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Cannabis and Cannabinoids (PDQ®): Complementary and alternative medicine - Health Professional Information [NCI]
This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
Cannabis and Cannabinoids
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.
- By federal law, the possession of Cannabis, also known as marijuana, is illegal in the United States; however, a growing number of states and the District of Columbia have enacted laws to legalize its medical use.
- The U.S. Food and Drug Administration has not approved Cannabis as a treatment for cancer or any other medical condition.
- 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.
- Commercially available cannabinoids, such as dronabinol and nabilone, are approved drugs for the treatment of cancer-related side effects.
- 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, which is oriented toward nonexperts. When a linked term is clicked, a definition will appear in a separate window.
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]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. Although few relevant surveys of practice patterns exist, it appears that physicians caring for cancer patients in the United States who recommend medicinal Cannabis predominantly do so for symptom management.[2]
Cannabinoids are a group of terpenophenolic compounds found in Cannabis species (e.g., Cannabis sativa L.). 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.
- Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.
- Doblin RE, Kleiman MA: Marijuana as antiemetic medicine: a survey of oncologists' experiences and attitudes. J Clin Oncol 9 (7): 1314-9, 1991.
Cannabis use for medicinal purposes dates back at least 3,000 years.[1,2,3,4,5] 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 $1 per ounce for medicinal use of Cannabis and $100 per 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 harmful 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.[1,2,3,4] Although federal law prohibits the use of Cannabis, the table below lists the localities that permit its use for certain medical conditions.
List of Localities That Permit Use ofCannabisfor Certain Medical Conditions
Alaska (AK) |
Arizona (AZ) |
California (CA) |
Colorado (CO) |
Connecticut (CT) |
Delaware (DE) |
District of Columbia (DC) |
Hawaii (HI) |
Illinois (IL) |
Maine (ME) |
Maryland (MD) |
Michigan (MI) |
Montana (MT) |
Nevada (NV) |
New Hampshire (NH) |
New Jersey (NJ) |
New Mexico (NM) |
Oregon (OR) |
Rhode Island (RI) |
Vermont (VT) |
Washington (WA) |
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 available at the time.[7] Dronabinol was also studied for its ability to stimulate weight gain in patients with AIDS in the late 1980s. Thus, the indications were expanded to include treatment of anorexia associated with human immunodeficiency virus infection in 1992. Clinical trial results showed no statistically significant weight gain, although patients reported an improvement in appetite.[8,9]
Within the past 20 years, the neurobiology of cannabinoids has been analyzed.[10,11,12,13] The first cannabinoid receptor, CB1, was 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]
Spasticity is a common symptom of multiple sclerosis for which existing therapy is unsatisfactory and may include muscle stiffness, reduced mobility, and pain. In Canada, New Zealand, and some countries in Europe, nabiximols (a THC:cannabidiol extract) is approved for the treatment of spasticity associated with multiple sclerosis via oromucosal administration.[14,15]
- Abel EL: Marihuana, The First Twelve Thousand Years. New York: Plenum Press, 1980. Also available online. Last accessed March 25, 2014.
- Joy JE, Watson SJ, Benson JA, eds.: Marijuana and Medicine: Assessing the Science Base. Washington, DC: National Academy Press, 1999. Also available online. Last accessed March 25, 2014.
- Mack A, Joy J: Marijuana As Medicine? The Science Beyond the Controversy. Washington, DC: National Academy Press, 2001. Also available online. Last accessed March 25, 2014.
- Booth M: Cannabis: A History. New York, NY: St Martin's Press, 2003.
- 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.
- 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. Last accessed March 25, 2014.
- 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.
- Gorter R, Seefried M, Volberding P: Dronabinol effects on weight in patients with HIV infection. AIDS 6 (1): 127, 1992.
- 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.
- 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.
- 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.
- Pertwee RG: Pharmacology of cannabinoid CB1 and CB2 receptors. Pharmacol Ther 74 (2): 129-80, 1997.
- Felder CC, Glass M: Cannabinoid receptors and their endogenous agonists. Annu Rev Pharmacol Toxicol 38: 179-200, 1998.
- Zajicek JP, Apostu VI: Role of cannabinoids in multiple sclerosis. CNS Drugs 25 (3): 187-201, 2011.
- Howard P, Twycross R, Shuster J, et al.: Cannabinoids. J Pain Symptom Manage 46 (1): 142-9, 2013.
Laboratory / Animal / Preclinical Studies
Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis species (e.g., Cannabis sativa L.) .[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 (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, 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 (HCC) 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.[5,6,7,8]
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9,10,11,12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents.[13,14] 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.[15]
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC.[16] Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma [17] and breast cancer.[18]
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic, mammary cells.[19]
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[20] In the experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.[21]
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
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.[22] 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. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[23,24]
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.[25] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[26,27,28,29]
CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[30] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells.
