Can CBD oil help with stomach ulcers, and if so, how?

Stomach ulcers, also known as gastric ulcers, are a type of peptic ulcer disease. ‘Peptic’ ulcer is the umbrella term for any ulcer affecting the stomach and the small intestines.

The stomach usually produces acid to help with the digestion of food and protect against bacteria and other microbes.

Meanwhile, cells on the inside lining of the stomach and first portion of the small intestine (duodenum) produce a natural mucus barrier to protect the tissues of the body from this acid. 

There is usually a balance between the amount of acid that the body makes and the mucus defence barrier – as well as the amount of base produced by the pancreas.

Ulcers may develop if there is an alteration in this balance, allowing the acid to damage the lining of the stomach or duodenum.

Stomach ulcers are characterized by open sores in the lining of the stomach. While small ulcers may not cause noticeable symptoms, larger ones can cause pain and discomfort (1)

Ulcer symptoms are often worse on an empty stomach and at night. Ulcer symptoms include:

  • Discomfort or burning pain in the upper abdomen
  • Feeling bloated
  • Burping
  • Nausea
  • Vomiting
  • Heartburn
  • Weight loss and lack of appetite
  • Dark black stools

CBD for Stomach Ulcers: What The Research Says 

There is evidence that cannabinoids like CBD and THC have a positive physiological impact on stomach pathology, including ulcers. 

According to research, there is evidence that CB1 receptor stimulation with cannabinoids inhibits gastric acid secretion in humans and experimental animals (2).

Studies have shown that CBD can decrease gastric acid and increase blood flow to the lining of the stomach.

Researchers of a 2016 study published in Current Neuropharmacology found that direct activation of CB1 receptors by cannabinoids effectively reduces both gastric acid secretion and gastric motor activity and decreases the formation of lesions on the stomach lining (3).

A study examined how cannabinoids impact the gastrointestinal tract of some species, like the mouse, rat, guinea pig, and humans (4).

In another study published in Pharmacology Journal, researchers found that delta-9-tetrahydrocannabinol (THC) inhibited ulcer formation in animal models (5). 

Although the studies did not focus on the cannabinoid CBD, the results are still encouraging. The authors believe the endocannabinoid system represents a promising target in the treatment of gastric mucosal lesions, ulceration and inflammation.

CBD  for Pain Relief

Prescription medication is not the only reliable scientific solution to treating conditions, such as stomach ulcers. 

Chemical-based painkillers have even been known to cause stomach ulcers in the first place.

According to the National Health Service (NHS) of the United Kingdom, taking non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or aspirin, can cause stomach or duodenal ulcers, particularly if these pharmaceuticals are taken for an extended period or at high doses (6). 

Meanwhile, CBD may also help provide effective pain relief from the invasion of stomach ulcers. 

Studies have shown that CBD may have promise in helping provide pain relief. CBD may be useful in treating different types of chronic pain (7). 

Chronic pain, particularly neuropathic pain, is a problem that is difficult to treat, according to the author of a study on neuronal mechanisms for neuropathic pain (8).

CBD for Nausea

Nausea is a feeling or urge to vomit. It can develop for several reasons, including medications, chemotherapy, food poisoning, morning sickness, general anesthesia, and migraines (9).

Nausea and vomiting both play an essential, defensive role by rejecting the ingestion or digestion of potentially harmful substances.

Cannabis has long been known to prevent or regulate nausea and vomiting from a variety of causes (10).

The studies demonstrated that primary cannabinoids, tetrahydrocannabinol (THC) and cannabidiol (CBD), have both been useful at regulating vomiting and nausea because they interact with cannabinoid receptor 1 (CBB1) of the endocannabinoid system. 

Activating the CB1 receptor suppresses vomiting, as noted in the review published in the journal Psychopharmacology (11). 

Studies have shown that CBD’s effectiveness at producing anti-nausea effects may also be in part of its indirect activation of the 5-HT-1A autoreceptors in the “vomiting center” or “chemoreceptor trigger zone” of the brain stem (12).

Activation of 5-HT1A heteroreceptors in these areas releases serotonin  (13). 

Serotonin is found mostly in the digestive system, although it is also in blood platelets and throughout the central nervous system.

Serotonin is sometimes called “the happy chemical” because it contributes to feelings of well-being and happiness.

Conclusion

CBD’s purported therapeutic benefits may help with symptoms of stomach ulcers. However, more research is needed to validate the results of the studies.

WHO states that CBD “is generally well-tolerated with a good safety profile.” (14) Still, the long-term effects of CBD remain unknown, and the compound may also interact with other pharmaceuticals.

Thus, individuals looking to try CBD for the first time, or intend to use CBD as an adjunct therapy, should first consult with a doctor experienced in cannabis use for advice.


