An observational study by investigators at the University of California at San Francisco (UCSF) revealed that patients afflicted with hepatitis C who used cannabis were significantly more likely to adhere to their treatment regimen than patients who did not use it. However, no clinical trials assessing cannabinoid use for this indication are available in the scientific literature.

It is indicated by preclinical data that endocannabinoid system could moderate aspects of chronic liver disease and inflammation could be reduced by cannabinoids in experimental models of hepatitis. Nevertheless, other clinical reviews have reported a positive association between cannabis use on a daily basis and the progression of liver fibrosis (excessive tissue build up) and steatosis (excessive fat build up) in select hepatitis C patients.

Investigators from Canada and Germany, writing in the October 2006 issue of the European Journal of Gastroenterology, concluded that cannabis’ “potential benefits of a higher likelihood of treatment success [for hepatitis c patients] appear to outweigh [its] risks.”

References:

[1] Schnelle et al. 1999. Results of a standardized survey on the medical use of cannabis products in the German-speaking area. Forschende Komplementarmedizin (Germany) 3: 28-36.
[2] David Berstein. 2004. “Hepatitis C – Current state of the art and future directions.” MedScape Today.
[3] Sylvestre et al. 2006. Cannabis use improves retention and virological outcomes in patients treated for hepatitis C. European Journal of Gastroenterology & Hepatology. 18: 1057-1063.
[4] Zamora-Valdes et al. 2005. The endocannabinoid system in chronic liver disease (PDF). Annals of Hepatology 4: 248-254.
[5] Gabbey et al. 2005. Endocannabinoids and liver disease – review. Liver International 25: 921-926.
[6] Lavon et al. 2003. A novel synthetic cannabinoid derivative inhibits inflammatory liver damage via negative cytokine regulation. Molecular Pharmacology 64: 1334-1344.
[7] Hezode et al. 2005. Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C. Hepatology 42: 63-71.
[8] Ishida et al. 2008. Influence of cannabis use on severity of hepatitis C disease. Clinical Gastroenterology and Hepatology 6: 69-75.
[9] Parfieniuk and Flisiak. 2008. Role of cannabinoids in liver disease. World Journal of Gastroenterology 14: 6109-6114.
[10] Fischer et al. 2006. Treatment for hepatitis C virus and cannabis use in illicit drug user patients: implications and questions. European Journal of Gastroenterology & Hepatology. 18: 1039-1042.
[11] Schwabe and Siegmund. 2005. op. cit.
[12] Hezode et al. 2005. op. cit.
[13] David Berstein. 2004. op. cit.
[14] Hezode et al. 2008. Daily cannabis use: a novel risk factor of steatosis severity in patients with chronic hepatitis C. Gastroenterology 134: 432-439.
[15] Purohit et al. 2010. Role of cannabinoids in the development of fatty liver (steatosis). The AAPS Journal 12: 233-237.

An absence of clinical trials investigating the use of cannabinoids for ALS treatment was revealed by a review of the scientific literature. However, it is indicated by recent preclinical findings that cannabinoids may delay progression of the disease, lending support to anecdotal reports by patients that cannabinoids may be efficacious in moderating the disease’s development and in alleviating certain ALS-related symptoms like depression, drooling, appetite loss, and pain.

Investigators at the California Pacific Medical Center in San Francisco, writing in the March 2004 issue of the journal Amyotrophic Lateral Sclerosis & Other Motor Neuron Disorders, reported that the administration of THC both before and after the onset of ALS symptoms staved disease progression and prolonged survival in animals compared to untreated controls.

The administration of other naturally occurring and synthetic cannabinoids may also moderate disease progression but not necessarily impact survival, according to additional trials in animal models of Amyotrophic Lateral Sclerosis. A recent study has demonstrated that blocking the CB1 cannabinoid receptor did extend life span in an ALS mouse model, indicating that the beneficial effects of cannabinoids on ALS could be mediated by non-CB1 receptor mechanisms.

A team of investigators writing in the American Journal of Hospice & Palliative Medicine in 2010 reported, “Based on the currently available scientific data, it is reasonable to think that cannabis might significantly slow the progression of ALS, potentially extending life expectancy and substantially reducing the overall burden of the disease.” They concluded, “There is an overwhelming amount of preclinical and clinical evidence to warrant initiating a multicenter randomized, double-blind, placebo-controlled trial of cannabis as a disease-modifying compound in ALS.”

