Australian & New Zealand Journal of Psychiatry 46(11) 1019–1025 DOI: 10.1177/0004867412464063 © The Royal Australian and New Zealand College of Psychiatrists 2012 Reprints and permission: sagepub.co.uk/journalsPermissions.nav anp.sagepub.com Australian & New Zealand Journal of Psychiatry, 46(11) Introduction The observation that bipolar disorder (BD) is gradually expanding is not at all new. The boundaries of bipolarity have been gradually shifting outwards from episodic manic depression for decades, starting with the proposal of bipolar II disorder (BD-II) in the 1970s, steadily annexing more and more phenomenology under the aegis of ‘soft bipolarity’ or the ‘bipo- lar spectrum’, and culminating in ‘bipolar spectrum disorder’, which can be diagnosed in the absence of elevation (Baldessarini, 2000; Ghaemi et al., 2002). Rather than a single ill- ness, we now have a spectrum model that links major depressive disorder (MDD) to BD, in which a steadily greater bipolar diathesis manifests as increased likelihood of subsyndromal mood instability (bipolar disorder not otherwise specified (BD-NOS) or subthreshold BD), hypomania (BD-II) and ultimately mania (bipolar I disor- der; BD-I) (Figure 1). The new bipolar spectrum is a broad church. First, it allows any form of mood instability, including brief hypomanic episodes, cyclothymic or hyperthymic personality, and mood swings within a day, and can even trump personality disorder (Akiskal et al., 2000). Second, it is potentially behind a substantial proportion of depressive illness, where it covers a wide phenomenological field including irritable/dysphoric, anxious, agitated, or atypical symptomatology (Akiskal, 2005), as well as psychosis (Ghaemi et al., 2002), and may therefore drive presentations as distinct as brief depressive episodes with preserved mood reactivity and severe psychotic depression (Ghaemi et al., 2002). It has also been linked to difficult or treatment-resistant depressions via early onset, recurrence, and failure to respond to antidepressants (Ghaemi et al., 2002). Finally, bipolarity has been suggested as a component of nearly every disorder we recognise, from psychosis (Keshavan et al., 2011) to personality disorder (Akiskal et al., 2000), anxiety (Akiskal et al., 2006), attention deficit hyperactivity disor- der (ADHD) (Zdanowicz and Myslinski, 2010), eating disorders (Lunde et al., 2009), substance use (Maremmani et al., 2006), autistic spectrum disorder (Ragunath et al., 2011), somatisation (Tavormina, 2011), dissociation (Oedegaard et al., 2008), conversion disorder (Ghosal et al., 2009) and dementia (Ng et al., 2008). It even contributes to whether or not we smoke, drink coffee, or eat chocolate (Maremmani et al., 2011). Perhaps unsurprisingly, in such expan- sive forms, bipolarity is present in 30–55% of all depressive illness (Akiskal et al., 2000) and in 25% of the community (Angst et al., 2003). More conservative estimates place the life- time bipolar spectrum prevalence much lower, at approximately 2.5% (Merikangas et al., 2011), but it remains clear that prevalence of bipo- lar diagnosis in the first world is rising sharply (Moreno et al., 2007). Unfortunately, such broad-spec- trum bipolarity seems to be a trou- bled diagnosis. As we expand the phenotype to include briefer or less severe mood swings, the diagnostic field steadily shifts away from episodic elevation towards affective instability (Goldberg et al., 2008), which is itself interesting insofar as this is presently a DSM (Diagnostic and Statistical Manual of Mental Disorders) criterion for bor- derline personality disorder (BPD) rather than bipolarity. This also has important diagnostic implications. It is notably unclear who should fall within the new ‘soft bipolar’ group and how we should dissect that out from per- sonality disorder. The research offers little guidance on this front, either explicitly ignoring the possibility that personality disorder might need to be modelled diagnostically (Angst et al., 2003), or suggesting as-yet unvali- dated operationalised criteria (such as the presence of two or more concur- rent manic symptoms), which do not address the overlap and produce markedly different prevalence esti- mates in different settings (Merikangas et al., 2011). However, it is of even more con- cern that the shift towards affective instability may be leading to a soft- ening of the way in which existing DSM-IV diagnoses are applied, such that 30–60% of North American patients who are diagnosed with bipo- larity in the community subsequently have that diagnosis retracted on for- mal research assessment (Zimmerman, 2010). As a result, DSM-IV bipolar dis- orders are now demonstrably overdi- agnosed in patients with disorders that phenomenologically overlap with Why is soft bipolar disorder so hard to define? Sandy Kuiper 1,2 , Genevieve Curran 1,2 and Gin S Malhi 1,2 1 CADE Clinic, Department of Psychiatry, Royal North Shore Hospital, Sydney, Australia 2 Discipline of Psychiatry, Sydney Medical School, University of Sydney, Sydney, Australia Corresponding author: Gin S Malhi, CADE Clinic, Lvl 5, Building 36, Royal North Shore Hospital, St Leonards, NSW 2065, Australia. Email: gin.malhi@sydney.edu.au 464063ANP 46 11 10.1177/0004867412464063ANZJP PerspectivesKuiper et al. 2012 Editorial