“I first got high in Charlestown on nutmeg. My cellmate was among at least a hundred nutmeg men who, for money or cigarettes, bought from kitchen-worker inmates penny matchboxes full of stolen nutmeg. I grabbed a box as though it were a pound of heavy drugs. Stirred into a glass of cold water, a penny matchbox full of nutmeg had the kick of three or four reefers.”
The Autobiography of Malcolm X
Nutmeg has long been prized for many properties, both real and imagined. First brought to Europe in the 12th century by Arab merchants and later the focus of fierce trade wars among the major European sea powers, the spice was at one time the third most valuable commodity in the world after gold and silver.
Nutmeg was used to preserve and flavor food. As a bonus, it was said to protect against plague and to be an aphrodisiac. Various systems of medicine recommended nutmeg for treating rheumatism, cholera, gastrointestinal disorders, and flatulence. Early descriptions of nutmeg toxicity were of women who ingested large amounts in attempts to induce abortion. And, of most interest to toxicologists, nutmeg had a well-established reputation for its hallucinogenic and psychotropic properties.
Nutmeg is the seed of the aromatic evergreen Myristica fragrans, a tree native only to the Banda Islands, a small archipelago in Indonesia. Today, M. fragrans is also cultivated in the Caribbean and Malaysia. Although it contains a number of volatile oils such as myristicin, safrole, and eugenol that might contribute to its toxicity and psychogenic properties, the exact pharmacology of nutmeg has not been decoded. It is possible that some of the components of nutmeg may inhibit monoamine oxidase or be transformed into amphetamine-like metabolites, but neither of these hypotheses has been proven.
Signs and symptoms of nutmeg toxicity are quite similar to those of anticholinergic poisoning. Patients often present with abdominal pain, nausea and vomiting, dry mouth, flushing, tachycardia, bizarre behavior, and delirium. Central nervous system stimulation and depression can occur. Some articles state that a distinguishing feature is the size of the pupils: dilated with anticholinergics, constricted with nutmeg. Case reports in the literature make it clear, however, that this is an inconsistent finding after ingestion of nutmeg. Meiosis, mydriasis, and normal pupil size have all been described. Hallucinations can be visual, auditory, and tactile. Users sometimes report a sense of dread or impending doom.
Onset of action for nutmeg ingestion is generally three to six hours. Duration is approximately 12 hours, but can be longer. Many individuals who take nutmeg once as an available, inexpensive high vow never to do it again. The experience is almost universally described as unpleasant, and requires ingestion of a large unpalatable dose.
A remarkable report from the University of Maryland was published in the early 1960s. (J Neuropsych 1961;2:205.) One of the authors, a psychiatrist, ingested 15 g of nutmeg at 9 a.m. on a Thursday morning. He describes the experiences that followed:
“I had been angry about a particular situation. By 10:30, the anger was dispelled. I felt at peace with the world. After lunch I went to a store downtown. … While driving to the stone cutter's, and especially returning, I noticed that I was having difficulty concentrating. I experienced increasing feelings of being detached and somewhat depersonalized. My mouth was becoming noticeably dry. … [I had] the very strange feeling of being completely lost.”
On returning to his office, our protagonist discovers that his pulse rate is 124 bpm, and he calls colleagues for advice:
“I was apparently very suggestible because one person suggested a drink of whiskey, and I took a small drink of whiskey. Another suggested a dextro-amphetamine, and I took a methamphetamine tablet. Another person suggested dimenhydrinate, and I took one of those tablets. By this point, I was unable to think clearly.”
Many textbook chapters and articles state that there has been one reported death caused by nutmeg ingestion. This belief stems from an unreferenced comment in a review article from 1908. The source of this comment is undoubtedly an even earlier brief report in The Medical Record (Nov. 12, 1887; p. 624) describing an 8-year-old boy who apparently ate two whole nutmegs:
“I found him in a semi-comatose condition, and immediately administered an emetic and diffusible stimulants. He vomited freely, but the coma increased until it was soon impossible to give anything by mouth. Hypodermic injections of brandy, ammonia, and small doses of sulph. of atropia were given, and artificial respirations were continued all night, but the little fellow did not rally, and died at an early hour the following morning.”
I suspect the child actually died of aspiration and the seemingly bizarre (at least by today's standards) treatments, not from nutmeg poisoning itself.
There is no specific antidote. Although nutmeg poisoning can mimic the anticholinergic toxidrome, physostigmine is not indicated, and has potential risks. Appropriate supportive care includes antiemetics for nausea and vomiting, benzodiazepines for anxiety and agitation, and fluids as needed. Most patients will be better by 12 hours, and, unlike the inmates described by Malcolm X, will not be inclined to repeat the experience.
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