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cannabis international

A Resource For The Dietary And Medicinal Study And Use Of Cannabis

CANNABIS INTERNATIONAL

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DR. WILLIAM COURTNEY / KRISTEN COURTNEY

Cannabis and Cannabinoids

This article is a mirror of this page on the National Cancer Institute's site.

Overview

This complementary and alternative medicine (CAM) information summary provides an overview of the use of Cannabis and its components as a treatment for people with cancer -related symptoms caused by the disease itself or its treatment.

This summary contains the following key information:

  • Cannabis has been used for medicinal purposes for thousands of years prior to its current status as an illegal substance.

  • Chemical components of Cannabis, called cannabinoids, activate specific receptors found throughout the body to produce pharmacologic effects, particularly in the central nervous system and the immune system.

  • Cannabinoids may have benefits in the treatment of cancer-related side effects.

Many of the medical and scientific terms used in this summary are hypertext linked (at first use in each section) to the NCI Dictionary of Cancer Terms 1, which is oriented toward nonexperts. When a linked term is clicked, a definition will appear in a separate window. All linked terms and their corresponding definitions will appear in a glossary in the printable version of the summary.

Reference citations in some PDQ CAM information summaries may include links to external Web sites that are operated by individuals or organizations for the purpose of marketing or advocating the use of specific treatments or products. These reference citations are included for informational purposes only. Their inclusion should not be viewed as an endorsement of the content of the Web sites, or of any treatment or product, by the PDQ Cancer CAM Editorial Board or the National Cancer Institute.

General Information

Cannabis, also known as marijuana, originated in Central Asia but is grown worldwide today. In the United States, it is a controlled substance and is classified as a Schedule I agent (a drug with increased potential for abuse and no known medical use). The Cannabis plant produces a resin containing psychoactive compounds called cannabinoids. The highest concentration of cannabinoids is found in the female flowers of the plant.[1] As a botanical, Cannabis is difficult to study because of the lack of standardization of the botanical product due to the many climates and environments in which it is grown. Clinical trials conducted on medicinal Cannabis are limited. The U.S. Food and Drug Administration (FDA) has not approved the use of Cannabis as a treatment for any medical condition. To conduct clinical drug research in the United States, researchers must file an Investigational New Drug (IND) application with the FDA.

The potential benefits of medicinal Cannabis for people living with cancer include antiemetic effects, appetite stimulation, pain relief, and improved sleep. Though no relevant surveys of practice patterns exist, it appears that physicians caring for cancer patients who prescribe medicinal Cannabis predominantly do so for symptom management.

Cannabinoids are a group of terpenophenolic compounds found in Cannabis species (Cannabis sativa L. and Cannabis indica Lam.). This summary will review the role of Cannabis and the cannabinoids in the treatment of people with cancer and disease-related or treatment-related side effects.

References

  1. Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996. [PUBMED Abstract]



History

Cannabis use for medicinal purposes dates back at least 3,000 years.[1-5] It was introduced into Western medicine in the 1840s by W.B. O'Shaughnessy, a surgeon who learned of its medicinal properties while working in India for the British East Indies Company. Its use was promoted for reported analgesic, sedative, anti-inflammatory, antispasmodic, and anticonvulsant effects.

In 1937, the U.S. Treasury Department introduced the Marihuana Tax Act. This Act imposed a levy of one dollar an ounce for medicinal use of Cannabis and one hundred dollars an ounce for recreational use. Physicians in the United States were the principal opponents of the Act. The American Medical Association (AMA) opposed the Act because physicians were required to pay a special tax for prescribing Cannabis, use special order forms to procure it, and keep special records concerning its professional use. In addition, the AMA believed that objective evidence that Cannabis was addictive was lacking and that passage of the Act would impede further research into its medicinal worth.[6] In 1942, Cannabis was removed from the U.S. Pharmacopoeia because of persistent concerns about its potential to cause harm.[2,3]

In 1951, Congress passed the Boggs Act, which for the first time, included Cannabis with narcotic drugs. In 1970, with the passage of the Controlled Substances Act, marijuana was classified as a Schedule I drug. Drugs in this category are distinguished as having no accepted medicinal use. Other Schedule I substances include heroin, LSD, mescaline, methaqualone, and gamma-hydroxybutyrate.

Despite its designation as having no medicinal use, Cannabis was distributed to patients by the U.S. government on a case-by-case basis under the Compassionate Use Investigational New Drug program established in 1978. Distribution of Cannabis through this program was discontinued in 1992.[1-4] In 2010, the U.S. Department of Veteran Affairs approved marijuana use for patients in states where its medicinal use is legal.

The main psychoactive constituent of Cannabis was identified as delta-9-tetrahydrocannabinol (THC). In 1986, synthetic delta-9-THC in sesame oil was licensed and approved for the treatment of chemotherapy -associated nausea and vomiting under the generic name dronabinol. Clinical trials determined that dronabinol was as effective as or better than other antiemetic agents.[7] Dronabinol was also studied for its ability to stimulate weight gain in patients with AIDS in the late 1980s. Clinical trial results showed no significant weight gain, although patients reported an improvement in appetite. [8,9]

Within the past 20 years, the neurobiology of cannabinoids has been analyzed.[10-13] The first cannabinoid receptor, CB1, was pharmacologically identified in the brain in 1988. A second cannabinoid receptor, CB2, was identified in 1993. The highest concentration of CB2 receptors is located on B lymphocytes and natural killer cells, suggesting a possible role in immunity. Endogenous cannabinoids (endocannabinoids) have been identified and appear to have a role in pain modulation, control of movement, feeding behavior, and memory.[11]

References

  1. Abel EL: Marihuana, The First Twelve Thousand Years. New York: Plenum Press, 1980. Also available online 2. Last accessed March 17, 2011.

  2. Joy JE, Watson SJ, Benson JA, eds.: Marijuana and Medicine: Assessing the Science Base. Washington, DC: National Academy Press, 1999. Also available online 3. Last accessed March 17, 2011.

