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The mechanisms of both subacute and idiosyncratic VHT remain incompletely understood, but it has been believed since the early 1980s – based on limited experimental and clinical evidence [53-56] – that hypocarnitinaemia, subsequent imbalance between β-oxidation and ω-oxidation, and accumulation of 4-en-VPA are involved

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and this pathway is modulated by, and in turn modulates many other systems that are commonly disrupted in psychiatric disorders, including immune, endocrine, metabolic, and hormonal systems [219]