Table 3.

Trigger patterns and hypothesized mechanistic domains (hypothesis-generating).

Trigger	Domain(s) most likely implicated	Physiological rationale
Cold exposure	Endothelial/microvascular dysfunction; dysautonomia	Impaired vasoconstrictive regulation or abnormal vascular reactivity may exaggerate perfusion instability
Heat exposure	Dysautonomia; endothelial dysfunction	Heat-induced vasodilation increases orthostatic stress and may unmask autonomic instability
Standing (Orthostatic stress)	Dysautonomia	Autonomic reflex failure or exaggerated sympathetic activation may impair blood pressure and heart rate regulation
Supine intolerance	Dysautonomia; neuroendocrine dysregulation	Altered baroreflex signaling or fluid redistribution may provoke autonomic or stress-axis symptoms
Meals (general)	Gut Dysbiosis; mast cell activation; dysautonomia	Post-prandial blood flow shifts, enteric–autonomic coupling, and mediator release may amplify systemic symptoms
Carbohydrate-heavy meals	Gut dysbiosis; bioenergetic dysfunction	Rapid glucose flux may exacerbate metabolic instability or post-prandial inflammatory signaling
High-fiber meals	Gut dysbiosis	Fermentation shifts and microbial metabolite production may transiently alter immune and autonomic tone
Emotions/Stress	Neuroendocrine dysregulation; dysautonomia	HPA axis activation and sympathetic signaling may amplify inflammatory and autonomic instability
Physical exertion	Mitochondrial/bioenergetic dysfunction; endothelial dysfunction	Impaired oxidative phosphorylation, redox recovery, or oxygen delivery may precipitate delayed symptom exacerbation