Salvia officinalis L. (Lamiaceae)
Sage Leaf (British Ph 2009, European Ph 2008); Sage Oil (British Ph 2009); Sage Tincture (British Ph 2009, European Ph 2008); Spanish Sage Oil (British Ph 2009, European Ph 2008); Three-lobed Sage Leaf (British Ph 2009, European Ph, 6th ed., 2008 and Supplements 6.1, 6.2, 6.3 and 6.4).
The major constituents of sage are flavonoids including luteolin and derivatives, caffeic acid derivatives, diterpenes and triterpenes.
The essential oil components vary according to species and origin. Salvia officinalis contains the monoterpene hydrocarbons alpha- and beta-thujones as the major components, together with 1,8-cineole, camphor and borneol, and others. Salvia lavandulifolia does not contain thujones, and Salvia triloba only small amounts, making these oils less toxic.
Use and indications
Sage is used traditionally to reduce ‘hot flushes’ and hyperhidrosis associated with the menopause. It has antiseptic and spasmolytic properties, and a tea infusion is used as a gargle for sore throats. Extracts are also strongly antioxidant. Sage (Salvia lavandulifolia in particular because of the absence of thujones) has recently generated interest as a cognition enhancer due to its anticholinesterase properties. The oil may be applied topically as an antiseptic and rubefacient but it should not be taken internally, applied externally in large amounts or used by pregnant women. Note that sage is widely used as a flavouring in foods.
An in vitro study found that sage does not have a clinically significant inductive effect on the cytochrome P450 isoenzymes CYP1A2, CYP2D6 and CYP3A4. Other in vitro studies. have found that sage does not inhibit CYP2D6, hepatic CYP3A4 or P-glycoprotein to a clinically relevant extent, although it may have some potentially clinically relevant effects on intestinal CYP3A4. In contrast, a further in vitro study found that sage had inhibitory effects on CYP2C9, CYP2C19, CYP2D6 and CYP3A4, but these findings should be interpreted with caution, as the study also found St John’s wort to be a CYP3A4 inhibitor, whereas, clinically, it is a CYP3A4 inducer. Therefore sage appears to have a low potential for causing interactions by these mechanisms, although the potential for a clinically relevant effect on intestinal CYP3A4 warrants further study.