Many essential oils (EOs) have anticonvulsant activity and might benefit people with epilepsy. Lemongrass, lavender, clove, dill, and other EOs containing constituents such as asarone, carvone, citral, eugenol, or linalool are good candidates for evaluation as antiepileptic drugs. On the other hand, some EOs have convulsant effects and may trigger seizures in both epileptic and healthy individuals. Internal use of EOs like sage, hyssop, rosemary, camphor, pennyroyal, eucalyptus, cedar, thuja, and fennel can cause epileptic seizures because they contain thujone, 1,8-cineole, camphor, or pinocamphone, which have been identified as convulsive agents. While more research is needed to confirm their mechanisms of action, it appears that the convulsant or anticonvulsant properties of essential oils are largely due to (1) their ability to modulate the GABAergic system of neurotransmission and (2) their capacity to alter ionic currents through ion channels. This review presents a systematic analysis of the current research on EOs and epilepsy, including human case studies, animal models, andin vitrostudies.

Cinnamon has been used as a flavoring and medicinal agent for centuries. Much research has focused on cinnamon bark powder, which contains antioxidants, flavonoids, carotenoids, vitamins, minerals, fiber, and small amounts of essential oil. However, isolated and concentrated cinnamon essential oil may also have important medicinal qualities, particularly in antidiabetic therapy. Some of the most common essential oil constituents identified in the literature include cinnamaldehyde, eugenol, and beta-caryophyllene. Due to their high concentration in cinnamon essential oil, these constituents are hypothesized to have the most significant physiological activity. Here, we present a brief review of literature on cinnamon oil and its constituents as they relate to glucose metabolism and diabetic pathogenesis. We also present molecular docking simulations of these cinnamon essential oil constituents (cinnamaldehyde, eugenol, beta-caryophyllene) that suggest interaction with several key enzymes in glucometabolic pathways.

No abstract

Aromatic compounds have a long history of use as medicines in most recorded cultures. An increasing interest in these therapeutic volatile molecules in both scientific and lay communities has led to the advancement of essential oils as phytomedicines. Recent discoveries suggest essential oils augment the endocannabinoid system in a positive manner to mitigate various pathologies. However, the exact mechanisms whereby essential oils influence endocannabinoid system activity are not fully known, these studies provide a glimpse into their involvement and warrant further evaluation. Additional study of the interaction between essential oils and the endocannabinoid system may lead to promising phytomedicines for the treatment of diseases and conditions involving dysregulation or activation of the endocannabinoid system.

Mono‐ and sesquiterpenoids are the main chemical constituents of essential oils. Essential oils and their constituents have received increasing attention for lipid‐lowering properties in both cell and animal models. Despite the chemical diversity of essential oil compounds, the effects of many of these compounds on cholesterol metabolism are highly similar. In this report, we review the literature regarding the effects of essential oils and their terpenoid constituents on cholesterol homeostasis, and explore likely mechanisms using protein–ligand docking. We identified 98 experimental and seven clinical studies on essential oils, isolated compounds, and blends; 100 of these described improvements either in blood cholesterol levels or in sterol metabolic pathways. Our review and docking analysis confirmed two likely mechanisms common to many essential oil compounds: (1) direct agonism of peroxisome‐proliferator‐activated receptors, and (2) direct interaction with sterol‐sensing domains, motifs found in key sterol regulatory proteins including sterol regulatory element binding protein cleavage activating protein and HMG‐CoA reductase. Notably, these direct interactions lead to decreased transcription and accelerated degradation of HMG‐CoA reductase. Our work suggests that terpene derivatives in essential oils have cholesterol‐lowering activity and could potentially work synergistically with statins, however, further high quality studies are needed to establish their clinical efficacy.