Cannabis and Cannabinoids
This article is a mirror of this page on the website of the National Cancer Institute.
General Information
Story
Laboratory / Animal / Preclinical Studies
Antitumor Effects
appetite stimulation
Analgesia
Human / Clinical Studies
Cannabis Pharmacology
cancer risk
Cancer Treatment
antiemetic effect
Cannabinoids
Cannabis
appetite stimulation
Cannabinoids
Cannabis
Analgesia
Cannabinoids
Cannabis
Stress and sleep
Cannabis
Side Effects
Cannabinoids
Cannabis
Overall Level of evidence for Cannabis and Cannabinoids
Changes to This Summary (03/28/2011)
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This complementary and alternative medicine (CAM) information summary provides an overview of the use of cannabis and its constituents as a treatment for people with cancer-related symptoms caused by the disease itself or its treatment.
This summary contains the following key elements:
Cannabis has been used for medicinal purposes for thousands of years before the current status as an illegal substance.
Chemical components of cannabis, called cannabinoid energopoiouneidika receptors are found throughout the body to produce pharmacological effects, particularly central nervous system and toanosopoiitiko 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 Terms toLexiko NCI Cancer 1, which is oriented towards nonexperts.Otan a term that is clicked, a definition will appear in separate parathyro.Ola related terms and their corresponding definitions will appear in a glossary in the printed version of the summary.
Reference citations in some PDQ CAM information summaries may include links to external websites operated by individuals or organizations for marketing or support the use of specific products or treatments. These references are included for reference and informational purposes only. Their inclusion should not be regarded as an indication of the content of websites, or of any treatment or product, by the Board Cancer PDQ CAM Editor 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, is a controlled substance and is classified as a Schedule I agent (enafarmako with increased potential for abuse and no known medical use). Ikannavi plant produces a resin containing psychoactive compounds called cannabinoids. The highest concentration of cannabinoid is in female flowers of the plant. [1] In botany, cannabis is difficult to study because of the lack of standardization of herbal products because of 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 Investigational New Drug (IND) application with the FDA.
The potential benefits of medicinal Cannabis for people living mekarkino include antiemetic effects, appetite stimulation, pain relief, and improved sleep. Though no relevant surveys of practice patterns, it appears that physicians caring for cancer patients who prescribe medicinal cannabis do mainly for the management of symptoms.
Cannabinoids are a group of compounds found terpenophenolic stinkannavi species (Cannabis sativa L. and Cannabis indica Lam.). This summary will review the role of cannabis and cannabinoids in the treatment of people with cancer and diseases associated with or related to therapeiaanepithymites actions.
References
L. Adams, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.Ê [PUBMED Abstract]
Story
Cannabis use for medicinal purposes dates back at least 3,000 years [.1 - 5] was introduced into Western medicine in the 1840s by WB O'Shaughnessy, a surgeon who learned of its medicinal properties while working in India for the British Society East India. The use of promoted for reported analgesic, sedative, anti-inflammatory, antispasmodic and anticonvulsant effects.
In 1937, the U.S. Treasury introduced the Tax Act Marihuana. This Act imposed a levy of one U.S. dollar an ounce for medicinal use of cannabis and one hundred U.S. dollars an ounce for recreational use. Giatroistis the United States were the main opponents of the law. The American Medical Association (AMA) opposed the act because physicians were required to pay a special tax for prescribing Cannabis, use special forms to obtain and keep a separate record of professional chrisi.Epipleon, AMA believed that there is objective evidence that cannabis was addictive was lacking and that passage of the law would prevent further research on medicinal value. [6] In 1942, cannabis was removed from IPAFarmakopoiias because of persistent concerns about its potential to cause harm. [2, 3]
In 1951, Congress passed the Act Boggs, which for the first time, included Cannabis with narcotic drugs. In 1970, with the enactment of the Law on pesticides, marijuana is classified as Annex I of drugs. Drugs of this class are distinguished as having no accepted medical use. Other Annex I substances include heroin, LSD, mescaline, methaqualone, and gamma-hydroxybutyrate.
