The early hype about acupuncture was so extreme (bathwater) that I stopped looking for the medical baby within. Part of the hype was a reaction against all things western.
However when stimulation of a mouse at the knee point (ST36) decreases mortality due to exposure to lipopolysaccharide by 40%, it’s time to sit up and take notice [ Nature vol. 598 pp. 573 – 574, 641 – 645 ’21 ].
Not only that but the authors found the neurons responsible for the effect. These neurons in the dorsal root ganglion express the G Protein Coupled Receptor (Prokr2) which is a receptor for prokineticin, a secreted protein which increases gut motility.
Stimulation of these neurons (or the point behind the knee they innervate) produces anti-inflammatory effects. Destruction of these neurons (by expressing diphtheria toxin in them) prevents low intensity stimulation of ST36 from dampening inflammation.
The paper even gives a possible explanation for some of the irreproducible results in the field. High intensity of stimulation of ST36 activates the sympathetic system, while low intensity stimulation activates the parasympathetic nervous system. The latter activates the vagus nerve which stimulates the adrenal medulla to produce catecholamines (which are anti-inflammatory). So high intensity stimulation of the same site produces no useful therapeutic effect.
I never thought I’d see high quality work like this on acupuncture, but there it is. More is sure to follow.
Chemiotics II 