Significant changes that I would suggest are:  less lag-time between assessment of outcome and therapy, more clearly defined and independent treatment protocols, and fewer measurements of outcome.  Although the large sample size was a positive aspect, a smaller sample would not compromise the results.

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com

References:

Barber, J., L. Luborsky, P. Crits-Christoph, M. Thase, R. Weiss, A. Frank, L. Onken, R. Gallop (1999),  Therapeutic alliance as a predictor of outcome in treatment of cocaine dependence.  Psychotherapy Research 9(1), pp. 54-73.

Written by Julie Myers, PsyD, MSCP

July 23, 2011 at 7:32 am

Cocaine and its Negative Side Effects

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Cocaine and its Negative Side Effects

by Julie Myers, PsyD, MSCP

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

 

As with other drugs, cocaine affects the nerve cells of the ventral segmental area, which extends into the nucleus accumbens, one of the reward centers of the brain.  Cocaine acts as a reuptake inhibitor of dopamine, whose increased presence creates the euphoria associated with cocaine.  The euphoric effects of cocaine are generally shorter acting than other drugs, lasting anywhere from a few minutes to a few hours, depending on the route of administration.  Because of its short duration, it is not uncommon for users to administer repeated doses (“binging”.)

In the short-term with small amounts, cocaine acts similarly to amphetamines, making the user feel euphoric, energetic, talkative, and mentally alert. It dilates pupils and increases vital signs such as temperature, heart rate, and blood pressure. With larger doses, the user can experience tremors, vertigo, and twitches.  A user may experience increasing irritability and restlessness.  Bizarre, erratic, and violent behaviors are associated with cocaine.  Chronic use can cause severe psychiatric symptoms, including anxiety, depression and psychosis.  Full-blown psychosis may result with paranoia, hallucinations, and delusions.

Medical complications associated with cocaine use include cardiovascular effects.  “Cocaine causes the blood vessels to thicken and constrict, reducing the flow of oxygen to the heart.  At the same time, cocaine causes the heart muscle to work harder, leading to heart attack or stroke, even in healthy people” (CAMH, 2007.)  It raises blood pressure, which can explode the weakened blood vessels in the brain.  It may also cause abdominal pain, nausea, and blurred vision.

As with other drugs, the route of administration can produce different adverse effects. Snorting cocaine can cause nasal effects, including loss of sense of smell, nosebleeds, problems with swallowing, hoarseness, and an even a perforated nasal septum.  Ingested cocaine can cause severe bowel gangrene, due to reduced blood flow. Smoking cocaine can cause “crack lung”, which includes severe chest pain and breathing problems.

When cocaine is mixed with alcohol, the two drugs are converted by the body to cocaethylene, a cocaine metabolite.  Cocaethylene appears to have more cardiovascular toxicity and hepatoxity than either drug alone.

Even though a user becomes tolerant to cocaine, they may not become sensitized to its anesthetic and convulsant effect, which may explain some cocaine deaths.  Overdose can cause seizures, heart failure, and arrest breathing. Withdrawal can include exhaustion, sleepiness or sleeplessness, hunger, irritability, depression.  Cocaine has a small index of tolerability.

 – Julie Myers, PsyD, MSCP    (www.DrJulieMyers.com)

The bulk of the information for this article was taken from NIDA (2004) and CAMH (2007.)  These resources offer a wealth of up-to-date information about the different drugs of abuse and are one of the first places to look for the most current information about any drug. I urge you to check out these resources for the latest information on addiction.

References:

CAMH (2007), Centre for Addiction and Mental Health, Do You Know… Cocaine

Castane, A., F. Berrendero, & R. Maldonado (2005), The role of the cannabinoid system in nicotine addiction Pharmacol Biochem Behav. 81(2), pp. 381-6.

NIDA (2004), NIDA Research Report – Cocaine Abuse and Addiction: NIH Publication No. 99-4342..

NIDA (2006), Research Report – Tobacco Addiction: NIH Publication No. 06-4342.1346417

Picciolo, M., D. Gigante, & A. Nunziata (2005), Nicotine addiction and current therapy of smoking cessation Clin Ter. 156(4), pp.159-71.

Written by Julie Myers, PsyD, MSCP

July 23, 2011 at 7:22 am

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

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

by Julie Myers, PsyD, MSCP

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

Treatment (cont.)

Psychoeducation is universally accepted as an integral part of the psychosocial treatment protocol and includes learning aspects of healthy habits, behavioral changes, symptom management, and adherence (Colom & Vieta, 2006). Colom and colleagues (2003) designed a 21-session program, which educates patients about all aspects of their illness, such as treatment, symptoms, drug use, life style and stress management.  Other common goals of psychosocial treatment include decreasing denial, challenging assumption, monitoring moods, managing environmental triggers, relapse prevention and enhancing social and occupational functioning (Miklowitz, 2006).

