Elsevier

Phytomedicine

Volume 12, Issue 8, 2 August 2005, Pages 607-611
Phytomedicine

Review
Gastrointestinal clinical pharmacology of peppermint oil

https://doi.org/10.1016/j.phymed.2004.10.006Get rights and content

Abstract

In nine studies, 269 healthy subjects or patients underwent exposure to peppermint oil (PO) either by topical intraluminal (stomach or colon) or oral administration by single doses or 2 weeks treatment (n=19). Methods used to detect effects were oro-cecal transit time by hydrogen expiration, total gastrointestinal transit time by carmine red method, gastric emptying time by radiolabelled test meal or sonography, direct observation of colonic motility or indirect recording through pressure changes or relieve of colonic spasms during barium enema examination. The dose range covered in single dose studies is 0.1–0.24 ml of PO/subject. With one exception, which show an unexplained potentiation of neostigmine stimulated colon activity, all other studies result in effects, indicating a substantial spasmolytic effect of PO of the smooth muscles of the gastrointestinal tract. Pharmacokinetic studies reveal that fractionated urinary recovery of menthol is dependent on the kind of formulation used for the application of PO. Optimal pH triggered enteric coated formulations start releasing PO in the small intestine extending release over 10–12 h thus providing PO to the target organ in irritable bowel syndrome, i.e. the colon. The hypothesis is supported by anecdotal observations in patients with achlorhydria or ileostoma, respectively.

Introduction

Peppermint oil (Menthae piperitae aetheroleum, PO) is obtained from the fresh leaves of peppermint, Mentha piperita L. by steam distillation. The major constituents of the oil include the terpenes (−)-menthol (30–55%), (−)-menthone (14–32%), (+)-isomenthone (1.5–10%), (−)-menthyl acetate (2.8–10%), (+)-menthofuran (1.0–9.0%) and 1,8-cineol (3.5–14%). Due to its calcium antagonistic properties (−)-menthol has been made responsible spasmolytic effect of PO (Hawthorn et al., 1988). The Food and Drug Administration lists peppermint and PO as “generally recognized as safe” (GRAS; Food and Drugs, 1998).

The purpose of this review is to analyze in detail the pharmacodynamic effects of PO on the gastrointestinal tract with a focus on its use in irritable bowel syndrome (IBS; ESCOP, 1997) as well as oral pharmacokinetics.

Section snippets

Pharmacodynamics

In Table 1 pharmacodynamic studies and results thereof relevant to the use of PO in the gastrointestinal tract are summarized. In nine studies 269 subjects underwent exposure to PO either by topical intraluminal (stomach or colon) or oral administration by single doses or 2 weeks (Wildgrube, 1988) treatment. Methods used to detect effects were oro-cecal transit time by hydrogen expiration, total gastrointestinal transit time by carmine red method, gastric emptying time by radiolabelled test

Pharmacokinetics

In rats PO is relatively rapidly absorbed and eliminated mainly via the bile. The major biliary metabolite is menthol glucuronide, which undergoes enterohepatic circulation. The urinary metabolites result from hydroxylation at the C-7 methyl group at C-8 and C-9 of the isopropyl moiety, forming a series of mono- and dihydroxymenthols and carboxylic acids, some of which are excreted in part as glucuronic acid conjugates (Yamaguchi et al., 1994).

Menthol (30–55% of natural PO) and other plant

Discussion

There is reasonable evidence that PO exerts a spasmolytic effect on the smooth vasculature of the intestinal tract. The duration of effect is limited to approximately 20 min. Furthermore, there is evidence that the typical adverse events of PO (e.g. heartburn) do occur if PO is released in the upper gastrointestinal tract. If the target organ like in IBS is the colon immediate release formulations are inadequate. A sustained release formulation is required which releases PO in the lower GI

References (17)

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