Myristicin: A Comprehensive Reference
1. Identity and Chemical Characterization
Nomenclature and Chemical Properties
Myristicin (molecular formula C11H12O3) is formally known as 5-allyl-1-methoxy-2,3-methylenedioxybenzene, or methoxysafrole; it is a metabolite of the phenylpropenes family, a subclass of phenylpropanoids. It is assigned CAS Registry Number 607-91-0. Myristicin, or methoxysafrole, is a benzodioxole with slight MAO-inhibiting properties.
The naturally occurring alkenylbenzene myristicin is a volatile, fragrant, and colorless oil. It has a specific gravity of 1.1416 g/mL at 20°C, a melting point lower than −20°C, a boiling point of 276.5°C, and a vapor pressure of 0.00646 mmHg at 25°C. As a member of the alkoxy-substituted allylbenzene family, myristicin shares many physical and chemical properties with the food additives apiole, safrole, elemicin, estragole, and methyleugenol. Myristicin is soluble in benzene and ether, slightly soluble in ethanol, and insoluble in water.
Myristicin belongs to the methylenedioxyphenyl or allyl-benzene family of compounds, which are found widely in plants of the Umbelliferae family, such as parsley and carrot. Myristicin contains a methylenedioxyphenyl substructure, and this specific structural feature may allow compounds to cause a mechanism-based inhibition of cytochrome P450 enzymes and produce reactive metabolites.
Myristicin first appeared in the chemical literature in 1890 in an article by Friedrich Wilhelm Semmler at the University of Greifswald, Germany. He isolated the compound from nutmeg oil and mace oil and determined its physical properties. In the 1900s, pharmacists O. K. Richter and M. Karmazin confirmed its structure. It was not until 1939 that the synthesis of myristicin was reported.
Botanical Sources
Myristicin is a natural alkenylbenzene compound that is commonly found in nutmeg, mace, black pepper, carrot, parsley, and celery seeds. Principally, myristicin is derived from the tropical evergreen tree Myristica fragrans Houtt. (Myristicaceae). Myristicin is a major constituent in essential oil extracted from either the seed (0.25% to 3.28%), which is the source of the spice nutmeg, or the aril covering the seed (0.25% to 5.92%), which is the source of the spice mace.
Myristicin is also in the oleoresin fraction of nutmeg and mace; one study reported 4.5% and another reported 8.1% myristicin in nutmeg oleoresin. Other notable components of nutmeg oil include elemicin, safrole, eugenol, isoeugenol, and methyleugenol. Besides M. fragrans, the chemical myristicin is present in some plants of the Apiaceae family, including dill and parsley, as well as in celery, carrot, and parsnip. The largest sources being nutmeg and mace. The percentage of myristicin in dill herb aromatic fraction is 2.81% to 7.63% and in essential oil from parsley leaf, myristicin is as low as 1% and as high as 60%.
Myristicin comprises 1.14% to 2.54% of powdered nutmeg and 2.59% to 7.55% of powdered mace. Myristicin, elemicin, and safrole account for the majority (85–95%) of the compounds in the aromatic fraction, and myristicin represents about 4–12% of the compounds present in the essential oil.
Myristicin is a major key constituent of many species, like Myristica fragrans Houtt. (nutmeg), Foeniculum vulgare Mill. (fennel), Anethum graveolens L. (dill weed), Petroselinum crispum (Mill.) Fuss (parsley), Apium nodiflorum (L.) Lag. (water celery), and Echinophora spinosa L. Myristicin can be found in the essential oil of nutmeg, black pepper, kawakawa, and many members of the Umbelliferae family, including anise, carrots, parsley, celery, dill, and parsnip. Trace amounts have also been isolated from a variety of plant species including Ridolfia segetum (harvest fennel) and species of the Oenanthe genus.
Common Forms and Preparations
Essential oil extracted from nutmeg is used as a flavoring in various products, including soft drinks and cigarettes, sauces, baked goods, processed foods, and condiments, and as a fragrance in perfumes and cosmetics. Exposure to myristicin is largely via ingestion, although inhalation and dermal exposure may be secondary routes, especially for those involved in the farming, transport, or processing of nutmeg.
Pure myristicin may be isolated from natural products, synthesized from pine oil, or derived synthetically from eugenol for research purposes. It is used as a flavoring agent and is often present in beverages and herb-containing products such as cola drinks.
