The introduction of bipolar II as a clinical concept was a logical and pragmatic step informed by the limited information available at the time. Originally bipolar II was developed as a practical ‘model’, which would undergo refinement in light of emergent evidence. This approach is in keeping with the framework for diagnoses proposed by Robins and Guze (Robins and Guze 1970). But no new insights have come to light and the concept has not been refined. Instead, it has been reified in the absence of any substantive corroborative research. Remarkably, after more than four decades of research, there is no unequivocal evidence to support the division of bipolar disorder along the lines of bipolar I and bipolar II. In fact, research has time and again produced results similar to the current study—suggesting that the disorder should not be dichotomised (See Fig. 1).
Perhaps even more surprising is the fact that the solution is staring us in the face. The logical interpretation of research findings that accords with the clinical reality that we see, is that “there is no category of bipolar II”. And that when this term is used in clinical practice it merely captures, in a somewhat haphazard manner, milder forms of bipolar disorder that are invariably harder to differentiate from comorbid illnesses such as personality disorder and anxiety. In addition, these diagnoses are more easily obscured by substance misuse, and hence form a diagnostic cloud that surrounds bipolar II diagnosis in clinical practice. Indeed, we appreciate the difficulty in identifying and managing the full spectrum of bipolar presentations, and we therefore recommend readers consult the recently published guidelines for the management of mood disorders (Malhi et.al. 2021), which include treatment advice for all manifestations of bipolar disorder. The fact of the matter is that the evidence is clear and straightforwardly interpretable. The difficulty is that the solution seems to be unpalatable, and it is not completely clear why this is so. Possible reasons include the concern that too much has been invested in subtyping the disorder and that over nearly half a century, too many people have already been assigned a diagnosis of bipolar II.
Nevertheless, we continue to champion a dimensional perspective, in which the duration criteria could be lowered, and the number of days patients experience manic symptoms could simply be specified rather than arbitrarily drawing artificial lines at 4 days and 7 days. We suggest that perhaps future research should invest in returning to not having a priori assumptions as regards categories, and instead examine clinical data along with biological and psychological data sets using modern methods of establishing linkages such as network analyses (that have been applied to symptoms) (Bryant et.al. 2017). Further, it may be possible to harness the benefits of analyses drawing on artificial intelligence to interrogate data to determine new means of drawing connections that have clinical salience; however, this does require relinquishing our dependence on the current taxonomies.
An alternative hybrid model remains in which there are semblances of categories reflecting underlying variance at subordinate levels, but because these overlap considerably at the phenomenological level, they blur into a continuum that is difficult to dissect using clinical parameters alone. This possibility needs to be borne in mind but should not determine clinical practice as yet, until such purported subgroupings can be identified, and even then, they only carry import if they confer clinical advantage. And so, while we respect the attempt to address the question using research, we remain unconvinced by the findings of this particular study, which to our minds supports our dimensional perspective and negates the concept of bipolar II further.