Cognitive behavioral techniques are useful, since bipolar patients have distinct attributional styles and cognitive distortions.   Research linking stress and lowered social support to bipolar episodes suggest treatment target stress reduction, improvement of relationships, and altering perceptions, and treatment that addresses these psychosocial vulnerabilities may help alter the course of Bipolar I disorder (Cohen, Hammen, Henry, & Daley, 2004).   Patients are then taught to plan for potential events and learn new ways of resolving interpersonal difficulties.  This approach has shown great promise for the treatment of BD (Colom & Vieta, 2006).  Combination CBT and medication has shown to delay relapse, improve symptoms, and sometimes increase social functioning (Miklowitz, 2006).

Interpersonal Social Rhythm Therapy revolves around the notion that sleep-wake cycles are primary to symptoms and disruption of the cycles can act as a stressor.  Social rhythms, such as exercise and personal habit routines, social stimulation, and work, affect the sleep cycle (Miklowitz, 2006).  Social routines may actually entrain circadian rhythms; disruption may cause bipolar episodes, suggesting that minimization of stressful and social rhythm disruptions may prevent episodes (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000). The client is encouraged to track mood, sleep, and events that lead to a disruption of the social-rhythm, such as a lost night of sleep.   Bipolar manic episodes may be more sensitive to social rhythm disruption and life events, as compared to other types of bipolar and unipolar episodes (Malkoff-Schwartz, Frank, Anderson, Hlastala, Luther, & Houck, 2000

Other treatment modalities are available.  Family-focused therapy focuses on family interactions and use of family members as allies in the treatment process (Miklowitz, 2006).  Skill training is used to reduce negative expression of emotion, which result in stress.  Group therapy is also used, which help patients learn to feel accepted and learn self-care strategies from one another.

I am personally interested in the use of biofeedback and neurofeedback to treat BD. Although there is no real “hard” evidence about its effectiveness with BD, largely due to the difficulty in replicating treatment in controlled experiments, anecdotal information from such people as Siegfried Othmer (one of the “fathers” of neurofeedback) convince me that the possibility for treating BD with neurofeedback are just beginning to emerge.   The use of biofeedback techniques for stress management in those with BD are useful, but must be administered with care.   Over-activation of the parasympathetic or sympathetic nervous system may induce a bipolar event.

Of direct implication from the kindling hypothesis is the timing of intervention.  Intervention may be much more effective at the initial stages of expression than at later stages (Monroe & Harkness, 2005, p. 442).  By tackling the stressful life situations of those at risk early on, the course of the disorder may be changed.  How much of the developmental process is a reaction to life course and how much is an independent psychobiological process is as yet unknown, but begs for further investigation.  “The key implication of this study is that childhood adversity may be related to a more challenging presentation of bipolar disorder, with an earlier age at onset and greater vulnerability to experiencing recurrences of mood episodes in the face of even mild stress. Earlier onset and a more difficult course of bipolar disorder may have serious consequences for both the efficacy of treatment of bipolar disorder and for the functioning of bipolar individuals.  If childhood adversity is a trigger of earlier onset and sensitizes individuals to stress, preventing stress exposure in high risk families, or promoting coping capabilities in such youngsters might have positive consequences on the course of illness”  (Dienes, Hammen, Henry, Cohen, & Daley, 2006, p. 49).  Prevention of stress and early intervention may be critical in reducing the severity of the disorder in later life.

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com

References

Akiskal, H. (2006). The Scope of Bipolar Disorders. In H. Akiskal, & M. Tohen, Bipolar Psychopharmacotherapy (pp. 1-8). West Sussex, England: John Wiley & Sons Ltd.

Akiskal, H., Mendlowicz, M., Jean-Louis, G., Rapaport, M., Kelsoe, J., Gillin, J., et al. (2000). TEMPS-A: validation of a short version of a self-related instrument designed to measure variations in temperament. J. of Affective Disorders , 85 (1-2), 45-52.

Angst, J., & Gamma, A. (2002). Prevalence of bipolar disoders: traditional and novel approaches. Clinical Approaches in Bipolar Disorder , 1, 10-14.

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Berk, M., Malhi, G., Cahill, C., Carman, C., Hadzi-Pavlovic, D., Hawkins, M., et al. (2007). The Bipolar Depression Rating Scale (BDRS): its defvlopment, validation and utility. Bipolar Disorders , 9 (6), 571-579.

