What is CBD?
It has displayed sedative effects in animal tests. Some research, however, indicates that CBD can increase alertness. It may decrease the rate of THC clearance from the body, perhaps by interfering with the metabolism of THC in the liver.
Medically, it has been shown to relieve convulsion, inflammation, anxiety, and nausea, as well as inhibit cancer cell growth. Recent studies have shown cannabidiol to be as effective as atypical antipsychotics in treating schizophrenia. Studies have also shown that it may relieve symptoms of dystonia.
A 2008 study published in the British Journal of Psychiatry showed significant differences in Oxford-Liverpool Inventory of Feelings and Experiences scores between three groups: The first consisted of non-cannabis users, the second consisted of users with ?9-THC detected, and the third consisted of users with both ?9-THC and CBD detected. The ?9-THC only group scored significantly higher for unusual experiences than the ?9-THC and CBD group, whereas the ?9-THC and CBD group had significantly lower introvertive anhedonia scores than the ?9-THC only group and non-cannabis user group. This research indicates that CBD acts as an anti-psychotic and may counteract the potential effects of THC on individuals with latent schizophrenia.
Cannabidiol is shown to decrease activity of the limbic system and to decrease social isolation induced by THC. It’s also shown that Cannabidiol reduces anxiety in social anxiety disorder.   In April 2005, Canadian authorities approved the marketing of Sativex, a mouth spray for multiple sclerosis to alleviate pain. Sativex contains tetrahydrocannabinol together with cannabidiol. It is marketed in Canada by GW Pharmaceuticals.
In 1985 a single case study suggested that CBD may be effective in the management of levodopa-induced dyskinesia in a Parkinson’s Disease patient. 
Studies have shown that CBD may reduce schizophrenic symptoms in patients, likely due to their apparent ability to stabilize disrupted or disabled NMDA receptor pathways in the brain, which are shared and sometimes contested by norepinephrine and GABA. Leweke et al. performed a double blind, 4 week, explorative controlled clinical trial to compare the effects of purified cannabidiol and the atypical antipsychotic amisulpride on improving the symptoms of schizophrenia in 42 patients with acute paranoid schizophrenia. Both treatments were associated with a significant decrease of psychotic symptoms after 2 and 4 weeks as assessed by Brief Psychiatric Rating Scale and Positive and Negative Syndrome Scale. While there was no statistical difference between the two treatment groups, cannabidiol induced significantly less side effects (extrapyramidal symptoms, increase in prolactin, weight gain) when compared to amisulpride.
Cannabidiol has also been shown as being effective treating an often drug-induced set of neurological movement disorders known as dystonia. In one study, five out of five participants showed noted improvement in their dystonic symptoms by 20-50%. CBD also appears to protect against ‘binge’ alcohol induced neurodegeneration.
Cannabidiol has no affinity for CB1 and CB2 receptors but acts as an indirect antagonist of cannabinoid agonists. Recently it was found to be an antagonist at the putative new cannabinoid receptor, GPR55, a GPCR expressed in the caudate nucleus and putamen. Cannabidiol has also been shown to act as a 5-HT1A receptor agonist, an action which is involved in its antidepressant, anxiolytic, and neuroprotective effects. Cannabidiol is also an allosteric modulator at the Mu and Delta opioid receptor sites.
Cannabidiol has also been shown to inhibit cancer cell growth with low potency in non-cancer cells. Although the inhibitory mechanism is not yet fully understood, Ligresti et al. suggest that “cannabidiol exerts its effects on these cells through a combination of mechanisms that include either direct or indirect activation of CB2 and TRPV1 receptors, and induction of oxidative stress, all contributing to induce apoptosis.” In November 2007, researchers at the California Pacific Medical Center reported that CBD shows promise for controlling the spread of metastatic breast cancer. In vitro CBD downregulates the activity of the gene ID1 which is responsible for tumor metastasis.
Cannabidiol is insoluble in water but soluble in organic solvents, such as pentane. At room temperature it is a colorless crystalline solid. In strongly basic medium and the presence of air it is oxidized to a quinone. Under acidic conditions it cyclizes to THC. The synthesis of cannabidiol has been accomplished by several research groups.