  3. Mack A, Joy J: Marijuana As Medicine? The Science Beyond the Controversy. Washington, DC: National Academy Press, 2001. Also available online 4. Last accessed March 17, 2011.

  4. Booth M: Cannabis: A History. New York, NY: St Martin's Press, 2003.

  5. Russo EB, Jiang HE, Li X, et al.: Phytochemical and genetic analyses of ancient cannabis from Central Asia. J Exp Bot 59 (15): 4171-82, 2008. [PUBMED Abstract]

  6. Schaffer Library of Drug Policy.: The Marihuana Tax Act of 1937: Taxation of Marihuana. Washington, DC: House of Representatives, Committee on Ways and Means, 1937. Available online 5. Last accessed March 17, 2011.

  7. Sallan SE, Zinberg NE, Frei E 3rd: Antiemetic effect of delta-9-tetrahydrocannabinol in patients receiving cancer chemotherapy. N Engl J Med 293 (16): 795-7, 1975. [PUBMED Abstract]

  8. Gorter R, Seefried M, Volberding P: Dronabinol effects on weight in patients with HIV infection. AIDS 6 (1): 127, 1992. [PUBMED Abstract]

  9. Beal JE, Olson R, Laubenstein L, et al.: Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage 10 (2): 89-97, 1995. [PUBMED Abstract]

  10. Devane WA, Dysarz FA 3rd, Johnson MR, et al.: Determination and characterization of a cannabinoid receptor in rat brain. Mol Pharmacol 34 (5): 605-13, 1988. [PUBMED Abstract]

  11. Devane WA, Hanus L, Breuer A, et al.: Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 258 (5090): 1946-9, 1992. [PUBMED Abstract]

  12. Pertwee RG: Pharmacology of cannabinoid CB1 and CB2 receptors. Pharmacol Ther 74 (2): 129-80, 1997. [PUBMED Abstract]

  13. Felder CC, Glass M: Cannabinoid receptors and their endogenous agonists. Annu Rev Pharmacol Toxicol 38: 179-200, 1998. [PUBMED Abstract]



Laboratory/Animal/Preclinical Studies

Cannabinoids are a group of 21 carbon terpenophenolic compounds produced uniquely by Cannabis sativa and Cannabis indica species.[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol, cannabichromene, cannabigerol, tetrahydrocannabivirin, and delta-8-THC. Cannabidiol, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.

Antitumor Effects

One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors. [3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]

Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis. [9-11] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor. [10,11]

In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[12] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects.

In addition, both plant-derived and endogenous cannabinoids have been studied for anti- inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation. [13] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the prevention and treatment of colorectal cancer has been developed.[14]

Another study has shown delta-9-THC is a potent and selective antiviral agent against Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8.[15] The researchers concluded that additional studies on cannabinoids and herpesviruses are warranted, as they may lead to the development of drugs that inhibit the reactivation of these oncogenic viruses. Subsequently, another group of investigators reported increased efficiency of KSHV infection of human dermal microvascular epithelial cells in the presence of low doses of delta-9-THC.[16]

Appetite Stimulation

Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[17] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[18]

Analgesia

Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in sections of the brain that regulate nociceptive processing.[19] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[20,21]

Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[22-24]

References

  1. Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996. [PUBMED Abstract]

  2. Grotenhermen F, Russo E, eds.: Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Binghamton, NY: The Haworth Press, 2002.

  3. National Toxicology Program .: NTP Toxicology and Carcinogenesis Studies of 1-Trans-Delta(9)-Tetrahydrocannabinol (CAS No. 1972-08-3) in F344 Rats and B6C3F1 Mice (Gavage Studies). Natl Toxicol Program Tech Rep Ser 446 (): 1-317, 1996. [PUBMED Abstract]

  4. Bifulco M, Laezza C, Pisanti S, et al.: Cannabinoids and cancer: pros and cons of an antitumour strategy. Br J Pharmacol 148 (2): 123-35, 2006. [PUBMED Abstract]

  5. Snchez C, de Ceballos ML, Gomez del Pulgar T, et al.: Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Res 61 (15): 5784-9, 2001. [PUBMED Abstract]

  6. McKallip RJ, Lombard C, Fisher M, et al.: Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood 100 (2): 627-34, 2002. [PUBMED Abstract]

  7. Casanova ML, Blzquez C, Martnez-Palacio J, et al.: Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest 111 (1): 43-50, 2003. [PUBMED Abstract]

  8. Blzquez C, Gonzlez-Feria L, Alvarez L, et al.: Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Res 64 (16): 5617-23, 2004. [PUBMED Abstract]

  9. Guzmn M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003. [PUBMED Abstract]

  10. Blzquez C, Casanova ML, Planas A, et al.: Inhibition of tumor angiogenesis by cannabinoids. FASEB J 17 (3): 529-31, 2003. [PUBMED Abstract]

  11. Vaccani A, Massi P, Colombo A, et al.: Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism. Br J Pharmacol 144 (8): 1032-6, 2005. [PUBMED Abstract]

  12. Preet A, Ganju RK, Groopman JE: Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 27 (3): 339-46, 2008. [PUBMED Abstract]

  13. Massa F, Marsicano G, Hermann H, et al.: The endogenous cannabinoid system protects against colonic inflammation. J Clin Invest 113 (8): 1202-9, 2004. [PUBMED Abstract]

  14. Patsos HA, Hicks DJ, Greenhough A, et al.: Cannabinoids and cancer: potential for colorectal cancer therapy. Biochem Soc Trans 33 (Pt 4): 712-4, 2005. [PUBMED Abstract]

  15. Medveczky MM, Sherwood TA, Klein TW, et al.: Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro. BMC Med 2: 34, 2004. [PUBMED Abstract]

  16. Zhang X, Wang JF, Kunos G, et al.: Cannabinoid modulation of Kaposi's sarcoma-associated herpesvirus infection and transformation. Cancer Res 67 (15): 7230-7, 2007. [PUBMED Abstract]

