Campbell Iain H, Frye Mark A, Campbell Harry
Division of Psychiatry, Centre for Clinical Brain Sciences, University of Edinburgh, Room FU214, Chancellors Building, Royal Infirmary of Edinburgh, Edinburgh, EH16 4SB, UK.
Professor of Psychiatry, Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, 55905, USA.
Mol Psychiatry. 2025 Jul 19. doi: 10.1038/s41380-025-03123-9.
The emerging field of metabolic psychiatry has brought mechanisms of metabolic dysfunction into focus in bipolar disorder research. In this manuscript, we propose that the metabolic features of bipolar disorder provide a new vector from which to understand the role of circadian dysfunction in this condition. A notable feature of bipolar disorder is the photoperiod driven, seasonal occurrence of symptoms and episodes mediated by circadian systems, with mania occurring more frequently in the spring and autumn at times of rapid rate of change in photoperiod, and depression being more prevalent in the winter when photoperiod is attenuated. In this manuscript we note that seasonal adaptations in metabolism are highly conserved evolutionary traits across diverse taxa. Several of the underlying mechanisms mediating seasonal changes in metabolism are conserved in human biology and are implicated in bipolar disorder pathophysiology. Such mechanisms encompass targets of lithium involved in insulin signaling (the phosphatidylinositol cycle, GSK3β and Akt), clock genes (CLOCK and BMAL1), targets of psychiatric and metabolic medications (mTOR and AMPK) and hormonal signaling (melatonin and cortisol). We propose that bipolar disorder may represent a dysregulation of conserved mechanisms of chronometabolic regulation and provide a discussion of the evolutionary context of such mechanisms. Genetic predisposition coupled to novel environmental inputs to human biology including artificial light at night and sustained refined sugar and carbohydrate intake may contribute to states of metabolic and circadian dysregulation in bipolar disorder underlying episodes of mania and depression.
代谢精神病学这一新兴领域已将代谢功能障碍机制纳入双相情感障碍研究的焦点。在本手稿中,我们提出双相情感障碍的代谢特征提供了一个新的切入点,用以理解昼夜节律功能障碍在这种疾病中的作用。双相情感障碍的一个显著特征是症状和发作由昼夜节律系统介导,受光周期驱动且具有季节性,躁狂在光周期快速变化的春季和秋季更频繁发生,而抑郁在光周期减弱的冬季更为普遍。在本手稿中,我们指出代谢的季节性适应是不同生物分类群中高度保守的进化特征。介导代谢季节性变化的一些潜在机制在人类生物学中是保守的,并且与双相情感障碍的病理生理学有关。这些机制包括参与胰岛素信号传导的锂靶点(磷脂酰肌醇循环、GSK3β和Akt)、生物钟基因(CLOCK和BMAL1)、精神科和代谢药物的靶点(mTOR和AMPK)以及激素信号传导(褪黑素和皮质醇)。我们提出双相情感障碍可能代表了保守的时间代谢调节机制的失调,并对这些机制的进化背景进行了讨论。遗传易感性加上包括夜间人造光以及持续摄入精制糖和碳水化合物在内的新型人类生物学环境输入,可能导致双相情感障碍中躁狂和抑郁发作背后的代谢和昼夜节律失调状态。