A vagal–immune convergence framework for the autonomic, peripheral immune and central neuroimmune effects of meditation

Meditation is widely reported to reduce physiological markers of stress, yet the field lacks a mechanistic account that connects specific meditative practices to specific immune outcomes. This review integrates four literatures: (1) autonomic effects of meditation, framed by the neurovisceral integration model; (2) the molecular architecture of the efferent pathways through which the brain restrains inflammation — vagal–splenic cholinergic (α7 nicotinic receptor, JAK2–STAT3, NF-κB), sympathetic–adrenergic and glucocorticoid-receptor signalling; (3) afferent and central mechanisms, including vagal cytokine sensing, insular representation of inflammation and microglial priming and reprogramming; and (4) trial, transcriptomic and epigenetic evidence on meditation and immunity. Meta-analyses show small and heterogeneous effects on vagally mediated heart rate variability and circulating C-reactive protein and interleukin-6, with more consistent down-regulation of NF-κB-related gene expression. We argue that part of this heterogeneity reflects the conflation of mechanistically distinct practices. Focused-attention, open-monitoring, loving-kindness/compassion and slow-breath/mantra practices have dissociable neural signatures, but direct evidence that they produce different immune signatures is currently limited to a few endocrine and transcriptomic findings. We therefore present a Vagal–Immune Convergence framework in which each link is graded by the strength of its evidence, distinguish established mechanisms from hypotheses, and extend the framework to central neuroimmune targets. The framework yields falsifiable predictions, for example, that socio-affective training will reduce stress-evoked interleukin-6 more than attention-based training, and that baseline heart rate variability will moderate attention-based but not breath-based effects, and specifies designs to test them.