Despite its name as it has no medical use, cannabis was distributed to patients by the U.S. government on a case-by tinparigoritiki use Investigational New Drug program established in 1978.Dianomi Cannabis through this program was discontinued in 1992 [. 1 to 4] In 2010, the U.S. Department of Veterans Affairs approved the use of marijuana for patients in countries where medical use is legal.
The main psychoactive ingredient 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 kaiemeto under the generic name dronabinol. Clinical trials determined that dronabinol was as effective as or better than other antiemetikonparagonton. [7] Dronabinol has also been studied for its ability to stimulate weight gain in patients with AIDS at the end of 1980. Clinical trial results showed no significant weight gain, although patients reported improvement in appetite. [8, 9]
Over the last 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 higher concentration of receptor CB2 is BSE lymphocytes and natural killer cells, suggesting a possible role in immunity. Endogenous cannabinoids have (endocannabinoids) have been identified and appear to have a role in regulating pain management, control of movement, feeding behavior, and memory. [11]
References
Abel EL: Marihuana, the first twelve thousand years. New York: Plenum Press, 1980. Also available online 2. Last accessed on March 17 2011.Ê
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 on March 17 2011.Ê
Mack A, J Joy: Marijuana as medicine? Science Beyond the controversy. Washington, DC:. National Academy Press, 2001 Also available online 4. Last accessed on March 17 2011.Ê
Booth M: Cannabis: A History. New York, New York: ST Martin, 2003.Ê
Russo EB, Jiang HE, Li X, et al:. Phytochemical and genetic analyzes of ancient cannabis from Central Asia. J Exp Bot 59 (15): 4171-82, 2008.Ê [PUBMED Abstract]
Schaffer Library of Drug Policy:. The Marihuana Tax Act of 1937: Taxation of Marihuana. Washington, DC: House of Representatives, Committee on ways and means of 1937.Diathesimo online 5. Last accessed on March 17 2011.Ê
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.Ê [PUBMED Abstract]
Gorter R, Seefried M, Volberding P: Dronabinol effects on weight in patients infected with HIV. AIDS 6 (1): 127, 1992.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
Devane WA, Dysarz FA third, Johnson MR, et al:. Identification and characterization of a cannabinoid receptor in rat brain. Mol Pharmacol 34 (5): 605-13, 1988.Ê [PUBMED Abstract]
Devane WA, Hanus L, Breuer A, et al:. Isolation and structure of an element of the brain associated with cannabinoid receptors. Science 258 (5090): 1946-9, 1992.Ê [PUBMED Abstract]
Pertwee RG: Pharmacology of cannabinoid receptors CB1 and CB2. There Pharmacol 74 (2): 129-80, 1997.Ê [PUBMED Abstract]
Felder CC, Glass M: cannabinoid receptors and endogenous agonists tous.Annu Rev Pharmacol Toxicol 38: 179-200, 1998.Ê [PUBMED Abstract]
Laboratory / Animal / Preclinical Studies
Cannabinoids are a group of 21 terpenophenolic carbon compounds produced exclusively from cannabis sativa and Cannabis indica species. [1, 2] These plant compounds may be referred to as phytocannabinoids. While delta-9-tetrahydrocannabinol (THC) is the principal psychoactive ingredient, other known compounds having biological activity is kannavinoli, cannabidiol, cannabichromene, cannabigerol, tetrahydrocannabivirin, and delta-8-THC.Kannavidiolis, specifically, is believed to have significant analgesic and anti -inflammatory activity without the psychoactive effect (high) of delta-9-THC.
Results against ogkouMia 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 administered various doses of THC by gavage. A dose dependent reduction in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was seen in mice. Reduced cases of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also observed in rats. In another study, delta-9-THC, delta-8-THC, cannabinol, and 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 to 8]
Cannabinoids may cause antitumor effects by various mechanisms, including the induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and tismetastasis. [9 - 11], cannabinoids appear to kill tumor cells, but do not affect non-transformed counterparts and may even protect from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce ypochorisiton 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] The tumor growth was inhibited by 60% in THC-treated mice compared to vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects.