Daily intake of myristicin by ingestion from all sources is estimated to not exceed 1 mg. Myristicin production or distribution is not regulated; moreover, natural and synthetic sources of myristicin are all generally recognized as safe.
2. Traditional and Historical Use
South and Southeast Asia
M. fragrans is indigenous to Southeast Asia, with primary cultivation established in tropical regions including India and Malaysia. Introduced cultivation occurs in China's Hainan and Yunnan provinces. Nutmeg is an important ethnomedicinal resource with both dietary and therapeutic significance in traditional Asian medical systems. Its use dates back to its introduction into China around the 3rd–4th centuries CE. Classical medical texts document its core functions of "warming the middle jiao to promote qi flow, and astringing the intestines to relieve diarrhea."
In Indian Ayurvedic medicine, nutmeg has been used to treat anxiety, nausea, diarrhea, cholera, stomach cramps, parasites, paralysis, and rheumatism and is also used as an aphrodisiac. In Pakistani traditional medicine, the nutmeg plant has been used to treat hypertension.
Traditional Uses Across Cultures
Plant parts of myristicin-containing species have been used in traditional medicine and as flavoring seasoning for cooking. Myristicin has been related with several biological effects, such as anticarcinogenic, anti-inflammatory, antimicrobial, antioxidant, antidiabetic, analgesic, and hepatoprotective. The traditional uses include the treatment of complications related to the gastrointestinal tract, respiratory system, and gynecological disorders.
In the seventeenth century, physicians claimed that a nutmeg pomander was a cure for the bloody flux and the sweating sickness, later called the black plague, and nutmeg was also supposed to have aphrodisiac properties.
Since the Crusades, nutmeg seeds had been used as a hallucinogen and, unsuccessfully, also as an abortifacient. Although nutmeg was historically rumored to have abortifacient properties, these claims have not been substantiated in the recent scientific literature.
According to Stein et al. (2011), the first case of nutmeg poisoning was described in 1576 by Lobel, who reported the ingestion of 10–12 nutmegs (approximately 70–84 g) by a pregnant English lady to induce inebriety.
3. Key Constituents and Context Within the Whole Plant
Phytochemical investigations of Myristica fragrans have identified a total of 328 compounds, with lignans and phenylpropanoids such as macelignan and myristicin recognized as key bioactive substances.
Several compounds were identified in nutmeg and mace, with terpinen-4-ol, β-pinene, and limonene being the dominant compounds common to volatile oil in all species. Although myristicin was found to be responsible for most of the pharmacological effects of nutmeg and mace, it was also reported, together with elemicin, to cause toxic effects.
It is believed that myristicin is mainly responsible for the benefits described with the use of nutmeg, as well as for its toxic effects, since it is the largest compound present in this spice.
The plant is rich in various bioactive compounds, mainly including lignans (macelignan, nectandrin B), phenylpropanoids (methoxyeugenol, myristicin), and volatile oils (sabinene, eugenol).
4. Mechanisms of Action
Monoamine Oxidase (MAO) Inhibition
Myristicin is defined as a naturally occurring compound found in mace and nutmeg, as well as in various other plants, that acts as a weak inhibitor of monoamine oxidase (MAO) and is associated with psychotropic effects, including euphoria and increased alertness, alongside potential toxicological symptoms at high doses. Myristicin is known to be a weak inhibitor of monoamine oxidase (MAO), an enzyme in humans that metabolizes neurotransmitters such as serotonin, dopamine, epinephrine, and norepinephrine. It lacks the basic nitrogen atom that is typical of monoamine oxidase inhibitors (MAOIs), potentially explaining a weaker inhibitory effect.
Cytochrome P450 Enzyme Modulation
Rats administered myristicin (10 to 500 µmol/kg) intraperitoneally exhibited a dose-dependent increase in microsomal cytochrome P450 (CYP) activity, including CYP1A1/1A2, CYP2B1/2B2, and CYP2E1. In mouse cells, myristicin was found to induce CYP1A1.
Biotransformation of myristicin in human liver microsomes to one of its major metabolites, 5-allyl-1-methoxy-2,3-dihydroxy-benzene, was found to be catalyzed by CYP3A4 and, to a lesser extent, CYP1A2.
