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Non-alcoholic fatty liver disease is a progressive disease, without effective intervention, can gradually deteriorate into non-alcoholic steatohepatitis, fatty liver fibrosis, liver cirrhosis and even liver cancer, and may become the main cause of end-stage liver disease in the future [11]

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CVOs enable diet induced excess of Glu to enter the CNS and create a Glu (excitatory)/GABA (inhibitory) imbalance to precipitate not only POTS but also symptoms that involve decreased oxytocin, vasopressin (ADH), CRH for ACTH, and gonadotropin releasing hormone (GnRH for LH, FSH)

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