Several biological systems are implicated in the neuroprogression of bipolar disorder including but
not limited to cytokine levels, oxidative stress markers, monoamine levels, tryptophan catabolite and
glutamate-mediated excitotoxicity, microglial activation as well as structural and functional changes. The high
rate of smoking behaviour in individuals with bipolar disorder provides the impetus for exploring shared and
discrete pathogenetic mechanisms. In addition to contributing to increased mortality, smoking activates several
neurobiological effector systems implicated in the progression of bipolar disorder. Here, a narrative review
provides evidence and putative mechanisms of comorbid effects of BD, cigarette use, and nicotine
dependence, and discusses the clinical implications of these interactions.