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Nevertheless, supplementation should ideally be guided by clinical assessment and, where appropriate, blood testing to confirm deficiency before commencing long-term high-dose therapy

TSH (thyroid) and HbA1c (blood sugar) on file

Macrophages derived from Nox2-deficient (gp91phox/) mice produced marginal amounts of superoxide radical and are more susceptible to parasite infection than those macrophages derived from wild-type mice

Ferroptosis (iron-dependent lipid peroxidation) is also implicated as a mechanistic bridge by emerging evidence: GPX4 dysfunction and iron accumulation increase lipid peroxides, which sensitize neurons to ferroptotic death and provide extra DAMP-like signals that increase inflammasome activation [58, 59]