Induced ketosis (or ketone body ingestion) can ameliorate several changes associated with neuroprogressive disorders, including schizophrenia, bipolar disorder, and major depressive disorder. Thus, the effects of glucose hypometabolism can be bypassed through the entry of beta-hydroxybutyrate, providing an alternative source of energy to glucose. The weight of evidence suggests that induced ketosis reduces levels of oxidative stress, mitochondrial dysfunction, and inflammation—core features of the above disorders. There are also data to suggest that induced ketosis may be able to target other molecules and signaling pathways whose levels and/or activity are also known to be abnormal in at least some patients suffering from these illnesses such as peroxisome proliferator-activated receptors, increased activity of the Kelch-like ECH-associated protein/nuclear factor erythroid 2-related factor 2, Sirtuin-1 nuclear factor-κB p65, and nicotinamide adenine dinucleotide (NAD). This review explains the mechanisms by which induced ketosis might reduce mitochondrial dysfunction, inflammation, and oxidative stress in neuropsychiatric disorders and ameliorate abnormal levels of molecules and signaling pathways that also appear to contribute to the pathophysiology of these illnesses. This review also examines safety data relating to induced ketosis over the long term and discusses the design of future studies.

中文翻译：

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诱导酮症作为治疗神经进行性疾病的方法：深思熟虑？

诱导性酮症（或酮体摄入）可以改善与神经进行性障碍相关的几种变化，包括精神分裂症、双相情感障碍和重度抑郁症。因此，可以通过β-羟基丁酸的进入来绕过葡萄糖代谢减退的影响，为葡萄糖提供替代能源。大量证据表明，诱导性酮症可降低氧化应激、线粒体功能障碍和炎症的水平——上述疾病的核心特征。还有数据表明，诱导性酮症可能能够靶向其他分子和信号通路，这些分子和信号通路的水平和/或活性也已知在至少一些患有这些疾病的患者中异常，例如过氧化物酶体增殖物激活受体，Kelch 样 ECH 相关蛋白/核因子红细胞 2 相关因子 2、Sirtuin-1 核因子-κB p65 和烟酰胺腺嘌呤二核苷酸 (NAD) 的活性增加。这篇综述解释了诱导酮症可能减少神经精神疾病中的线粒体功能障碍、炎症和氧化应激的机制，并改善似乎也有助于这些疾病的病理生理学的分子和信号通路的异常水平。本综述还检查了与长期诱导酮症相关的安全性数据，并讨论了未来研究的设计。神经精神疾病中的氧化应激和改善分子和信号通路的异常水平，这些异常水平似乎也有助于这些疾病的病理生理学。本综述还检查了与长期诱导酮症相关的安全性数据，并讨论了未来研究的设计。神经精神疾病中的氧化应激和改善分子和信号通路的异常水平，这些异常水平似乎也有助于这些疾病的病理生理学。本综述还检查了与长期诱导酮症相关的安全性数据，并讨论了未来研究的设计。