Mind-body therapies and control of inflammatory biology: A descriptive review

Abstract

The use of mind-body therapies, including Tai Chi, Qigong, yoga, and meditation, has grown steadily in recent years. These approaches have been shown to be effective in reducing symptoms and improving quality of life, and research has begun to examine the impact of these therapies on biological processes, including inflammation. A review of 26 randomized controlled trials was conducted to describe the effects of mind-body therapies (MBTs) on circulating, cellular, and genomic markers of inflammation. This qualitative evaluation showed mixed effects of MBTs on circulating inflammatory markers, including CRP and IL-6, and on measures of stimulated cytokine production. More consistent findings were seen for genomic markers, with trials showing decreased expression of inflammation-related genes and reduced signaling through the proinflammatory transcription factor NF-κB. Potential mechanisms for these effects are discussed, including alterations in neuroendocrine, neural, and psychological and behavioral processes.

Keywords: Inflammation; Meditation; Qigong; Review; Tai Chi; Yoga.

Figure 1

Potential pathways linking mind-body therapies and inflammatory biology, focusing on neuroendocrine mechanisms. Mind-body interventions may influence neural regions that regulate downstream stress response pathways, including the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal (HPA) axis. The ANS and the HPA axis may, in turn, influence the production of proinflammatory cytokines via effects of their ligands on adrenergic, cholinergic, and glucocorticoid receptors on immune cells. Stimulation of adrenergic receptors by epinephrine and norepinephrine can activate proinflammatory transcription factors such as NF-kB, whereas stimulation of GC receptors can inhibit proinflammatory cytokine production. Randomized controlled trials of mind-body therapies have demonstrated reduced pro-inflammatory signaling through NF-kB and increased anti-inflammatory GR signaling, suggesting that these approaches may modulate gene expression to reduce inflammation. However, effects on stimulated production of proinflammatory cytokines and circulating cytokine concentrations are mixed.