Moreover, both of vegetable origin and endogenous cannabinoids have been studied for anti-inflammatory effects. One study showed that mouse endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation. [13] As a result, a case phytocannabinoids endocannabinoids and may be useful in the treatment of prolipsikai colon cancer has developed. [14]
Another study has shown delta-9-THC is a potent and selective ionparagonta by Kaposi's sarcoma-related herpesvirus (KSHV), also known as human herpesvirus 8. [15] The researchers concluded that additional studies are warranted to cannabinoids and herpesviruses, as they can lead to the development of drugs that inhibit the reactivation of these oncogenic viruses. Subsequently, another group of researchers reported increased efficiency of KSHV infection of human dermal microvascular epithelial cells in the presence of low doses of delta-9-THC. [16]
Stimulation of orexisPolles animal studies have previously shown that the delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase feed intake. Believed that the endogenous cannabinoid system can serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice. [17] In addition, CB1ypodocheis the hypothalamus may be involved in motivation or reward aspects of eating. [18]
AnalgisiaTin understanding of the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids kaisynthetikon agonists and antagonists. The CB1 receptor is both stokentriko nervous system (CNS) and peripheral nerve terminals. Similar meopioeidon receptors, increased levels of CB1 receptors found in the brain that regulate nociceptive processing. [19] CB2 receptors are located primarily in peripheral tissue, present in 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 regulation of pain has been obtained. [20, 21]
Cannabinoids can also contribute to the modulation of pain through an anti-inflammatory mechanism; A cannabinoid CB2 effect acting giaistiokyttaro receptors weaken the release of inflammatory factors, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids is described [. 22 to 24]
References
L. Adams, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.Ê [PUBMED Abstract]
Grotenhermen F, E Russo, eds:. Cannabis and Cannabinoids: Pharmacology, Toxicology, and therapeutic potential. Binghamton, NY: The Haworth Press, 2002.Ê
National Toxicology Program:. NTP Toxicology and carcinogenesis studies of 1-Trans-Delta (9)-tetrahydrocannabinol (No. CAS 03/08/1972) F344 rats and mice B6C3F1 (Ypersitisiiou Studies). Natl Toxicol Program Tech Rep Ser 446 (): 1-317, 1996.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
S ‡ nchez C, de Ceballos ML, Gomez del Pulgar T, et al:. Inhibition of growth of glioma in vivo by selective activation of CB (2) cannabinoid receptor. Cancer Res 61 (15): 5784-9, 2001.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
Casanova ML, Bl ‡ zquez C, Mart'nez-Palacio J, et al:. Inhibition of tumor growth of the skin and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest 111 (1): 43-50, 2003.Ê [PUBMED Abstract]
Bl ‡ zquez C, GONZ ‡ lez-Feria L, Alvarez L, et al:. Cannabinoids inhibit the pathway of vascular endothelial growth factor in gloiomata.Cancer Res 64 (16): 5617-23, 2004.Ê [PUBMED Abstract]
Guzm ‡ n M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003.Ê [PUBMED Abstract]
Bl ‡ zquez C, Casanova ML, Planas A, et al:. Inhibition of tumor angiogenesis of cannabinoids. FASEB J 17 (3): 529-31, 2003.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
Preet A, Ganju RK, Groopman JE: Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro, and the growth and metastasis in vivo. Oncogene 27 (3): 339-46, 2008.Ê [PUBMED Abstract]
Massa F, G Marsicano, Hermann H, et al:. The endogenous cannabinoid system protects against colonic inflammation. J Clin Invest 113 (8): 1202-9, 2004.Ê [PUBMED Abstract]