Female A/J mice orally administered 30 mg myristicin over the course of 6 days exhibited increased levels of hepatic and intestinal glutathione S-transferase (GST) activity. A similar GST activity induction was observed in albino mice, which exhibited a preferential induction of GSTµ expression over GSTπ and GSTα.
Anti-inflammatory Pathways
In general, experimental tests show that myristicin is a potent anti-inflammatory. Several studies report that it is able to inhibit the production of prostaglandins (PGE2), one of the main substances involved in the inflammatory process.
The anti-inflammatory effect of myristicin on double-stranded RNA (dsRNA)-stimulated macrophages has been examined. Myristicin did not reduce the cell viability of RAW 264.7 mouse macrophages at concentrations of up to 50 µM.
Apoptotic and Antiproliferative Signaling
Myristicin inhibited cell proliferation and induced apoptosis in Huh-7 and HCCLM3 hepatocellular carcinoma cells; it suppressed cell migration and invasion ability, and increased E-cadherin expression and decreased N-cadherin expression, thereby inhibiting epithelial–mesenchymal transition (EMT). Additionally, myristicin decreased phosphorylated (p)-mTOR and p-AKT expression at the protein level.
In laboratory studies, myristicin stimulates cytochrome c release, which activates caspase cascades and induces early apoptosis in cells.
Hepatoprotective Mechanisms
Myristicin was found to possess extraordinarily potent hepatoprotective activity. It markedly suppressed lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced enhancement of serum TNF-alpha concentrations and hepatic DNA fragmentation in mice. These findings suggest that the hepatoprotective activity of myristicin might be, at least in part, due to the inhibition of TNF-alpha release from macrophages.
Psychoactive Metabolite Hypothesis
Myristicin and elemicin may be biotransformed into MMDA (3-methoxy-4,5-dimethylene-dioxamphetamine) and TMA (3,4,5-trimethoxyamphetamine), respectively, both consisting of a difference of only an amine group added to the side chain. There has been speculation that myristicin might be converted into the psychedelic MMDA, but this has not been demonstrated in humans. Two nitrogen-containing metabolites of myristicin have been identified in the urine of rats and guinea pigs following oral or intraperitoneal administration. The major basic ninhydrin-positive urinary metabolite of myristicin in the rat is 3-piperidyl-1-(3′methoxy-4′,5′-methylenedioxyphenyl)-1-propanone, while in the guinea pig it is 3-pyrrolidinyl-1-(3′methoxy-4′,5′-methylenedioxyphenyl)-1-propanone.
Whether these aminated metabolites are responsible for the reported psychoactive and psychedelic effects from botanical sources of these allylbenzenes is not known.
5. Scientific Evidence by Area of Use
Important overarching note: No human clinical studies have been performed on myristicin as an isolated compound. Myristicin is a molecule that is still poorly studied and is still not used in therapy, but the few available data point to a promising therapeutic potential. Some reported pharmacological properties of M. fragrans include anticancer, antidepressant, antidiabetic, antiobesity, anti-inflammatory, analgesic, antimicrobial, antioxidant, hepatoprotective, and memory enhancing; however, the clinical efficacy of this plant on various ailments is still to be investigated. All evidence described below is therefore preclinical (in vitro or animal-based) unless otherwise stated.
5.1 Anti-inflammatory Activity
Evidence level: Preclinical (in vitro and in vivo animal studies only)
The anti-inflammatory activity of myristicin in several pathways of the inflammation process is remarkable based on current in vitro and in vivo data. A key in vitro study examined myristicin's behavior in virus-mimetic conditions: the anti-inflammatory effect of myristicin on dsRNA-stimulated macrophages was examined, and myristicin did not reduce the cell viability of RAW 264.7 mouse macrophages at concentrations of up to 50 µM. The analgesic action of myristicin has also been evaluated. Tests conducted with Pycnocycla bashagardiana essential oil containing myristicin did not result in analgesic activity in hot plate tests with mice, despite its good anti-inflammatory action (reduction of paw edema). No human clinical trials exist for myristicin as an anti-inflammatory agent.