  17. Mechoulam R, Berry EM, Avraham Y, et al.: Endocannabinoids, feeding and suckling--from our perspective. Int J Obes (Lond) 30 (Suppl 1): S24-8, 2006. [PUBMED Abstract]

  18. Fride E, Bregman T, Kirkham TC: Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood. Exp Biol Med (Maywood) 230 (4): 225-34, 2005. [PUBMED Abstract]

  19. Walker JM, Hohmann AG, Martin WJ, et al.: The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999. [PUBMED Abstract]

  20. Meng ID, Manning BH, Martin WJ, et al.: An analgesia circuit activated by cannabinoids. Nature 395 (6700): 381-3, 1998. [PUBMED Abstract]

  21. Walker JM, Huang SM, Strangman NM, et al.: Pain modulation by release of the endogenous cannabinoid anandamide. Proc Natl Acad Sci U S A 96 (21): 12198-203, 1999. [PUBMED Abstract]

  22. Facci L, Dal Toso R, Romanello S, et al.: Mast cells express a peripheral cannabinoid receptor with differential sensitivity to anandamide and palmitoylethanolamide. Proc Natl Acad Sci U S A 92 (8): 3376-80, 1995. [PUBMED Abstract]

  23. Ibrahim MM, Porreca F, Lai J, et al.: CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids. Proc Natl Acad Sci U S A 102 (8): 3093-8, 2005. [PUBMED Abstract]

  24. Richardson JD, Kilo S, Hargreaves KM: Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral CB1 receptors. Pain 75 (1): 111-9, 1998. [PUBMED Abstract]



Human/Clinical Studies


Cannabis Pharmacology

When Cannabis is ingested by mouth, there is a low (6%20%) and variable oral bioavailability. [1,2] Peak plasma concentrations of delta-9-tetrahydrocannabinol (THC) occur after 1 to 6 hours and remain elevated with a terminal half-life of 20 to 30 hours. Taken by mouth, delta-9-THC is initially metabolized in the liver to 11-OH-THC, a potent psychoactive metabolite. When inhaled, cannabinoids are rapidly absorbed into the bloodstream with a peak concentration in 2 to 10 minutes, declining rapidly for a period of 30 minutes and with less generation of the psychoactive 11-OH metabolite.

Cannabinoids are known to interact with the hepatic cytochrome P450 enzyme system.[3,4] In one study, 24 cancer patients were treated with intravenous irinotecan (600 mg, n = 12) or docetaxel (180 mg, n = 12), followed 3 weeks later by the same drugs concomitant with medicinal Cannabis taken in the form of an herbal tea for 15 consecutive days, starting 12 days before the second treatment.[4] The administration of Cannabis did not significantly influence exposure to and clearance of irinotecan or docetaxel, although the herbal tea route of administration may not reproduce the effects of inhalation or oral ingestion of fat- soluble cannabinoids.

Cancer risk

A number of studies have yielded conflicting evidence regarding the risks of various cancers associated with Cannabis use. A case- cohort study of men in northwestern Africa showed a significantly increased risk of lung cancer among tobacco smokers who also inhaled Cannabis. A large retrospective cohort study from the United States found that Cannabis use was not associated with tobacco-related cancers and a number of other common malignancies, but did find that among nonsmokers of tobacco, ever having used Cannabis was associated with an increased risk of prostate cancer.[5] A population-based case-control study of the association between Cannabis use and the risk of lung and aerodigestive tract cancers in Los Angeles found no positive associations with any cancer type (oral, pharyngeal, laryngeal, lung, or esophagus) when adjusting for several confounders including cigarette smoking.[6] A comprehensive Health Canada monograph on Marihuana (Marijuana, Cannabis): Information for Health Care Professionals concludes that while there are many cellular and molecular studies that provide strong evidence that inhaled marijuana is carcinogenic, the epidemiologic evidence of a link between marijuana use and cancer is still inconclusive. [7]

Cancer Treatment

No clinical trials of Cannabis as a treatment for cancer in humans were identified in a PubMed search.

Antiemetic Effect

Cannabinoids

Despite advances in pharmacologic and nonpharmacologic management, nausea and vomiting (N/V) remain distressing side effects for cancer patients and their families. Dronabinol was approved in the United States in 1986 as an antiemetic to be used in cancer chemotherapy. Nabilone, another synthetic form of delta-9-THC, was first approved in Canada in 1982 and is now also available in the United States.[8] Both dronabinol and nabilone have been approved by the U.S. Food and Drug Administration for the treatment of N/V associated with cancer chemotherapy in patients who have failed to respond to conventional antiemetic therapy. Numerous clinical trials and meta-analyses have shown that dronabinol and nabilone are effective in the treatment of N/V induced by chemotherapy.[9-12]

One systematic review studied 30 randomized comparisons of delta-9-THC preparations with placebo or other antiemetics from which data on efficacy and harm were available.[13] Oral nabilone, oral dronabinol, and intramuscular levonantradol (a synthetic analog of dronabinol) were tested. Inhaled Cannabis trials were not included. Among all 1,366 patients included in the review, cannabinoids were found to be more effective than the conventional antiemetics prochlorperazine, metoclopramide, chlorpromazine, thiethylperazine, haloperidol, domperidone, and alizapride. Cannabinoids, however, were not more effective for patients receiving very low or very high emetogenic chemotherapy. Side effects included a feeling of being high, euphoria, sedation or drowsiness, dizziness, dysphoria or depression, hallucinations, paranoia, and hypotension. [13]

Another analysis of 15 controlled studies compared nabilone with placebo or available antiemetic drugs.[14] Among 600 cancer patients, nabilone was found to be superior to prochlorperazine, domperidone, and alizapride, with nabilone favored for continuous use.