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.[31] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[32]
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 regions of the brain that regulate nociceptive processing.[33] 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.[34,35]
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.[36,37,38] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[39]
- Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.
- Grotenhermen F, Russo E, eds.: Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Binghamton, NY: The Haworth Press, 2002.
- 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.
- 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.
- Sánchez 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.
- 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.
- Casanova ML, Blázquez C, Martínez-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.
- Blázquez C, González-Feria L, Alvarez L, et al.: Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Res 64 (16): 5617-23, 2004.
- Guzmán M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003.
- Blázquez C, Casanova ML, Planas A, et al.: Inhibition of tumor angiogenesis by cannabinoids. FASEB J 17 (3): 529-31, 2003.
- 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.
- Ramer R, Bublitz K, Freimuth N, et al.: Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1. FASEB J 26 (4): 1535-48, 2012.
- Velasco G, Sánchez C, Guzmán M: Towards the use of cannabinoids as antitumour agents. Nat Rev Cancer 12 (6): 436-44, 2012.
- Cridge BJ, Rosengren RJ: Critical appraisal of the potential use of cannabinoids in cancer management. Cancer Manag Res 5: 301-13, 2013.
- Torres S, Lorente M, Rodríguez-Fornés F, et al.: A combined preclinical therapy of cannabinoids and temozolomide against glioma. Mol Cancer Ther 10 (1): 90-103, 2011.
- Vara D, Salazar M, Olea-Herrero N, et al.: Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. Cell Death Differ 18 (7): 1099-111, 2011.
- Preet A, Qamri Z, Nasser MW, et al.: Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis. Cancer Prev Res (Phila) 4 (1): 65-75, 2011.
- Nasser MW, Qamri Z, Deol YS, et al.: Crosstalk between chemokine receptor CXCR4 and cannabinoid receptor CB2 in modulating breast cancer growth and invasion. PLoS One 6 (9): e23901, 2011.
- Shrivastava A, Kuzontkoski PM, Groopman JE, et al.: Cannabidiol induces programmed cell death in breast cancer cells by coordinating the cross-talk between apoptosis and autophagy. Mol Cancer Ther 10 (7): 1161-72, 2011.
- Aviello G, Romano B, Borrelli F, et al.: Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. J Mol Med (Berl) 90 (8): 925-34, 2012.
- Romano B, Borrelli F, Pagano E, et al.: Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol. Phytomedicine 21 (5): 631-9, 2014.
- 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.
- Zhu LX, Sharma S, Stolina M, et al.: Delta-9-tetrahydrocannabinol inhibits antitumor immunity by a CB2 receptor-mediated, cytokine-dependent pathway. J Immunol 165 (1): 373-80, 2000.
- McKallip RJ, Nagarkatti M, Nagarkatti PS: Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response. J Immunol 174 (6): 3281-9, 2005.
- Massa F, Marsicano G, Hermann H, et al.: The endogenous cannabinoid system protects against colonic inflammation. J Clin Invest 113 (8): 1202-9, 2004.
- 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.
- Liu WM, Fowler DW, Dalgleish AG: Cannabis-derived substances in cancer therapy--an emerging anti-inflammatory role for the cannabinoids. Curr Clin Pharmacol 5 (4): 281-7, 2010.
- Malfitano AM, Ciaglia E, Gangemi G, et al.: Update on the endocannabinoid system as an anticancer target. Expert Opin Ther Targets 15 (3): 297-308, 2011.
- Sarfaraz S, Adhami VM, Syed DN, et al.: Cannabinoids for cancer treatment: progress and promise. Cancer Res 68 (2): 339-42, 2008.
- Nabissi M, Morelli MB, Santoni M, et al.: Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents. Carcinogenesis 34 (1): 48-57, 2013.
- 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.
- 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.
- Walker JM, Hohmann AG, Martin WJ, et al.: The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999.
- Meng ID, Manning BH, Martin WJ, et al.: An analgesia circuit activated by cannabinoids. Nature 395 (6700): 381-3, 1998.
- 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.
- 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.
- 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.
- Richardson JD, Kilo S, Hargreaves KM: Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral CB1 receptors. Pain 75 (1): 111-9, 1998.
- Khasabova IA, Gielissen J, Chandiramani A, et al.: CB1 and CB2 receptor agonists promote analgesia through synergy in a murine model of tumor pain. Behav Pharmacol 22 (5-6): 607-16, 2011.
