Why Your Brain Fog Won't Lift: The Six Mechanisms of Cognitive Dysfunction in Chronic Illness, and Why Standard Interventions Keep Failing — Why Standard Interventions Plateau

If the framework above is correct, the failure profile of standard brain fog treatment becomes predictable. Caffeine and other stimulants increase arousal without addressing any of the six mechanisms. They mask the symptom temporarily. Tolerance develops within weeks. The underlying lesion continues to advance. Nootropics (racetams, modafinil, methylphenidate, amphetamine variants) increase monoaminergic signaling or affect specific neurotransmitter systems. They produce dramatic short term benefit. They do not address the gut layer, the inflammation layer, the mitochondrial layer, the cofactor layer, the mast cell layer, or the hormonal layer except indirectly. The benefit plateaus or requires escalating doses. Long term cognitive function is often not improved despite years of use. SSRIs and SNRIs raise central monoamine availability downstream of depleted pools. They help when the dominant lesion is serotonergic or noradrenergic insufficiency that the upstream system cannot correct. They do not move the upstream lesion. Discontinuation usually produces a return of symptoms. Vagus nerve stimulation and polyvagal exercises modulate the autonomic side of the gut to brain axis but do not change the gut afferent drive that established the dysregulated set point. The benefit is real but does not accumulate, as I described in Why Every Protocol Stops Working After Two Weeks. Methyl