A Sativa have a THC/CBD ratio 20 times that of an Indica. Marijuana with relatively high ratios of CBD:THC is less likely to induce anxiety than marijuana with low CBD:THC ratios, due to CBD’s antagonist effects at the cannabidanoid receptor, compared to THC’s partial agonist effect.  The relatively large amount of CBD contained in Cannabis Indica, means, compared to a sativa, the effects are modulated significantly. Sedative and anxiolytic effects are attenuated, while alterations in space and time perception are not as perceptible as with an equal dose of a similar potency sativa.
In Canada Cannabidiol is a Schedule 2 Drug, a category that encompasses quantities of cannabis less than 30 grams, and various related synthetic derivatives and preparations. In the United States it is Schedule I. 
- ^ McPartland JM, Russo EB. (2001). Cannabis and Cannabis Extracts: Greater Than the Sum of Their Parts?. Journal of Cannabis Therapeutics. 1(3/4):103-132.
- ^ Grlie, L (1976). “A comparative study on some chemical and biological characteristics of various samples of cannabis resin”. Bulletin on Narcotics 14: 37–46.
- ^ Pickens JT (1981). “Sedative activity of cannabis in relation to its delta’-trans-tetrahydrocannabinol and cannabidiol content”. Br. J. Pharmacol. 72 (4): 649–56. PMC 2071638. PMID 6269680.
- ^ Nicholson, AN; C Turner, BM Stone, and PJ Robson (June 2004). “Effect of Delta-9-tetrahydrocannabinol and cannabidiol on nocturnal sleep and early-morning behavior in young adults” (fee required). J Clin Psychopharmacol 24 (3): 305–13. doi:10.1097/01.jcp.0000125688.05091.8f. ISSN 0271-0749. PMID 15118485. Retrieved 2007-05-03.
- ^ a b Mechoulam, R.; M. Peters, Murillo-Rodriguez (21 Aug 2007). “Cannabidiol – recent advances”. Chemistry & Biodiversity 4 (8): 1678–1692. doi:10.1002/cbdv.200790147. PMID 17712814.
- ^ a b Zuardi, A.W; J.A.S. Crippa, J.E.C. Hallak, F.A. Moreira, F.S. Guimarães (2006). “Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug” (PDF). Braz. J. Med. Biol. Res. 39 (4): 421–429. doi:10.1590/S0100-879X2006000400001. PMID 16612464.
- ^ a b Consroe, P.; Sandyk, R.; Snider, S. R. (1986). “Open label evaluation of cannabidiol in dystonic movement disorders”. The International journal of neuroscience 30 (4): 277–282. doi:10.3109/00207458608985678. PMID 3793381. edit
- ^ a b Snider, Stuart R. and Consroe, Paul. (1985). “Beneficial and Adverse Effects of Cannabidiol in a Parkinson Patient with Sinemet-Induced Dystonic Dyskinesia“. Neurology. (Suppl 1) p. 201.
- ^ Celia J. A. Morgan, PhD and H. Valerie Curran, PhD, DClinPsy Effects of cannabidiol on schizophrenia-like symptoms in people who use cannabis
- ^ José Alexandre de Souza Crippa, Antonio Waldo Zuardi, Griselda E J Garrido, Lauro Wichert-Ana, Ricardo Guarnieri, Lucas Ferrari, Paulo M Azevedo-Marques, Jaime Eduardo Cecílio Hallak, Philip K McGuire and Geraldo Filho Busatto (October 2003). “Effects of Cannabidiol (CBD) on Regional Cerebral Blood Flow”. Neuropsychopharmacology 29 (2): 417–426. doi:10.1038/sj.npp.1300340. PMID 14583744.
- ^ Daniel Thomas Malone, Dennis Jongejana and David Alan Taylora (August 2009). “Cannabidiol reverses the reduction in social interaction produced by low dose ?9-tetrahydrocannabinol in rats”. Pharmacology Biochemistry and Behavior 93 (2): 91–96. doi:10.1016/j.pbb.2009.04.010. PMID 19393686.