Human / Clinical Studies
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 pooled analysis of three case-cohort studies of men in northwestern Africa (430 cases and 778 controls) showed a significantly increased risk of lung cancer among tobacco smokers who also inhaled Cannabis.[5]
A large, retrospective cohort study of 64,855 men aged 15 to 49 years from the United States found that Cannabis use was not associated with tobacco-related cancers and a number of other common malignancies. However, the study did find that, among nonsmokers of tobacco, ever having used Cannabis was associated with an increased risk of prostate cancer.[6]
A population-based 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 and found no positive associations with any cancer type (oral, pharyngeal, laryngeal, lung, or esophagus) when adjusting for several confounders, including cigarette smoking.[7]
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 inhalation and lung cancer after adjusting for tobacco use.[8]
Epidemiologic studies examining one association of Cannabis use with head and neck squamous cell carcinomas have also been inconsistent in their findings. A pooled analysis of nine case-control studies from the U.S./Latin American International Head and Neck Cancer Epidemiology (INHANCE) Consortium included information from 1,921 oropharyngeal cases, 356 tongue cases, and 7,639 controls. Compared with those who never smoked Cannabis, Cannabis smokers had an elevated risk of oropharyngeal cancers and a reduced risk of tongue cancer. These study results both reflect the inconsistent effects of cannabinoids on cancer incidence noted in previous studies and suggest that more work needs to be done to understand the potential role of human papillomavirus infection.[9]
With a hypothesis that chronic marijuana use produces adverse effects on the human endocrine and reproductive systems, the association between marijuana use and incidence of testicular germ cell tumors (TGCTs) has been examined.[10,11,12] Three population-based case-control studies report an association between marijuana use and elevated risk of TGCTs, especially nonseminoma or mixed-histology tumors.[10,11,12] However, the sample sizes in these studies were inadequate to address marijuana dose by addressing associations with respect to recency, frequency, and duration of use. These early reports of marijuana use and TGCTs establish the need for larger, well-powered, prospective studies, especially studies evaluating the role of endocannabinoid signaling and cannabinoid receptors in TGCTs.
A comprehensive Health Canada monograph on marijuana concluded 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.[13]
Cancer Treatment
No clinical trials of Cannabis as a treatment for cancer in humans were identified in a PubMed search; however, a single, small study of intratumoral injection of delta-9-THC in patients with recurrent glioblastoma multiforme reported potential antitumoral activity.[14,15]
Antiemetic Effect
Despite advances in pharmacologic and nonpharmacologic management, nausea and vomiting (N/V) remain distressing side effects for cancer patients and their families. Dronabinol, a synthetically produced delta-9-THC, was approved in the United States in 1986 as an antiemetic to be used in cancer chemotherapy. Nabilone, a synthetic derivative of delta-9-THC, was first approved in Canada in 1982 and is now also available in the United States.[16] 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.[17,18,19,20] The National Comprehensive Cancer Network Guidelines recommend cannabinoids as breakthrough treatment for chemotherapy-related N/V.
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.[21] 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.[21] Newer antiemetics (e.g., 5-HT3 receptor antagonists) have not been directly compared with Cannabis or cannabinoids in cancer patients.
Another analysis of 15 controlled studies compared nabilone with placebo or available antiemetic drugs.[22] Among 600 cancer patients, nabilone was found to be superior to prochlorperazine, domperidone, and alizapride, with nabilone favored for continuous use.
(Refer to the Cannabis section in the PDQ summary on Nausea and Vomiting for more information.)
Three trials have evaluated the efficacy of inhaled marijuana in chemotherapy-induced N/V.[23,24,25] 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,[23] but in the second trial, a statistically significant superior antiemetic effect of inhaled Cannabis versus placebo was found among patients receiving high-dose methotrexate.[24] 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.[25]
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.
Three 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.[22] 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.[26] 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 after 8 to 11 weeks of treatment. 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 group—food tasted better, appetite increased, and the proportion of calories consumed as protein was greater than in the placebo recipients.[27]
In a randomized clinical trial, researchers compared the safety and effectiveness of orally administered Cannabis extract (2.5 mg THC and 1 mg cannabidinol), THC (2.5 mg), or placebo for the treatment of cancer-related anorexia-cachexia in 243 patients with advanced cancer who received treatment twice daily for 6 weeks. Results demonstrated that although these agents were well tolerated by these patients, no differences were observed in patient appetite or quality of life among the three groups at this dose level and duration of intervention.[28]
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.[29]
In trials conducted in the 1980s that involved healthy control subjects, inhaling Cannabis led to an increase in caloric intake, mainly in the form of between-meal snacks, with increased intakes of fatty and sweet foods.[30,31] No published studies have explored the effect of inhaled Cannabis on appetite in cancer patients.