References:

[1] Amtmann et al. 2004. Survey of cannabis use in patients with amyotrophic lateral sclerosis. The American Journal of Hospice and Palliative Care 21: 95-104.
[2] Raman et al. 2004. Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. Amyotrophic Lateral Sclerosis & Other Motor Neuron Disorders 5: 33-39.
[3] Weydt et al. 2005. Cannabinol delays symptom onset in SOD1 transgenic mice without affecting survival. Amyotrophic Lateral Sclerosis & Other Motor Neuron Disorders 6: 182-184.
[4] Bilsland et al. 2006. Increasing cannabinoid levels by pharmacological and genetic manipulation delay disease progression in SOD1 mice. The FASEB Journal 20: 1003-1005.
[5] Ibid.
[6]Carter et al. 2010. Cannabis and amyotrophic lateral sclerosis: hypothetical and practical applications, and a call for clinical trials. American Journal of Hospice & Palliative Medicine 27: 347-356.

Twenty-eight patients had been included to investigate the effects of smoked cannabis on their pain in the original already published clinical study. Seven of these patients selected for investigating the blood levels of the hormones leptin, ghrelin, peptide YY, and insulin after exposition with cannabis and placebo in a cross-over design.

Cannabis administration, compared to placebo, was associated with significant increases in plasma levels of ghrelin and leptin, and decreases in peptide YY. It however did not significantly influence insulin levels. Authors stated that “cannabis-related changes in these hormones had a magnitude similar to what has been observed with food intake over the course of a day in normal volunteers, suggesting physiological relevance. “They concluded that “these findings are consistent with modulation of appetite hormones mediated through endogenous cannabinoid receptors, independent of glucose metabolism.”

Reference:

Riggs PK, Vaida F, Rossi SS, Sorkin LS, Gouaux B, Grant I, Ellis RJ. A pilot study of the effects of cannabis on appetite hormones in HIV-infected adult men. Brain Res. 2011 Nov 7. [in press])

Several recent clinical trials in the past have indicated that cannabinoid therapy could reduce incidents of incontinence. Investigators at Oxford’s Centre for Enablement in Britain, writing in the February 2003 issue of the journal Clinical Rehabilitation, reported that bladder control was improved by self-administered doses of whole-plant cannabinoid extracts when compared to placebo in patients suffering from MS and spinal cord injury.

These initial findings were followed by investigators at London’s Institute for Neurology in an open-label pilot study of cannabis-based extracts for bladder dysfunction in 15 patients with advanced multiple sclerosis. Investigators determined “urinary urgency, the number of and volume of incontinence episodes, frequency, and nocturia all decreased significantly” following cannabinoid therapy. “Cannabis-based medicinal extracts are a safe and effective treatment for urinary and other problems in patients with advanced MS.”

A multi-center, randomized placebo-controlled trial involving 630 patients administered oral doses of cannabis extracts or THC confirmed these findings in 2006. It was reported by researchers that subjects administered cannabis extracts experienced a 38 percent reduction in incontinence episodes from baseline to the end of treatment, while patients administered THC experienced a 33 percent reduction, suggesting a “clinical effect of cannabis on incontinence episodes.

“In light of these findings, experts have recommended the use of cannabinoids as potential ‘second-line’ agents to treat incontinence.

References:

[1] Wade et al. 2003. A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms. Clinical Rehabilitation 17: 21-29.
[2] Brady et al. 2004. An open label pilot study of cannabis-based extracts for bladder dysfunction in advanced multiple sclerosis. Multiple Sclerosis 10: 425-433.
[3] Freeman et al. 2006. The effect of cannabis on urge incontinence in patients with multiple sclerosis: a multicentre, randomized placebo-controlled trial. The International Urogynecology Journal 17: 636-641.
[4] University of Pittsburgh Medical Center Press Release. May 21, 2006. ” Marijuana-derived drug suppresses bladder pain in animal models.”
[5] Kalsi and Fowler. 2005. Therapy insight: bladder dysfunction associated with multiple sclerosis. Nature Clinical Practice Neurology 2: 492-501.

 The symptoms of gastrointestinal disorders often include cramping, abdominal pain, inflammation of the lining of the large and/or small intestine, rectal bleeding, chronic diarrhea, and weight loss.

Though several anecdotal reports and a handful of case reports exist in the scientific literature supporting the use of cannabinoids for treating symptoms of this disorder, virtually no clinical trial work has been performed in this area, aside from a 2007 clinical study assessing the impact of oral THC on colonic motility.

