Tag Archives: Cannabinoids

Study Claims Marijuana Tied to Lower Bladder Cancer Risk

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“Cannabis use only was associated with a 45 percent reduction in bladder cancer incidence, and tobacco use only was associated with a 52 percent increase in bladder cancer,” said study author Dr. Anil A. Thomas, a fellow in urology at Kaiser Permanente Medical Center in Los Angeles…

“The theory is that there are receptors in the bladder that are affected by cannabis,” he said.

The cannabinoids [compounds] in the marijuana may link with the cannabinoid receptors in the bladder and somehow protect against cell changes that can lead to cancer..”

More: http://www.healthfinder.gov/News/Article/676121/study-claims-marijuana-tied-to-lower-bladder-cancer-risk

“…using tobacco only was associated with an increased risk of bladder cancer, whereas cannabis use only was associated with a 45% reduction in bladder cancer… cannabis use may be inversely associated with bladder cancer risk…” http://www.ncbi.nlm.nih.gov/pubmed/25623697

http://www.thctotalhealthcare.com/category/bladder-cancer/

The Feds Finally Recognize The Anti-Cancer Potential Of Cannabis — 36 Years Too Late!

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3-24-2011: “Scientific trials have for decades documented the anti-cancer properties of cannabis and its constituents. Yet it took until this week for the website of the National Institute of Cancer, a component of the U.S. government’s National Institutes of Health, to finally acknowledged the herb’s therapeutic utility for patients living with disease or suffering from the adverse side-effects of cancer treatment.

In a newly added section to the website, entitled ‘Cannabis and Cannabinoids,’ the Institute states:

Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis. Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death.”

…The potential benefits of medicinal cannabis for people living with cancer include antiemetic effects, appetite stimulation, pain relief, and improved sleep. In the practice of integrative oncology, the health care provider may recommend medicinal cannabis not only for symptom management but also for its possible direct antitumor effect.”

It’s a stunning acknowledgment, given that the NIH is a branch of the very same government that presently maintains that the cannabis plant and all of its naturally-derived components have ‘no accepted medical use.’ Yet it also begs the question: Where has the National Institute of Cancer been all these years?

After all, the anti-tumor activity of cannabinoids were initially documented in 1975! That’s right; it’s taken 36 years for the Institute to get with the program.

Hopefully it won’t take them another 36 years to demand that the Feds finally assess whether these preclinical results are replicable in human trials.”

by Paul Armentano, NORML Deputy Director

http://blog.norml.org/2011/03/24/the-feds-finally-recognize-the-anti-cancer-potential-of-cannabis-36-years-too-late/

Marijuana Study Shows Brain Cancer Cells Eat Themselves

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“… a study released by researchers at the Complutense University in Madrid describes how marijuana’s active chemical, tetrahydrocannabinol, can aid anti-cancer therapies due to its ability to coax cancerous brain cells to self-digest.

The research involved stimulating cancer growth in mice and then injecting sites near the tumors with THC every day. An experimental trial involving two brain cancer patients were also analyzed by the researchers.

It studied how an aggressive brain tumor type was affected by THC, noting that the findings fell in line with the tests done on mice. They say the work shows how “a new family of potential antitumoral agent” exists among THC and related cannabinoids.”

http://www.shortnews.com/start.cfm?id=78020

“Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells”

Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/

Phytocannabinoids

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“Phytocannabinoids, also called ”natural cannabinoids”, ”herbal cannabinoids”, and ”classical cannabinoids”, are only known to occur naturally in significant quantity in the cannabis plant, and are concentrated in a viscous resin that is produced in glandular structures known as trichomes.

In addition to cannabinoids, the resin is rich in terpenes, which are largely responsible for the odour of the cannabis plant.

Phytocannabinoids are nearly insoluble in water but are soluble in lipids, alcohols, and other non-polar organic solvents. However, as phenols, they form more water-soluble phenolate salts under strongly alkaline conditions.

All-natural cannabinoids are derived from their respective 2-carboxylic acids (2-COOH) by decarboxylation (catalyzed by heat, light, or alkaline conditions).