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.[32] 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.[33,34]
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.[35] 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.[36] 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 nabiximols (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.[37] In a randomized, placebo-controlled, graded-dose trial, opioid-treated cancer patients with poorly controlled chronic pain demonstrated significantly better control of pain and sleep disruption with THC:CBD oromucosal spray at lower doses (1–4 and 6–10 sprays/day), compared with placebo. Adverse events were dose related, with only the high-dose group (11–16 sprays/day) comparing unfavorably with the placebo arm. These studies provide promising evidence of an "adjuvant analgesic" effect of THC:CBD in this opioid-refractory patient population and may provide an opportunity to address this significant clinical challenge.[38] An open-label extension study of 43 patients who had participated in the randomized trial found that some patients continued to obtain relief of their cancer-related pain with long-term use of the THC:CBD oromucosal spray without increasing their dose of the spray or the dose of their other analgesics.[39]
A randomized, placebo-controlled, crossover pilot study of nabiximols in 16 patients with chemotherapy-induced neuropathic pain showed no significant difference between the treatment and placebo groups. A responder analysis, however, demonstrated that five patients reported a reduction in their pain of at least 2 points, suggesting that a larger follow-up study may be warranted.[40]
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.[41]
Animal studies have suggested a synergistic analgesic effect when cannabinoids are combined with opioids. The results from one pharmacokinetic interaction study have been reported. In this study, 21 patients with chronic pain were administered vaporized Cannabis along with sustained-release morphine or oxycodone for 5 days.[42] The patients who received vaporized Cannabis and sustained-release morphine had a statistically significant decrease in their mean pain score over the 5-day period; those who received vaporized Cannabis and oxycodone did not. These findings should be verified by further studies before recommendations favoring such an approach are warranted in general clinical practice.
Neuropathic pain is a symptom cancer patients may experience, especially if treated with platinum-based chemotherapy or taxanes. To date, no clinical trial has examined the effectiveness of cannabinoid preparations in the treatment of chemotherapy-induced neuropathic pain.
Two randomized controlled trials of inhaled Cannabis in patients with peripheral neuropathy or neuropathic pain of various etiologies found that pain was reduced in patients who received inhaled Cannabis, compared with those who received placebo.[43,44] Two additional trials of inhaled Cannabis have also demonstrated the benefit of Cannabis over placebo in HIV-associated neuropathic pain.[45,46]
Anxiety and Sleep
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.[47]
Another common effect of Cannabis is sleepiness. In a trial of a sublingual spray, a Cannabis-based mixture was able to improve sleep quality.[48] 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.[27]
Current Clinical Trials
Check NCI's list of cancer clinical trials for cancer CAM clinical trials on dronabinol, marijuana, nabiximols and nabilone that are actively enrolling patients.
General information about clinical trials is also available from the NCI Web site.
- Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.
- 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.
- 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.
- Engels FK, de Jong FA, Sparreboom A, et al.: Medicinal cannabis does not influence the clinical pharmacokinetics of irinotecan and docetaxel. Oncologist 12 (3): 291-300, 2007.
- Berthiller J, Straif K, Boniol M, et al.: Cannabis smoking and risk of lung cancer in men: a pooled analysis of three studies in Maghreb. J Thorac Oncol 3 (12): 1398-403, 2008.
- 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.
- 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.
- 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.
- Marks MA, Chaturvedi AK, Kelsey K, et al.: Association of marijuana smoking with oropharyngeal and oral tongue cancers: pooled analysis from the INHANCE consortium. Cancer Epidemiol Biomarkers Prev 23 (1): 160-71, 2014.
- Daling JR, Doody DR, Sun X, et al.: Association of marijuana use and the incidence of testicular germ cell tumors. Cancer 115 (6): 1215-23, 2009.
- Trabert B, Sigurdson AJ, Sweeney AM, et al.: Marijuana use and testicular germ cell tumors. Cancer 117 (4): 848-53, 2011.
- Lacson JC, Carroll JD, Tuazon E, et al.: Population-based case-control study of recreational drug use and testis cancer risk confirms an association between marijuana use and nonseminoma risk. Cancer 118 (21): 5374-83, 2012.
- Health Canada: Marihuana (Marijuana, Cannabis): Dried Plant for Administration by Ingestion or Other Means. Ottawa, Canada: Health Canada, 2010. Available online. Last accessed March 25, 2014.
- Guzmán M, Duarte MJ, Blázquez C, et al.: A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. Br J Cancer 95 (2): 197-203, 2006.
- Velasco G, Sánchez C, Guzmán M: Towards the use of cannabinoids as antitumour agents. Nat Rev Cancer 12 (6): 436-44, 2012.