Nevertheless, it has been demonstrated by numerous preclinical studies that activation of the CB1 and CB2 cannabinoid receptors exert biological functions on the gastrointestinal tract. In animals, effects of their activation include suppression of gastrointestinal motility, reduced acid reflux, inhibition of intestinal secretion, protection from inflammation, and promotion of epithelial wound healing in human tissue.

As a result, it is believed by many experts that cannabinoids and/or modulation of the endogenous cannabinoid system represents a novel therapeutic approach for the treatment of numerous GI disorders — including inflammatory bowel diseases, functional bowel diseases, gastro-oesophagael reflux conditions, secretory diarrhea, gastric ulcers, and colon cancer.

References:
[1] Gahlinger, Paul M. 1984. Gastrointestinal illness and cannabis use in a rural Canadian community. Journal of Psychoactive Drugs 16: 263-265.
[2] Swift et al. 2005. Survey of Australians using cannabis for medical purposes. Harm Reduction Journal 4: 2-18.
[3] Baron et al. 1990. Ulcerative colitis and marijuana. Annals of Internal Medicine 112: 471.
[4] Jeff Hergenrather. 2005. Cannabis alleviates symptoms of Crohn’s Disease. O’Shaughnessy’s 2: 3.
[5] Esfandyari et al. 2007. Effects of a cannabinoid receptor agonist on colonic motor and sensory functions in humans: a randomized, placebo-controlled study. American Journal of Physiology, Gastrointestinal and Liver Physiology 293: 137-145.
[6] Massa and Monory. 2006. Endocannabinoids and the gastrointestinal tract. Journal of Endocrinological Investigation 29 (Suppl): 47-57.
[7] Roger Pertwee. 2001. Cannabinoids and the gastrointestinal tract. Gut 48: 859-867.
[8] DiCarlo and Izzo. 2003. Cannabinoids for gastrointestinal diseases: potential therapeutic applications. Expert Opinion on Investigational Drugs 12: 39-49.
[9] Lehmann et al. 2002. Cannabinoid receptor agonism inhibits transient lower esophageal sphincter relaxations and reflux in dogs. Gastroenterology 123: 1129-1134.
[10] Massa et al. 2005. The endocannabinoid system in the physiology and pathophysiology of the gastrointestinal tract. Journal of Molecular Medicine 12: 944-954.
[11] Wright et al. 2005. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology 129: 437-453.
[12] Massa and Monory. 2006. op. cit.
[13] Izzo and Coutts. 2005. Cannabinoids and the digestive tract. Handbook of Experimental Pharmacology 168: 573-598.
[14] Izzo et al. 2009. Non-psychotropic plant cannabinoids: new therapeutic opportunities from an ancient herb. Trends in Pharmacological Sciences 30: 515-527.

Even independent labs and government agencies have confirmed that marijuana does not constitute a danger to public safety and is the safest and the most useful drug known to the mankind. If marijuana was bad, why does the U.S. federal government owns a patent (number 6630507) for the medicinal use of marijuana? Time for a rethink!

The Drug Enforcement Administration’s own administrative law judge, Francis L. Young, held that “marijuana has been accepted as capable of relieving the distress of great numbers of very ill people, and doing so with safety under medical supervision. It would be unreasonable, arbitrary and capricious for DEA to continue to stand between those sufferers and the benefits of this substance in light of the evidence in this record.”

It is worthwhile to note here that marijuana, unlike other drugs, is quite safe to be used recreationally by responsible adults. Moreover, it is non-addictive in nature, has not caused a single death, and could not be over-dosed. If that is not all, medical marijuana has been allowing patients across the world.

Marijuana has been and is commonly used for treating health diseases such as obsessive compulsive disorder (OCD), chemotherapy-related nausea, migraine, depression, skin cancer, prostate cancer, lung cancer, breast cancer, attention deficit/hyperactivity disorder (ADHD), amyotrophic lateral sclerosis (ALS), autism, multiple sclerosis, and trauma.  In addition to this, medical marijuana has also demonstrated effectiveness in treating complications such as stuttering, HIV, AIDS, post polio syndrome, malignant melanoma, testicular cancer, diabetic peripheral vascular disease, obesity, autoimmune diseases, schizophrenia, writers’ cramp, alcohol abuse, tobacco dependence, Tourette’s syndrome, and persistent insomnia.

