This post will look at Bipolar Disorder (BD) and where possible focus on the variant Bipolar Disorder II. It will examine its genetic and psychosocial aetiologies, and consider its diagnosis and treatment. A brief visit will be paid to online spaces for treatment. The post will conclude that Bipolar Disorder is a pernicious illness but that hope remains for the sufferer that with good management and strong support they can lead a productive life.
This author is a sufferer of Bipolar II Disorder (BDII) and this post will be written within the Personal Narrative framework (Nash, 2004), wherein it is a narrative that is honest, self-disclosing and scholarly, all at the same time. As Nash says,
I contend that what you have lived, loved, loathed and learned in a lifetime of extraordinary (or ordinary) challenges and satisfactions can be of enormous benefit to others (p. 24).
Therefore this review will include personal insight and experience where such disclosure feels warranted and useful.
Bipolar Disorder is a neurobiological disorder that according to leading Australian BD researchers at the Black Dog Institute affects up to six percent of the Australian population (Black Dog Institute, 2012). Onset age can be as early as mid teens (Barlow & Durand, 2015) and the disorder only slightly preferences females over males (Black Dog Institute, 2012).
A comprehensive review of BDII by Berk and Dodd (2005) noted that depression is often the presenting symptom and that comorbidity with, inter alia, substance or alcohol abuse is often present, clouding the initial diagnosis. This is certainly true in my case; I originally presented to my GP with persistent depression and on subsequent initial interview with a psychiatrist my reliance on alcohol for self-medication was considered. It wasn’t until much later that my drinking got out of control (by my standards), threatening my marriage, and I realised I had a problem and so stopped drinking altogether. By this time I was consuming two bottles of wine a night.
A review of BDII
Ghaemi et al. (2000) reported that 60% of a primary care psychiatric sample had bipolar spectrum disorder and that 56% of subjects diagnosed with unipolar depression were subsequently found to have bipolar spectrum disorders upon further assessment, leading one to think that bipolar spectrum disorders may be much more common that hitherto appreciated. The chronicity of BDII has been demonstrated, with high rates of occupational, leisure and relationship dysfunction. There are higher rates of family dysfunction, divorce and separation than in either bipolar I disorder or unipolar disorder. An early age of onset of BDII has been associated with an increase in severity, a poorer treatment response and a poorer prognosis (Berk & Dodd, 2005). Substantial suicide risk is a clinical feature that is a recurrent theme in studies describing the illness; at least 25% to 50% of patients with bipolar disorder also attempt suicide at least once (Jamison, 2000). On polysomnography, BDII patients have more hypersomnia, higher rapid eye movement latencies and more non-REM time than unipolar patients. Angst (1986; cited in Berk and Dodd, 2005) described a number of features that differentiate unipolar from bipolar disorder, including longer length of illness, lower rates of recovery, shorter cycles, greater number of episodes, and a more chronic outcome. Substance abuse occurs in up to 50% of people with BDII, with alcohol the most common agent of abuse (Feinman & Dunner, 1996; cited in Berk & Dodd, 2005). In BDII most of the clinical spectrum is in the depressive phase, which is certainly where I spend a considerable part of my time. Periods of relative calm are enjoyed for what they are—fleeting and enjoyable.
There has only been one study conducted on the genetics of BD (Baum et al., 2008) and the participants were all BDI sufferers. There have so far been no genetic studies on the difference, if any, between BDI and BDII. It seems that there is no one gene that stands out as highly significant for BD, but rather a number of genes that individually have small effect appear to influence disease risk. Predominant amongst this small collection is the gene DGKH, which showed significance at the P<0.05 level. The gene encodes dgkh, a key protein in a lithium-sensitive pathway. Baum et al. (2008) note that no one gene appears to be necessary or sufficient for the disease, implying that major gene effects in BD are very uncommon, if they exist at all.
Park and Park (2014) note that a lack of social support and high levels of social strain can impact negatively on the BDII sufferer. They also cite other studies that implicate childhood sexual abuse, childhood trauma, heightened expressed emotion and high criticism.
Building on the work of Riedel, Heiby, & Kopetskie (2001), Park and Park (2014) posited 17 factors regarding the aetiology of BDI based on psychological behaviourism theory (Staats, 1996) (see Table 1).