5.2 Anticancer / Antiproliferative Activity
Evidence level: Preclinical (in vitro and limited in vivo animal studies only)
The antiproliferative activity of myristicin has been studied in recent years. Literature data report that myristicin is responsible for the anticancer activity of some medicinal plants and is a cancer chemopreventive agent. Crude extract and isolated myristicin were tested in vitro for their antiproliferative activity, at a concentration of 100 µg/mL, against K-562 (human chronic myeloid leukemia), NCI-H460 (human non-small cell lung adenocarcinoma), and MCF-7 (human breast adenocarcinoma) cells using the MTT assay. The extracts and isolated myristicin showed significant antiproliferative activity in the tested cancer cell lines, with inhibition of 50% to 100% of cells at different concentrations.
In the context of hepatic carcinoma, an in vitro study using human hepatic carcinoma cell lines (Huh-7 and HCCLM3) treated myristicin at concentrations of 0.5, 1, and 5 mM for 24, 48, and 72 hours: myristicin inhibited cell proliferation and induced apoptosis; suppressed cell migration and invasion ability; and increased E-cadherin expression and decreased N-cadherin expression, thereby inhibiting EMT. Findings indicated that myristicin decreased phosphorylated mTOR and AKT expression at the protein level. Myristicin exerts an effect on hepatic carcinoma cells by suppressing the PI3K/Akt/mTOR signalling pathway.
Myristicin was shown to induce apoptosis in MCF-7 breast cancer cells by regulating the apoptotic signaling pathway, suggesting potential as an anticancer agent.
Earlier animal research established that myristicin can act as a chemopreventive agent: myristicin induces glutathione S-transferase and inhibits tumorigenesis caused by benzo[a]pyrene in the mouse lung. These findings are considered exploratory; no human cancer trials have been conducted with isolated myristicin.
5.3 Hepatoprotective Activity
Evidence level: Preclinical (in vitro and animal models only)
Myristicin has shown hepatoprotective effects in laboratory rats, as demonstrated in 2003 by Kimio Sugiyama and collaborators at Shizuoka University and the Kagome Company. They found that of 21 spices fed to rats with liver damage, nutmeg showed the most potent protective activity. Mechanistically, myristicin markedly suppressed LPS/D-GalN-induced enhancement of serum TNF-alpha concentrations and hepatic DNA fragmentation in mice, suggesting that the hepatoprotective activity of myristicin might be, at least in part, due to the inhibition of TNF-alpha release from macrophages. However, further studies are needed to elucidate the hepatoprotective mechanism(s) of myristicin.
Myristicin also completely prevented carbon tetrachloride-induced hepatotoxicity in mice. No controlled human trials of hepatoprotection by isolated myristicin have been conducted.
5.4 Antioxidant Activity
Evidence level: Preclinical (in vitro and animal studies only)
Nutmeg kernel extract has demonstrated antioxidant, anti-inflammatory, and anti-apoptotic properties, and its hepatoprotective effect is linked to its ability to promote the nuclear factor erythroid 2-related factor (Nrf2) pathway. Myristicin could effectively modulate important stress and inflammatory effectors and protect mucosal DNA from oxidative damage, serving as a promising candidate for the treatment of ulcerative colitis. These conclusions derive from animal and cell-based models; no human clinical evidence currently exists.
5.5 Antimicrobial Activity
Evidence level: Preclinical (in vitro only)
Myristicin emerged as the key contributor to antimicrobial and antibiofilm activity in essential oil of Athamanta sicula. The results highlight the relevance of this essential oil as a myristicin-rich oil with notable in vitro biological activity. Myristicin has been known to have anti-cholinergic, antibacterial, and hepatoprotective effects. Evidence in this area is limited to in vitro microbial inhibition assays, with no human infection trials.
5.6 Psychoactive and Central Nervous System (CNS) Effects
Evidence level: Case reports and animal studies; no controlled human trials
Myristicin is active at the 5-HT receptors in the brain, and has been shown to have hypotensive, sedative, anti-depressant, anesthetic, hallucinogenic, and serotonergic properties in preclinical settings. Large doses generally cause hyper-excitability, followed by CNS depression.
Rats and guinea pigs dosed with myristicin (5 to 20 mg/kg intraperitoneal injection) were hyperactive for the first 30 minutes after exposure and then became sedated and nonresponsive for up to 2 hours.
These components demonstrate multiple pharmacological activities, including neuroprotective, gastrointestinal regulatory, and hypoglycemic effects in preclinical models. Network pharmacology studies have preliminarily revealed potential targets and pathways of nutmeg in the nervous system, anti-inflammatory effects, and metabolic regulation. All such data derive from preclinical work.