Patsos HA, DJ Hicks, Greenhough A, et al:. Cannabinoids and cancer: potential for the treatment of colon. Biochem Soc Trans 33 (Pt 4): 712-4, 2005.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
Zhang X, Wang JF, Kunos G, et al:. Cannabinoids differentiation sarcoma-Kaposi, associated herpesvirus infection and transformation. Cancer Res 67 (15): 7230-7, 2007.Ê [PUBMED Abstract]
. Mechoulam R, Berry EM, Avraham Y, et al: endocannabinoids, nutrition and breastfeeding - from our side. Int J Obes (Lond) 30 (Suppl 1): S24-8, 2006.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
Walker JM, Hohmann AG, Martin WJ et al,. The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999.Ê [PUBMED Abstract]
Meng ID, BH Manning, Martin WJ et al,. Analgesia A circuit activated by cannabinoids. Nature 395 (6700): 381-3, 1998.Ê [PUBMED Abstract]
Walker JM, Huang SM, NM Strangman, et al:. Modulation of pain through the release of endogenous cannabinoid anandamide. Proc Natl Acad Sci USA 96 (21): 12198-203, 1999.Ê [PUBMED Abstract]
Facci L, Dal Toso R, Romanello S, et al:. Mast cells express a peripheral cannabinoid receptor with differential sensitivity to anandamide and palmitoulaithanolamidio. Proc Natl Acad Sci USA 92 (8): 3376-80, 1995.Ê [PUBMED Abstract]
Ibrahim MM, Porreca F, Lai J, et al:. CB2 receptor activation of cannabinoid produce perception of pain by stimulating peripheral release of endogenous opioids. Proc Natl Acad Sci USA 102 (8): 3093-8, 2005.Ê [PUBMED Abstract]
Richardson JD, S kilo, Hargreaves KM: Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral receptors CB1. Pain 75 (1): 111-9, 1998.Ê [PUBMED Abstract]
Human / Clinical Studies
Cannabis FarmakologiasOtan hemp was ingested by mouth, there is a low (6% D20%) and variable oral bioavailability. [1, 2] Maximum plasmasygkentroseis of delta-9-tetrahydrocannabinol (THC) occur after 1 to 6 hours and remain elevated with a half-life of 20 to 30 ores.Lamvanetai oral delta-9-THC is initially metabolized in liver to 11-OH-THC, a potent psychoactive metabolite. When inhaled, cannabinoids rapidly absorbed into the bloodstream, with a peak concentration of 2 to 10 minutes, rapidly decreases for a period of 30 minutes and less production of psychoactive 11-OH metabolite.
Cannabinoids are known to interact with the hepatic cytochrome P450 enzyme. [3, 4] In one study, 24 cancer patients treated with intravenous irinotecan (600 mg, n = 12) or docetaxel followed (180 mg, n = 12), 3 weeks later, the same drugs concomitant with medicinal cannabis taken in the form of herbal tea for 15 consecutive days, starting 12 days before the second treatment. [4] The administration tisKannavis not significantly affect the exposure and clearance of irinotecan or docetaxel, while the route of administration herbal tea can not reproduce the effects of inhalation or oral ingestion of fat-dialytakannavinoeidi.
The risk karkinouMia number of studies have provided conflicting evidence on the risks of various cancers associated with cannabis use. A case-study group 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 host of other common malignancies, but found that among non-smokers from tobacco smoke, have never used kannavisyschetistike with increased risk of prostate cancer. [5] A plithysmiakimeleti-control of the association between cannabis use and risk toupnefmona and respiratory tract cancer in Los Angeles found no positive correlation with any type of cancer (mouth, pharynx, larynx, lung, or esophagus) when adjusting for various confounding factors such as cigarette smoking [. 6] A comprehensive Health Canada monograph on Marihuana (Marijuana, Cannabis): Information for Healthcare Professionals concludes that while there are many cellular and molecular studies provide strong evidence that inhaled marijuana is carcinogenic, the epidemiologic evidence of a link between of marijuana use and cancer is still unclear. [7]
Treatment karkinouDen no clinical trials of cannabis as a treatment for cancer in humans were identified in a search PubMed.
