1. Is Mindfulness Based Cognitive Therapy Effective in a Bipolar Disorder Population?
By Carole Kirwood

2. Abstract
This essay has critically reviewed the literature and argued the role of MBCT to manage the various
psychological factors associated with Bipolar Disorder. The impact of comorbidities on
symptomology of Bipolar Disorder was examined, and the link between stressors effecting daily life
was also explored. Lastly, the overall impacts of recurrent mood instability and subsequent relapse
was considered. Psychological distress was found to be particularly strong in patients living with
BD. Moreover, MBCT was seen to enable patients to more successfully self-manage their unique
BD symptomology. Despite many positive reports from the literature on MBCT for BD it is not
conclusive, and more research is needed to assist clinicians to better streamline future interventions.

3. Bipolar Disorder (BD) is a multifaceted mood disorder that results in considerable costs, at
both societal and personal levels. Moreover, recent statistics by Sane Australia (2016) indicate that
1 in 50 Australians will develop a form of BD over the course of their lifetime. While
pharmacological treatments are the primary form of treatment (Williams et al., 2008), 73% of
patients will relapse within five years despite adhering to their medication regime (Gitlin,
Swendsen, Heller, & Hammen, 1995). Williams et al., specifies that comorbidities are common
with BD (i.e., anxiety disorder and substance-use disorder) and further complicate the patient
experience. Psychological interventions, such as Mindfulness-based Cognitive Therapy, have
assumed growing attention as a way to manage the mood instability that accompanies the highs and
lows of this condition (Williams et al., 2008). This aim of this essay is to critically review the
evidence to determine if Mindfulness-based Cognitive Therapy is effective in a BD population.
Definition and Diagnosis of Bipolar Disorder
Bipolar disorder (BD) is severe and chronic in nature; characterised by fluctuating mood
and patterns of activity to alternate between mixed-mood, major depressive, manic or hypomanic
episodes interspersed with times of recovery (Hölzel, 2014; Van den Heuvel, Goossens, Terlouw,
Van Achterberg, & Schoonhoven, 2015). The Diagnostic and Statistical Manual of Mental
Disorders (5th
ed.; DSM-5; American Psychiatric Association, 2013) categorises a diagnosis of
bipolar disorder (BDI) when a manic episode has been experienced, and bipolar disorder II (BDII)
when at least one hypomanic episode is accompanied by one or more major depressive episode.
Notably, DSM-5 advises that BDII is not simply a milder version of BDI, due to the fact that
depressive episodes tend to be more frequent and last longer in BII. To indicate that mania tends to
be the predominant mood disturbance in BDI, and depression tends to be the predominant mood

4. 2
disturbance in BDII, and it is the extremes in deregulated mood that make both spectrums of BD
equally disabling.
Manic, Hypomanic and Major Depressive Symptoms
DSM-5 provides specific criterion to diagnose each state of BD. A manic episode is
characterised by a week or more of markedly elevated, expansive and euphoric mood, whereas a
hypomanic episode is less extreme lasting for a minimum four days (American Psychiatric
Association, 2013). In addition, a specified number of additional symptoms must be witnessed
during specified timeframes (e.g., “inflated self-esteem or grandiosity” and “decreased need for
sleep”), as well as significant impairment of social or occupational functioning, or behaviour that
necessitates hospitalisation. It is noteworthy that the DSM-5 criterion for mania and hypomania are
identical, and it is the duration of time that the symptom is experienced that provides differentiation.
A major depressive episode is characterised by its own set of unique symptoms of which
there are nine in total. DSM-5 indicates that at least five symptoms must be present within a given
2-week period, and represent a change in normal functioning. At least one of these symptoms must
be either depressed mood or loss of interest or pleasure. These symptoms must cause significant
impairment of functioning in one of three ways; social, occupational or other important areas. The
DSM-5 criterion for mania, hypomania and manic depression also indicate that the episode must not
be attributable to the physical effects of substance use or another medical condition. Although, the
causes of BD are not fully understood some predisposing factors have been identified.
Causal and predisposing factors of BD
It is assumed that the presentation of BD is the result of a complex interaction between
biological and genetic vulnerability, as well as environmental factors (Alloy et al., 2005). The
biological foundations of BD are slowly being revealed and a strong genetic contribution has been