Cannabis

Three trials have evaluated the efficacy of inhaled marijuana in chemotherapy-induced N/V.[15-17] In two of the studies, inhaled Cannabis was made available only after dronabinol failure. In the first trial, no antiemetic effect was achieved with marijuana in patients receiving cyclophosphamide or doxorubicin, [15] but in the second trial, a statistically significant superior antiemetic effect was found among patients receiving high- dose methotrexate compared with those receiving placebo.[16] The third trial was a randomized, double-blind, placebo-controlled cross-over trial involving 20 adults in which both inhaled marijuana and oral THC were evaluated. One-quarter of the patients reported a favorable antiemetic response to the cannabinoid therapies. This latter study was reported in abstract form in 1984. A full report, detailing the methods and outcomes apparently has not been published, which limits a thorough interpretation of the significance of these findings.[17]

Appetite Stimulation

Anorexia, early satiety, weight loss, and cachexia are problems experienced by cancer patients. Such patients are faced not only with the disfigurement associated with wasting but also with an inability to engage in the social interaction of meals.

Cannabinoids

Two controlled trials demonstrated that oral THC has variable effects on appetite stimulation and weight loss in patients with advanced malignancies and human immunodeficiency virus (HIV) infection. [14] One study evaluated whether dronabinol alone or with megestrol acetate was greater, less, or equal in efficacy to megestrol acetate alone for managing cancer-associated anorexia.[18] In this randomized double-blind study of 469 adults with advanced cancer and weight loss, patients received 2.5 mg of oral THC twice daily, 800 mg of oral megestrol daily, or both. Appetite increased by 75% in the megestrol group and weight increased by 11%, compared with a 49% increase in appetite and a 3% increase in weight in the oral THC group. These two differences were statistically significant. Furthermore, the combined therapy did not offer additional benefits beyond those provided by megestrol acetate alone. The authors concluded that dronabinol did little to promote appetite or weight gain in advanced cancer patients compared with megestrol acetate. However, a smaller placebo-controlled trial of dronabinol in cancer patients demonstrated improved and enhanced chemosensory perception in the cannabinoid groupfood tasted better, appetite increased, and the proportion of calories consumed as protein was greater than in the placebo recipients.[19]

Another clinical trial that involved 139 patients with HIV or AIDS and weight loss found that, compared with placebo, oral dronabinol was associated with a statistically significant increase in appetite after 4 to 6 weeks of treatment. Patients receiving dronabinol tended to have weight stabilization, whereas patients receiving placebo continued to lose weight.[20]

Cannabis

Anecdotally, in trials conducted in the 1970s that involved healthy control subjects, inhaling Cannabis led to an increase in caloric intake, mainly in the form of between meal snacks, with increased intake of fatty and sweet foods. No published studies have explored the effect of inhaled Cannabis on appetite in cancer patients.

Analgesia

Cannabinoids

Pain management improves a patient's quality of life throughout all stages of cancer. Through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists, the mechanisms of cannabinoid-induced analgesia have been analyzed. The CB1 receptor is found in the central nervous system (CNS) and in peripheral nerve terminals.[21] CB2 receptors are located mainly in peripheral tissue and are expressed in only low amounts in the CNS. Whereas only CB1 agonists exert analgesic activity in the CNS, both CB1 and CB2 agonists have analgesic activity in peripheral tissue.[22,23]

Cancer pain results from inflammation, invasion of bone or other pain-sensitive structures, or nerve injury. When cancer pain is severe and persistent, it is often resistant to treatment with opioids.

Two studies examined the effects of oral delta-9-THC on cancer pain. The first, a double-blind placebo- controlled study involving ten patients, measured both pain intensity and pain relief.[24] It was reported that 15 mg and 20 mg doses of the cannabinoid delta-9-THC were associated with substantial analgesic effects, with antiemetic effects and appetite stimulation.

In a follow-up single-dose study involving 36 patients, it was reported that 10 mg doses of delta-9-THC produced analgesic effects during a 7-hour observation period that were comparable to 60 mg doses of codeine, and 20 mg doses of delta-9-THC induced effects equivalent to 120 mg doses of codeine.[25] Higher doses of THC were found to be more sedative than codeine.

Another study examined the effects of a whole-plant extract with controlled cannabinoid content in an oromucosal spray. In a multicenter, double-blind, placebo-controlled study, the THC:cannabidiol (THC:CBD) extract and THC extract alone were compared in the analgesic management of patients with advanced cancer and with moderate-to-severe cancer-related pain. Patients were assigned to one of three treatment groups: THC:CBD extract, THC extract, or placebo. The researchers concluded that the THC:CBD extract was efficacious for pain relief in advanced cancer patients whose pain was not fully relieved by strong opioids.[26]

An observational study assessed the effectiveness of nabilone in advanced cancer patients who were experiencing pain and other symptoms (anorexia, depression, and anxiety). The researchers reported that patients who used nabilone experienced improved management of pain, nausea, anxiety, and distress when compared with untreated patients. Nabilone was also associated with a decreased use of opioids, nonsteroidal anti-inflammatory drugs, tricyclic antidepressants, gabapentin, dexamethasone, metoclopramide, and ondansetron. [27]

Cannabis

Neuropathic pain is a symptom cancer patients may experience, especially if treated with platinum-based chemotherapy or taxanes. A randomized controlled trial of inhaled Cannabis compared with placebo in 50 patients with HIV-related peripheral neuropathy found that pain was reduced by more than 30% in 52% of patients in the Cannabis group and in 24% of patients in the placebo group. This difference was statistically significant.[28] To date, no clinical trial has examined the effectiveness of cannabinoid preparations in the treatment of chemotherapy-induced neuropathic pain.