  1. WakeMed. Stomach Ulcers. Retrieved from https://www.wakemed.org/stomach-ulcers.
  2. Abdel-Salam O. Gastric acid inhibitory and gastric protective effects of Cannabis and cannabinoids. Asian Pac J Trop Med. 2016;9(5):413–419. DOIi:10.1016/j.apjtm.2016.04.021.
  3. Gyires K, Zádori ZS. Role of Cannabinoids in Gastrointestinal Mucosal Defense and Inflammation. Curr Neuropharmacol. 2016;14(8):935–951. DOI:10.2174/1570159×14666160303110150.
  4. Pertwee RG. Cannabinoids and the gastrointestinal tract. Gut. 2001;48(6):859–867. DOI:10.1136/gut.48.6.859.
  5. Sofia RD, Diamantis W, Harrison JE, Melton J. Evaluation of antiulcer activity of delta9-tetrahydrocannabinol in the Shay rat test. Pharmacology. 1978;17(3):173–177. DOI:10.1159/000136851.
  6. NHS Inform. (2020, Feb 14). Stomach Ulcer. Retrieved from https://www.nhsinform.scot/illnesses-and-conditions/stomach-liver-and-gastrointestinal-tract/stomach-ulcer.
  7. Grinspoon, P. (2019, Aug 27). Cannabidiol (CBD) — what we know and what we don’t. Retrieved from https://www.health.harvard.edu/blog/cannabidiol-cbd-what-we-know-and-what-we-dont-2018082414476.
  8. Zhuo M. Neuronal mechanism for neuropathic pain. Mol Pain. 2007;3:14. Published 2007 Jun 6. DOI:10.1186/1744-8069-3-14.
  9. ECHO. (2017, Feb 17). Nausea: Cannabinoids and CBD Research Overview. Retrieved from https://echoconnection.org/nausea-medical-cannabis-and-cbd-research-overview/.
  10. Parker, L.A., Rock, E.M., Sticht, M.A., Wills, K.L., and Limebeer, C.L. (2015). Cannabinoids suppress acute and anticipatory nausea in preclinical rat models of conditioned gaping. Clinical Pharmacology and Therapeutics, 97(6), 559-61;  Sharkey, K.A., Darmani, N.A., and Parker, L.A. (2014). Regulation of nausea and vomiting by cannabinoids and the endocannabinoid system. European Journal of Pharmacology, 722, 134-4.
  11. Parker, L.A., Mechoulam, R., Schlievert, C., Abbott, L., Fudge, M.L., and Burton, P. (2003, March). Effects of cannabinoids on lithium-induced conditioned rejection reactions in a rat model of nausea. Psychopharmacology, 166(2), 156-62.
  12. Rock EM, Bolognini D, Limebeer CL, et al. Cannabidiol, a non-psychotropic component of cannabis, attenuates vomiting and nausea-like behaviour via indirect agonism of 5-HT(1A) somatodendritic autoreceptors in the dorsal raphe nucleus. Br J Pharmacol. 2012;165(8):2620–2634. DOI:10.1111/j.1476-5381.2011.01621.x.  
  13. Garcia-Garcia AL, Newman-Tancredi A, Leonardo ED. 5-HT(1A) [corrected] receptors in mood and anxiety: recent insights into autoreceptor versus heteroreceptor function [published correction appears in Psychopharmacology (Berl). 2014 Feb;231(4):637]. Psychopharmacology (Berl). 2014;231(4):623–636. doi:10.1007/s00213-013-3389-x.
  14. WHO. Expert Committee on Drug Dependence. (2017, Nov 6-10). Cannabidiol (CBD). Retrieved from https://www.who.int/medicines/access/controlled-substances/5.2_CBD.pdf.  

More Info

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CIMETIDINE

(Group 3)

For definition of Groups, see Preamble Evaluation.

 

VOL.: 50 (1990) (p. 235)

 

CAS No.: 51481-61-9

Chemical Abstr. Name: Guanidine N-cyano-N’-methyl-N”-(2-{[(5-methyl-1H-imidazol-

4-yl)methyl]thio}ethyl)-

 

  1. Summary of Data Reported and Evaluation

5.1 Exposure data

Cimetidine is a histamine H2-receptor antagonist which inhibits gastric acid secretion. Since its introduction in the mid-1970s, it has been used widely by oral administration for the treatment of duodenal and gastric ulcers.

 

Although cimetidine can be nitrosated in vitro in the presence of nitrite under acidic conditions to form N-nitrosocimetidine, no study in experimental animals or in humans has demonstrated that this reaction occurs in vivo.

 

5.2 Experimental carcinogenicity data

Cimetidine was tested for carcinogenicity by oral administration in single studies in mice, rats and dogs. In the experiment in mice, dams were treated throughout life beginning two weeks prior to pregnancy, with no increase in tumour incidence. In female progeny that were exposed throughout life from conception, there was an increase in the incidence of lymphomas, although these tumours also occurred at relatively high rates in control animals. In rats, an increase in the incidence of benign Leydig-cell tumours of the testis was observed in the low- and high-dose groups but not in the mid-dose group. The study in dogs was inadequate for evaluation.

 

In a study in which mice were exposed from conception throughout life to a combination of cimetidine and sodium nitrite, males had an increased incidence of lung neoplasms, although these tumours also occurred at a high frequency in control animals.

 

N-Nitrosocimetidine was tested for carcinogenicity by oral administration in mice and rats and by skin application in mice. The experiments in rats and three of the studies in mice were inadequate for evaluation. In one study by oral administration in mice, there was no increase in the incidence of tumours.

 

5.3 Human carcinogenicity data

In a large number of case reports, cancer, particularly gastric cancer, was diagnosed at various intervals after the start of cimetidine therapy. These reports are difficult to interpret because gastric cancer is a common malignancy and cimetidine is a commonly used drug, and coincidence cannot be ruled out.

 

Three cohort studies showed increased incidences of gastric cancer but also of other gastrointestinal cancers among cimetidine users; however, as for the case reports, the association could well have been due to the drug being given for symptoms of pre-existing cancers. This interpretation is supported by a diminution of the association with increasing duration of follow-up. Two of the studies also showed an association between cimetidine use and lung cancer, but confounding with cigarette smoking could well have been the explanation.

 

5.4 Other relevant data

Cimetidine has been associated with reversible impotence and other antiandrogenic effects in men.

 

N-Nitrosocimetidine is rapidly converted to cimetidine in vivo in experimental animals.

 

Cimetidine did not induce single-strand breaks in DNA from rats treated in vivo, nor did it methylate DNA in a variety of tissues of rats in vivo. It did not induce single-strand breaks in the DNA of rat cells treated in vitro. Cimetidine was not mutagenic to and did not cause DNA damage in Salmonella typhimurium or Escherichia coli. Cimetidine hydrochloride induced single-strand breaks and unscheduled DNA synthesis in rat but not human cells in vitro. It did not cause sister chromatid exchange in human cells in vitro.

 

Cimetidine in combination with sodium nitrite did not induce DNA damage in vivo or methylate DNA in a variety of tissues of rats in vivo. Gastric juice from cimetidine-treated patients was mutagenic to bacteria when enriched with nitrite.

