A quarter of people with depression showed circadian disturbances in an Australian study

Having read the article, I think that stating [in the press release] that ‘a new subtype of depression has been identified’ is completely exaggerated and inaccurate. It has been known for decades that some people with depression exhibit symptoms linked to biological rhythms: the DSM itself describes patients with a ‘seasonal pattern’, and a traditional subtype of depression, known as ‘atypical depression’, includes many of the symptoms described in the article, such as daytime hypersomnia. There are also references to ‘seasonal affective disorder’ and its greater response to light therapy in studies from the 1980s and 1990s by Rosenthal, Lewy and other authors.

The study does provide a genetic correlate to the clinical description, suggesting a greater but non-specific genetic component (a higher genetic burden for bipolar disorder and ADHD, amongst other conditions); however, the proportion of variance explained by genetics is very small and heterogeneous to support the claim that this constitutes a subtype of depression.

In summary, the study has its merits, but it in no way supports a new concept or disease; rather, it reinforces some classic clinical observations with further biological data.

This is a rigorous study of scientific interest, based on a large sample of over 11,000 people with a history of depression, which combines clinical and genetic information to advance our understanding of the heterogeneity of this disorder. The results are consistent with previous evidence regarding the relationship between circadian rhythm disturbances and depression. Approximately 23 per cent of participants exhibited a profile characterised by various sleep- and circadian rhythm-related disturbances, associated with an earlier onset of the illness, greater clinical severity, genetic predispositions and a lower perceived efficacy of certain antidepressants.

However, rather than identifying a completely new subtype, the study provides further evidence for a clinical profile that had already been proposed in previous research. The main limitations are its cross-sectional design and the use of self-reported and retrospective data. The classification is based on sleep and behavioural characteristics, without direct physiological measurements of circadian rhythms, and differences in response to antidepressants are derived from subjective assessments rather than comparative clinical trials. Furthermore, the genetic associations are generally modest, and the sample exhibits characteristics that limit the generalisability of the results.

Therefore, it cannot yet be concluded that this profile constitutes a distinct biological subtype, nor that individuals exhibiting it respond better to treatments targeting the biological clock. It will be necessary to replicate the findings in independent populations and verify their ability to predict therapeutic response. Although the study opens up interesting possibilities for progress towards more personalised treatments, for the time being it does not justify changing standard clinical recommendations.