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The interaction is primarily facilitated by contacts with the substituted -helix in the original protein, underscoring the effective structural mimicry of this protein segment

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The clinical presentation and progression of NAION manifests through: Sudden, painless monocular vision loss occurring over hours to days, often discovered upon awakening Altitudinal visual field defects affecting either the superior or inferior visual field Visual acuity loss ranging from mild (20/30) to severe (counting fingers or worse) Optic disc edema during the acute phase, progressing to optic atrophy over 4-6 weeks Risk of bilateral involvement, with 15% of patients developing NAION in the second eye within five years No effective treatment to restore vision once damage occurs Permanent disability requiring lifestyle adaptations and assistive technologies The pathophysiology of NAION involves impaired perfusion to the anterior portion of the optic nerve head, though the exact mechanism remains incompletely understood

Its common that feelings of fatigue and tiredness will reduce after a week or two once the body adapts to the reduced calorie intake and change in metabolism