Anxiety and Sleep

Cannabis

Patients often experience mood elevation after exposure to Cannabis, depending on their prior experience. In a five-patient case series of inhaled marijuana that examined the analgesic effects of THC, it was reported that patients administered THC had improved mood, improved sense of well-being, and less anxiety.[29]

Another common effect of Cannabis is sleepiness. In a trial of a sublingual spray, a Cannabis-based mixture was able to improve sleep quality.[30] A small placebo-controlled study of dronabinol in cancer patients with altered chemosensory perception also noted increased quality of sleep and relaxation in THC-treated patients.[19]

References

  1. Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996. [PUBMED Abstract]

  2. Agurell S, Halldin M, Lindgren JE, et al.: Pharmacokinetics and metabolism of delta 1-tetrahydrocannabinol and other cannabinoids with emphasis on man. Pharmacol Rev 38 (1): 21-43, 1986. [PUBMED Abstract]

  3. Yamamoto I, Watanabe K, Narimatsu S, et al.: Recent advances in the metabolism of cannabinoids. Int J Biochem Cell Biol 27 (8): 741-6, 1995. [PUBMED Abstract]

  4. Watanabe K, Matsunaga T, Yamamoto I, et al.: Involvement of CYP2C in the metabolism of cannabinoids by human hepatic microsomes from an old woman. Biol Pharm Bull 18 (8): 1138-41, 1995. [PUBMED Abstract]

  5. Sidney S, Quesenberry CP Jr, Friedman GD, et al.: Marijuana use and cancer incidence (California, United States). Cancer Causes Control 8 (5): 722-8, 1997. [PUBMED Abstract]

  6. Hashibe M, Morgenstern H, Cui Y, et al.: Marijuana use and the risk of lung and upper aerodigestive tract cancers: results of a population-based case-control study. Cancer Epidemiol Biomarkers Prev 15 (10): 1829-34, 2006. [PUBMED Abstract]

  7. Health Canada.: Marihuana (Marijuana, Cannabis): Dried Plant for Administration by Ingestion or Other Means. Ottawa, Canada: Health Canada, 2010. Available online 6. Last accessed March 17, 2011.

  8. Sutton IR, Daeninck P: Cannabinoids in the management of intractable chemotherapy-induced nausea and vomiting and cancer-related pain. J Support Oncol 4 (10): 531-5, 2006 Nov-Dec. [PUBMED Abstract]

  9. Ahmedzai S, Carlyle DL, Calder IT, et al.: Anti-emetic efficacy and toxicity of nabilone, a synthetic cannabinoid, in lung cancer chemotherapy. Br J Cancer 48 (5): 657-63, 1983. [PUBMED Abstract]

  10. Chan HS, Correia JA, MacLeod SM: Nabilone versus prochlorperazine for control of cancer chemotherapy-induced emesis in children: a double-blind, crossover trial. Pediatrics 79 (6): 946-52, 1987. [PUBMED Abstract]

  11. Johansson R, Kilkku P, Groenroos M: A double-blind, controlled trial of nabilone vs. prochlorperazine for refractory emesis induced by cancer chemotherapy. Cancer Treat Rev 9 (Suppl B): 25-33, 1982. [PUBMED Abstract]

  12. Niiranen A, Mattson K: A cross-over comparison of nabilone and prochlorperazine for emesis induced by cancer chemotherapy. Am J Clin Oncol 8 (4): 336-40, 1985. [PUBMED Abstract]

  13. Tramr MR, Carroll D, Campbell FA, et al.: Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review. BMJ 323 (7303): 16-21, 2001. [PUBMED Abstract]

  14. Ben Amar M: Cannabinoids in medicine: A review of their therapeutic potential. J Ethnopharmacol 105 (1-2): 1-25, 2006. [PUBMED Abstract]

  15. Chang AE, Shiling DJ, Stillman RC, et al.: A prospective evaluation of delta-9-tetrahydrocannabinol as an antiemetic in patients receiving adriamycin and cytoxan chemotherapy. Cancer 47 (7): 1746-51, 1981. [PUBMED Abstract]

  16. Chang AE, Shiling DJ, Stillman RC, et al.: Delata-9-tetrahydrocannabinol as an antiemetic in cancer patients receiving high-dose methotrexate. A prospective, randomized evaluation. Ann Intern Med 91 (6): 819-24, 1979. [PUBMED Abstract]

  17. Levitt M, Faiman C, Hawks R, et al.: Randomized double blind comparison of delta-9-tetrahydrocannabinol and marijuana as chemotherapy antiemetics. [Abstract] Proceedings of the American Society of Clinical Oncology 3: A-C354, 91, 1984.

  18. Jatoi A, Windschitl HE, Loprinzi CL, et al.: Dronabinol versus megestrol acetate versus combination therapy for cancer-associated anorexia: a North Central Cancer Treatment Group study. J Clin Oncol 20 (2): 567-73, 2002. [PUBMED Abstract]

  19. Brisbois TD, de Kock IH, Watanabe SM, et al.: Delta-9-tetrahydrocannabinol may palliate altered chemosensory perception in cancer patients: results of a randomized, double-blind, placebo-controlled pilot trial. Ann Oncol : , 2011. [PUBMED Abstract]

  20. Beal JE, Olson R, Laubenstein L, et al.: Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage 10 (2): 89-97, 1995. [PUBMED Abstract]

  21. Walker JM, Hohmann AG, Martin WJ, et al.: The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999. [PUBMED Abstract]

  22. Calignano A, La Rana G, Giuffrida A, et al.: Control of pain initiation by endogenous cannabinoids. Nature 394 (6690): 277-81, 1998. [PUBMED Abstract]

  23. Fields HL, Meng ID: Watching the pot boil. Nat Med 4 (9): 1008-9, 1998. [PUBMED Abstract]

  24. Noyes R Jr, Brunk SF, Baram DA, et al.: Analgesic effect of delta-9-tetrahydrocannabinol. J Clin Pharmacol 15 (2-3): 139-43, 1975 Feb-Mar. [PUBMED Abstract]

  25. Noyes R Jr, Brunk SF, Avery DA, et al.: The analgesic properties of delta-9-tetrahydrocannabinol and codeine. Clin Pharmacol Ther 18 (1): 84-9, 1975. [PUBMED Abstract]

  26. Johnson JR, Burnell-Nugent M, Lossignol D, et al.: Multicenter, double-blind, randomized, placebo-controlled, parallel-group study of the efficacy, safety, and tolerability of THC:CBD extract and THC extract in patients with intractable cancer-related pain. J Pain Symptom Manage 39 (2): 167-79, 2010. [PUBMED Abstract]