Types

At least 66 cannabinoids have been isolated from the cannabis plant. To the right the main classes of natural cannabinoids are shown. All classes derive from cannabigerol-type compounds and differ mainly in the way this precursor is cyclized.

Tetrahydrocannabinol (THC), cannabidiol (CBD) and cannabinol (CBN) are the most prevalent natural cannabinoids and have received the most study. Other common cannabinoids are listed below:

  • CBG Cannabigerol
  • CBC Cannabichromene
  • CBL Cannabicyclol
  • CBV Cannabivarin
  • THCV Tetrahydrocannabivarin
  • CBDV Cannabidivarin
  • CBCV Cannabichromevarin
  • CBGV Cannabigerovarin
  • CBGM Cannabigerol Monoethyl Ether

Tetrahydrocannabinol

Tetrahydrocannabinol (THC) is the primary psychoactive component of the plant. It appears to ease moderate pain (analgetic) and to be neuroprotective. THC has approximately equal affinity for the CB1 and CB2 receptors. Its effects are perceived to be more cerebral.

”Delta”-9-Tetrahydrocannabinol (Δ9-THC, THC) and ”delta”-8-tetrahydrocannabinol (Δ8-THC), mimic the action of anandamide, a neurotransmitter produced naturally in the body. The THCs produce the ”high” associated with cannabis by binding to the CB1 cannabinoid receptors in the brain.

Cannabidiol

Cannabidiol (CBD) is not psychoactive, and was thought not to affect the psychoactivity of THC. However, recent evidence shows that smokers of cannabis with a higher CBD/THC ratio were less likely to experience schizophrenia-like symptoms.

This is supported by psychological tests, in which participants experience less intense psychotic effects when intravenous THC was co-administered with CBD (as measured with a PANSS test).

It has been hypothesized that CBD acts as an allosteric antagonist at the CB1 receptor and thus alters the psychoactive effects of THC.

It appears to relieve convulsion, inflammation, anxiety, and nausea. CBD has a greater affinity for the CB2 receptor than for the CB1 receptor.

Cannabigerol

Cannabigerol (CBG) is non-psychotomimetic but still affects the overall effects of Cannabis. It acts as an α2-adrenergic receptor agonist, 5-HT1A receptor antagonist, and CB1 receptor antagonist. It also binds to the CB2 receptor.

Tetrahydrocannabivarin

Tetrahydrocannabivarin (THCV) is prevalent in certain South African and Southeast Asian strains of Cannabis. It is an antagonist of THC at CB1 receptors and attenuates the psychoactive effects of THC.

Cannabichromene

Cannabichromene (CBC) is non-psychoactive and does not affect the psychoactivity of THC It is found in nearly all tissues in a wide range of animals.

Two analogs of anandamide, 7,10,13,16-docosatetraenoylethanolamide and ”homo”-γ-linolenoylethanolamine, have similar pharmacology.

All of these are members of a family of signalling lipids called ”N”-acylethanolamides, which also includes the noncannabimimetic palmitoylethanolamide and oleoylethanolamine, which possess anti-inflammatory and orexigenic effects, respectively. Many ”N”-acylethanolamines have also been identified in plant seeds and in molluscs.

  • 2-arachidonoyl glycerol (2-AG)

Another endocannabinoid, 2-arachidonoyl glycerol, binds to both the CB1 and CB2 receptors with similar affinity, acting as a full agonist at both, and there is some controversy over whether 2-AG rather than anandamide is chiefly responsible for endocannabinoid signalling ”in vivo”.

In particular, one ”in vitro” study suggests that 2-AG is capable of stimulating higher G-protein activation than anandamide, although the physiological implications of this finding are not yet known.

  • 2-arachidonyl glyceryl ether (noladin ether)

In 2001, a third, ether-type endocannabinoid, 2-arachidonyl glyceryl ether (noladin ether), was isolated from porcine brain.

Prior to this discovery, it had been synthesized as a stable analog of 2-AG; indeed, some controversy remains over its classification as an endocannabinoid, as another group failed to detect the substance at “any appreciable amount” in the brains of several different mammalian species.