 

N-Nitrosocimetidine has not been demonstrated in gastric juice of humans; however, increased gastric concentrations of nitrite and total N-nitroso compounds have been reported in some studies of patients taking cimetidine. N-Nitrosocimetidine induced DNA damage, sister chromatid exchange, chromosomal aberrations and morphological transformation in mammalian cells in vitro and caused DNA damage and mutation in bacteria. Radiolabelled N-nitrosocimetidine methylated DNA in a variety of tissues of rats in vivo.

 

5.5 Evaluation

There is inadequate evidence for the carcinogenicity of cimetidine in humans.

 

There is inadequate evidence for the carcinogenicity of cimetidine in experimental animals.

 

Overall evaluation

Cimetidine is not classifiable as to its carcinogenicity to humans (Group 3).

 

For definition of the italicized terms, see Preamble Evaluation.

 

Synonyms

Acibilin

Aciloc

Acinil

Altramet

Cianosel

‘Cim’

Cimal

Cimegan

Cimet

Cimetid

Cimetidina

Cimetin

Cimetum

Cinamet

Cinulcus

Citimid

Citius

Climatidine

2-Cyano-1-methyl-3-[2-(5-methylimidazo-4-ylmethylthio)ethyl]guanidine

Dina

Duncamet

Duogastril

Duractin

Dyspamet

Edalene

Etidine

Eureceptor

Evicer

Fisiol

Fremet

Gasmetin

Gastrobitan

Gastro H2

Gastromet

Himetin

Itacem

Lucimet

Lucomet

Mansal

Nimus (Udine) gadol

Notrul

Novocimetine

Peptol

Prometidine

Regastric

SKF 92334

Stomakon

Tagacid

Tagama

Tagagel

Tagamet

Tametin

Temic

Tratul

Tratul Retard (SR)

Ulcedine

Ulcenon

Ulcerdine

Ulcerfen

Ulcestop

Ulcidin

Ulcimet

Ulcodina

Ulcomedina

Ulhys

Vagolisal

Valmagen

Last updated: 11 November 1997

    

 

Myristica fragrans Houtt.