  27. Maida V, Ennis M, Irani S, et al.: Adjunctive nabilone in cancer pain and symptom management: a prospective observational study using propensity scoring. J Support Oncol 6 (3): 119-24, 2008. [PUBMED Abstract]

  28. Abrams DI, Jay CA, Shade SB, et al.: Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial. Neurology 68 (7): 515-21, 2007. [PUBMED Abstract]

  29. Noyes R Jr, Baram DA: Cannabis analgesia. Compr Psychiatry 15 (6): 531-5, 1974 Nov-Dec. [PUBMED Abstract]

  30. Russo EB, Guy GW, Robson PJ: Cannabis, pain, and sleep: lessons from therapeutic clinical trials of Sativex, a cannabis-based medicine. Chem Biodivers 4 (8): 1729-43, 2007. [PUBMED Abstract]



Adverse Effects


Cannabinoids

Cannabinoids have a favorable drug safety profile.[1-4] Unlike opioid receptors, cannabinoid receptors are not located in the brainstem areas controlling respiration; therefore, lethal overdoses due to respiratory suppression do not occur. Because cannabinoid receptors are present in tissues throughout the body, not just in the central nervous system, adverse effects include tachycardia, hypotension, conjunctival injection, bronchodilation, muscle relaxation, and decreased gastrointestinal motility.

Although cannabinoids are considered by some to be addictive drugs, their addictive potential is considerably lower than that of other prescribed agents or substances of abuse.[4] The brain develops a tolerance to cannabinoids.

Withdrawal symptoms, such as irritability, insomnia with sleep electroencephalogram disturbance, restlessness, hot flashes, and rarely, nausea and cramping have been observed, but these symptoms appear to be mild compared with withdrawal symptoms associated with opiates or benzodiazepines, and the symptoms usually dissipate after a few days.

Unlike other commonly used drugs, cannabinoids are stored in adipose tissue and excreted at a low rate (half-life 13 days), so even abrupt cessation of cannabinoid intake is not associated with rapid declines in plasma concentrations that would precipitate severe or abrupt withdrawal symptoms or drug cravings.

Cannabis

In clinical trials of Cannabis, euphoria is often scored as an adverse effect.[1,2]

In a retrospective cohort study of 64,855 men aged 15 to 49 years, participants were divided into cohorts based on their use of tobacco and marijuana: never inhaled either, inhaled only Cannabis, inhaled only tobacco, and inhaled tobacco and Cannabis.[5] Among the nonsmokers, two cases of lung cancer were diagnosed during the follow-up period. Among the men who inhaled tobacco either alone or in addition to marijuana, the risk of lung cancer increased tenfold. In the follow-up of men who inhaled marijuana alone, no cases of lung cancer were documented.

A case-control study of 611 lung cancer patients revealed that chronic low Cannabis exposure was not associated with an increased risk of lung cancer or other upper aerodigestive tract cancers.[6] A standardized questionnaire used during face-to-face interviews collected information on marijuana use expressed in joint-years, where 1 joint-year is the equivalent of inhaling one marijuana cigarette per day for 1 year. The results showed that, although using marijuana for 30 years or longer was positively associated in the crude analysis with each cancer type studied except pharyngeal cancer, no positive associations were found when adjusting for several confounders including cigarette smoking.[6]

Furthermore, a systematic review assessing 19 studies that evaluated premalignant or malignant lung lesions in persons 18 years or older who inhaled marijuana concluded that observational studies failed to demonstrate statistically significant associations between marijuana inhaling and lung cancer after adjusting for tobacco use.[7]

References

  1. Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996. [PUBMED Abstract]

  2. Grotenhermen F, Russo E, eds.: Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Binghamton, NY: The Haworth Press, 2002.

  3. Sutton IR, Daeninck P: Cannabinoids in the management of intractable chemotherapy-induced nausea and vomiting and cancer-related pain. J Support Oncol 4 (10): 531-5, 2006 Nov-Dec. [PUBMED Abstract]

  4. Guzmn M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003. [PUBMED Abstract]

  5. Sidney S, Quesenberry CP Jr, Friedman GD, et al.: Marijuana use and cancer incidence (California, United States). Cancer Causes Control 8 (5): 722-8, 1997. [PUBMED Abstract]

  6. Hashibe M, Morgenstern H, Cui Y, et al.: Marijuana use and the risk of lung and upper aerodigestive tract cancers: results of a population-based case-control study. Cancer Epidemiol Biomarkers Prev 15 (10): 1829-34, 2006. [PUBMED Abstract]

  7. Mehra R, Moore BA, Crothers K, et al.: The association between marijuana smoking and lung cancer: a systematic review. Arch Intern Med 166 (13): 1359-67, 2006. [PUBMED Abstract]



Overall Level of Evidence for Cannabis and Cannabinoids

To assist readers in evaluating the results of human studies of complementary and alternative medicine (CAM) treatments for people with cancer, the strength of the evidence (i.e., the levels of evidence) associated with each type of treatment is provided whenever possible. To qualify for a level of evidence analysis, a study must:

Separate levels of evidence scores are assigned to qualifying human studies on the basis of statistical strength of the study design and scientific strength of the treatment outcomes (i.e., endpoints) measured. The resulting two scores are then combined to produce an overall score. An overall level of evidence score cannot be assigned to cannabinoids because there has been insufficient clinical research to date. For an explanation of possible scores and additional information about levels of evidence analysis of CAM treatments for people with cancer, refer to Levels of Evidence for Human Studies of Cancer Complementary and Alternative Medicine 7.

Cannabinoids

Cannabis

  • There have been only three small clinical trials on the use of Cannabis in cancer patients. All three studies assessed antiemetic activity but each explored a different patient population and chemotherapy regimen. One study demonstrated no effect, the second study showed a positive effect versus placebo, and the report of the third study did not provide enough information to characterize the overall outcome as positive or neutral. Consequently, there are insufficient data to provide an overall level of evidence assessment for the use of Cannabis for chemotherapy-induced N/V. Apparently, there are no published data on the use of Cannabis for other cancer-related or cancer treatmentrelated symptoms.