It binds to the CB1 cannabinoid receptor (”K”i = 21.2 nmol/L) and causes sedation, hypothermia, intestinal immobility, and mild antinociception in mice. It binds primarily to the CB1 receptor, and only weakly to the CB2 receptor.

Like anandamide, NADA is also an agonist for the vanilloid receptor subtype 1 (TRPV1), a member of the vanilloid receptor family.

  • Virodhamine (OAE)

A fifth endocannabinoid, virodhamine, or ”O”-arachidonoyl-ethanolamine (OAE), was discovered in June 2002. Although it is a full agonist at CB2 and a partial agonist at CB1, it behaves as a CB1 antagonist ”in vivo”.

In rats, virodhamine was found to be present at comparable or slightly lower concentrations than anandamide in the brain, but 2- to 9-fold higher concentrations peripherally.

Function

Endocannabinoids serve as intercellular ‘lipid messengers’, signaling molecules that are released from one cell and activate the cannabinoid receptors present on other nearby cells.

Although in this intercellular signaling role they are similar to the well-known monoamine neurotransmitters, such as acetylcholine and dopamine, endocannabinoids differ in numerous ways from them. For instance, they use retrograde signaling.

Furthermore, endocannabinoids are lipophilic molecules that are not very soluble in water. They are not stored in vesicles, and exist as integral constituents of the membrane bilayers that make up cells. They are believed to be synthesized ‘on-demand’ rather than made and stored for later use.

The mechanisms and enzymes underlying the biosynthesis of endocannabinoids remain elusive and continue to be an area of active research.

The endocannabinoid 2-AG has been found in bovine and human maternal milk.

Retrograde signal

Conventional neurotransmitters are released from a ‘presynaptic’ cell and activate appropriate receptors on a ‘postsynaptic’ cell, where presynaptic and postsynaptic designate the sending and receiving sides of a synapse, respectively.

Endocannabinoids, on the other hand, are described as retrograde transmitters because they most commonly travel ‘backwards’ against the usual synaptic transmitter flow.

They are, in effect, released from the postsynaptic cell and act on the presynaptic cell, where the target receptors are densely concentrated on axonal terminals in the zones from which conventional neurotransmitters are released.

Activation of cannabinoid receptors temporarily reduces the amount of conventional neurotransmitter released.

This endocannabinoid mediated system permits the postsynaptic cell to control its own incoming synaptic traffic.

The ultimate effect on the endocannabinoid-releasing cell depends on the nature of the conventional transmitter being controlled.

For instance, when the release of the inhibitory transmitter GABA is reduced, the net effect is an increase in the excitability of the endocannabinoid-releasing cell.

On the converse, when release of the excitatory neurotransmitter glutamate is reduced, the net effect is a decrease in the excitability of the endocannabinoid-releasing cell.

Range

Endocannabinoids are hydrophobic molecules. They cannot travel unaided for long distances in the aqueous medium surrounding the cells from which they are released, and therefore act locally on nearby target cells. Hence, although emanating diffusely from their source cells, they have much more restricted spheres of influence than do hormones, which can affect cells throughout the body.

Other thoughts

Endocannabinoids constitute a versatile system for affecting neuronal network properties in the nervous system.

”Scientific American” published an article in December 2004, entitled “The Brain’s Own Marijuana” discussing the endogenous cannabinoid system.

The current understanding recognizes the role that endocannabinoids play in almost every major life function in the human body.

U.S. Patent # 6630507

In 2003 The U.S.A.’s Government as represented by the Department of Health and Human Services was awarded a patent on cannabinoids as antioxidants and neuroprotectants. U.S. Patent 6630507.”

http://www.news-medical.net/health/Phytocannabinoids.aspx

Synthetic and Patented Cannabinoids

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“Historically, laboratory synthesis of cannabinoids were often based on the structure of herbal cannabinoids, and a large number of analogs have been produced and tested, especially in a group led by Roger Adams as early as 1941 and later in a group led by Raphael Mechoulam.