  1. NAME

   1.1 Scientific name

   1.2 Family

   1.3 Common name(s) and synonym(s)

  1. SUMMARY

   2.1 Main risks and target organs

   2.2 Summary of clinical effects

   2.3 Diagnosis

   2.4 First-aid measures and management principles

   2.5 Poisonous parts

   2.6 Main toxins

  1. CHARACTERISTICS

   3.1 Description of the plant

      3.1.1 Special identification features

      3.1.2 Habitat

      3.1.3 Distribution

   3.2 Poisonous parts of the plant

   3.3 The toxin(s)

      3.3.1 Name(s)

      3.3.2 Description, chemical structure, stability

      3.3.3 Other physico-chemical characteristics

   3.4 Other chemical contents of the plant

  1. USES/CIRCUMSTANCES OF POISONING

   4.1 Uses

      4.1.1 Uses

      4.1.2 Description

   4.2 High risk circumstances

   4.3 High risk geographical areas

  1. ROUTES OF EXPOSURE

   5.1 Oral

   5.2 Inhalation

   5.3 Dermal

   5.4 Eye

   5.5 Parenteral

   5.6 Others

  1. KINETICS

   6.1 Absorption by route of exposure

   6.2 Distribution by route of exposure

   6.3 Biological half-life by route of exposure

   6.4 Metabolism

   6.5 Elimination and excretion

  1. TOXINOLOGY

   7.1 Mode of action

   7.2 Toxicity

      7.2.1 Human data

         7.2.1.1 Adults

         7.2.1.2 Children

      7.2.2 Relevant animal data

      7.2.3 Relevant in vitro data

   7.3 Carcinogenicity

   7.4 Teratogenicity

   7.5 Mutagenicity

   7.6 Interactions

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

   8.1 Material sampling plan

      8.1.1 Sampling and specimen collection

         8.1.1.1 Toxicological analyses

         8.1.1.2 Biomedical analyses

         8.1.1.3 Arterial blood gas analysis

         8.1.1.4 Haematological analyses

         8.1.1.5 Other (unspecified) analyses

      8.1.2 Storage of laboratory samples and specimens

         8.1.2.1 Toxicological analyses

         8.1.2.2 Biomedical analyses

         8.1.2.3 Arterial blood gas analysis

         8.1.2.4 Haematological analyses

         8.1.2.5 Other (unspecified) analyses

      8.1.3 Transport of laboratory samples and specimens

         8.1.3.1 Toxicological analyses

         8.1.3.2 Biomedical analyses

         8.1.3.3 Arterial blood gas analysis

         8.1.3.4 Haematological analyses

         8.1.3.5 Other (unspecified) analyses

   8.2 Toxicological Analyses and Their Interpretation

      8.2.1 Tests on toxic ingredient(s) of material

         8.2.1.1 Simple Qualitative Test(s)

         8.2.1.2 Advanced Qualitative Confirmation Test(s)

         8.2.1.3 Simple Quantitative Method(s)

         8.2.1.4 Advanced Quantitative Method(s)

      8.2.2 Tests for biological specimens

         8.2.2.1 Simple Qualitative Test(s)

         8.2.2.2 Advanced Qualitative Confirmation Test(s)

         8.2.2.3 Simple Quantitative Method(s)

         8.2.2.4 Advanced Quantitative Method(s)

         8.2.2.5 Other Dedicated Method(s)

      8.2.3 Interpretation of toxicological analyses

   8.3 Biomedical investigations and their interpretation

      8.3.1 Biochemical analysis

         8.3.1.1 Blood, plasma or serum

         8.3.1.2 Urine

         8.3.1.3 Other fluids

      8.3.2 Arterial blood gas analyses

      8.3.3 Haematological analyses

      8.3.4 Interpretation of biomedical investigations

   8.4 Other biomedical (diagnostic) investigations and their interpretation

   8.5 Overall interpretation of all toxicological analyses and toxicological investigations

   8.6 References

  1. CLINICAL EFFECTS

   9.1 Acute poisoning:

      9.1.1 Ingestion

      9.1.2 Inhalation

      9.1.3 Skin exposure

      9.1.4 Eye contact

      9.1.5 Parenteral exposure

      9.1.6 Other

   9.2 Chronic poisoning

      9.2.1 Ingestion

      9.2.2 Inhalation

      9.2.3 Skin exposure

      9.2.4 Eye contact

      9.2.5 Parenteral exposure

      9.2.6 Other

   9.3 Course, prognosis, cause of death

   9.4 Systematic description of clinical effects

      9.4.1 Cardiovascular

      9.4.2 Respiratory

      9.4.3 Neurological

         9.4.3.1 Central nervous system (CNS)

         9.4.3.2 Peripheral nervous system

         9.4.3.3 Autonomic nervous system

         9.4.3.4 Skeletal and smooth muscle

      9.4.4 Gastrointestinal

      9.4.5 Hepatic

      9.4.6 Urinary

         9.4.6.1 Renal

         9.4.6.2 Other

      9.4.7 Endocrine and reproductive systems

      9.4.8 Dermatological

      9.4.9 Eye, ear, nose, throat: local effects

      9.4.10 Haematological

      9.4.11 Immunological

      9.4.12 Metabolic

         9.4.12.1 Acid-base disturbances

         9.4.12.2 Fluid and electrolyte disturbances

         9.4.12.3 Others

      9.4.13 Allergic reactions

      9.4.14 Other clinical effects

      9.4.15 Special risks

   9.5 Other

   9.6 Summary

  1. MANAGEMENT

   10.1 General principles

   10.2 Life supportive procedures and symptomatic/specific treatment

   10.3 Decontamination

   10.4 Enhanced elimination

   10.5 Antidote/antitoxin treatment

      10.5.1 Adults

      10.5.2 Children

   10.6 Management discussion

  1. ILLUSTRATIVE CASES

   11.1 Case reports from literature

  1. ADDITIONAL INFORMATION

   12.1 Specific preventative measures

   12.2 Other

  1. REFERENCES
  2. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)

 

    MYRISTICA FRAGRANS

 

    International Programme on Chemical Safety

    Poisons Information Monograph 355

    Plant

 

  1. NAME

 

        1.1  Scientific name

 

             Myristica fragrans Houtt.

 

        1.2  Family

 

             Myristicaceae

 

        1.3  Common name(s) and synonym(s)

 

             mace (UK); muscadier (France); Muskatbaum

             (Germany); myristica; nuez moscada (Uruguay, Spain);

             nutmeg (UK); nutmeg tree (UK); nux moschata;

             Myristica officinalis L.

 

  1. SUMMARY

 

        2.1  Main risks and target organs

 

             -transient psychosis

    

             -possibility of fatty liver and hepatic necrosis

    

             -transient renal toxicity

    

             -possible carcinogen and teratogen

    

             -possibility of death occurring

 

        2.2  Summary of clinical effects

 

             Nutmeg intoxication resembles anticholinergic

             intoxication, e.g. profuse sweating, flushed face, delirium,

             dry throat etc.  There is always an altered state of mind,

             e.g. hallucinations, confusion and an impending sense of

             doom.  Clinical symptoms may be contradictory depending on

             the length of time lapsed after ingesting the toxin. 

             Symptoms also vary according to the dose taken and the

             variability between different samples of nutmegs.

 

        2.3  Diagnosis

 

             Blood: for electrolytes, liver enzymes and renal

             function tests; plus urinalysis.

 

        2.4  First-aid measures and management principles

 

             Management

    

             Treatment is symptomatic and supportive.  The use of

             cathartics, gastric lavage or ipecac may be beneficial if

             they are not contraindicated.  A sedative and anticonvulsant

             may be administered to calm the patient and combat seizures

             should they occur.  A liquid diet high in protein and

             carbohydrate, but low in fat, is recommended.

 

        2.5  Poisonous parts

 

             The seeds (nutmeg) and, to a lesser extent, the aril

             (mace).

 

        2.6  Main toxins

 

             Myristicin and elemicin, but intoxication is not thought

             to be due to these alone.

 

  1. CHARACTERISTICS

 

        3.1  Description of the plant

 

             3.1.1  Special identification features

 

  1. fragrans is a spreading aromatic evergreen

                    tree usually growing to around 5 to 13 metres high,

                    occasionally 20 metres.  The bark contains watery pink

                    or red sap.  The pointed dark green leaves (5 to 15 cm

                    × 2 to 7 cm) are arranged alternately along the

                    branches and are borne on leaf stems about 1 cm long. 

                    Upper leaf surfaces are shiny.  Flowers are usually

                    single sexed; occasionally male and female flowers are

                    found on the same tree.  Female flowers arise in

                    groups of 1 to 3; males in groups of 1 to 10.  Flowers

                    are pale yellow, waxy, fleshy and bell-shaped.  Male

                    flowers are 5 to 7 mm long; female flowers are up to

                    1 cm long.  The fruits are fleshy, drooping, yellow,

                    smooth, 6 to 9 cm long with a longitudinal ridge. 

                    When ripe, the succulent yellow fruit coat splits into

                    2 valves revealing a purplish-brown, shiny seed

                    (nutmeg) surrounded by a red aril (mace).  Seeds

                    (nutmegs) are broadly ovoid (2 to 3 cm long), firm,

                    fleshy, whitish and transversed by red-brown veins. 

                    When fresh, the aril (mace) is bright scarlet becoming

                    more horny, brittle and a yellowish-brown colour when

                    dried (Purseglove, 1968).

    

 

                    The tree does not flower until around 9 years old,

                    when it fruits; it can continue to do so for a further

                    75 years.  The tree bears 2 to 3 crops a year.  The

                    seeds (nutmegs) need 3 to 6 weeks to dry before they

                    are ready for use.

 

             3.1.2  Habitat

 

                    Grows wild on rich volcanic soils in lowland

                    tropical rain forests.  Its cultivation as a crop is

                    largely confined to islands in the hot, humid tropics

                    at altitudes up to 4,500 metres (Purseglove,

                    1968).

 

             3.1.3  Distribution

 

                    Indigenous to the Moluccas and Banda Islands in

                    the South Pacific although it is seldom found truly

                    wild.  It is now cultivated in tropical regions,

                    especially Indonesia, Grenada in the West Indies and

                    Sri Lanka (Purseglove, 1968; Bown, 1995).

