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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

 

Written by Julie Myers, PsyD, MSCP

June 27, 2011 at 5:09 pm

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