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Weve known for over 20 years that large doses of carnitine given intravenously in people within hours of a heart attack may have an antiarrhythmic effect, presumably by facilitating glucose oxidation in the failing heart muscle
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When activated, Nrf2 disassociates from its repressor protein KEAP1 that reacts with oxidative radicals, translocates to the nucleus, binds to antioxidant response element and induces the transcription of defensive genes
It is essential to start with a lower dose and gradually titrate up to assess tolerance, particularly for patients with severe ME/CFS who may be highly sensitive to metabolic shifts
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