 

        3.2  Poisonous parts of the plant

 

             Seeds (nutmegs) and to a lesser extent the aril

             (mace).

    

             Nutmeg oil:

    

             Nutmeg oil is also known as oleum myristicae, ol. myrist.,

             myristica oil, essence de muscade, atheririsches muskatol,

             essencia de moscada and essencia de nuez moscada.  It is a

             volatile oil obtained by steam distillation from the seed. 

             It is a colourless or pale yellow liquid with an odour and

             taste of nutmeg.  It is scarcely distinguishable from the

             volatile oil of mace and frequently no commercial distinction

             is made between the two.  There are two types of nutmeg oil,

             mainly East Indian Nutmeg Oil and West Indian Nutmeg Oil. 

             The East Indian Nutmeg Oil has a weight of 0.885 to 0.915

             g/mL and is soluble in 90% alcohol at a ratio of 1 part oil

             to 3 parts alcohol.  West Indian Nutmeg Oil has a weight of

             0.86-0.88 g/mL and is soluble in 90% alcohol at a ratio of 1

             part oil to 4 parts alcohol.  Nutmeg oil should be stored in

             a cool place in well filled airtight containers and protected

             from light.

    

             Nutmeg Butter:

    

             Nutmeg butter, also known as balsam of nutmegs, oil of mace,

             butter of mace, Banda soap and oleum myristicae expressum is

             the fixed oil component of the seed (nutmeg).  It accounts

             for 25 to 40% of the nutmeg’s weight and it is a solid at

 

             room temperature.  Sometimes it occurs in the form of

             prismatic crystals.  It is obtained by exposing the nuts to

             hydraulic pressure and heat.

    

             Pharmacologically active parts of the plant:

    

             The most important part of the plant in terms of its

             pharmacological activity and also in commerce, is of course

             the dried kernel (seed), the nutmeg.  Intoxication from the

             use of the aril of the fruit (seed case), generally known as

             mace, has also been reported, but only rarely.  The oil of

             nutmeg has also been used for medicinal purposes and it is

             this fraction of the nutmeg which is strongly suspected of

             harbouring the pharmacologically active components of

             nutmeg.

 

        3.3  The toxin(s)

 

             No single component of the nutmeg has been identified as

             responsible for all the symptoms seen during intoxication. 

             It is widely believed that myristicin is the major component

             responsible, however, it alone cannot reproduce all the

             symptoms.  Shulgin (1966) suggests that myristicin and

             elemicin may not be the active ingredients but they may be

             metabolized in the body to 3-methoxy-4,5-methylenedioxy

             amphetamine (MMDA) and elemicine, an ether analogous to

             myristicin, 3,4,5-trimethoxy amphetamine (TMA).

 

             3.3.1  Name(s)

 

                    Myristicin:

                    CAS number:   607-91-0

                    Molecular formula: C11H12O3

                    Molecular weight: 192.21

    

                    Elemicin:

                    CAS number:  487-11-6

                    Molecular formula:  C12H16O3

                    Molecular weight: 208.26

                    (Harborne & Baxter, 1996).

 

             3.3.2  Description, chemical structure, stability

 

                    Components of nutmeg

    

                    The major components in M. fragrans are terpenes,

                    terpene alcohols and phenolic ethers.  The major

                    phenolic ether is myristicin (4-methoxy-6-(2-

                    propenyl)-1,3-benzadioxole) accompanied by safrole

                    (5-(2-propenyl)-3-benzodioxole) and eugenol methyl

                    ether (3,4,-dimethoxy-(2-propenyl)-benzene). 

                    Myristicin accounts for about 2.12 to 2.88% of the

                    total weight of the nutmeg where as safrole accounts

 

                    for 0.27 to 0.39%.  The volatile oil content of nutmeg

                    depends on the geographical origin and length of

                    storage.  Chemical analysis has shown that even though

                    there is a real variability between the quality

                    (differences in composition) and quantity of nutmeg

                    oil from various samples of nutmegs oil accounts for

                    84 to 95% of the total aromatic fraction of the

                    volatile oil from all the samples tested.  In the

                    samples, myristicin, safrole and elemicin accounted

                    for 3.86 to 12.7%, 0.53 to 3.42% and 0.02 to 2.36%,

                    respectively of the nutmeg oil samples.  Early work on

                    myristicin used myristicin distilled from nutmeg oil. 

                    It has been subsequently proven that myristicin

                    extracted from nutmeg via this method is not elemicin

                    free and therefore the effects reported may be due to

                    either substances found in the extract.

 

             3.3.3  Other physico-chemical characteristics

 

                    No data available.

 

        3.4  Other chemical contents of the plant

 

             No data available.

 

  1. USES/CIRCUMSTANCES OF POISONING

 

        4.1  Uses

 

             4.1.1  Uses

 

                    Miscellaneous pharmaceutical product

                    Other therapeutic preparation

                    Food; 

                    general

                    Beverage; general

 

             4.1.2  Description

 

                    Medicinal:

    

                    Used as an anti-diarrhoea agent for patients with

                    medullary carcinoma of the thyroid.  The effectiveness

                    of the treatment may be due to the inhibition of

                    prostaglandin synthesis in the mucosa and submucosa of

                    the colon.  The dosage given was 9 tablespoons orally

                    per day but it may vary between patients to avoid

                    toxic symptoms.

    

                    Domestic:

    

                    Used as a spice in various dishes, as components of

                    teas and soft drinks or mixed in milk and alcohol.

                    Traditional and folk medicine:

    

 

                    It is widely used as a traditional medicine in the

                    Middle East and Asia.

    

                    In Western medicine nutmeg is sometimes used as a

                    stomachic, stimulant, carminative as well as for

                    intestinal catarrh and colic, to stimulate appetites,

                    to control flatulence, and it has a reputation as a

                    emmenagogue and abortifacient.