Medical studies have also confirmed that marijuana shows great promise in offering significant relief to patients suffering from nightmares, non-psychotic organic brain disorder, post traumatic stress disorder, Parkinson’s disease, epilepsy, paralysis, Bell’s palsy, muscular dystrophies, glaucoma, and chronic sinusitis.

In addition to these medical benefits, legalizing marijuana could easily open new avenues of employment and wealth from an economy’s point of view. By regulating and taxing marijuana, the United States alone could earn $40 billion to $100 billion in new revenue. Moreover, legalization of marijuana could easily prevent drug users and sellers from being termed as “criminals.” Legalizing marijuana would also promote entrepreneurial spirit among marijuana sellers and help them become respectable and accepted individuals in our society. In addition to that, governments could easily control how marijuana is consumed by increasing or decreasing the taxes on the drug, once it is legalized.

With governments scrambling to identify new sources of revenue to pay for important social objectives and recession hitting almost every segment of the economy, the time is not far when the nature’s great gift (marijuana) would be legalized. This is primarily because legalization of marijuana would inevitably add a new and powerful industry to our draining economy.

All in all, legalizing marijuana is the best thing that could be done to save the mankind from diseases, constraints, and stigma.

References:

Marijuanainfo.com
Marijuana Mission
Marijuana Policy Project (MPP) Library
MedicalMJ.org – Medical Marijuana News and Facts
Students for Sensible Drug Policy
The Drug Reform Coordination Network
The Hemp & Cannabis Foundation

Marijuana is one of the most commonly used drugs across the world, yet it is given an illegal status by some countries. The valid reason for this illegality is none and the valid reasons for granting it the legal status are endless.

If you have been wondering why marijuana is an illegal drug, this is because big pharmaceuticals are threatened by marijuana, the wonder drug, which could be used to treat almost every medical complication known to the mankind. Drug cartels in Mexico and beer distributors in California opposed the legalization of marijuana as they feared it would reduce their profits.

If that is not all, some politicians oppose legalization of marijuana as they are afraid they will be accused of being “pro-drug”, labeled as weak on crime, and believe that marijuana is not a wonder drug (even if that means overriding scientific and medical evidences without any valid reason and proof). Moreover, how would court expenses that are paid by marijuana offenders be justified and how would the police departments justify their budgets fighting marijuana and making a lot of money by seizing property during marijuana busts?

Why Legalize Marijuana?
Legalization of marijuana would not only create thousands of jobs based on a clean and sustainable source of fuel, medicine, and fiber, but it would also help the treasury earn taxes worth billions. Moreover, legalizing marijuana would save taxpayers’ money by the elimination of the money spent on law enforcement, the courts, and the prisons. More importantly, it would help individuals and families who have been criminalized by a system that promotes arrests, fines, and confiscation.

Legalizing marijuana would not only restore social consent and help billions of people worldwide get cured of medical complications, but to also avoid lives of people getting ruined by unjustified arrest and confiscation.

The belief that people who advocate marijuana use are either uninformed or their jobs depend upon the mandatory acceptance of marijuana prohibition is nothing but a pure myth. This is primarily because the laws against marijuana are arbitrary, unjust, and wrong and the findings that gave birth to these laws are biased towards big pharmaceutical companies that are threatened by the greatest gift of the Mother Nature, marijuana.

The findings of the Canadian Senate Special Committee (on Illegal Drugs. 2002. Cannabis: Summary Report: Our Position for a Canadian Public Policy. Ottawa) says it all. “We believe … that the continued prohibition of cannabis jeopardizes the health and well-being of Canadians much more than does the substance itself or the regulated marketing of the substance. In addition, we believe that the continued criminalization of cannabis undermines the fundamental values set out in the Canadian Charter of Rights and Freedoms and confirmed in the history of a country based on diversity and tolerance.

… It is for this reason that the Committee recommends that the Government of Canada amend the Controlled Drugs and Substances Act to create a criminal exemption scheme, under which the production and sale of cannabis would be licensed, [and] … to permit persons over the age of 16 to procure cannabis and its derivatives at duly licensed distribution centers.”

In short, marijuana prohibition is nothing but unjust, the epitome of unwarranted big government intrusion into and interference with our private lives, and a huge waste of police, legal, and taxpayer resources. The time is not far when marijuana would be made easily accessible for adults who choose to use it, whether for medical use or pleasure and relaxation.