Newer compounds are no longer related to natural cannabinoids or are based on the structure of the endogenous cannabinoids.

Synthetic cannabinoids are particularly useful in experiments to determine the relationship between the structure and activity of cannabinoid compounds, by making systematic, incremental modifications of cannabinoid molecules.

Medications containing natural or synthetic cannabinoids or cannabinoid analogs:

  • Dronabinol (Marinol), is Δ9-tetrahydrocannabinol (THC), used as an appetite stimulant, anti-emetic, and analgesic
  • Nabilone (Cesamet), a synthetic cannabinoid and an analog of Marinol. It is Schedule II unlike Marinol, which is Schedule III
  • Sativex, a cannabinoid extract oral spray containing THC, CBD, and other cannabinoids used for neuropathic pain and spasticity in Canada and Spain. Sativex develops whole-plant cannabinoid medicines
  • Rimonabant (SR141716), a selective cannabinoid (CB1) receptor antagonist used as an anti-obesity drug under the proprietary name Acomplia. It is also used for smoking cessation

Other notable synthetic cannabinoids include:

  • CP-55940, produced in 1974, this synthetic cannabinoid receptor agonist is many times more potent than THC
  • Dimethylheptylpyran
  • HU-210, about 100 times as potent as THC
  • HU-331 a potential anti-cancer drug derived from cannabidiol that specifically inhibits topoisomerase II.
  • SR144528, a CB2 receptor antagonists
  • WIN 55, a potent cannabinoid receptor agonist
  • JWH-133, a potent selective CB2 receptor agonist
  • Levonantradol (Nantrodolum), an anti-emetic and analgesic but not currently in use in medicine”

http://www.news-medical.net/health/Synthetic-and-Patented-Cannabinoids.aspx

Cannabinoids – What are Cannabinoids?

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“Cannabinoids are a group of terpenophenolic compounds present in Cannabis (”Cannabis sativa”) and occur naturally in the nervous and immune systems of animals.

The broader definition of cannabinoids refers to a group of substances that are structurally related to tetrahydrocannabinol (THC) or that bind to cannabinoid receptors.

The chemical definition encompasses a variety of distinct chemical classes: the classical cannabinoids structurally related to THC, the nonclassical cannabinoids, the aminoalkylindoles, the eicosanoids related to the endocannabinoids, 1, quinolines and arylsulphonamides, and additional compounds that do not fall into these standard classes but bind to cannabinoid receptors.

The term ”cannabinoids” also refers to a unique group of secondary metabolites found in the cannabis plant, which are responsible for the plant’s peculiar pharmacological effects.

At the present time, there are three general types of cannabinoids: ”phytocannabinoids” occur uniquely in the cannabis plant; ”endogenous cannabinoids” are produced in the bodies of humans and other animals; and ”synthetic cannabinoids” are similar compounds produced in a laboratory.”

http://www.news-medical.net/health/Cannabinoids-What-are-Cannabinoids.aspx

Cannabinoid Receptors

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“Before the 1980s, it was often speculated that cannabinoids produced their physiological and behavioral effects via nonspecific interaction with cell membranes, instead of interacting with specific membrane-bound receptors.

The discovery of the first cannabinoid receptors in the 1980s helped to resolve this debate.

These receptors are common in animals, and have been found in mammals, birds, fish, and reptiles.

At present, there are two known types of cannabinoid receptors, termed CB1 and CB2, with mounting evidence of more.

Cannabinoid receptor type 1

CB1 receptors are found primarily in the brain, to be specific in the basal ganglia and in the limbic system, including the hippocampus.

They are also found in the cerebellum and in both male and female reproductive systems. CB1 receptors are absent in the medulla oblongata, the part of the brain stem responsible for respiratory and cardiovascular functions. Thus, there is not a risk of respiratory or cardiovascular failure as there is with many other drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis.

Cannabinoid receptor type 2

CB2 receptors are almost exclusively found in the immune system, with the greatest density in the spleen.