Table 1. Hypotheses regarding the aetiology of BD based on Psychological Behaviourism Theory
|Factors (see Riedel et al., 2001)||Sub-Factors||Hypotheses|
|Past psychosocial factors||1. Learning risky activities||Bipolar individuals have had developmental histories in which significant others modelled and shaped risky types of activities, such as gambling, crime, or substance abuse|
|2. Reinforcing impulsivity||Significant others punished a cautious or realistic attitude towards the future and modelled and reinforced impulsivity and, perhaps, denial or disregard of consequences|
|S1-1: Elation||3. Grandiose self-labelling||Bipolar individuals learned to use grandiose self-labelling and denial as ways to cope with stress as well as to enhance feelings of elation and confidence in response to superficial successes|
|Past psychosocial factors||4. Exposure to irritability||Bipolar individuals were exposed to family members’ irritability|
|S1-2: Irritability||5. Punishment of negative emotions||Bipolar individuals used to be punished for expressing negative emotions including anger|
|Concurrent psychosocial factors||6. Euphoria-triggering experience||Manic episodes involving euphoria may be triggered by pleasant events|
|7. Lack of social support||Bipolar individuals may lack adequate social support systems that involve significant others who model and reinforce euthymic emotions, veridical self-labelling and cautionary statements, and safe behaviours|
|S2||8. Reinforcement for elevated emotions||Significant others may provide reinforcement for elevated emotions, grandiose self-labelling, and risky behaviour|
|Transient concurrent organic factors||9. Sleep problems||Medical problems, such as sleep deprivation, may precipitate the onset of bipolar symptoms|
|O3||10. Antidepressant problems||Medical treatment, such as antidepressant medication, may be iatrogenic|
|e-m BBR||11. Manic emotional response||Bipolar emotional responses to certain stimulus situations are excessive|
|12. Positive arousal to threat||Bipolar individuals respond with positive emotional arousal to situations that others would find threatening or anxiety provoking|
|s-m BBR||13. Manipulative skill||Bipolar individuals have above-average skills for engaging in risky types of activities, which produce short-term reinforcement and long-term punishment. These may include persuasive conversational techniques or social manipulativeness|
|14. Lack of social skills||Bipolar individuals have a deficit in social skills for maintaining adequate social support networks|
|l-c BBR||15. Short-term pleasure seeking||Bipolar individuals have a deficit in estimating long-term negative consequences|
|16. Denial of negative emotions||Bipolar individuals tend to employ grandiose self-labelling and denial to elevate mood|
|17. Lack of problem-solving skills||Bipolar individuals have poor cognitive problem-solving skills|
I look at the above hypotheses and find very little that resonates with me. But I have no doubt from my readings of Jamison (Jamison, 1997, 2000) and others (Gelenberg, Hirschfeld, Jefferson, Potter, & Thase, 1995; O’Hagan, 2009; Styron, 1990, inter alia) that I am Bipolar II.
According to the DSM-5 (American Psychiatric Association, 2013) diagnosis requires a 4-day duration of a persistently elevated, expansive or irritable mood. But this is not without controversy; studies have shown that an episodic duration of between one and three days is prevalent (Wicki & Angst, 1991; Akiskal et al. 1995; both cited in Berk & Dodd, 2005), suggesting that the DSM-5 may be missing a clinically relevant sub-group.
Some patients who present with recurrent depressions (and this was initially my presentation) subsequently report earlier episodes of mania or hypomania. These individuals tend to have shorter ‘well’ intervals, a younger age of onset (mine was about thirteen or fourteen, even arguably as young as ten), and an unstable work history (mine has been one of shorter employment periods that have been cut short by depression or anxiety, interspersed by a series of attempts at self-employment, some more successful than others).
Although BDII and Major Depressive Disorder (MDD) have similar initial diagnoses, BDII differs from MDD in key areas. Younger age of onset, not having taken medication for depression, and alcohol abuse or dependence were identified (Bega, Schaffer, Goldstein, & Levitt, 2012). Additionally, a regression of symptoms during a depressive episode demonstrated that appetite loss, psychomotor retardation, guilt feelings and being argumentative were predictive of BDII. All of these features are part of my own psychological makeup.
Parker (2015) outlines from extensive clinical practice some of the shortcomings of the DSM-5’s delineation of BDI and BDII and gives several suggestions as to how to not over-diagnose BDII (a concern of the DSM-5) but how to effectively diagnose BDII. The interested reader is strongly recommended to access Parker’s paper to read a short and enlightening first-hand account of diagnosing BDII.
Guidelines for treatment of BD have been produced by the Texas Consensus Conference Panel (Suppes et al.; cited in Berk & Dodd, 2005) and the World Federation of Societies of Biological Psychiatry (Grunze et al., 2002, 2003; cited in Berk & Dodd, 2005). Although not specific to BDII, Berk and Dodd (2005) report on their usefulness to the clinician. They also note that BDII seems to phenomenologically straddle bipolar I and unipolar disorders. It was noted (Colom et al., 2003) that in a trial of BD patients, psychoeducation or weekly group meetings demonstrated the efficacy of psychoeducation in recurrence prevention. Antidepressant therapy is effective in the short and medium term. The risk of relapse of bipolar depression was shown to be lower in patients who continued treatment with adjunctive antidepressant therapy, compared with patients who were treated with mood stabilisers. Berk and Dodd (2005) also note that controlled data on the long-term effects of antidepressant therapy is absent. Antidepressants come with dangers, however; some patients report increased episodes of mania or hypomania. It is a difficult decision for a clinician to withhold antidepressants in a depressed bipolar patient.