References:

Dr David Bearman’s Home Page
Dr Tod Mikuriya’s Home Page
Eugene (Oregon) – Compassion Center
Falcon Cove Biology Laboratory
Forfeiture Endangers American Rights

The term medical marijuana took on a dramatic new meaning in February 2000 when researchers in Madrid made an announcement that they had destroyed incurable brain cancer tumors in rats by injecting them with the active ingredient in cannabis, THC.
It was revealed:

“All the rats left untreated uniformly died 12-18 days after glioma (brain cancer) cell inoculation … Cannabinoid (THC)-treated rats survived significantly longer than control rats. THC administration was ineffective in three rats, which died by days 16-18. Nine of the THC-treated rats surpassed the time of death of untreated rats, and survived up to 19-35 days. Moreover, the tumor was completely eradicated in three of the treated rats.”

In a local section of the Washington Post on August 18, 1974, under the headline, “Cancer Curb Is Studied,” it was reported, “The active chemical agent in marijuana curbs the growth of three kinds of cancer in mice and may also suppress the immunity reaction that causes rejection of organ transplants, a Medical College of Virginia team has discovered.” The researchers “found that THC slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent.”

The Spanish researchers were led by Dr. Manuel Guzman of Complutense University and the findings were reported in an issue of “Nature Medicine.”
The following studies also demonstrated that marijuana is highly effective in treating cancer.

1. “Cannabinoids, the active components of Cannabis sativa and their derivatives, act in the organism by mimicking endogenous substances, the endocannabinoids, that activate specific cannabinoid receptors. Cannabinoids exert palliative effects in patients with cancer and inhibit tumour growth in laboratory animals.
“The best-established palliative effect of cannabinoids in cancer patients is the inhibition of chemotherapy-induced nausea and vomiting. ….
“Other potential palliative effects of cannabinoids in cancer patients — supported by Phase III clinical trials — include appetite stimulation and pain inhibition. ….
“Cannabinoids inhibit tumor growth in laboratory animals. They do so by modulating key cell-signaling pathways, thereby inducing direct growth arrest and death of tumor cells, as well as by inhibiting tumor angiogenesis and metastasis.

“Cannabinoids are selective antitumor compounds, as they can kill tumor cells without affecting their non-transformed counterparts. It is probable that cannabinoid receptors regulate cell-survival and cell-death pathways differently in tumor and non-tumor cells.
“Cannabinoids have favorable drug-safety profiles and do not produce the generalized toxic effects of conventional chemotherapies. … “

Source:
Guzman, Manuel, “Cannabinoids: Potential Anticancer Agents.” Nature Reviews: Cancer (October 2003), p. 746.

http://www.brainlife.org/reprint/2003/guzm%C3%A1n_m031000.pdf

2. “Our results, which were obtained in a clinically relevant animal model of ErbB2-positive breast cancer, suggest that these highly aggressive and low responsive tumors could be efficiently treated with nonpsychoactive CB2-selective agonists without affecting the surrounding healthy tissue.”
From the abstract: “Conclusions: Taken together, these results provide a strong preclinical evidence for the use of cannabinoid-based therapies for the management of ErbB2-positive breast cancer.”

Sources:
Caffarel, María M; Andradas, Clara; Mira, Emilia; Pérez-Gómez, Eduardo; Cerutti; Camilla; Moreno-Bueno, Gema; Flores, Juana; García-Realm, Isabel; Palacios, José; Mañes, Santos; Guzmán, Manuel; Sánchez, Cristina, “Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition,” Molecular Cancer (London, United Kingdom: July 22, 2010), p. 1 and P. 8.

http://www.molecular-cancer.com/content/9/1/196

www.ncbi.nlm.nih.gov/pmc/articles/PMC2917429/pdf/1476-4598-9-196.pdf

3. “In conclusion, our data indicate that cannabidiol, and possibly Cannabis extracts enriched in this natural cannabinoid, represent a promising nonpsychoactive antineoplastic strategy. In particular, for a highly malignant human breast carcinoma cell line, we have shown here that cannabidiol and a cannabidiol-rich extract counteract cell growth both in vivo and in vitro as well as tumor metastasis in vivo. 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.”