- 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.
- 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.
- 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.
- 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.
- 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.
- Tramèr 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.
- Ben Amar M: Cannabinoids in medicine: A review of their therapeutic potential. J Ethnopharmacol 105 (1-2): 1-25, 2006.
- 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.
- Chang AE, Shiling DJ, Stillman RC, et al.: Delta-9-tetrahydrocannabinol as an antiemetic in cancer patients receiving high-dose methotrexate. A prospective, randomized evaluation. Ann Intern Med 91 (6): 819-24, 1979.
- 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.
- 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.
- 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 22 (9): 2086-93, 2011.
- Strasser F, Luftner D, Possinger K, et al.: Comparison of orally administered cannabis extract and delta-9-tetrahydrocannabinol in treating patients with cancer-related anorexia-cachexia syndrome: a multicenter, phase III, randomized, double-blind, placebo-controlled clinical trial from the Cannabis-In-Cachexia-Study-Group. J Clin Oncol 24 (21): 3394-400, 2006.
- 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.
- Foltin RW, Brady JV, Fischman MW: Behavioral analysis of marijuana effects on food intake in humans. Pharmacol Biochem Behav 25 (3): 577-82, 1986.
- Foltin RW, Fischman MW, Byrne MF: Effects of smoked marijuana on food intake and body weight of humans living in a residential laboratory. Appetite 11 (1): 1-14, 1988.
- Walker JM, Hohmann AG, Martin WJ, et al.: The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999.
- Calignano A, La Rana G, Giuffrida A, et al.: Control of pain initiation by endogenous cannabinoids. Nature 394 (6690): 277-81, 1998.
- Fields HL, Meng ID: Watching the pot boil. Nat Med 4 (9): 1008-9, 1998.
- 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.
- 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.
- 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.
- Portenoy RK, Ganae-Motan ED, Allende S, et al.: Nabiximols for opioid-treated cancer patients with poorly-controlled chronic pain: a randomized, placebo-controlled, graded-dose trial. J Pain 13 (5): 438-49, 2012.
- Johnson JR, Lossignol D, Burnell-Nugent M, et al.: An open-label extension study to investigate the long-term safety and tolerability of THC/CBD oromucosal spray and oromucosal THC spray in patients with terminal cancer-related pain refractory to strong opioid analgesics. J Pain Symptom Manage 46 (2): 207-18, 2013.
- Lynch ME, Cesar-Rittenberg P, Hohmann AG: A double-blind, placebo-controlled, crossover pilot trial with extension using an oral mucosal cannabinoid extract for treatment of chemotherapy-induced neuropathic pain. J Pain Symptom Manage 47 (1): 166-73, 2014.
- 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.
- Abrams DI, Couey P, Shade SB, et al.: Cannabinoid-opioid interaction in chronic pain. Clin Pharmacol Ther 90 (6): 844-51, 2011.
- Wilsey B, Marcotte T, Deutsch R, et al.: Low-dose vaporized cannabis significantly improves neuropathic pain. J Pain 14 (2): 136-48, 2013.
- Wilsey B, Marcotte T, Tsodikov A, et al.: A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain. J Pain 9 (6): 506-21, 2008.
- 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.
- Ellis RJ, Toperoff W, Vaida F, et al.: Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial. Neuropsychopharmacology 34 (3): 672-80, 2009.
- Noyes R Jr, Baram DA: Cannabis analgesia. Compr Psychiatry 15 (6): 531-5, 1974 Nov-Dec.
- 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.
Adverse Effects
Cannabisand Cannabinoids
Because cannabinoid receptors, unlike opioid receptors, are not located in the brainstem areas controlling respiration, lethal overdoses from Cannabis and cannabinoids do not occur.[1,2,3,4] However, cannabinoid receptors are present in other tissues throughout the body, not just in the central nervous system, and 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. However, 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 1–3 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.
Since Cannabis smoke contains many of the same components as tobacco smoke, there are valid concerns about the adverse pulmonary effects of smoked Cannabis. A longitudinal study in a noncancer population evaluated repeated measurements of pulmonary function over 20 years in 5,115 men and women whose smoking histories were known.[5] While tobacco exposure was associated with decreased pulmonary function, the investigators concluded that occasional and low-cumulative Cannabis use was not associated with adverse effects on pulmonary function (forced expiratory volume in the first second of expiration [FEV1] and forced vital capacity [FVC]).
- Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.
- Grotenhermen F, Russo E, eds.: Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Binghamton, NY: The Haworth Press, 2002.
- 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.
- Guzmán M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003.
