been more encouraging. The trial should therefore not be regarded as a definitive dismissal of the promise of these or related agents. 3 Theoretically, depression in bipolar disorder is a more heterogeneous construct than mania, which is more monothematically biological in its causation. Depression is driven by a far wider array and admixture of biological factors, consequences of behaviours while manic, losses in domains such as educational and vocational horizons, relationships, personality, finances, guilt, stigma, and self-stigma, among others. Therefore, it is arguably ambitious at the outset to expect a singular biological therapy targeting one biological marker of the disorder to address all phenotypes of this heterogeneous clinical presentation. The complexity of bipolar depression might be an explanation more broadly for the relatively common failure of singular treatment approaches. These failures suggest that polyvalent and personalised therapies predicated on individualised profiles are needed to select from the diverse pharmacological, neurostimulatory, nutraceutical, lifestyle, and psychological approaches that are available. 10 In sum, this might not be the last word on the potential role of anti-inflammatory drugs in the treatment of bipolar depression, but notwithstanding the methodological issues that accompany any clinical trial, the promise of targeting the inflammation pathway in the management of this challenging condition is today somewhat weaker.

No abstract

No abstract

No abstract

No abstract