Acupuncture really does help relieve stress. And now, a new study is giving a closer look at why. The new study explores the biological mechanisms involved in acupuncture’s stress-relieving abilities. The researchers discovered that stress hormones were lower in rats that had received electronic acupuncture. Results were published in the Journal of Endocrinology.
Dr. Ladan Eshkevari, an associate professor of nursing at Georgetown University School of Nursing and Health Studies, said that many practitioners of acupuncture have observed that this ancient practice can reduce stress in their patients, but there is a lack of biological proof of how or why this happens. We’re starting to understand what’s going on at the molecular level that helps explain acupuncture’s benefit. Please see the following abstract.
Acupuncture blocks cold stress-induced increases in the hypothalamus–pituitary–adrenal axis in the rats
School of Nursing and Health Studies, Georgetown University Medical Center, 421 St Mary’s Hall, 3700 Reservoir Road NW, Washington, District of Columbia 20007 1USA Departments of Histopathology 2Pharmacology and Physiology, Georgetown University Medical Center, Washington, District of Columbia 20007, USA
Electroacupuncture (EA) is used to treat chronic stress; however, its mechanism(s) of action in allaying stress remains unclear. The interplay of stress hormones of the hypothalamus–pituitary–adrenal axis (HPA) and the sympathetic nervous system (SNS) is critical in the stress response. Our objective was to determine whether EA at acupoint, stomach 36 (EA St36) is effective in preventing chronic cold stress-induced increased hormone levels in the rat by examining four groups of animals, three of which were exposed to cold and one of which was a non-treatment control group. Before exposure to the cold, two groups were treated with either EA St36, or Sham-EA, before 10 days of cold stress. The EA St36 animals demonstrated a significant decrease in peripheral HP hormones (ACTH and CORT) compared with stress animals (P<0.05). These effects were specific; rats receiving Sham-EA had elevation of these hormones, similar to the stress-only animals. These effects were mirrored centrally in the brain; CRH levels were significantly (P<0.05) reduced in EA St36 animals compared with the other animals. Finally, EA effect on peripheral and adrenal SNS hormones (norepinephrine (NE) and neuropeptide Y (NPY) respectively) was examined, with no significant difference noted in adrenal tyrosine hydroxylase or circulating NE in any of the groups. However, EA St36 was effective in preventing stress-induced elevation is adrenal Npy mRNA. These results indicate that EA St36 blocks the chronic stress-induced elevations in the HPA and the sympathetic NPY pathway, which may be a mechanism for its specific stress-allaying effects.