Panax ginseng and Eleutherococcus senticosus may exaggerate an already existing biphasic response to stress via inhibition of enzymes which limit the binding of stress hormones to their receptors

Med Hypotheses. 2001 May;56(5):567-72. doi: 10.1054/mehy.2000.1163.


A mechanism of action for Panax ginseng (PG) and Eleutherococcus senticosus (ES) is proposed which explains how they could produce the paradoxical effect of sometimes increasing and sometimes decreasing the stress response. The mechanism suggests that this biphasic effect results from increased occupancy of positive and negative feedback stress hormone receptors by their natural ligands due to inhibition of specific enzymes which function to limit receptor occupancy. Specifically, it is suggested that PG inhibits 11-beta hydroxysteroid dehydrogenase one and ES inhibits catechol- O -methyl transferase, both of which reside in close proximity to stress hormone receptors and catalyse the degradation of stress hormones into inactive compounds. In addition, it is suggested that the increased energy said to result from PG and ES may be a consequence of their increasing the occupancy of stress hormone receptors which function to redistribute the body's energy reserves from regeneration to activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1
  • Animals
  • Catechol O-Methyltransferase Inhibitors
  • Eleutherococcus
  • Enzyme Inhibitors / pharmacology*
  • Hormones / metabolism*
  • Hydroxysteroid Dehydrogenases / antagonists & inhibitors
  • Panax*
  • Plant Extracts*
  • Plants, Medicinal*
  • Protein Binding
  • Receptors, Steroid / metabolism*
  • Stress, Physiological / enzymology
  • Stress, Physiological / therapy*


  • Catechol O-Methyltransferase Inhibitors
  • Enzyme Inhibitors
  • Hormones
  • Plant Extracts
  • Receptors, Steroid
  • Hydroxysteroid Dehydrogenases
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1