- ^ Mateus M Bergamaschi, Regina Helena Costa Queiroz, Marcos Hortes Nisihara Chagas, Danielle Chaves Gomes de Oliveira, Bruno Spinosa De Martinis, Flávio Kapczinski, João Quevedo, Rafael Roesler, Nadja Schröder, Antonio E Nardi, Rocio Martín-Santos, Jaime Eduardo Cecílio (may 2011). “Cannabidiol Reduces the Anxiety Induced by Simulated Public Speaking in Treatment-Naïve Social Phobia Patients”. Neuropsychopharmacology 36 (6): 1219–1226. doi:10.1038/npp.2011.6. PMC 3079847. PMID 21307846.
- ^ Crippa JA, Derenusson GN, Ferrari TB, Wichert-Ana L, Duran FL, Martin-Santos R, Simões MV, Bhattacharyya S, Fusar-Poli P, Atakan Z, Santos Filho A, Freitas-Ferrari MC, McGuire PK, Zuardi AW, Busatto GF, Hallak JE. (January 2011). “Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder: a preliminary report”. J Psychopharmacol. 25 (1): 121–130. doi:10.1177/0269881110379283. PMID 20829306.
- ^ Snider, SR; Consroe P (1985). “Beneficial and adverse effects of cannabidiol in a Parkinson patient with sinemet-induced dystonic dyskinesia”. Neurology 35: 201.
- ^ http://www.nature.com/npp/journal/v31/n4/abs/1300838a.html
- ^ Leweke, FM; Koethe D, Pahlisch F, Schreiber D, Gerth1 CW, Nolden1 BM, Klosterkötter J, Hellmich M and Piomelli D. (2009). “Antipsychotic effects of cannabidiol” (PDF). European Psychiatry 17th EPA Congress 24 (1): s207. doi:10.1016/S0924-9338(09)70440-7.
- ^ http://dx.doi.org/10.1124/jpet.105.085779 Comparison of Cannabidiol, Antioxidants, and Diuretics in Reversing Binge Ethanol-Induced Neurotoxicity
- ^ http://www.ncbi.nlm.nih.gov/pubmed/19631736 White matter integrity in adolescents with histories of marijuana use and binge drinking.
- ^ http://www.nature.com/news/2010/101001/full/news.2010.508.html
- ^ Ryberg E, Larsson N, Sjögren S, et al. (2007). “The orphan receptor GPR55 is a novel cannabinoid receptor”. British Journal of Pharmacology 152 (7): 1092–101. doi:10.1038/sj.bjp.0707460. PMC 2095107. PMID 17876302.
- ^ Russo EB, Burnett A, Hall B, Parker KK (August 2005). “Agonistic properties of cannabidiol at 5-HT1a receptors”. Neurochemical Research 30 (8): 1037–43. doi:10.1007/s11064-005-6978-1. ISBN 1106400569781. PMID 16258853.
- ^ Zanelati T, Biojone C, Moreira F, Guimarães F, Joca S (December 2009). “Antidepressant-like effects of cannabidiol in mice: possible involvement of 5-HT1A receptors”. British Journal of Pharmacology 159 (1): 122–8. doi:10.1111/j.1476-5381.2009.00521.x. PMC 2823358. PMID 20002102.
- ^ a b Resstel LB, Tavares RF, Lisboa SF, Joca SR, Corrêa FM, Guimarães FS (January 2009). “5-HT1A receptors are involved in the cannabidiol-induced attenuation of behavioural and cardiovascular responses to acute restraint stress in rats”. British Journal of Pharmacology 156 (1): 181–8. doi:10.1111/j.1476-5381.2008.00046.x. PMC 2697769. PMID 19133999.
- ^ Campos AC, Guimarães FS (August 2008). “Involvement of 5HT1A receptors in the anxiolytic-like effects of cannabidiol injected into the dorsolateral periaqueductal gray of rats”. Psychopharmacology 199 (2): 223–30. doi:10.1007/s00213-008-1168-x. ISBN 2130081168. PMID 18446323.