5. 3
established (McGuffin et al., 2003; Mitchell, Malhi, & Ball, 2004; Mortensen, Pedersen, Melbye,
Mors, & Ewald, 2003) and some epigenetic evidence indicated (Pishva et al., 2014). Although, a
2003 meta-analysis was unable to identify the specific chromosomes linked to BD, the same study
found regions linked to schizophrenia which provides some promise for future BD gene
identification (Levinson, Levinson, Segurado, & Lewis, 2003). A 2013 meta-analysis confirmed
that functional polymorphism (5-HTTLPR) in the serotonin-transporter gene increases
susceptibility to BD, and some evidence indicates that alleles of different ethnicity may also lead to
BD susceptibility (Jiang et al., 2013; Kunugi et al., 1997). Some environmental factors in the
literature include early childhood trauma (Pishva et al., 2014; Watson et al., 2014) and life events
that disrupt daily rhythms and schedules (e.g., mealtimes and bedtimes) in at risk individuals
(Alloy, Boland, Ng, Whitehouse, & Abramson, 2015).
Living with BD; the patient experience
Impacts of stress
Stressors and challenges are part of everyday living for BD patients and their carers
(Granek, Danan, Bersudsky, & Osher, 2016). Acute phases often end with devastating
consequences, such as unemployment or early retirement (Van den Heuvel et al., 2015) and high
rates of divorce and instability in relationships (Granek et al., 2016). Stressful life events are linked
to increased risk of mood episode relapse (Hammen & Gitlin, 1997) and increased time taken to
recover (Johnson & Miller, 1997).
Increased self-awareness increases self-management skill
Perception of life events plays an important role in a BD patient’s everyday experience. BD patients
who are aware of prodromal (warning) signs cultivate increased choice, and an opportunity to create

6. 4
change in their lives (Van den Heuvel et al., 2015). Indeed, BD patients astute to warning signs
recognised increased social activities prevented depressive episodes, and avoiding the same
environment prevented mania and hypomania.
Impacts of relapse
The frequency of recurrent episodes contributes to morbidity across the many forms of BD
(Van den Heuvel et al., 2015), indeed the statistics show that 15% of hospitalised bipolar
successfully suicide (Hawton, Sutton, Haw, Sinclair, & Harriss, 2005). Notably, the depressive
aspect of BD is highlighted in this alarming statistic, with approximately 80% of suicide attempts
and subsequent death resulting from a major depressive episode (Mitchell & Malhi, 2004).
Mindfulness-based cognitive therapy (MBCT) is a depressive relapse prevention program
integrating aspects of cognitive therapy and mindfulness training (Weber et al., 2010).
Definition of MBCT
MBCT is an 8 week group program that teaches skills training, integrating aspects of
MBSR with elements of Cognitive Behaviour Therapy (Beck, 1979) which was initially developed
specifically to prevent unipolar depressive relapse (Segal, 2002). The mindfulness aspect of MBCT
increases awareness and teaches people to observe their thoughts without judging them. This means
BD patients who train in mindfulness learn to lessen the impact of their negative thoughts, and
reduce the destructive cycle of ruminating and catastrophising to avoid lowered mood and relapse
(Williams et al., 2008). The cognitive behaviour therapy aspect of MBCT focuses on early
recognition of warning symptoms and using behavioural regulation strategies to prevent relapse
(Ives-Deliperi, Howells, Stein, Meintjes, & Horn, 2013). There is extensive literature to evaluate the
effectiveness of MBCT in a BD population.
Reviewing the effectiveness of MBCT in a BD population

7. 5
MBCT demonstrates benefits to patients who have experienced three or more MDD
episodes, which Teasdale, Segal, and Williams (2003) indicates is due their proneness to engage in
ruminative thinking. A 2011 meta-analysis of the literature confirmed these findings (Piet &
Hougaard, 2011). A pilot study was conducted to assess the benefits of MBCT for BD patients
(Weber et al., 2010). This randomised control trial consisted of MBCT patients presenting with a
history of suicidal behaviour or ideation. No conclusion was reached on the efficacy of MBCT for
BD in this initial study as participation was not associated with improvement in their sample.
However, when patient self-report evaluations were assessed the majority of participants indicated
the benefits of MBCT, and in particular, that it was helpful to cope with obtrusive thoughts and
emotions. This initial study concluded that BD should not be excluded from MBCT criterion in
future studies.
Ives-Deliperi et al. (2013) observed the effects of MBCT on BD patients anticipating
improvements in cognitive function and clinical measures of mindfulness, as well as reduced
symptoms of mood instability and anxiety. The study found that MBCT teaches BD patients to
notice and observe their fluctuations in mood and symptom changes, and learn to respond in a
regulated way to these signs. In addition, Ives-Deliperi examined a functional MRI investigation to
conclude that MBCT increases emotional regulation and mindfulness in BD, while also reducing
anxiety which corresponded to activation increase in the medial PFC, a region associated with
flexibility in cognition and previously implicated as a key area of pathophysiology in BD.
Williams et al. (2008) studied the effects MBCT on BD patients with a history of suicidal
ideation or behaviour. Participants completed a number of assessments pre and post intervention to
measure their between-episode depressive and anxiety symptoms. The results suggest that the
increasing anxiety was significantly limited over time, and successful reduction of depressive