While found only in the peripheral nervous system, a report does indicate that CB2 is expressed by a subpopulation of microglia in the human cerebellum.

CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.”

http://www.news-medical.net/health/Cannabinoid-Receptors.aspx

Cannabis News: The Cannabinoid System Reverses Dementia, Treats PTSD and Controls Diabetes Top May’s News Digest from Publius

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“The Cannabinoid System’s role in reversing dementia, treating PTSD and controlling diabetes highlight May’s cannabis news from Publius, the pen name used by the authors of The Cannabis Papers – Federal ignorance goes on unabated.”

“The Cannabinoid System’s (CS) role in reversing dementia, treating PTSD and controlling diabetes highlight May’s cannabis news from Publius, the pen name used by the authors of The Cannabis Papers: A citizen’s guide to cannabinoids (2011).”

More: http://www.prweb.com/releases/2013/5/prweb10787154.htm

Cannabinoids Attenuate Cancer Pain and Proliferation in a Mouse Model

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“Oral cancer represents 3% of all cancers and its overall survival rate of 50% places it among the worst of all cancers

For many years cannabinoids have been used for medicinal and recreational purposes.

Recently, studies have focused on the therapeutic effects of cannabinoids on different cancers. The current study was the first to investigate the therapeutic effects of synthetic cannabinoids on oral cancer.

We investigated the effects of cannabinoid receptor agonists on (1) oral cancer cell viability in vitro and (2) oral cancer pain and tumor growth in a mouse cancer model.

Here we demonstrate the anti-nociceptive and anti-proliferative effects of systemic administration of cannabinoid receptor agonists on human oral cancer cells.

Our results suggest that systemic administration of cannabinoids decease oral cancer pain.

Our findings suggest a direct role for cannabinoid mechanisms in oral cancer pain and proliferation.

The systemic administration of cannabinoid receptor agonists may have important therapeutic implications wherein cannabinoid receptor agonists may reduce morbidity and mortality of oral cancer.

The present findings suggest that cannabinoid treatment may be a promising alternative therapy for oral cancer pain management. Furthermore, CBr2 agonism is not only palliative, but it may also be effective in inhibiting oral cancer growth, making the agonist a particularly desirable therapeutic agent.”

Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099480/

Study: No Association Between The Cumulative Consumption Of Cannabis Smoke And The Risk Of Lung Cancer

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“In a recent presentation given at the annual meeting of the American Association of Cancer Research, investigators from the university of California, Los Angeles provided the latest data reaffirming that cannabis consumption is not associated with an elevated risk of lung cancer. Below is a summary of the findings from The Oncology Report:

The study included data from six case-control studies conducted from 1999 to 2012 in the United States, Canada, the United Kingdom, and New Zealand, with a subject pool of 2,159 lung cancer cases and 2,985 controls. All of the studies were part of the International Lung Cancer Consortium (ILCCO), an international group of lung cancer researchers with the aim of sharing comparable data from ongoing and recently completed lung cancer studies from different geographical areas and ethnicities.

Dr. Zhang of the University of California, Los Angeles, performed two analyses. One compared all lung cancer cases and all controls, regardless of concurrent or past tobacco use. Then, to reduce confounding by tobacco, she restricted the analysis to those who had never smoked tobacco.

… When compared with cannabis smokers who also used tobacco, habitual pot smokers had no significant increase in cancer risk. In an analysis of marijuana smokers that excluded tobacco smokers, there were no significant differences in any of the comparisons, including habitual vs. nonhabitual use; number of joints smoked per day; duration of up to 20 years or duration of more than 20 years.

The abstract of the presentation, which concludes “Our pooled results showed no significant association between the intensity, duration, or cumulative consumption of cannabis smoke and the risk of lung cancer overall or in never smokers,” is available online here.

Numerous preclinical studies have documented that cannabinoids possess potent anti-cancer properties, including the inhibition of lung cancer cell growth.”

More: http://enewspf.com/latest-news/health-and-fitness/43037-study-no-association-between-the-cumulative-consumption-of-cannabis-smoke-and-the-risk-of-lung-cancer.html