5.7 Insecticidal Activity
Evidence level: In vitro / ex vivo laboratory studies
Isolated myristicin has proven an effective insecticide against many agricultural pests, including Aedes aegypti mosquito larvae, Spilosoma obliqua (hairy caterpillars), Epilachna varivestis (Mexican bean beetles), Acyrthosiphon pisum (pea aphids), mites, and Drosophila melanogaster (fruit flies). Myristicin was shown to be an effective repellent, and to cause mortality via direct and systemic exposure.
6. Body Systems and Health Areas of Association
- Gastrointestinal system: Nutmeg was used in ancient times (in India and other regions of Asia) to treat anxiety, stomach cramps, nausea, and diarrhea.
- Hepatic (liver) system: Myristicin demonstrates potent hepatoprotective effects against toxin-induced liver injury in animal models, through inhibition of TNF-alpha and modulation of antioxidant pathways.
- Oncology (experimental): Preclinical antiproliferative activity across multiple cancer cell lines via PI3K/Akt/mTOR pathway suppression and induction of apoptosis.
- Central nervous system / neurological: Myristicin has been shown to have hypotensive, sedative, anti-depressant, anesthetic, hallucinogenic, and serotonergic properties in preclinical settings, with known MAO-inhibitory activity.
- Immune and inflammatory system: Reduction of PGE2, TNF-alpha, and NO production demonstrated in cell-based models.
- Antimicrobial: In vitro inhibition of bacterial and biofilm growth across multiple studies.
- Respiratory system: Traditional uses include the treatment of complications related to the gastrointestinal tract, respiratory system, and gynecological disorders.
7. Dosage Forms and Reported Dosages in Studies
Daily intake of myristicin by ingestion from all sources is estimated to not exceed 1 mg. Dosages used in specific preclinical studies include:
- Rats administered myristicin intraperitoneally at 10 to 500 µmol/kg exhibited dose-dependent increases in CYP enzyme activity.
- Female A/J mice given 30 mg myristicin orally over 6 days exhibited increased hepatic and intestinal GST activity.
- Myristicin did not reduce the cell viability of RAW 264.7 mouse macrophages at concentrations up to 50 µM in in vitro studies.
- Myristicin was tested in vitro against multiple cancer cell lines at a concentration of 100 µg/mL using the MTT assay.
- Human hepatic carcinoma cell lines were treated with myristicin at concentrations of 0.5, 1, and 5 mM for 24, 48, and 72 hours in the hepatocellular carcinoma study.
- Rats and guinea pigs dosed with myristicin at 5 to 20 mg/kg by intraperitoneal injection in CNS effect studies.
- In the toxicological context, the minimum dosage of nutmeg that can cause a psychogenic effect is 5 g (ground nutmeg) with 1 to 2 mg myristicin content, which is considered a 'toxic dose.'
No established therapeutic or supplemental dosage for isolated myristicin in humans exists in the peer-reviewed literature.
8. Safety, Toxicology, and Drug Interactions
Overview of Toxicological Profile
Toxic outcomes related to myristicin in humans are largely associated with acute overdoses of nutmeg. Ingestion of excessive amounts of nutmeg (as little as one and a half seeds and up to 19 seeds) can result in a delirious stupor, with a combination of stimulation and drowsiness or weakness similar to opium and other narcotics. Patients with nutmeg overdose present with facial flushing, tachycardia, hypertension, blurred vision, dry mouth, psychoactive hallucinations, and feelings of euphoria, anxiety, and fear; symptoms typically subside after 24 to 36 hours.
Those symptoms usually occur 3 to 6 hours after ingestion of myristicin or foodstuffs containing it, and effects may persist up to 72 hours.
Acute Poisoning and Fatalities
In recent years, many cases of nutmeg poisoning have been reported, including several fatal myristicin cases. Such poisonings can result not only from the toxic effect of myristicin itself but also from the combined toxic effects of its use with other substances.
In literature, cases of nutmeg abuse have been described repeatedly, but only one fatal case of poisoning was reported. In this case, myristicin (4 µg/ml) was detected in the postmortem serum of a 55-year-old woman. Identification was achieved with UV-VIS spectroscopy and TLC; for quantification, HPLC was used. Because flunitrazepam (0.072 µg/ml) was also found, death had probably been due to the combined toxic effect of both substances.