  • An increasing number of trials are evaluating the sublingual administration of whole Cannabis plant extract with fixed concentrations of cannabinoid components.

  • At present, there is insufficient evidence to recommend inhaling Cannabis as a treatment for cancer-related symptoms or cancer treatmentrelated side effects outside the context of well-designed clinical trials.

Changes to This Summary (03/28/2011)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

This is a new summary.

More Information

Additional Information about CAM Therapies

About PDQ

Other PDQ Summaries

Important:

This information is intended mainly for use by doctors and other health care professionals. If you have questions about this topic, you can ask your doctor, or call the Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

About This PDQ Summary


Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the use of Cannabis and cannabinoids in the treatment of people with cancer. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Cancer Complementary and Alternative Medicine Editorial Board 19. Board members review recently published articles each month to determine whether an article should:

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewer for Cannabis and Cannabinoids is:

  • Donald I. Abrams, MD (UCSF Osher Center for Integrative Medicine)

Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form 20. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Cancer Complementary and Alternative Medicine Editorial Board uses a formal evidence ranking system 7 in developing its level-of-evidence designations.

Permission to Use This Summary

PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]."

The preferred citation for this PDQ summary is:

National Cancer Institute: PDQ Cannabis and Cannabinoids. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional. Accessed <MM/DD/YYYY>.

Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online 21, a collection of over 2,000 scientific images.

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The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Coping with Cancer: Financial, Insurance, and Legal Information page 22 page.

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More information about contacting us or receiving help with the Cancer.gov Web site can be found on our Contact Us for Help 23 page. Questions can also be submitted to Cancer.gov through the Web site's Contact Form 20.



