Recreational abuse of the spice nutmeg for psychoactive effect has smoldered along, largely under the radar, for over a century. Although it usually keeps a low profile compared to other drugs of abuse and alcohol, it occasionally enjoys a swift rise in popularity, followed by a crash because of its unreliable success and unpleasant side effects. Recent internet challenges have instructed teenagers to consume large quantities of nutmeg and share their experiences using social media. Clinicians need to be alert to this phenomenon in order to recognize its toxicity in their patients.
Nutmeg as a spice is found both pre-ground and as a whole nut to be freshly grated. It has a unique, intense, warm flavor that enhances both sweet and savory dishes, particularly during the winter holidays. (Think pumpkin pie and eggnog dusted with nutmeg.) Therefore, it can often be found in the home’s kitchen, conveniently accessible for free to teens and pre-teens, or purchased in grocery stores quite inexpensively. It may be ingested as a paste, mixed with a beverage like a milkshake, or packed into gelatin capsules to make it easier to swallow.
In folk medicine, nutmeg was a fairly useless treatment for various conditions such as rheumatism, diarrhea, pregnancy, and inadequate sexual desire. It is currently recommended in “pinch” amount to improve sleep on natural health websites. Therapeutic dosing of nutmeg is not supported by clinical data for any indication.
In excess, nutmeg in has multiple actions involving primarily the CNS and GIT but sparing the CV system for the most part.
NUTMEG SOURCE AND COMPOSITION
Nutmeg is the central kernel of the fruit produced by the Myristica fragrans, an evergreen tree indigenous to parts of Indonesia. The majority is cellulose to provide structure and the rest is extractable oil: 20 to 40% “fixed” oil (triglycerides and fatty acids) and 8 to 15% “volatile” or “essential” oil. The components of the volatile oil fraction are responsible for the toxic effects of nutmeg and include myristicin, elemicin, safrole, eugenol and various aromatic terpenes.
MECHANISM OF TOXICITY
While the mechanisms of nutmeg toxicity are not well understood, all of the main volatile oils and some of their metabolites are believed to be active and work in combination. Myristicin has structural similarities to MMDA (Ecstasy-like drug) and mescaline. It appears to be psychoactive and hallucinogenic via serotonergic receptor activity, boosted by its weak monoamine oxidase inhibitor properties. In animal studies, myristicin alone produced psychoactive effects but effects were always stronger when it was combined with the other components of the volatile oil. For example, elemicin and safrole are hypothesized to be responsible for the anxiogenic properties of nutmeg.
Some of the other terpene aromatics are structurally related to known CNS stimulants, such camphor and thujone (an inhibitor of GABA A receptors). They may also modulate neurotransmitter release in the brain through interference with calcium channels that enable vesicles to fuse with the synaptic membrane. This broad mechanism could account for the wide range of symptoms.
Toxic effects are myriad and unpredictable, which is likely a function of both the amount ingested and the actual volatile-oil composition and potency of the particular nutmeg. Composition and potency vary considerably based on source, growing conditions, processing, and age in storage.
Dosing is inexact because of the variation in bulk volume and weight as well as composition and freshness. An intact nutmeg weighs 6-7 grams, and 1 to 1½ nuts is the recommended recreational dose. For ground nutmeg the dose ranges from 5 to 30 grams, and this is difficult to translate into spoonsful. A typical 4-inch-tall spice jar contains 60 grams of ground nutmeg; half a bottle is often taken. Underdosing and overdosing are common, resulting in either a disappointing attempt or an unpleasant toxic day or two. Both of these outcomes discourage additional experimentation with nutmeg, so the flurry of interest quickly dies out.
Gastrointestinal symptoms including burning epigastric and mid-chest pain and nausea and vomiting occur first, and are thought to be due to direct irritant effect on the mucosa.
CNS symptoms usually begin within 3-8 hours with concurrent features suggestive of anticholinergia, CNS excitation, CNS depression, and psychosis. In severe cases of toxicity, patients may experience significant psychological effects.
Anticholinergic-like symptoms may include tachycardia, dry mouth, thirst, flushing, visual complaints, confusion, delirium, quiet bowel, and urinary retention.
Excitatory symptoms may include agitation, motor restlessness, anxiety, feeling of doom, panic, confusion, headache, tremor, and, very rarely, seizures.
CNS depression symptoms may include drowsiness, lethargy, stupor, ataxia, nystagmus, vertigo, and generalized weakness.
Psychotic symptoms may include hallucinations (auditory, visual, tactile), perceptual disturbances, depersonalization/dissociation, delirium, incoherent speech, mutism, and behavioral dyscontrol.
The pupils may display miosis, mydriasis, or normal size and so are an unreliable sign of nutmeg effect.
Characteristically the patient displays alternating periods of delirium and stupor. The entire episode resolves over 24 to 36 hours, leaving no sequalae.
MANAGEMENT OF TOXICITY
Unintentional ingestions of nutmeg, usually in children, are often managed at home. Patients are referred to a health care facility if they intentionally ingest a large amount of nutmeg or develop persistent vomiting or significant CNS effects. Patients with CNS toxicity are normally admitted for observation since effects can last more than 24 hours.
Treatment of nutmeg toxicity involves good supportive care; there is no antidote. Decontamination is not indicated as the patient has most likely already been vomiting, and the onset of prominent toxic effects inducing the patient to seek medical care is delayed beyond the time of its usefulness. Treat nausea and vomiting with standard antiemetics. Patients with psychomotor agitation or anxiety may be managed with benzodiazepines, although caution is needed in view of the potential for lethargy or stupor to supervene. There is no experience and so no indication for a cholinesterase inhibitor for toxic delirium (physostigmine or rivastigmine) since it is likely to be multi-factorial, not necessarily anticholinergic.
Monitoring should include vital signs, mental status, and routine laboratory studies, although these are expected to be normal. A urine drug screen may reveal other drugs of abuse taken concurrently, as this is common among recreational users and experimenters.
If you have any questions about the adverse effects of nutmeg, please feel free to call the Missouri Poison Center at 1-800-222-1222. Our specially trained nurses, pharmacists, and toxicologists can provide the most up-to-date information regarding exposures and treatment.