From a pathophysiological perspective, my first thought is that this could reflect an indirect effect on peripheral nerve sensitivity, possibly related to: rapid shifts in glucoselipid metabolism, changes in nerve conduction due to electrolyte fluctuations, or even a centrally mediated effect, considering GLP-1 receptor expression in the CNS
In an environment characterized by oxidative stress and mitochondrial dysfunction, the presence of oxLDL further increases the secretion of proinflammatory cytokines (e.g., tumor necrosis factor , interleukin [IL]-6 and IL-1) and the expression of adhesion molecules (including vascular cell adhesion protein [VCAM]-1, monocyte chemoattractant protein [MCP]-1, intercellular adhesion molecule [ICAM]-1 and E-selectin) by monocytes and macrophages ( GLP-1 receptor stimulation appears to attenuate these processes in preclinical models and human studies in various ways
Eating more than usual while on the medications seems to be a common trigger
Semaglutide helps both groups, just at different scales