 

        4.2  High risk circumstances

 

             Abuse

    

             Nutmeg has been known for its hallucinogenic properties for a

             long time.  Adults may abuse the hallucinogenic properties of

             nutmeg.  Children may be at high risk at home, since nutmeg

             may be widely available as a cooking additive.  In the course

             of its use in traditional medicine, overdose may occur.

 

        4.3  High risk geographical areas

 

             No data available.

 

  1. ROUTES OF EXPOSURE

 

        5.1  Oral

 

             This is the most common method of consuming nutmeg, be

             it as a remedy, a spice or as a psychotropic drug.

 

        5.2  Inhalation

 

             Nutmeg is mixed with tobacco snuff in certain parts of

             southern India.  Intoxication through this method of

             administration is reported to be the same as for intoxication

             through oral administration, except that the onset of

             symptoms is faster.

 

        5.3  Dermal

 

             No data available.

 

        5.4  Eye

 

             No data available.

 

        5.5  Parenteral

 

             Reported only in experimental animals.  The effects are

             reported to be the same as those when given orally.

 

        5.6  Others

 

             No data available.

 

  1. KINETICS

 

        6.1  Absorption by route of exposure

 

             No detailed studies are available concerning the

             absorption of the active principles involved in nutmeg

             poisoning.  Current literature states that when nutmeg powder

             is administered orally, the toxic effects begin within 1 to

             12 hours.  The effects last generally for 24 hours but may

             continue for as long as a week or more.  When taken as a tea,

             the reaction is reported to be immediate.  Snuffing nutmeg is

             reported to produce a reaction within 15 minutes.

 

        6.2  Distribution by route of exposure

 

             No data available.

 

        6.3  Biological half-life by route of exposure

 

             No data available.

 

        6.4  Metabolism

 

             3,4,5,-trimethoxy amphetamine (TMA):

    

             It has been postulated that elemicin, a major component in

             nutmeg oil, could undergo oxidation of its oleficin side

             chain in the same manner that the mentioned side chain in

             safrole is also oxidized in the body.  This would produce a

             vinyl alcohol which could under go transamination to produce

             TMA.

    

             The potency of TMA is reported to be more than that of

             mescaline as a psychotropic drug.

    

             3-methoxy-4,5-methylenedioxy amphetamine (MMDA):

    

             It has been proposed that myristicin may be metabolized in

             the body to MMDA in a manner similar to the metabolism of

             elimicin into TMA.

    

             MMDA is reported to have a higher potency than TMA as a

             psychotropic  drug, that is, its potency is about three times

             the potency of mescaline.  It has almost the same properties

             as TMA, being both hallucinogenic and permitting total recall

             of the experience.

 

        6.5  Elimination and excretion

 

             No data available.

 

  1. TOXINOLOGY

 

        7.1  Mode of action

 

             3,4,5,-trimethoxy amphetamine (TMA):

 

             It has been postulated that elemicin, a major component in

             nutmeg oil, could undergo oxidation of its oleficin side

             chain in the same manner that the mentioned side chain in

             safrole is also oxidized in the body.  This would produce a

             vinyl alcohol which could under go transamination to produce

             TMA.

    

             The potency of TMA is reported to be more than that or

             mescaline as a psychotropic drug.

    

             3-methoxy-4,5-methylenedioxy amphetamine (MMDA):

    

             It has been proposed that myristicin may be metabolized in

             the body to MMDA in a manner similar to the metabolism of

             elimicin into TMA.

    

             MMDA is reported to have a higher potency than TMA as a

             psychotropic  drug, that is, its potency is about three times

             the potency of mescaline.  It has almost the same properties

             as TMA, being both hallucinogenic and permitting total recall

             of the experience.

    

             Nutmeg has monoamineoxidase inhibition properties (1963). 

             Nutmeg is also known to have anti-prostaglandin synthesis

             effects.

 

        7.2  Toxicity

 

             7.2.1  Human data

 

                    7.2.1.1  Adults

 

                             The dose needed to induce

                             intoxication varies according to the quality

                             and length of storage of the nutmeg.  1 to 3

                             nutmegs (5 to 15 g) is reported as the toxic

                             dose (Haddad & Winchester, 1983).

 

                    7.2.1.2  Children

 

                             Death by nutmeg intoxication has

                             been reported by Cushny (Weil, 1964) in an 8-

                             year-old boy after consuming 2 nutmegs.

 

             7.2.2  Relevant animal data

 

                    In cats, an oral dose of 24 mg nutmeg oil per

                    kg body weight was found to be lethal.

 

             7.2.3  Relevant in vitro data

 

                    No data available.

 

        7.3  Carcinogenicity

 

             Safrole is a known mild hepatocarcinogen.  Although

             safrole itself is not carcinogenic, it is metabolized to form

             1′-hydroxysafrole which is carcinogenic.  Data are not

             available on the carcinogenicity of nutmeg itself.

 

        7.4  Teratogenicity

 

             Verrett (Wulf et al., 1978) reports that myristicin may

             be a strong teratogen.

 

        7.5  Mutagenicity

 

             No data available.

 

        7.6  Interactions

 

             Consideration should be given to possible nutmeg-ethanol

             interaction since nutmeg has hallucinogenic and MAO

             inhibition effects.

 

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

 

        8.1  Material sampling plan

 

             8.1.1  Sampling and specimen collection

 

                    8.1.1.1  Toxicological analyses

 

                    8.1.1.2  Biomedical analyses

 

                    8.1.1.3  Arterial blood gas analysis

 

                    8.1.1.4  Haematological analyses

 

                    8.1.1.5  Other (unspecified) analyses

 

             8.1.2  Storage of laboratory samples and specimens

 

                    8.1.2.1  Toxicological analyses

 

                    8.1.2.2  Biomedical analyses

 

                    8.1.2.3  Arterial blood gas analysis

 

                    8.1.2.4  Haematological analyses

 

                    8.1.2.5  Other (unspecified) analyses

 

             8.1.3  Transport of laboratory samples and specimens

 

                    8.1.3.1  Toxicological analyses

 

                    8.1.3.2  Biomedical analyses

 

                    8.1.3.3  Arterial blood gas analysis

 