- Pletcher MJ, Vittinghoff E, Kalhan R, et al.: Association between marijuana exposure and pulmonary function over 20 years. JAMA 307 (2): 173-81, 2012.
Summary of the 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:
- Be published in a peer-reviewed scientific journal.
- Report on therapeutic outcome or outcomes, such as tumor response, improvement in survival, or measured improvement in quality of life.
- Describe clinical findings in sufficient detail for a meaningful evaluation to be made.
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.
Several controlled clinical trials have been performed, and meta-analyses of these support a beneficial effect of cannabinoids (dronabinol and nabilone) on chemotherapy -induced nausea and vomiting (N/V) compared with placebo. Both dronabinol and nabilone are approved by the U.S. Food and Drug Administration for the prevention or treatment of chemotherapy-induced N/V in cancer patients but not for other symptom management or off-label use. |
- 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 treatment–related 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 treatment–related side effects.
Changes to This Summary (05 / 13 / 2014)
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.
Laboratory/Animal/Preclinical Studies
Added text to state that a subsequent study found that the antiproliferative effect of cannabidiol was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors (cited Romano et al. as reference 21).
This summary is written and maintained by the PDQ Cancer Complementary and Alternative Medicine Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.
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, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
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 reviewers for Cannabis and Cannabinoids are:
- Donald I. Abrams, MD (UCSF Osher Center for Integrative Medicine)
- Nagi B. Kumar, PhD, RD, FADA (Fellow of the American Dietetic Association)
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. 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 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, a collection of over 2,000 scientific images.
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.
Contact Us
More information about contacting us or receiving help with the Cancer.gov Web site can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the Web site's Contact Form.
Last Revised: 2014-05-13
This information does not replace the advice of a doctor. Healthwise, Incorporated disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use. How this information was developed to help you make better health decisions.
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text:
NH Fish & Game plans $695,000 tracking project to study moose population's rapid decline
Normandeau estimated that the moose population in the state is 4,500 at this point, which is considered a low number.
Using helicopters and net-guns, the wildlife biologists capture and radio-collar cow and calf moose, and then use GPS technology to track their movements.
Ted Walski, a Fish and Game biologist, recently told the Keene Sentinel that sightings are down 20 to 30 percent in recent years.
They are hunted in October for nine days through a state lottery that this year granted permits to 275 people from a pool of 13,000 applicants.
"It's completely gone," he said. "And other areas are experiencing similar declines while other areas are doing well. We're trying to figure out what is going on, and if there are things we can do, long-term, to ensure we have moose in the future."
In other action, the council voted to:
• Confirm Perry Plummer to continue as director of Homeland Security and Emergency Management, after applauding his recent response to flooding in various parts of the state.

subset: commoncrawl


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GOP calls Shaheen letter a 'stunt'
"That issuer has eliminated ten of the state's 26 hospitals from its provider network for all plans issued through the marketplace, including in the multi-state program plan," Shaheen, D-NH, wrote in a letter to U.S. Health and Human Services Secretary Kathleen Sebelius. "As a result, I have heard from consumers who have been left without access to the provider with whom they had built a long-standing relationship."
"Once again, Senator Jeanne Shaheen is trying to distract from her blind support for the President's failed policies and her deciding vote for ObamaCare with another desperate election-year stunt," Horn said in a statement. "Senator Shaheen is directly responsible for imposing this terrible law on New Hampshire and forcing thousands of her constituents to give up their doctors and lose their health insurance."


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Intel To Launch 4.5W Haswell Processors Later This Year
Tue, Jul 23, 2013 - 2:25 PMIntel disclosed that they will be coming out with a 4.5W SDP (Scenario Design Power) variant of Haswell during an analyst briefing that took place this morning. Intel did not give any specifics when it comes to clock speeds, or the price of this ultra low power processor, but did say that it would be coming out later this year in limited volumes. SDP refers to power draw during sustained workloads, whereas traditional TDP ratings measure power usage during shorter bursts of activity. Previously leaked documents show this unnamed processor being a Y-series model thanks to the TDP Spec table below that was discovered. Intel says that the 4.5W SDP processor will be used in select fanless tablets & 2-in-1 detachables.
Intel PR Statement Made Today:
- At Computex we disclosed 4th gen Core would operate as low as 6 watts SDP. In fact, parts as low as 4.5 watts will be in the market later this year in limited volumes. The 4.5 watt parts enable incredibly thin and fanless designs with all day battery life and great performance.
- The 4.5W SDP Y processors enable Intel Core architecture in select fanless tablets & 2-in-1 detachables. The 6W SDP Y processors will feature in detachables and thin convertibles 2-in-1s that while being super thin, will still need some fanned cooling. Both Y processors will offer balanced performance and mobility across productivity & tablet workloads.
