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This allows the remaining cancer cells to be synchronized towards a purely glycolytic phenotype, driving a form of metabolic inflexibility

Together, these two mechanisms explain why low-dose atropine can paradoxically enhance vagal effects and slow sinoatrial node firing before higher doses shift the balance toward the expected anticholinergic tachycardia

10.1016/j.phymed.2022.154240 81 XingZ.XiaZ.PengW.LiJ.ZhangC.FuC.et al (2016)

Individual responses vary widely, and a compounded formula's role is supportive

Ann Rheum Dis (2013) 72(1):1107

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