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Genetics of chronic fatigue syndrome
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=== The IDO Metabolic Trap Hypothesis for the Etiology of ME/CFS === A new hypothesis, the indolamine-2,3-dioxygenase ([[IDO]]) [[metabolic trap]], was developed and formulated as a mathematical model. The historical occurrence of [[List of myalgic encephalomyelitis and chronic fatigue syndrome outbreaks|ME/CFS outbreaks]] is a singular feature of the disease and implies that any predisposing genetic mutation must be common. A database search for common damaging mutations in human enzymes produces 208 hits, including IDO2 with four such mutations. Non-functional IDO2, combined with well-established substrate inhibition of [[IDO1]] and kinetic asymmetry of the large neutral amino acid transporter, LAT1, yielded a mathematical model of tryptophan metabolism that displays both physiological and pathological steady-states. Escape from the pathological one requires an exogenous perturbation. This model also identifies a critical point in cytosolic tryptophan abundance beyond which descent into the pathological steady-state is inevitable.<ref name="Kashi2019" />
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