Lavender: Background

2010

Common Name

Lavender

Other Names

Common lavender, English lavender, French lavender, garden lavender, Spanish lavender, spike lavender, true lavender

Botanical Name / Family

Lavandula angustifolia (synonyms: Lavandula officinalis, Lavandula vera, Lavandula spica); L. dentata; L. latifolia; L. pubescens; L. stoechas (family Labiatae)

Plant Parts Used

Flower

Historical Note

Lavender was used as an antiseptic in ancient Arabian, Greek and Roman medicines. Its generic name comes from the Latin lavare, to wash, and it was used as a bath additive as well as an antiseptic in the hospitals and sick rooms of ancient Persia, Greece and Rome. In the 17th century, Culpeper described lavender as having ‘use for pains in the head following cold, cramps, convulsions, palsies and faintings’. Lavender was also used traditionally to scent bed linen and to protect stored clothes from moths. This was such a well-accepted practice that the phrase ‘laying up in lavender’ was used metaphorically to mean ‘putting away in storage’. Lavender is now widely used to scent perfumes, potpourri, toiletries and cosmetics, as well as to flavour food. Lavender is commonly adulterated with related species that can vary in their constituents. Spike lavender yields more oil but is of lower quality. Lavandin is a hybrid of spike lavender and true lavender.

Chemical Components

Lavender flowers contain between 1% and 3% essential oil. The oil is a complex mixture of many different compounds, the amounts of which can vary between species. The most abundant compounds include linalyl acetate (30-55%), linalool (20-35%), cineole, camphor, coumarins and tannins (5-10%), together with 1,8-cineole, thymol and carvacrol. Perillyl alcohol and D-limonene have been shown to exert anticancer effects (see clinical note).

Clinical note — Perillyl alcohol and anticancer effects?

Perillyl alcohol and D-limonene are monoterpenes found in lavender (also cherries, mint and celery seeds) and have shown chemotherapeutic and chemoprotective effects in a wide variety of in vitro and animal models and are currently being examined in human clinical trials. Perillyl alcohol treatment has resulted in 70-99% inhibition of ‘aberrant hyperproliferation’, a late-occurring event preceding mammary tumourigenesis in vivo and, together with limonene, perillyl alcohol has been shown to induce the complete regression of rat mammary carcinomas by what appears to be a cytostatic and differentiation process. Perillyl alcohol has also been shown to inhibit human breast cancer cell growth in vitro and in vivo and inhibit the expression and function of the androgen receptor in human prostate cancer cells.

A variety of mechanisms has been proposed to explain these effects. The compounds may act via interfering with RAS signal transduction pathways that regulate malignant cell proliferation and have been found to promote apoptosis in pancreatic adenocarcinoma cells and liver tumours in vivo. Perillyl alcohol, together with D-limonene, has been found to preferentially inhibit HMG-CoA reductase in tumour cells, as well as inhibit ubiquinone synthesis and block the conversion of lathosterol to cholesterol, which may add to its antitumour activity. Limonene is oxidised by the CYP2C9 and CYP2C19 enzymes in human liver microsomes and there are reported sex-related differences in the oxidative metabolism of limonene by liver microsomes in rats.

Although in vitro and animal studies have demonstrated the ability of perillyl alcohol to inhibit tumourigenesis in the mammary gland, liver, and pancreas, the results are not yet conclusive and one animal study testing perillyl alcohol detected a weakly promoting effect early in nitrosamine-induced oesophageal tumourigenesis in rats. In initial phase II clinical trials, perillyl alcohol administered orally, four times daily, at a dose of 1200 mg/m2 had no clinical antitumour activity on advanced ovarian cancer, metastatic androgen-independent prostate cancer, or metastatic colorectal cancer.