Antiemetic effect
KannavinoeidiPara advances in pharmacologic and nonpharmacologic management, nausea kaiemeto (N / V) remain distressing side effects for cancer patients and their families. Dronabinol was approved in the United States in 1986 osantiemetiko for use in cancer chemotherapy. Nabilone, one allosynthetiko form of delta-9-THC, was first approved in Canada in 1982 and is now available in the United States. [8] Both dronabinol nabilone and 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. Polyarithmesklinikes treatment trials and meta-analyzes have shown that dronabinol and nabilone are effective in the treatment of N / V chemotherapy induced [. 9 -12]
One systematic review studied 30 randomized comparisons of delta-9-THC preparations with placebo or other antiemetics from which data on the efficacy and harm were available. [13] Oral nabilone, oral dronabinol, and intramuscular levonantradol (a synthetic analog of dronabinol) tested. Inhaled Cannabis trials were not included. Among all 1366 patients included in the review, cannabinoids found to be more effective than the conventional antiemetic prochlorperazine, metoclopramide, chlorpromazine, triaithyloperazini, haloperidol, domperidone, and alizapride. Cannabinoids, however, was more effective in patients receiving very low or very high emetogenic chemotherapy. Side effects include a sense of being high, euphoria, sedation or somnolence, dizziness, malaise or depression, hallucinations, paranoia, and hypotension. [13]
Another analysis of 15 controlled studies compared nabilone with placebo or available antiemetic drugs. [14] Among 600 patients with cancer, nabilone found to be superior to prochlorperazine, domperidone, and alizapride, with nabilone favored for continuous use.
KannaviTreis studies have evaluated the efficacy of inhaled marijuana in chemotherapy-induced N / V. [15 to 17] In two 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 test, enastatistika significant antiemetic effect was higher among patients receiving high-dose methotrexate compared with those who received placebo. [16] The third study was a randomized, double-blind, placebo-controlled cross-over study involving 20 adults in which both inhaled and oral THC marijuana evaluated. A quarter of patients reported a positive response to the cannabinoid antiemetic treatments. This latter study reported in abstract form in 1984. A full report detailing the methods and results apparently unpublished, which limits a thorough interpretation of the significance of these findings. [17]
OrexisAnorexia stimulation, early satiety, weight loss and cachexia are problems experienced by patients with cancer. These patients face not only the deformation associated with waste, and the inability to participate in social interaction meals.
KannavinoeidiDyo controlled trials showed that oral THC has variable effects on appetite stimulation and weight loss in patients with advanced malignancies Kull human immunodeficiency (HIV) infection. [14] A study evaluated whether dronabinol alone or with megestrol acetate was higher, lower, or equal in activity to megestrol acetate only to the management of cancer related anorexia. [18] In this randomized double-blind study of 469 adults with advanced cancer and weight loss, patients received 2,5 mg orally twice daily THC, 800 mg orally daily megestrol, or both . Appetite increased by 75% in the megestrol and weight increased by 11%, compared to a 49% increase in appetite and a 3% increase in weight at the oral THC group. These two differences were statistically significant. Furthermore, the combination therapy did not provide additional benefits beyond those provided by megestrol acetate only. The authors concluded that dronabinol did little to promote appetite or weight gain in patients with advanced cancer compared with megestrol acetate. However, a smaller placebo-controlled trial dronabinol in cancer patients demonstrated improved and enhanced chemosensory perception in the cannabinoid groupÑfood better taste, increased appetite, and the proportion of calories consumed as protein was greater than in placebo recipients. [19]
Another clinical trial involving 139 patients with HIV or AIDS, and weight loss was found that, compared to placebo, oral dronabinol was associated with a statistically significant increase in appetite after 4 to 6 weeks. Patients receiving dronabinol tended to stabilize the weight, while patients receiving placebo continued to lose weight. [20]
KannaviAnecdotally in trials conducted in the 1970's involved healthy control subjects, inhaling Cannabis led to an increase tisthermidikis recruitment, mainly in the form of between meals, with increased intake of fatty and sugary foods. No published studies have investigated the effect of inhaled cannabis on appetite in patients with cancer.