Brown, G., McBride, L., Bauer, j., & Willifor, W. (2005). Impact of childhood abuse on the course of bipolar disorder:A replication study in U.S. veterans B. J. of Affecgtive Disorders , 89, 57-67.

Brudick, K., Funke, B., Goldberg, J., Bates, J., Jaeger, J., Kucherlapati, R., et al. (2007). COMT genotype increases risk of bipolar I disorder and influences neurocontive performance. Bipolar Disorders , 9 (4), 370-376.

Cohen, A., Hammen, C., Henry, R., & Daley, S. (2004). Effects of stress and social suport on recurrence in bipolar disorder. J. of Affegtive Disorders , 82, 143-47.

Colom, F., & Vieta, E. (2006). The pivotal role of psychoeducation in the long-term treatment of bipolar disorder. In H. Akiskal, & M. Tohen, Bipolar Psycopharmacotherapy: Caring for the Patiens (pp. 331-345). West Sussex: John Wiley & Sons, Ltd.

Colom, F., Vieta, E., Sanchez-Moreno, J., Reinares, M., Martinez-Aran, A., Torrent, C., et al. (2003). Psychoeducatio efficacy in bipolar disorders beyond compliance enhancement. J Clin Psychiatry , 6, 294-298.

Correll, C., Penzner, J., Lencz, T., Auther, A., Smith, C., Malhotra, C., et al. (2007). Early identificaiton and high-risk strategies for bipolar disorder. Bipolar Disorders , 9 (4), 324-338.

DelBello, M., & Geller, B. (2001). Review of studies of child and adolescent offspring of bipolar parents. Bipolar Disorders , 3, 325-334.

Dienes, K., Hammen, C., Henry, R., Cohen, A., & Daley, S. (2006). The stress sensitization hypothesis: Understanding the course of bipolar disorder. Journal of affective Disorders , 95, 43-49.

Faraone, S., Lasky-Su, J., Glatt, S., Van Eerdewegh, P., & Tsuang, M. (2006). Early ongset bipolar disorer: Possible linkage to chromosome 9q34. Bipolar Disorder , 8, 144-151.

Gottesman, I., & Gould, T. (2003). The endophenotype concept in psychiatiry: Etymology and strategic intentions. Am J Psychiatry , 160, 636-645.

Hammen, C., & Gitlin, M. (1997). Stress reactivity in bipolar patients and its relation to prior hisotry of disorder. Am J Psychiatry , 154, 856-857.

Hammen, C., & Gitlin, M. (1997). Stress reactivity in bipolar patients and its relation to prior history of disorder. Am J Psychiatry , 154 (6), 856-7.

Hillergers, M., Burger, H., Wals, M., Reichart, C. V., Nolen, W., & Ormel, J. (2004). Impact of stressful life events, familial loading and their interaction on the onset of mood disorders: Study in a high-risk cohort of adolescent offspring of parents with bipolar disorder. British J. of Psychiatry , 185, 97-101.

Hirschfeld, R., & Vornik, L. (2004). recognition and diagnosis of bipolar disorder. J of Clinical Psychiatry , 65 (Supp 15), 5-8.

Hlastala, S., Frank, E., Kowlaski, J., Sherril, J., Tu, X., Anderson, B., et al. (2000). Sressful life events, bipolar disorder, and teh “kinlding model”. J Abnormal Psychol , 109 (4), 777-86.

Kessler, R., Rubinow, D., Holmes, C., Abelson, J., & Ahao, S. (1997). The epidemiology of DSM-III-R bipolar I disorder in a gerneal population survey. Psychol Med (27), 1079-1089.

kilbourne, A., Rofey, D., McCarthy, F., Post, E., Welsh, D., & Blow, F. (2007). nutrition and exercise behavior amongh patients with bipolar disorer. Bipolar Disorders , 9 (5), 443-452.

Kim, E., Miklowitz, d., Biuckians, A., & Mullen, K. (2007). Life stress and the course of early-onset bipolar disorder. J of affective Disorders , 99, 37-44.

Koukopoulos, A. (2006). The Primacy of Mania. In H. Akiskal, & M. Tohen, Bipolar p2006sychopharmacotherapy: Caring for the patient (pp. 169-192). West Sussex, England: John Wiley & Sons, Ltd.

Kupka, R., Altshuler, L., Nolaen, W., Suppes, T., Luckenbaugh, D., Leverich, G., et al. (2007). Three times more days depressed than manic or hypomanic in both bipolar I and bipolar II disorder. Bipolar Disorders , 9 (5), 531-535.

Leahy, R. (. (2006). Contemporary Cognitive Therapy. New York: Guilford Press.