- We're focused on bringing the power down in a big way to deliver on more mobile and fanless designs. This is yet another step to move the industry in that direction. The Thermal Design Power (TDP) for the Y processors is 11.5W, same TDP as on the 6W Y processors.
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You are hereCobb County Clarifies: Teach Only Science in Science Classes
On January 8, 2003, the Cobb County, Georgia, School District issued guidelines that clarify the new "Theories of Origins" policy. WGBH Evolution Series Receives Award
The National Association of Science Writers has awarded Richard Hutton, producer of the NOVA/Clear Blue Skies Evolution series, its Science in Society award in the Television category. Evolution, first broadcast September 24-27, 2001, but rebroadcast in 2002, was honored "for recognizing the impact the science of evolution has had on society for well over 100 years. AAAS: "Intelligent Design" Not Smart for Science Classes
The American Association for the Advancement of Science, the world's largest general scientific organization, recently announced the top ten key science and technology policy issues to emerge in 2002. Among them: 5) INTELLIGENT DESIGN--NOT SMART FOR SCIENCE CLASSES: Voices for Evolution
Over seventy-five years after the Scopes trial, the controversy over the teaching of creationism in the public schools continues unabated. On the front lines of the controversy is the National Center for Science Education — NCSE — the only organization entirely devoted to defending the teaching of evolution in the public schools. Among the tools that NCSE provides for those wishing to defend the teaching of evolution is its publication Voices for Evolution, published first in 1989 and then in a revised edition in 1995. AIG Analyzes ID
Stating some of the same criticisms NCSE has raised about Intelligent Design, Carl Wieland of the young-earth creationist organization Answers in Genesis (AiG), criticizes the ID movement for not having a "'story of the past" – of lacking a coherent narrative of "what happened", and focusing only on the mechanism (of natural selection.) As Wieland points out, "if the origins debate is not about a 'story of the past', what is it about?" The reason for the lack of a coherent position on "what happened" is "a necessity, because they do not agree within themselves on a st Pages |
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In certain cases of navicular disease, drilling a hole into the navicular bone--a procedure called core decompression that's commonly used to treat human osteonecrosis (bone death caused by poor blood supply to the area)--might provide a new treatment option for veterinarians. According to Carl Kirker-Head, MA, Vet MB, Dipl. ACVS, ECVS, associate professor of equine surgery at Tufts University's
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Known as the City of Roses, Pasadena possesses a family-friendly quality of life that is rare in the sprawling city of Los Angeles. With a population of 137,222 according to the U.S. Census Bureau, and located just 10 miles northeast of downtown LA, all of the conveniences of a metropolis are at your fingertips without the jostle of the city. As one of the larger neighborhoods in the county, people looking for Pasadena apartments for rent should have no problems in their search, since the area is largely residential.
Settled by the Spanish San Gabriel Mission in 1771 and once part of Mexican territory, the Latino community has been a major influence on the local culture and cuisine of Pasadena. Until California was granted statehood in 1850, the area was populated by many prosperous Mexican families.
Pasadena slowly grew into a lavish, touristy winter playground for the nouveau riche in the Roaring 20s. As Hollywood's film industry blossomed during this time, the city began to expand and Pasadena became incorporated into the city of Los Angeles. The tourists moved out, and many Californians moved in. Many public works projects, including the Rose Bowl Stadium, were built in the area at this time.
As LA continued to sprawl into the late 20th century, Pasadena stayed true to its familial roots. Although many proposals wanted to tear down the Spanish-style building, which makes Pasadena unique, to build skyscrapers, neighborhood and preservation groups struck down the measures and kept Pasadena the quiet, residential oasis that it has always been.
Major corporations like AT&T, Bank of America and Ameron International are among some of the city's top employers. Those looking for Pasadena rentals will have no problems getting to and from work, even if their business is elsewhere in the LA area. With an immediate freeway and mass transit access, Pasadena has always been an attractive city for many businesses.
One of the best schools in the country is located right in the heart of Pasadena. Students from all over the country flock to the California Institute of Technology (known as CalTech by locals) every fall, so if you are a student looking for apartments in the area, it would be wise to begin your search as early as July to make sure that you find the perfect pad.
Ask any Californian and he or she will say that living in Pasadena can be quite expensive. According to city-data.com, the cost of living is comparable to many communities in the Los Angeles area. However, in 2009 the average household income in Pasadena was more than $60,000, with the average rent set at $1,269; so, there are plenty of options for most Pasadena residents to live comfortably.