                    8.1.3.4  Haematological analyses

 

                    8.1.3.5  Other (unspecified) analyses

 

        8.2  Toxicological Analyses and Their Interpretation

 

             8.2.1  Tests on toxic ingredient(s) of material

 

                    8.2.1.1  Simple Qualitative Test(s)

 

                    8.2.1.2  Advanced Qualitative Confirmation Test(s)

 

                    8.2.1.3  Simple Quantitative Method(s)

 

                    8.2.1.4  Advanced Quantitative Method(s)

 

             8.2.2  Tests for biological specimens

 

                    8.2.2.1  Simple Qualitative Test(s)

 

                    8.2.2.2  Advanced Qualitative Confirmation Test(s)

 

                    8.2.2.3  Simple Quantitative Method(s)

 

                    8.2.2.4  Advanced Quantitative Method(s)

 

                    8.2.2.5  Other Dedicated Method(s)

 

             8.2.3  Interpretation of toxicological analyses

 

        8.3  Biomedical investigations and their interpretation

 

             8.3.1  Biochemical analysis

 

                    8.3.1.1  Blood, plasma or serum

 

                             “Basic analyses”

                             “Dedicated analyses”

                             “Optional analyses”

 

                    8.3.1.2  Urine

 

                             “Basic analyses”

                             “Dedicated analyses”

                             “Optional analyses”

 

                    8.3.1.3  Other fluids

 

             8.3.2  Arterial blood gas analyses

 

             8.3.3  Haematological analyses

 

                    “Basic analyses”

                    “Dedicated analyses”

                    “Optional analyses”

 

             8.3.4  Interpretation of biomedical investigations

 

        8.4  Other biomedical (diagnostic) investigations and their

             interpretation

 

        8.5  Overall interpretation of all toxicological analyses and

             toxicological investigations

 

        8.6  References

 

  1. CLINICAL EFFECTS

 

        9.1  Acute poisoning:

 

             9.1.1  Ingestion

 

                    In the toxic state, the patient first feels

                    excited and may have psychedelic hallucinations.  This

                    is followed by a period of drowsiness, delirium and,

                    possibly, unconsciousness.  Thirst has been reported.  

                    Mental concentration may either be impaired or

                    enhanced;  delirium with agitation, disorientation and

                    incoherence may develop.  Prison inmates taking nutmeg

                    “trips” have compared it to alcohol, heroin and

                    marihuana and referred to it as making them feel

                    “high”, relaxed and drowsy.  Some reported a sleepy

                    feeling, others, restlessness and tense.  Most

                    patients with accidental nutmeg intoxication

                    experience an impending sense of doom after the

                    initial excitation.  The effects of nutmeg are most

                    often compared to those of marihuana.  Although the

                    hallucinogenic effects of nutmeg are satisfactory, the

                    side effects often discourage its use as such an

                    agent.  One reported case of nutmeg intoxication after

                    drinking nutmeg tea, states that the reaction is

                    immediate.

 

             9.1.2  Inhalation

 

                    The effects by inhalation are generally similar

                    to those experienced via oral administration with the

                    exception that onset is faster by 15 minutes.

 

             9.1.3  Skin exposure

 

                    No data available.

 

             9.1.4  Eye contact

 

                    No data available.

 

             9.1.5  Parenteral exposure

 

                    Parenteral exposure in animals has shown to

                    produce the same general effect as that of oral

                    exposure.

 

             9.1.6  Other

 

                    No data available.

 

        9.2  Chronic poisoning

 

             9.2.1  Ingestion

 

                    Chronic poisoning by oral administration has

                    caused temporary (up to six months) psychosis in

                    prison inmates.

 

             9.2.2  Inhalation

 

                    No data available.

 

             9.2.3  Skin exposure

 

                    No data available.

 

             9.2.4  Eye contact

 

                    No data available.

 

             9.2.5  Parenteral exposure

 

                    No data available.

 

             9.2.6  Other

 

        9.3  Course, prognosis, cause of death

 

             Not all the symptoms listed below appear in every case

             of poisoning.  Contradicting symptoms may occur at different

             times during the course of intoxication.

    

             The subject initially feels excited, then drowsy before a

             delirious state sets in.  This is followed by a deep sleep. 

             During this period, cyanosis of the extremities and

             convulsions may occur.  Generally there is tachycardia and an

             increase in blood pressure.  Acidosis may set in because of

             diarrhoea and vomiting which is usually present along with

             various other gastrointestinal symptoms such as abdominal

             cramps.  The subject may or may not be hallucinating but

             usually expresses a feeling of impending doom.  Nutmeg

             intoxication usually clears by itself within 24 hours,

             however, it has been reported that psychosis may set in. 

             Transient renal toxicity has also been reported causing an

             increase in albumin and non-protein nitrogen content in the

             urine, returning to normal within 24 hours.

    

             Nutmeg has been proven to cause fatty liver in cats which

             have later died from the dose of nutmeg oil but, in the case

             of humans, this is not clear since only one death has been

             attributed to nutmeg toxicity: an 8-year-old boy who became

             comatose and later died after ingesting two nutmegs.

 

        9.4  Systematic description of clinical effects

 

             9.4.1  Cardiovascular

 

                    Tachycardia.

                    Hypertension or hypotension may occur.

                    Chest pains or tightness in chest.

 

             9.4.2  Respiratory

 

                    No data available.

 

             9.4.3  Neurological

 

                    9.4.3.1  Central nervous system (CNS)

 

                             Severe headaches.

                             Drowsiness several hours after taking nutmeg.

                             Fitful sleep/convulsions.

                             Hallucinations (predominantly visual). Colour

                             distortion may also occur.

                             Delirium.

                             Unconsciousness/coma.

                             Agitation.

                             Disorientation.

                             Incoherence.

    

 

                             Sedation.

                             Euphoria.

                             Concentration may be impaired or improved.

                             Excitation resembling that caused by

                             anticholinergic intoxication.

                             Florid paranoia.

                             Belligerence.

                             Vertigo.

                             Stupor.

                             Feeling of impending doom.