Glossary Terms

activate (AK-tih-vayt)
In biology, to stimulate a cell in a resting state to become active. This causes biochemical and functional changes in the activated cell.
AIDS
A disease caused by the human immunodeficiency virus (HIV). People with AIDS are at an increased risk for developing certain cancers and for infections that usually occur only in individuals with a weak immune system. Also called acquired immunodeficiency syndrome.
analgesic (AN-ul-JEE-zik)
A drug that reduces pain. Analgesics include aspirin, acetaminophen, and ibuprofen.
anti-inflammatory (AN-tee-in-FLA-muh-TOR-ee)
Having to do with reducing inflammation.
anticonvulsant (AN-tee-kun-VUL-sunt)
A drug or other substance used to prevent or stop seizures or convulsions. Also called antiepileptic.
antiemetic (AN-tee-eh-MEH-tik)
A drug that prevents or reduces nausea and vomiting.
appetite (A-peh-tite)
A desire to satisfy a physical or mental need, such as for food, sex, or adventure.
bioavailable
The ability of a drug or other substance to be absorbed and used by the body. Orally bioavailable means that a drug or other substance that is taken by mouth can be absorbed and used by the body.
cancer (KAN-ser)
A term for diseases in which abnormal cells divide without control and can invade nearby tissues. Cancer cells can also spread to other parts of the body through the blood and lymph systems. There are several main types of cancer. Carcinoma is a cancer that begins in the skin or in tissues that line or cover internal organs. Sarcoma is a cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue. Leukemia is a cancer that starts in blood-forming tissue such as the bone marrow, and causes large numbers of abnormal blood cells to be produced and enter the blood. Lymphoma and multiple myeloma are cancers that begin in the cells of the immune system. Central nervous system cancers are cancers that begin in the tissues of the brain and spinal cord. Also called malignancy.
central nervous system (SEN-trul NER-vus SIS-tem)
The brain and spinal cord. Also called CNS.
chemical (KEH-mih-kul)
A substance made up of elements, such as hydrogen or sodium.
chemotherapy (KEE-moh-THAYR-uh-pee)
Treatment with drugs that kill cancer cells.
clinical trial (KLIH-nih-kul TRY-ul)
A type of research study that tests how well new medical approaches work in people. These studies test new methods of screening, prevention, diagnosis, or treatment of a disease. Also called clinical study.
compassionate use trial (kum-PA-shuh-nut yoos TRY-ul)
A way to provide an investigational therapy to a patient who is not eligible to receive that therapy in a clinical trial, but who has a serious or life-threatening illness for which other treatments are not available. Compassionate use trials allow patients to receive promising but not yet fully studied or approved cancer therapies when no other treatment option exists. Also called expanded access trial.
complementary and alternative medicine (KOM-pleh-MEN- tuh-ree... all-TER-nuh-tiv MEH-dih-sin)
Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices generally are not considered standard medical approaches. Standard treatments go through a long and careful research process to prove they are safe and effective, but less is known about most types of CAM. CAM may include dietary supplements, megadose vitamins, herbal preparations, special teas, acupuncture, massage therapy, magnet therapy, spiritual healing, and meditation. Also called CAM.
concentration (KON-sun-TRAY-shun)
In science, the amount of a substance, such as a salt, that is in a certain amount of tissue or liquid, such as blood. A substance becomes more concentrated when less water is present. For example, the salt in urine may become more concentrated when a person doesn't drink enough water.
cytochrome P450 enzyme system (SY-tuh-krome ... EN-zime SIS-tem)
A group of enzymes involved in drug metabolism and found in high levels in the liver. These enzymes change many drugs, including anticancer drugs, into less toxic forms that are easier for the body to excrete.
dronabinol (droh-NAH-bih-nol)
A synthetic pill form of delta-9-tetrahydrocannabinol (THC), an active ingredient in marijuana that is used to treat nausea and vomiting associated with cancer chemotherapy.
drug
Any substance, other than food, that is used to prevent, diagnose, treat or relieve symptoms of a disease or abnormal condition. Also refers to a substance that alters mood or body function, or that can be habit-forming or addictive, especially a narcotic.
generic (jeh-NEH-rik)
Official nonbrand names by which medicines are known. Generic names usually refer to the chemical name of the drug.
hepatic (heh-PA-tik)
Refers to the liver.
heroin (HAYR-uh-win)
A substance made from morphine. Heroin is very addictive and it is illegal to use or sell it in the United States. It is a type of opiate.
immune system (ih-MYOON SIS-tem)
The complex group of organs and cells that defends the body against infections and other diseases.
ingestion
Taking into the body by mouth.
inhalation
In medicine, refers to the act of taking a substance into the body by breathing.
investigational (in-VES-tih-GAY-shuh-nul)
In clinical trials, refers to a drug (including a new drug, dose, combination, or route of administration) or procedure that has undergone basic laboratory testing and received approval from the U.S. Food and Drug Administration (FDA) to be tested in human subjects. A drug or procedure may be approved by the FDA for use in one disease or condition, but be considered investigational in other diseases or conditions. Also called experimental.
liver (LIH-ver)
A large organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile.
marijuana (MAYR-uh-WAH-nuh)
The dried leaves and flowering tops of the Cannabis sativa plant, or an extract from the plant. Marijuana is being studied in the treatment of nausea and vomiting caused by chemotherapy or opiate drugs, such as morphine sulfate. Marijuana is also being studied in the treatment of pain.
metabolite (meh-TA-boh-lite)
A substance made or used when the body breaks down food, drugs or chemicals, or its own tissue (for example, fat or muscle tissue). This process, called metabolism, makes energy and the materials needed for growth, reproduction, and maintaining health. It also helps get rid of toxic substances.
narcotic (nar-KAH-tik)
A substance used to treat moderate to severe pain. Narcotics are like opiates such as morphine and codeine, but are not made from opium. They bind to opioid receptors in the central nervous system. Narcotics are now called opioids.
National Cancer Institute
The National Cancer Institute, part of the National Institutes of Health of the United States Department of Health and Human Services, is the Federal Government's principal agency for cancer research. The National Cancer Institute conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the National Cancer Institute Web site at http://www.cancer.gov. Also called NCI.
nausea
A feeling of sickness or discomfort in the stomach that may come with an urge to vomit. Nausea is a side effect of some types of cancer therapy.
oral (OR-ul)
By or having to do with the mouth.
ounce
A measure of weight (one-sixteenth pound) and volume (one-eighth cup).
PDQ
PDQ is an online database developed and maintained by the National Cancer Institute. Designed to make the most current, credible, and accurate cancer information available to health professionals and the public, PDQ contains peer-reviewed summaries on cancer treatment, screening, prevention, genetics, complementary and alternative medicine, and supportive care; a registry of cancer clinical trials from around the world; and directories of physicians, professionals who provide genetics services, and organizations that provide cancer care. Most of this information, and more specific information about PDQ, can be found on the NCI's Web site at http://www.cancer.gov/cancertopics/pdq. Also called Physician Data Query.
pharmacopoeia
A book describing chemicals, drugs, and other substances and how they are used as medicines. It is prepared by a recognized authority.
physician (fih-ZIH-shun)
Medical doctor.
plasma (PLAZ-muh)
The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma.
prescription (prih-SKRIP-shun)
A doctor's order for medicine or another intervention.
receptor (reh-SEP-ter)
A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell.
scientist
A person who has studied science, especially one who is active in a particular field of investigation.
sedative (SEH-duh-tiv)
A drug or substance used to calm a person down, relieve anxiety, or help a person sleep.
side effect
A problem that occurs when treatment affects healthy tissues or organs. Some common side effects of cancer treatment are fatigue, pain, nausea, vomiting, decreased blood cell counts, hair loss, and mouth sores.
significant
In statistics, describes a mathematical measure of difference between groups. The difference is said to be significant if it is greater than what might be expected to happen by chance alone. Also called statistically significant.
surgeon (SER-jun)
A doctor who removes or repairs a part of the body by operating on the patient.
symptom
An indication that a person has a condition or disease. Some examples of symptoms are headache, fever, fatigue, nausea, vomiting, and pain.
synthetic (sin-THEH-tik)
Having to do with substances that are man-made instead of taken from nature.
vomit (VAH-mit)
To eject some or all of the contents of the stomach through the mouth.
Western medicine (... MEH-dih-sin)
A system in which medical doctors and other healthcare professionals (such as nurses, pharmacists, and therapists) treat symptoms and diseases using drugs, radiation, or surgery. Also called allopathic medicine, biomedicine, conventional medicine, mainstream medicine, and orthodox medicine.

Table of Links

1http://www.cancer.gov/dictionary
2http://www.druglibrary.org/Schaffer/hemp/history/first12000/abel.htm
3http://books.nap.edu/openbook.php?isbn=0309071550
4http://books.nap.edu/openbook.php?isbn=0309065313#
5http://www.druglibrary.org/schaffer/hemp/taxact/woodward.htm
6http://www.hc-sc.gc.ca/dhp-mps/marihuana/how-comment/medpract/infoprof/index-en
g.php
7http://www.cancer.gov/cancertopics/pdq/levels-evidence-cam/HealthProfessional
8http://nccam.nih.gov
9http://www.cancer.gov/cam
10http://www.nlm.nih.gov/nccam/camonpubmed.html
11http://cancer.gov/cancerinfo/pdq/cancerdatabase
12http://cancer.gov/cancerinfo/pdq/adulttreatment
13http://cancer.gov/cancerinfo/pdq/pediatrictreatment
14http://cancer.gov/cancerinfo/pdq/supportivecare
15http://cancer.gov/cancerinfo/pdq/screening
16http://cancer.gov/cancerinfo/pdq/prevention
17http://cancer.gov/cancerinfo/pdq/genetics
18http://cancer.gov/cancerinfo/pdq/cam
19http://www.cancer.gov/cancertopics/pdq/cancer-cam-board
20http://www.cancer.gov/contact
21http://visualsonline.cancer.gov
22http://www.cancer.gov/cancertopics/coping/financial-legal
23http://www.cancer.gov/help