8. 6
symptoms was also seen. However, the researchers cautioned the conclusions drawn from this study
as this preliminary study had small sample sizes. Moreover, they indicate the promising results may
be at least partly due to increased medication adherence and/or improved life style changes.
Nonetheless, they recognise that MBCT is a mood regulation strategy in its own right and that
further investigation of MBCT for BD is warranted.
A randomised control trial by T. Perich, Manicavasagar, Mitchell, Ball, and Hadzi-
Pavlovic (2013) found conflicting results. To show that MBCT did not offer a protective benefit
against reoccurring episodes (depression or hypo/mania) when compared to patients receiving
normal treatment. Although, another study by some of the same researchers concluded that
meditation associated with MBCT was associated with improvements in anxiety and depression
(Tania Perich, Manicavasagar, Mitchell, & Ball, 2013). Nonetheless, this original 2013 study did
witness significantly lower scores for anxiety and achievement to suggest that MBCT helps BD
patients to self-manage anxiety and learn skills of non-striving towards achievement. The score of
dependency and rumination were also significant to suggest MBCT may help BD patients to be less
reliant on others to achieve personal happiness, and also less likely to get caught up in maladaptive
thoughts and emotions.
BD patients indicate that detection of prodromal signs is a key factor for successful self-
management (Van den Heuvel et al., 2015). Moreover, timely response to these warning signs
allowed patients to gain control. Notably, many improvements have been reported in BD patients
after participating in MBCT interventions. Participation in a MBCT intervention has been shown to
reduce comorbid anxiety and depression symptoms (T. Perich, Manicavasagar, Mitchell, Ball, &
Hadzi‐pavlovic, 2013), improve cognitive function (Stange et al., 2011), and enhance early

9. 7
information processing while reducing emotional disregulation (Howells, Ives-Deliperi, Horn, &
Stein, 2012).
MBCT was originally designed as a relapse prevention program for depression (Segal,
2002), and notably original trials excluded BD (Ma & Teasdale, 2004). Extensive literature exists
on the benefits of MBCT for depression (such as Jacob Piet & Esben Hougaard, 2011;Riemann,
Hertenstein, & Schramm, 2016; J. Williams & Kuyken, 2012), and this essay demonstrates some
strong evidence for MBCT and BD. As with all studies there are limitations, which include small
control groups and wide variation in group numbers (Ives-Deliperi et al., 2013). In addition, Tania
Perich et al. (2013) questioned the appropriateness of the Mindful Attention Awareness Scale
(MAAS; Brown & Ryan, 2003) recognising that it may not measure the domains of mindfulness
associated with meditation practice. As DSM-5 has now recognised BD in varying forms future
research would benefit from examining the effects of MBCT for BDI and BDII independently, as
well as, observing the effects of varying time spent meditating. This additional research will serve
to broaden the knowledge pool and inform future interventions for BD.
In conclusion, this essay has critically reviewed the literature regarding MBCT as a
concomitant intervention for BD. It was argued that there are many psychological factors that
contribute to decreased quality of life in BD patients, and some evidence to suggest MBCT can
offer some relief. The psychological factors that were explored were comorbidities, stress and
negative life events and mood instability. The tendency of BD patients to get caught up in
maladaptive thoughts, feelings and sensations made them prone to maladaptive behaviours. The
evidence was mostly consistent and supports MBCT as an intervention to increase awareness to
prodromal symptoms in order to bring change and return choice to the BD patient.