Source:
Ligresti, Alessia; Moriello, Aniello Schiano; Starowicz, Katarzyna; Matias, Isabel; Pisanti, Simona; De Petrocellis, Luciano; Laezza, Chiara; Portella, Giuseppe; Bifulco, Maurizio; and Di Marzo, Vincenzo, “Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma,” The Journal of Pharmacology and Experimental Therapeutics (Bethesda, MD: The American Society for Pharmacology and Experimental Therapeutics, March 2004) Vol. 318, No. 3, pp. 1386-1387.

http://jpet.aspetjournals.org/content/318/3/1375.full.pdf
4. “… we show that cannabinoid administration selectively down-regulates MMP-2 [matrix metalloproteinases] expression in mice bearing gliomas as well as in two patients with recurrent glioblastoma multiforme. Cannabinoid-induced inhibition of MMP-2 expression was also evident in cultured glioma cells, indicating that the changes observed in gliomas in vivo reflect—at least in part—the direct effect of cannabinoids on tumor cells. MMP-2 expression is upregulated in almost all human cancers, including gliomas, and this has been shown to be closely associated with negative prognosis.”

“As MMP-2 up-regulation is associated with high progression and poor prognosis of gliomas and many other tumors, MMP-2 downregulation constitutes a new hallmark of cannabinoid antitumoral activity.”

Source:
Cristina Bla´zquez, Mari´a Salazar, Arkaitz Carracedo, Mar Lorente, Ainara Egia, Luis Gonza´lez-Feria, Amador Haro, Guillermo Velasco, and Manuel Guzman, “Cannabinoids Inhibit Glioma Cell Invasion by Down-regulating Matrix Metalloproteinase-2 Expression,” Cancer Research (March 2008), pp. 1951 and 1945.

http://cancerres.aacrjournals.org/cgi/reprint/68/6/1945.pdf

5. “Cannabinoids have a favourable drug safety profile. Acute fatal cases due to cannabis use in humans have not been substantiated, and median lethal doses of THC in animals have been extrapolated to several grams per kilogram of body weight. Cannabinoids are usually well tolerated in animal studies and do not produce the generalized toxic effects of most conventional chemotherapeutic agents. For example, in a 2-year administration of high oral doses of THC to rats and mice, no marked histopathological alterations in the brain and other organs were found. Moreover, THC treatment tended to increase survival and lower the incidence of primary tumours. Similarly, long-term epidemiological surveys, although scarce and difficult to design and interpret, usually show that neither patients under prolonged medical cannabinoid treatment nor regular cannabis smokers have marked alterations in a wide array of physiological, neurological and blood tests.”

Source:
Guzman, Manuel, “Cannabinoids: Potential Anticancer Agents.” Nature Reviews: Cancer (October 2003), p. 752.

http://www.brainlife.org/reprint/2003/guzm%C3%A1n_m031000.pdf

6. “Cannabinoids, the active components of marijuana and their other natural and synthetic analogues have been reported as useful adjuvants to conventional chemotherapeutic regimens for preventing nausea, vomiting, pain, and for stimulating appetite. Before the discovery of specific cannabinoid systems and receptors, it was speculated that cannabinoids produced their effects via nonspecific interaction with cell membranes. Cannabinoids are proving to be unique based on their targeted action on cancer cells and their ability to spare normal cells. Variation in the effects of cannabinoids in different cell lines and tumor model could be due to the differential expression of CB1 and CB2 receptors. Thus, overexpression of cannabinoid receptors may be effective in killing tumors, whereas low or no expression of these receptors could lead to cell proliferation and metastasis because of the suppression of the antitumor immune response.”

Source:
Sarfaraz, Sami; Adhami, Vaqar M.; Syed, Deeba N.; Afaq, Farrukh; and Mukhtar, Hasan, “Cannabinoids for Cancer Treatment: Progress and Promise,” Cancer Research (Philadelphia, PA: American Association for Cancer Research, January 2008) Vol. 68, pp. 341-342.

http://cancerres.aacrjournals.org/cgi/reprint/68/2/339.pdf

The neuroprotective effects of a series of cannabinoid-based compounds with more selectivity for different elements of the cannabinoid signaling system in rats with unilateral lesions of nigrostriatal dopaminergic neurons caused by local application of 6-hydroxydopamine were evaluated for the research purposes.

The CB1 receptor agonist arachidonyl-2-chloroethylamide (ACEA), the CB2 receptor agonist HU-308, the non-selective agonist WIN55, 212-2, and the inhibitors of the endocannabinoid inactivation AM404 and UCM707 were used and all of them administered i.p. Daily administration of ACEA or WIN55, 212-2 did not reverse 6-hydroxydopamine-induced dopamine (DA) depletion in the lesioned side, whereas HU-308 produced a minor recovery supporting a likely involvement of CB2 but not CB1 receptors.