- ^ Mishima K, Hayakawa K, Abe K, et al. (May 2005). “Cannabidiol prevents cerebral infarction via a serotonergic 5-hydroxytryptamine1A receptor-dependent mechanism”. Stroke; a Journal of Cerebral Circulation 36 (5): 1077–82. doi:10.1161/01.STR.0000163083.59201.34. PMID 15845890.
- ^ Hayakawa K, Mishima K, Nozako M, et al. (March 2007). “Repeated treatment with cannabidiol but not Delta9-tetrahydrocannabinol has a neuroprotective effect without the development of tolerance”. Neuropharmacology 52 (4): 1079–87. doi:10.1016/j.neuropharm.2006.11.005. PMID 17320118.
- ^ Cannabidiol is an allosteric modulator at mu- and delta-opioid receptors. Kathmann M, Flau K, http://www.ncbi.nlm.nih.gov/pubmed/16489449Redmer A, Tränkle C, Schlicker E. Source Department of Pharmacology and Toxicology, School of Medicine, University of Bonn, Reuterstr. 2b, 53113 Bonn, Germany.
- ^ Ligresti A, Moriello AS, Starowicz K, et al. (2006). “Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma”. J. Pharmacol. Exp. Ther. 318 (3): 1375–87. doi:10.1124/jpet.106.105247. PMID 16728591.
- ^ McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY (2007). “Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells”. Mol. Cancer Ther. 6 (11): 2921–7. doi:10.1158/1535-7163.MCT-07-0371. PMID 18025276.
- ^ Jones PG, Falvello L, Kennard O, Sheldrick GM Mechoulam R (1977). “Cannabidiol”. Acta Cryst. B33 (10): 3211–3214. doi:10.1107/S0567740877010577.
- ^ Mechoulam R, Ben-Zvi Z (1968). “Hashish—XIII On the nature of the beam test”. Tetrahedron 24 (16): 5615–5624. doi:10.1016/0040-4020(68)88159-1. PMID 5732891.
- ^ Gaoni Y, Mechoulam R (1966). “Hashish—VII The isomerization of cannabidiol to tetrahydrocannabinols”. Tetrahedron 22 (4): 1481–1488. doi:10.1016/S0040-4020(01)99446-3.
- ^ Petrzilka T, Haefliger W, Sikemeier C, Ohloff G, Eschenmoser A (1967). “Synthese und Chiralität des (-)-Cannabidiols”. Helv. Chim. Acta 50 (2): 719–723. doi:10.1002/hlca.19670500235. PMID 5587099.
- ^ Gaoni Y, Mechoulam R (1985). “Boron trifluoride etherate on alumuna – a modified Lewis acid reagent. An improved synthesis of cannabidiol”. Tetrahedron Letters 26 (8): 1083–1086. doi:10.1016/S0040-4039(00)98518-6.
- ^ Kobayashi Y, Takeuchi A, Wang YG (2006). “Synthesis of cannabidiols via alkenylation of cyclohexenyl monoacetate”. Org. Lett. 8 (13): 2699–2702. doi:10.1021/ol060692h. PMID 16774235.
- ^ Marks, M.; Tian, L.; Wenger, J.; Omburo, S.; Soto-Fuentes, W.; He, J.; Gang, D.; Weiblen, G. et al (2009). “Identification of candidate genes affecting ?9-tetrahydrocannabinol biosynthesis in Cannabis sativa”. Journal of experimental botany 60 (13): 3715–3726. doi:10.1093/jxb/erp210. PMC 2736886. PMID 19581347. edit
- ^ J.E. Joy, S. J. Watson, Jr., and J.A. Benson, Jr, (1999). Marijuana and Medicine: Assessing The Science Base. Washington D.C: National Academy of Sciences Press. ISBN 0585058008.
- ^ http://laws.justice.gc.ca/en/showdoc/cs/C-38.8//20090606/en?command=search&caller=SI&fragment=schedule%201&search_type=all&day=6&month=6&year=2009&search_domain=cs&showall=L&statuteyear=all&lengthannual=50&length=50&offset=2
- ^ http://www.justice.gov/dea/pubs/scheduling.html