10. 8
References
Alloy, L. B., Abramson, L. Y., Urosevic, S., Walshaw, P. D., Nusslock, R., & Neeren, A. M.
(2005). The psychosocial context of bipolar disorder: Environmental, cognitive, and
developmental risk factors.(Report). Clinical Psychology Review, 25(8), 1043.
Alloy, L. B., Boland, E. M., Ng, T. H., Whitehouse, W. G., & Abramson, L. Y. (2015). Low Social
Rhythm Regularity Predicts First Onset of Bipolar Spectrum Disorders Among At-Risk
Individuals With Reward Hypersensitivity. Journal of Abnormal Psychology, 124(4), 944-
952. doi: 10.1037/abn0000107
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders
(DSM-5®): American Psychiatric Pub.
Beck, A. T. (1979). Cognitive therapy of depression: Guilford press.
Brown, K. W., & Ryan, R. M. (2003). The benefits of being present: Mindfulness and its role in
psychological well-being. Journal of Personality and Social Psychology, 84(4), 822-848.
doi: 10.1037/0022-3514.84.4.822
Gitlin, M., Swendsen, J., Heller, T., & Hammen, C. (1995). RELAPSE AND IMPAIRMENT IN
BIPOLAR DISORDER. Am. J. Psychiat., 152(11), 1635-1640.
Granek, L., Danan, D., Bersudsky, Y., & Osher, Y. (2016). Living with bipolar disorder: the impact
on patients, spouses, and their marital relationship. Bipolar Disorders, 18(2), 192-199. doi:
10.1111/bdi.12370
Hammen, C., & Gitlin, M. (1997). Stress reactivity in bipolar patients and its relation to prior
history of disorder. American Journal of Psychiatry, 154(6), 856-857.

11. 9
Hawton, K., Sutton, L., Haw, C., Sinclair, J., & Harriss, L. (2005). Suicide and attempted suicide in
bipolar disorder: a systematic review of risk factors. Journal of Clinical Psychiatry, 66(6),
693-704.
Hölzel, B., Deckersbach, T, Nierenberg, A, Lazar, S, Eisner, L. (2014). Mindfulness-based
cognitive therapy for bipolar disorder. In T. a. Deckersbach (Ed.). New York: New York :
Guilford Publications.
Howells, F. M., Ives-Deliperi, V. L., Horn, N. R., & Stein, D. J. (2012). Mindfulness based
cognitive therapy improves frontal control in bipolar disorder: a pilot EEG study. BMC
psychiatry, 12(1), 1.
Ives-Deliperi, V. L., Howells, F., Stein, D. J., Meintjes, E. M., & Horn, N. (2013). The effects of
mindfulness-based cognitive therapy in patients with bipolar disorder: A controlled
functional MRI investigation. Journal of Affective Disorders, 150(3), 1152-1157. doi:
10.1016/j.jad.2013.05.074
Jiang, H.-Y., Qiao, F., Xu, X.-F., Yang, Y., Bai, Y., & Jiang, L.-L. (2013). Meta-analysis confirms
a functional polymorphism (5-HTTLPR) in the serotonin transporter gene conferring risk of
bipolar disorder in European populations. Neuroscience Letters, 549, 191-196. doi:
10.1016/j.neulet.2013.05.065
Johnson, S. L., & Miller, I. (1997). Negative life events and time to recovery from episodes of
bipolar disorder. Journal of Abnormal Psychology, 106(3), 449.
Koenders, M. A., Giltay, E. J., Spijker, A. T., Hoencamp, E., Spinhoven, P., & Elzinga, B. M.
(2014). Stressful life events in bipolar I and II disorder: Cause or consequence of mood
symptoms? Journal of Affective Disorders, 161, 55-64. doi: 10.1016/j.jad.2014.02.036

12. 10
Kunugi, H., Hattori, M., Kato, T. a., Tatsumi, M., Sakai, T., Sasaki, T., . . . Nanko, S. (1997).
Serotonin transporter gene polymorphisms: ethnic difference and possible association with
bipolar affective disorder. Molecular psychiatry, 2(6).
Levinson, D., Levinson, M. D., Segurado, R., & Lewis, C. M. (2003). Genome scan meta-analysis
of schizophrenia and bipolar disorder, part I: Methods and power analysis. Am. J. Hum.
Genet., 73(1), 17-33.
Ma, S. H., & Teasdale, J. D. (2004). Mindfulness-based cognitive therapy for depression:
replication and exploration of differential relapse prevention effects.(Author Abstract).
Journal of Consulting and Clinical Psychology, 72(1), 31.
McGuffin, P., Rijsdijk, F., Andrew, M., Sham, P., Katz, R., & Cardno, A. (2003). The heritability
of bipolar affective disorder and the genetic relationship to unipolar depression. Archives of
general psychiatry, 60(5), 497-502.
Mitchell, P. B., & Malhi, G. S. (2004). Bipolar depression: phenomenological overview and clinical
characteristics. Bipolar Disorders, 6(6), 530-539.
Mitchell, P. B., Malhi, G. S., & Ball, J. R. (2004). Major advances in bipolar disorder. Medical
journal of Australia, 181, 207-210.
Mortensen, P. B., Pedersen, C., Melbye, M., Mors, O., & Ewald, H. (2003). Individual and familial
risk factors for bipolar affective disorders in Denmark. Archives of general psychiatry,
60(12), 1209-1215.
Perich, T., Manicavasagar, V., Mitchell, P. B., & Ball, J. R. (2013). The association between
meditation practice and treatment outcome in Mindfulness-based Cognitive Therapy for
bipolar disorder. Behaviour Research and Therapy, 51(7), 338-343. doi:
http://dx.doi.org/10.1016/j.brat.2013.03.006