AM404 produced a significant recovery of 6-hydroxydopamine-induced DA depletion and tyrosine hydroxylase deficit in the lesioned side, possibly caused by the antioxidant properties of AM404. The AM404 properties are derived from the presence of a phenolic group in its structure, rather than by the capability of AM404 to block the endocannabinoid transporter as another transporter inhibitor devoid of antioxidant properties, UCM707, did not produce the same effect.

The researchers also evaluated the timing for the effect of CBD in offering 6-hydroxydopamine-induced DA depletion when it was administered immediately after the lesion. However, it failed to do that when treatment was initiated a week later. Moreover, the effect of CBD implied an upregulation of mRNA levels for Cu, Zn-superoxide dismutase, a key enzyme in endogenous defenses against oxidative stress.

In short, the results indicate that those cannabinoids having antioxidant cannabinoid receptor-independent properties offer neuroprotection against the progressive degeneration of nigrostriatal dopaminergic neurons occurring in PD. Furthermore, the activation of CB2 (but not CB1) receptors, or other additional mechanisms, may also contribute to some extent to the potential of cannabinoids in Parkinson’s disease.

The study was conducted by García-Arencibia M, González S, de Lago E, Ramos JA, Mechoulam R, Fernández-Ruiz J. from Departamento de Bioquímica y Biología Molecular III, Facultad de Medicina, Universidad Complutense, 28040-Madrid, Spain.

Reference:
Brain Res., 2007 Feb 23;1134(1):162-70

Type 1 diabetes: People diagnosed with type 1 diabetes (also known as juvenile diabetes) are incapable to produce pancreatic insulin and must rely on insulin medication to survive.

Type 2 diabetes: People diagnosed with type 2 diabetes (also known as adult onset diabetes) produce inadequate insulin amounts.

Over a period of time, diabetes could result in blindness, kidney failure, nerve damage, hardening of the arteries, and even death.

A search of the scientific literature identified a small number of preclinical studies that indicated cannabinoids may modify the disease’s progression and provide symptomatic relief to those suffering from it.

Injections of 5 mg per day of the non-psychoactive cannabinoid CBD significantly minimized the incidence of diabetes in mice, according to a 2006 study published in the journal Autoimmunity. It was reported by investigators that 86% of untreated control mice in the study developed diabetes and only 30% of CBD-treated mice developed the disease, by contrast.

Researchers at the Medical College of Virginia while writing in the March 2006 issue of the American Journal of Pathology reported that rats treated with CBD for periods of one to four weeks experienced significant protection from diabetic retinopathy.
A pair of studies published in the journal Neuroscience Letters in 2004 suggested that “cannabinoids have a potential beneficial effect on experimental diabetic neuropathic pain.”

References:
[1] Croxford and Yamamura. 2005. Cannabinoids and the immune system: Potential for the treatment of inflammatory diseases. Journal of Neuroimmunology 166: 3-18.
[2] Lu et al. 2006. The cannabinergic system as a target for anti-inflammatory therapies. Current Topics in Medicinal Chemistry 13: 1401-1426.
[3] Weiss et al. 2006. Cannabidiol lowers incidence of diabetes in non-obese diabetic mice. Autoimmunity 39: 143-151.
[4] Ibid
[5] El-Remessy et al. 2006. Neuroprotective and blood-retinal barrier preserving effects of cannabidiol in experimental diabetes. American Journal of Pathology 168: 235-244.
[6] Dogrul et al. 2004. Cannabinoids block tactile allodynia in diabetic mice without attenuation of its antinociceptive effect. Neuroscience Letters 368: 82-86.
[7] Ulugol et al. 2004. The effect of WIN 55,212-2, a cannabinoid agonist, on tactile allodynia in diabetic rats. Neuroscience Letters 71: 167-170.
[8] Li et al. 2001. Examination of the immunosuppressive effect of delta-9-tetrahydrocannabinol in streptozotocin-induced autoimmune diabetes. International Immunopharmacology (Italy) 4: 699-712.
[9] Rajesh et al. 2010. Cannabidiol attenuates cardiac dysfunction, oxidative stress, fibrosis, and inflammatory and cell death signaling pathways in diabetic cardiomyopathy. Journal of the American College of Cardiology 56: 2115-2125.