    

                             Sometimes unusual behaviour occurs during

                             intoxication such as hysteria and wild

                             trashing of limbs, and behaviour resembling

                             that of a snarling dog.

 

                    9.4.3.2  Peripheral nervous system

 

                             Initial stimulation after

                             administration.

                             Strong tingling in the fingers and toes

                             shortly after snuffing some nutmeg.

                             Numbness in hand and feet half an hour after

                             snuffing nutmeg.

                             Absent limb reflexes.

 

                    9.4.3.3  Autonomic nervous system

 

                             Profuse sweating several hours after

                             administration possibly reflecting

                             amphetamine-type reaction.

                             Absence of salivation.

 

                    9.4.3.4  Skeletal and smooth muscle

 

                             Muscular excitation several hours

                             after administration.

 

             9.4.4  Gastrointestinal

 

                    Nausea.

                    Vomiting.

                    Diarrhoea.

                    Abdominal pain.

 

             9.4.5  Hepatic

 

                    Hepatic necrosis in heavy poisoning.

                    Fatty degradation of liver.

 

             9.4.6 Urinary

 

                    9.4.6.1  Renal

 

                             Transient renal toxicity producing

                             albuminuria.  Non-protein nitrogen content in

                             urine which returns to normal within 24

                             hours.

 

                    9.4.6.2  Other

 

                             No data available.

 

             9.4.7  Endocrine and reproductive systems

 

                    No data available.

 

             9.4.8  Dermatological

 

                    Flushed skin.

 

             9.4.9  Eye, ear, nose, throat:  local effects

 

                    Eyes: A drawing sensation over the eyes after

                    snuffing.

                    Miosis (initially or it may not occur)

                    Mydriasis (occurs less often than miosis)

    

                    Throat: Epigastric pain

 

             9.4.10 Haematological

 

                    No data available.

 

             9.4.11 Immunological

 

                    No data available.

 

             9.4.12 Metabolic

 

                    9.4.12.1 Acid-base disturbances

 

                             Acidosis may be attributed to

                             excessive diarrhoea and vomiting.

 

                    9.4.12.2 Fluid and electrolyte disturbances

 

                             Fluid and electrolyte disturbance

                             may develop because of diarrhoea and

                             vomiting.

 

                    9.4.12.3 Others

 

                             Hypothermia/hyperthermia.

 

             9.4.13 Allergic reactions

 

                    Oedema of eyelids.

                    Possible elevation in body temperature.

                    Marked flushing and itching of face.

                    Allergic reactions tend to subside quickly.

 

             9.4.14 Other clinical effects

 

                    Severe thirst.

 

             9.4.15 Special risks

 

                    Nutmeg has been used as an abortifacient but

                    there are no confirmed clinical accounts.

 

        9.5  Other

 

             No data available.

 

        9.6  Summary

 

  1. MANAGEMENT

 

        10.1 General principles

 

             Treatment is supportive.  Decontamination procedures,

             such as gastric lavage and cathartics, are theoretically

             beneficial within the first few hours but be aware of any

             contraindications before their administration.  Syrup of

             ipecac is not advisable because it may precipitate

             convulsions.  Milk or a demulcent may be given to alleviate

             gastric irritation.

 

        10.2 Life supportive procedures and symptomatic/specific treatment

 

             Nasal oxygen may be administered to patients suffering

             from vertigo.  Barbiturates or diazepam may be given for

             convulsions and analeptics such as chlorpromazine  (25 mg

             every 4 hours) for severe agitation.  Sedatives should be

             administered with caution since the patient goes through

             alternating periods of delirium and lethargy.  A liquid diet

             is recommended, high in protein and carbohydrate and low in

             fat.  Wash eyes if they are physically contaminated by nutmeg

             powder.  Monitor cardiac function and blood pressure and

             treat as necessary.

 

        10.3 Decontamination

 

             Decontamination procedures such as gastric lavage and

             cathartics are theoretically beneficial within the first few

             hours but be aware of any contraindications before their

             administration. Syrup of ipecac is not advisable because it

             may precipitate convulsions.  Milk or a demulcent may be

             given to alleviate gastric irritation.

 

        10.4 Enhanced elimination

 

             No data available.

 

        10.5 Antidote/antitoxin treatment

 

             10.5.1 Adults

 

                    No data available.

 

             10.5.2 Children

 

                    No data available.

 

        10.6 Management discussion

 

             No data available.

 

  1. ILLUSTRATIVE CASES

 

        11.1 Case reports from literature

 

             Two male college students, 19 and 20 years of age, each

             ingested 2 tablespoons (about 14 gm) of powdered nutmeg

             suspended in a glass of milk to produce a sense of

             exhilaration.  Five hours later, rapid heart rates and

             palpitations were noted and both complained of dry mouths and

             thirst.  Onlookers observed that one student became

             hyperactive, agitated and talked incoherently.  Their faces

             were “red as beets”.  Nausea, vomiting and abdominal cramps

             were absent.  60 hours were needed for full recovery.

    

             A 37 year old woman drank a nutmeg tea at a party.  The tea

             consisted of two ground nutmegs in a glass of warm water. 

             She had flushed skin, rapid pulse, incoherent speech and felt

             giddy after 4 hours.  Her vision was disturbed and she had

             hallucinations of faces laughing at her and monsters in the

             bed trying to engulf her.  Symptoms gradually diminished and

             recovery made within 24 hours.

 

  1. ADDITIONAL INFORMATION

 

        12.1 Specific preventative measures

 

             No information available.

 

        12.2 Other

 

             No information available

 

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        Elliott S and Brimacombe J (1987)  The medical plants of Gunung

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  1. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE

        ADDRESS(ES)

 

        Author: UKM

        Kuala Lumpur

        Malaysia

    

        Date: April 1991

    

        Peer Review: Singapore, November 1991

    

        General edit and botanical review:

    

        Christine Leon

        Medical Toxicology Unit

        Guy’s & St Thomas Hospital Trust

        c/o Royal Botanic Gardens, Kew

        Richmond

        Surrey

        TW9 3AB

        United Kingdom   

       

        July 1997

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