From 1996 to 1998, seven poisonings with nutmeg were recorded by the Erfurt Poison Information Centre. Even where higher doses (20–80 g of powder) had been ingested, a life-threatening situation was never observed.
Organ-Level Toxicity (Preclinical)
Increased liver weights (absolute and relative) occurred in the 100 mg/kg groups of male and female rats and mice in NTP studies, and centrilobular hepatocellular hypertrophy also occurred in 100 mg/kg female mice. The increases in liver weights and incidences of hepatocellular hypertrophy may have been due in part to the induction of cytochrome P450 enzyme systems. Myristicin has been shown to induce the P450 enzymes CYP1A1/2, CYP2B1/2, and CYP2E1.
In a 42-day study in adult Wistar rats, oral administration of nutmeg spice (500 and 1,000 mg/kg) displayed degeneration and atrophy of the kidney. However, in another study, male white rats administered 10 mg/kg myristicin per day for 26 days exhibited no changes in body weight and no abnormalities of the liver or kidney.
A dose-dependent reduction in cell viability occurs at myristicin concentration ≥0.5 mM in SK-N-SH (human neuroblastoma) cells. Apoptotic cell death was confirmed using DNA fragmentation, terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling, and DAPI staining. Western blotting revealed that the apoptosis triggered by myristicin was accompanied by an accumulation of cytochrome c and by the activation of caspase-3. The results suggest that myristicin induces cytotoxicity in human neuroblastoma SK-N-SH cells by an apoptotic mechanism.
Metabolic Activation and Reactive Metabolites
In the liver, myristicin has been metabolized by CYP450 enzymes to generate an active metabolite (1′-hydroxymyristicin) responsible for cytotoxic, genotoxic, and apoptotic effects (at 150 µM). Myristicin at 600 µM does not produce enough 1′-hydroxymyristicin to yield the final toxic metabolite.
A panel of predictive models developed using alkenylbenzene toxicology data from subchronic studies suggested that when compared against known hepatocarcinogenic alkenylbenzenes, myristicin would likely be a weak carcinogen if studied at a dose level of 2 mmol/kg body weight per day for 2 years in male F344 rats. To date, there have been no 2-year exposure studies on myristicin to investigate carcinogenicity.
Drug Interactions
Myristicin has also been shown to inhibit cytochrome P450 enzymes, which are responsible for metabolizing a variety of substrates including hormones and toxins, allowing these substrates to accumulate.
While smaller concentrations of MAOIs may not cause problems, there are additional warnings regarding drug interactions. Those taking antidepressants that are MAOIs (such as phenelzine, isocarboxazid, tranylcypromine, or selegiline) or taking selective serotonin reuptake inhibiting (SSRI) antidepressants should avoid essential oils rich in myristicin, such as those of nutmeg and anise.
Recreational Abuse and Intoxication
In the modern era, overdoses are more likely to occur due to intentional ingestion of nutmeg as an inexpensive and legal alternative or addition to other abuse substances. California Poison Control System electronic database data shows 72.3% of exposures between 1997 and 2008 were intentional for recreational purposes, predominantly among individuals between ages 13 and 20.
General Population Exposure
Myristicin poses no major risk to human health through the consumption of herbs and spices due to its presence in low amounts. The estimated intake of myristicin from dietary sources by the general population is a few mg daily.
9. Current Research Status and Evidence Gaps
Myristicin, a substance of natural origin, has shown several promising activities in a large number of in vitro and in vivo studies. Considering the need of the pharmaceutical industry to obtain new treatments for diseases such as cancer and infections, it becomes relevant to clinically evaluate the use of substances that have shown therapeutic potential in preliminary studies. Researchers are encouraged to explore this promising molecule and carry out more detailed studies about its mechanism of action, especially on its anti-inflammatory, antiproliferative, and antioxidant activities.
Most studies on the pharmacological properties of M. fragrans and its constituents focus on in vivo and in vitro models. Current clinical research remains limited. A 2019 study by the National Toxicology Program on the effects of myristicin on female and male rats and mice showed some minor physiological problems but no substantial adverse effects. No human studies have been performed on myristicin.
References
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