One of the best areas to explore the Spanish antiquity of the city is in the Old Pasadena Management District. A unique and vibrant experience, this downtown area has more than 100 shops, restaurants, bars, and public spaces that are modern, but stay true to Pasadena's Spanish and Mexican heritage.
The crowned jewel of the city of Pasadena is the Rose Bowl Stadium, the proud home of the prestigious NCAA football bowl game and historic parade that is televised every winter. Because of the temperate Southern California climate, roses here are larger than life and can be seen throughout the grounds. Although there are no public tours of the stadium, it does host several public events throughout the year, including the world's largest flea market and a spectacular Fourth of July celebration.
Each year on New Year's Day, many Americans turn their eyes to Pasadena for the now century-old Rose Parade, a nod to the community spirit that makes this area such a wonderful place to live. With 80,000 hours of manpower and a nationally televised broadcast before the historic Rose Bowl college football game, the entire country gets a chance to see the beautiful native roses of Pasadena on display in many of the handcrafted floats that have made this parade so popular.
To find your next rental apartment or house in Pasadena, take a look at our listings on Rent.com®.
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Rangers resume playoff push against familiar face
Garza opposes former Texas lefty Wilson in opener with Angels
Matt Garza will seek to get the Rangers back on track Friday after an off-day as Texas continues its postseason push against the Angels at Angel Stadium.
Texas dropped two of three to the A's in its last series and has a half-game lead on Oakland in the American League West. The Rangers went 20-7 in August, but are 2-4 in their last six games.
Garza helped produce one of those two wins Saturday, allowing just a run in seven innings against the Twins. It was his first quality start since July 29, and third with Texas.
"I got back into a nice tempo and a nice rhythm," Garza said. "I wasn't pitching bad, but I got back in rhythm and want to keep doing it every time out."
He is 3-2 with a 4.04 ERA in eight starts with the Rangers, and 10-12 with a 4.36 ERA in 32 career games (31 starts) in September. The right-hander hasn't been in a playoff push since his final season with the Rays in 2010.
"I just keep looking forward to pitching every five days and leaving it all out there," Garza said. "My job is to keep us in there, and I try to do it every time out. When you wake up and do what I do, you're always energized. It's a lot of fun coming to the yard, and there is a lot more intensity and energy circulating out there right now, so it's going to be a lot more fun."
The Angels will counter with former Rangers lefty C.J. Wilson, who is 0-2 with a 8.63 ERA in six career starts against his former team. He's faced the Rangers once this season, allowing six runs on 11 hits in four innings on July 30.
It goes against the success he's had facing the American League West this season. He's 8-2 with a 2.86 ERA and a .225 opposing batting average in 12 division starts. Wilson has a 2.64 ERA in his last 11 starts overall, a strong personal finish he hopes will also become indicative of the team.
"With some of the guys we have here, obviously the majority of them are returning, so if we can just kind of go into the last month with some momentum like this, it'll be a good way to head into the offseason," Wilson said after his last start. "Obviously, we started off poorly and haven't really played to our potential all year, but this has been a good showing the last couple of weeks."
Angels: Halos remain focused during stretch run
The Angels might be well out of the AL West race, but they're still focused on finishing strong.
"I think you need to always have that mindset of going out there to win a game," manager Mike Scioscia said. "I think that's that training that eventually gets you to championships."
Scioscia also said his club isn't interested in playing spoiler. The Angels have six games remaining against both the Rangers and A's.
"I don't know anything about a spoiler role," Scioscia said. "We are trying to win games every night no matter who we are playing. That's the challenge in front of us."
• With 95 runs scored, outfielder Mike Trout is five shy of becoming the third Angel to score 100 runs in consecutive seasons (Don Baylor, 1978-79; Troy Glaus, 2000-01). Trout would also become the seventh player in Major League history to score 100 runs in his age-20 and 21 seasons.
Rangers: Ogando returns from DL
• Alexi Ogando made his first outing Wednesday against the A's since he was activated off the disabled list. He pitched a scoreless inning with a strikeout in the seventh. Ogando has been on the DL three times this season with two different cases of shoulder inflammation and biceps tendinitis in his throwing arm.
• Shortstop Elvis Andrus, sidelined with tightness in his lower back, is expected to return to the lineup on Friday.
Worth noting
• The Rangers snapped a streak of 31 consecutive games allowing five or fewer runs Wednesday. It was longest streak in the AL in the designated hitter era.
• Texas lefty Martin Perez was named American League Rookie of the Month for August.
• The Angels have dropped seven straight to Texas, equaling their longest losing streak to the Rangers in club history.
Master Tesfatsion is an associate reporter for MLB.com. This story was not subject to the approval of Major League Baseball or its clubs.