13. 11
Perich, T., Manicavasagar, V., Mitchell, P. B., Ball, J. R., & Hadzi-Pavlovic, D. (2013). A
randomized controlled trial of mindfulness-based cognitive therapy for bipolar disorder.
Acta Psychiatrica Scandinavica, 127(5), 333-343. doi: 10.1111/acps.12033
Perich, T., Manicavasagar, V., Mitchell, P. B., Ball, J. R., & Hadzi‐pavlovic, D. (2013). A
randomized controlled trial of mindfulness‐based cognitive therapy for bipolar disorder.
Acta Psychiatrica Scandinavica, 127(5), 333-343. doi: 10.1111/acps.12033
Piet, J., & Hougaard, E. (2011). The effect of mindfulness-based cognitive therapy for prevention of
relapse in recurrent major depressive disorder: A systematic review and meta-analysis Clin.
Psychol. Rev. (Vol. 31, pp. 1032-1040).
Pishva, E., Kenis, G., van den Hove, D., Lesch, K.-P., Boks, M., van Os, J., & Rutten, B. (2014).
The epigenome and postnatal environmental influences in psychotic disorders. The
International Journal for Research in Social and Genetic Epidemiology and Mental Health
Services, 49(3), 337-348. doi: 10.1007/s00127-014-0831-2
Sane Australia. (2016). Bipolar disorder. from https://www.sane.org/mental-health-and-
illness/facts-and-guides/bipolar-disorder
Segal, Z. V. (2002). Mindfulness-based cognitive therapy for depression : a new approach to
preventing relapse. New York: New York : Guilford Press.
Stange, J. P., Eisner, L. R., Hölzel, B. K., Peckham, A. D., Dougherty, D. D., Rauch, S. L., . . .
Deckersbach, T. (2011). Mindfulness-based cognitive therapy for bipolar disorder: effects
on cognitive functioning. Journal of psychiatric practice, 17(6), 410.
Teasdale, J. D., Segal, Z. V., & Williams, J. M. G. (2003). Mindfulness training and problem
formulation. Clinical Psychology: Science and Practice, 10(2), 157-160.

14. 12
Van den Heuvel, S. C. G. H., Goossens, P. J. J., Terlouw, C., Van Achterberg, T., & Schoonhoven,
L. (2015). Identifying and describing patients' learning experiences towards self-
management of bipolar disorders: a phenomenological study.(Report). Journal of
Psychiatric and Mental Health Nursing, 22(10), 801.
Watson, S., Gallagher, P., Dougall, D., Porter, R., Moncrieff, J., Ferrier, I. N., & Young, A. H.
(2014). Childhood trauma in bipolar disorder. The Australian and New Zealand Journal of
Psychiatry, 48(6), 564-570. doi: 10.1177/0004867413516681
Weber, B., Jermann, F., Gex-Fabry, M., Nallet, A., Bondolfi, G., & Aubry, J. (2010). Mindfulness-
based cognitive therapy for bipolar disorder: A feasibility trial. Eur. Psychiat., 25(6), 334-
337. doi: 10.1016/j.eurpsy.2010.03.007
Williams, J. M. G., Alatiq, Y., Crane, C., Barnhofer, T., Fennell, M. J. V., Duggan, D. S., . . .
Goodwin, G. M. (2008). Mindfulness-based Cognitive Therapy (MBCT) in bipolar disorder:
Preliminary evaluation of immediate effects on between-episode functioning. Journal of
Affective Disorders, 107(1-3), 275-279. doi: 10.1016/j.jad.2007.08.022