Malkoff-Schwartz, S., Frank, E., Anderson, B., Hlastala, S., Luther, J. S., & Houck, P. K. (2000). Social rhythm disruption and stressful life events in the onset of bipolar and unipolar episodess. Psychol Med , 30 (5), 1005-6.

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Miklowitz, D. (2006). Psychosocial interventions in bipolar disorders: Rationale and effectivness. In H. Akiskal, & M. Tohen, Bipolar psychopharmacogtherapy: Caring for the Patient (pp. 313-332). West Sussex: John Wiley & Sons.

Monroe, S., & Harkness, K. (2005). Life stress, te “kindling” hypothesis, and the recurrence of depression: Considerations from a life stress perspesctive. Psychological Review , 112 (2), 417-445.

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Oquendo, M., Galfalvy, H., Russo, S., Ellis, S., Grunebaum, M., Burke, A., et al. (2004). Prospective study of clinical predictors of suicidal acts after a major depressive episode in patients with major depressive disorder or bipolar disorder. Am J Psychiatry , 161 (8), 1433-1441.

Parkikh, S., Velyvis, V., Yatham, L., Beaulieu, S., Cervantes, P., MacQueen, G., et al. (2007). Coping styles in proderomes of bipolar mania. Bipolar Disorders , 9 (6), 589-595.

Perugi, G., Ghaemi, N., & Akiskal, H. (2006). Diagnosis and clinical management approaches to bipolar depression, bipolar II and their comorbidities. In S. Hagop, & A. Tohen, Bipolar Psychopharmacotherapy: Caring for the Patient. John Wile & Sons, Ltd.

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Copyright (2011) Julie Myers, PsD

Written by Julie Myers, PsyD, MSCP

July 13, 2011 at 5:44 pm

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

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

 

by Julie Myers, PsyD, MSCP

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

 

Treatment

The treatment of BD is complex.   Psychosocial treatments are necessary but rarely sufficient for controlling relapse or acute symptoms.  From my observations, the treatment of BD is as much of an art as it is a science, with different researchers and clinicians having different ideas as to what is the appropriate formulation.   Critically important is the assessment of suicide throughout the treatment.  Suicidal ideation and suicide completion is a very real possibility in those with BD, both in depressed and hypomanic or manic states.   Suicidal acts in those with BD may be a tendency to develop pessimistic response to major life stressors (Oquendo, et al., 2004).

 Comorbid anxiety disorders should be treated concurrently.  Treatment of anxiety disorders may lessen the severity of the BD symptoms and possibly increase pharmacological response (Simon, Otto, & Wisneiewski, 2004).  According to Simon and colleagues (2004), there is a growing awareness of the need to address comorbid anxiety disorders, which should be integrated into the treatment of high-risk bipolar patients and suicide prevention.  However, few specific anxiety-targeted interventions for BD have been developed.  As of 2004, there was no data showing anxiety treatment efficacy for clinical course of BD.   There is also little known about how anxiety increases suicidality, although it may be that BD patients with severe anxiety are less able to tolerate negative affect and less capable of calling upon social supports or cognitive strategies.

 Psychopharmacological treatment focuses on controlling current acute symptoms and maintenance to prevent relapse.  Mood-stabilizers are administered for reducing episodes, anti-psychotics generally for reducing symptoms of mania, hypomania, aggression, and irritability, and anti-depressants for depressive phases (although generally only after mood-stabilizers are use.)  Psychopharmacological treatment also usually involves treatment of the co-occurring disorders.  However, because there is such a strong co-occurrence of substance abuse problems in those with BD, many of the anxiolytics are used with caution.  Benzodiazepines, although very effective for many of the anxiety disorders, can generate rapid physical dependence and are subject to abuse.  Particularly important, according to some researchers, is the discontinuation of any stimulants, even coffee.

 A wide array of psychosocial interventions are available including psychoeducational, cognitive-behavioral, family therapy, social rhythm therapy and interpersonal psychotherapies.  All of these techniques help to teach self-monitoring, identification of early warning signs of relapse, and enhance coping mechanisms (Parkikh, et al., 2007).  Early warning signs are associated with life-stressors.  A number of studies have identified the coping mechanisms involved with prodromal states as being particularly important in controlling symptoms, including Parkikh, et al. (2007) and Koukopoulus (2006).  A self-report questionnaire called the Coping Inventory for Prodroms of Mania (CIPM) has been developed to assess coping styles in the manic and hypomanic state (Wong & Lam, 1999).

(continued)

– Julie Myers, PsyD, MSCP

http://www.DrJulieMyers.com

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

 

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