Chemical Messengers

The Story

The thing Stina’s doctors kept getting wrong was timing. Her racing heart and dry mouthThe opening of the digestive tract where food enters and mastication begins. didn’t track with anxiety or caffeine — they tracked with her flares. When her inflammatory markers climbed, so did her autonomic chaos; when the fire banked, her body settled. That coupling pointed away from “nerves” in the colloquial sense and toward the actual chemistry of the autonomic synapses — chemistry that inflammation is known to disturb.

Autonomic signaling runs on two main neurotransmittersChemicals released by neurons to transmit signals across a synapse. and a small family of receptorsProteins located on the surface or inside cells that bind specific molecules (e.g., neurotransmitter. Every preganglionic neuron — sympathetic and parasympathetic alike — releases acetylcholinealso know as ACh A neurotransmitter that stimulates muscle contraction. (ACh) onto nicotinic receptorsCholinergic receptors found on postganglionic neurons and skeletal muscle; they respond to acetylcho at the ganglionA cluster of neuron cell bodies located in the peripheral nervous system (PNS).. From there the divisions diverge: parasympathetic postganglionic neuronsThe functional cells of the nervous system that transmit signals. release ACh again, this time onto muscarinic receptorsCholinergic receptors found on the effector organs of the parasympathetic nervous system; they media on the target organ, while most sympathetic postganglionic neurons release norepinephrineA neurotransmitter involved in attention, arousal, and the fight-or-flight response. (NE) onto adrenergic receptorsReceptors that bind norepinephrine and epinephrine; divided into α (alpha) and β (beta) types with. So three receptorA structure that detects stimuli. families do the work — nicotinic, muscarinic, and adrenergic — and the identity of the messenger and receptor determines whether an organ speeds up or slows down. Here is the FMF connection: inflammatory cytokines can alter neurotransmitterChemicals that transmit signals across synapses. release, shift receptor sensitivity, and bias the whole system toward sympathetic “revving.” Stina’s autonomic symptomsSubjective experiences reported by the patient (e.g., nausea, fatigue). rose and fell with her inflammation because the inflammation was, quite literally, tampering with the chemistry of her autonomic synapses.

From Stina’s chart: Stina’s autonomic symptoms wax and wane with her inflammation, not with her stress level. This page builds the chemistry that inflammation can disturb.