Of the few studies conducted on BDII patients, many report the utility of lithium, noting its association with a reduction in hypomanic and depressive symptoms. In addition, lithium has a prophylactic effect regarding suicide, with a 6.9-fold reduction in suicide risk. Since switching to lithium several years ago my hypomanic symptomology has shown a marked decrease, but this may be confounded by the mood stabilisers I am also taking. One side effect of these mood stabilisers is weight gain; I have gained 10-15 kilograms, with no loss of weight once I stopped drinking. Topiramate has been suggested (Chengappa et al., 2007; Mahmoudi-Gharaei et al., 2012; Vieta et al., 2001; Vieta et al., 2004) as a useful adjunctive therapy. Topiramate is associated with weight loss and as a result of research for this essay I will be approaching my psychiatrist, requesting a trial.
Deckersbach, Hansen and Holzel (2014) report on the new application of mindfulness-based cognitive therapy for BD. Several psychosocial interventions have been developed to treat bipolar disorder adjunctive to mood-stabilizing medication. These include cognitive-behavioral therapy (CBT) (see the comprehensive Basco & Rush, 2005), and family-focused therapy (FFT). Inder and colleagues (Inder et al., 2015) have tried interpersonal and social rhythm therapy (IPSRT) with young people, with some modest success. Leitan et al. (2015) have pointed out the potential for online self-managed delivery of psycho-education and group/individual support (see ‘Recovery and online spaces and tools’ below). Bowden and Singh (2005) note the lifelong need for treatment because of the lifelong nature of the illness. Brooks III, Sommer and Ketter (2010) point out that there are no specific treatments for the aged, despite their altered metabolism and challenging comorbid conditions.
My own experience of treatment has revolved around the pharmacological and brief introductions and courses on mindfulness/acceptance and commitment therapy (ACT) and CBT (particularly for alcohol abuse, run from the Kahlyn Centre). In CBT the underlying irrational and dysfunctional beliefs can be explored and restructured. My current expression of BDII involves bouts of intense anxiety, which is managed by medication and CBT, particularly through a smartphone app which helps me to breath slower and more deeply. Regular contact with my psychiatrist and a CBT-trained psychologist help me keep my anxiety and depression managed and under control.
Also of assistance has been this Masters program; it has distracted me from my personal woes and given me something positive to focus on. By lifting my mood the course has also helped me reconcile with my wife, from whom I separated in November 2013—my depression was a strong contributing factor to our marriage breakdown.
Reflecting on my studies so far, I feel that of all the counselling theories that I have so far encountered—psychoanalytic, cognitive-behavioural, humanistic, and Christian—it would be the psychoanalytic framework that would hold the least promise of relief from my psychological tensions. It focuses entirely on the inner world, not taking into account the biological and social factors that also contribute to my illness. The counselling theory with the greatest promise is CBT; the aforementioned Basco and Rush’s book (2005) on the subject gives great hope.
Recovery and online spaces and tools
We know that psychosocial treatments are effective adjuncts to pharmacotherapy for BD (Leitan et al., 2015), but effect sizes remain modest and more research is required to underpin the next generation of psychosocial interventions. Personal recovery—as distinct from clinical and functional recovery—is the process of individual psychological adaptation to the disorder, rather than the reduction of symptoms, relapse prevention or addressing functional difficulties (Cavelti et al., cited in Leitan et al., 2015). Recovery refers not only to overcoming the negative consequences of having the disorder, but also the positive goals of attaining a sense of agency and a meaningful life (Jones, Mulligan, Higginson, Dunn, & Morrison, 2013).
Research into the implications of the recovery construct for BD sufferers is only just starting. One of the primary goals of self-management is to empower individuals to take control of their illness, rather than relying solely on their mental health provider (Andresen, Caputi, & Oades, 2010; Richards, 2004; Sterling, von Esenwein, Tucker, Fricks, & Druss, 2010). One potential strategy is the use of ‘Web 2.0’ applications such as social networking platforms. The Black Dog Institute and Beyond Blue are just two Australian mental health organisations actively involved on Facebook and other social platforms, aiming to reach as many sufferers of mental illness as possible. Both organisations are also investigating content and service delivery via smartphone apps. Self-management of the recovery process offers an important alternative to traditional models which, while decreasing reliance on clinicians, also serves to empower and support a sense of agency. There seems scope for the thoughtful creation of a vibrant online community, staffed by trained therapists/counsellors and encouraging the input of the sufferer’s peers. To some extent this is what Beyond Blue, the Black Dog Institute, Russ Harris with his new ACTCompanion smartphone app and other mental health organisations have been attempting in Australia.
BDII is a pernicious illness. Although often ‘arriving’ in a person’s life during their mid-teens, it sometimes doesn’t wreak its full havoc until that person is in their mid-life, impacting severely on their family and career. With a high suicide rate, the sufferer can often have little to look forward to and much to concern them. Treatments available include pharmacological and CBT, and newer mindfulness approaches are also suggestive.
However, all is not doom and gloom for BDII sufferers; with proper management that includes both pharmaceutical and psychological interventions, as well as strong family and social support, the illness can be controlled. But just not eradicated. Unfortunately.
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