Analgesia
KannavinoeidiI pain management improves a patient's quality of life at all stadiatou 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 in the central nervous system (CNS) and peripheral nerve terminals. [21] The CB2 receptors are located primarily in peripheral tissues and expressed only in small amounts in the CNS. While 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 damage. When cancer pain is severe and persistent, are often resistant to treatment with opioids.
Two studies examined the effects of oral delta-9-THC with the threat of cancer. The first, a double-blind controlled study involving ten patients, measured as the intensity of pain and to relieve pain. [24] reported that 15 mg and 20 mg doses of cannabinoid delta-9-THC were associated with significant analgesic effects, with antiemetic effects and appetite stimulation.
In a single dose study was then comprising 36 patients, it was reported that 10 mg doses of delta-9-THC produced analgesic effects during a 7-hour observation period 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 whole-plant extract with controlled cannabinoid content in oral sprays. In a multicenter, double-blind, placebo-controlled study, THC: cannabidiol (THC: CBD) extract and THC extract alone in analgesic management of patients with advanced cancer and moderate to severe cancer-related pain. The patients were divided into one of three treatment groups: THC: CBD extract, THC, or placebo. The researchers concluded that the THC:. CBD extract was effective in relieving pain in patients with advanced cancer whose pain is not fully relieved by strong opioids [26]
An observational study evaluated the efficacy of nabilone in patients with advanced cancer who experience pain and allasymptomata (anorexia, depression, and anxiety). The researchers reported that patients who used nabilone experienced improved management of pain, nausea, anxiety and distress compared with untreated patients. Nabilone was also associated with reduced use of opioids, nonsteroidal anti-inflammatory drugs, tricyclic antidepressants, gabapentin, dexamethasone, metoclopramide, kaiondansetroni. [27]
KannaviO Neuropathic pain is a symptom of cancer patients may experience, especially if treated with platinum-based chemotherapy itaxanes. 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% to 52% of patients in the cannabis group and in 24% of patients in group placebo. 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.
Stress and sleep
KannaviOi patients often experience mood elevation after exposure to Cannabis, depending on their previous experience. In five patient case series of inhaled marijuana that examined the analgesic effects of THC, reported that patients administered THC had improved mood, improved sense of well-being, and less anxiety. [29]
Another common effect of cannabis is drowsiness. In a study of a sublingual spray, a cannabis-based mixture was able to improve the quality of sleep. [30] A small placebo-controlled study of dronabinol in cancer patients with altered chemosensory perception also improved the quality of sleep and relaxation in THC-treated patients. [19]
References
L. Adams, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.Ê [PUBMED Abstract]
Agurell S, M Halldin, 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.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
Watanabe T, T Matsunaga, 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.Ê [PUBMED Abstract]
Sidney S, Quesenberry CP Jr, GD Friedman, et al:. Marijuana use and cancer incidence (California, United States). Cancer Causes Control 8 (5): 722-8, 1997.Ê [PUBMED Abstract]
Hashibe M, H Morgenstern, 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.Ê [PUBMED Abstract]
Health Canada:. Marihuana (Marijuana, Cannabis): Dried Plant for Administration by ingestion or by other means. Ottawa, Canada: Health Canada, 2010. Available online 6. Last accessed on March 17 2011.Ê
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.Ê [PUBMED Abstract]
Ahmedzai S, Carlyle DL, Calder IT, et al:. Antiemetic efficacy and toxicity of nabilone, a synthetic cannabinoid, in chemotherapy for lung cancer. Br J Cancer 48 (5): 657-63, 1983.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract]
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.Ê [PUBMED Abstract
References
L. Adams, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.Ê [PUBMED Abstract]
Grotenhermen F, E Russo, eds:. Cannabis and Cannabinoids: Pharmacology, Toxicology, and therapeutic potential. Binghamton, NY: The Haworth Press, 2002.Ê
Guzm ‡ n M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003.Ê [PUBMED Abstract
Overall Level of evidence for Cannabis and Cannabinoids
Cannabinoids
Changes to This Summary (03/28/2011)
