Melissa Etheridge: Pot changed my life, singer advocates legalization of marijuana

WPTV Melissa Etheridge

“My friends have always told me that rock stardom was wasted on me.

To them it seemed that being a rock star was a free ticket to debauchery. It was sex, drugs and rock ‘n’ roll, and I was only taking advantage of two. Drugs were not a part of my rock ‘n’ roll lifestyle. I wasn’t even much of a drinker. I have never thrown up from being over intoxicated.

What kind of rock star is that? I had certainly encountered drugs during the ’80s, mostly cocaine, but nothing about grinding my teeth and rambling on about myself appealed to me. During the ’90s, I smoked an occasional joint. Those were usually fun social occasions. My work was a drug-free zone.

Then in 2004, I was diagnosed with breast cancer. The chemotherapy that was prescribed was called “dose dense”: a harsher, stronger chemo than the usual because I had the benefit of not having to work during the treatment. My close friends told me that, as an alternative, medical marijuana was a natural way to help with the excruciating side effects of chemo.

It worked. The entire experience changed my life. It opened my mind to a new way of thinking about my body, my health and the future.

This herb, this weed that is so strong it grows wild by the side of the road, has always been with us. In ancient times it was highly regarded and has even been found in tombs. It has even been put forth from some biblical scholars that Jesus may have used cannabis oil to heal.

Now, this herb, marijuana, is at center of a debate within our society….


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

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

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Cannabis ‘helped woman to sleep’

“A YOUNG mother using cannabis to help her sleep has been given the benefit of the probation act at Wexford District Court.

Shelly Donnelly, Moortown Great, Ballmitty, had pleaded guilty to the possession of cannabis at her home on June 11, 2010.

Judge Donnchadh O Buachalla heard that the property at Moortown Great was searched and a small quantity of cannabis herb was found. It was for Donnelly’s own use.

Eva Lalor, for Donnelly, said her client is 24years-old and has a fiveyear-old daughter with her long-term partner.

Ms Lalor said Donnelly was suffering from insomnia following a family bereavement and was using cannabis to help her sleep. Donnelly, who has no previous convictions, is now on medication to help her sleep.

Judge O Buachalla gave her the benefit of the probation act, saying that he hopes she has learnt her lesson from the experience.”

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Pharmacological exploitation of the endocannabinoid system: new perspectives for the treatment of depression and anxiety disorders?

 “Animal experiments suggest that drugs promoting endocannabinoid action may represent a novel strategy for the treatment of depression and anxiety disorders.

Because of its analgesic, antiemetic and tranquilizing effects, the herb Cannabis sativa has been used for medical purposes for centuries. In addition, preparations of cannabis, such as marijuana, hashish or skunk, have a long history as drugs of abuse.1 Typical effects of cannabis abuse are amnesia, sedation and a feeling of well-being described as “bliss”.2 In the middle of the last century, Raphael Mechoulam and colleagues identified Δ9-tetrahydrocannabinol (Δ9-THC) as the main psychoactive ingredient of this herb. Today, it is known that Cannabis sativa contains more than 60 substances, such as cannabidiol, cannabinol and cannabicromene, which are referred to as phytocannabinoids.3 Their lipid nature posed a significant obstacle to chemical experiments, which might explain why the discovery of phytocannabinoids occurred late compared to other natural compounds (e.g. morphine was isolated from opium in the XIX century). The molecular structure rendered it likely that Δ9-THC exerts its effects primarily by changing physico-chemical characteristics of cell membranes. Therefore it came as a surprise that specific binding sites could be identified within the mammalian brain,4 followed by isolation and characterization of endogenous binding substances, named endocannabinoids.5 The development of novel pharmacological compounds targeting receptors or ligand synthesis and degradation revealed a number of complex brain functions, which are tightly controlled by the endocannabinoid system. The aim of the present review is to briefly introduce this system and its pharmacology, to discuss its involvement in psychopathology and to illustrate its therapeutic potential.


 Malfunctions in the endocannabinoid system may promote the development and maintenance of psychiatric disorders such as depression, phobias and panic disorder. Thus, CB1 agonists or inhibitors of anandamide hydrolysis are expected to exert antidepressant and anxiolytic effects. Future studies should consider 1) the development of CB1 antagonists that cannot readily cross the blood-brain barrier, 2) shifts in the balance of CB1 vs. TRPV1 signalling, 3) the allosteric site of CB1 receptor and 4) the potential involvement of CB2 receptor in mood regulation. Striking similarities in (endo)cannabinoid action in animals and men render it likely that the new pharmacological principle outlined in the present article may find their way into clinical practice.”

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Pot Stirring – ELLE

“Some are using marijuana as their drug of choice to curb anxiety.”

Marijuana Anxiety Disorders

 “A thimbleful is all it takes. After a day’s work, I pinch off a small amount of marijuana and put it in a steel-tooth grinder. The flowers, covered in tiny white diamonds of THC, release a piney scent when crushed. I turn on the TV, and instead of taking a glass of wine with my evening news, I take out my vaporizer and set it on the coffee table.

Outside the walls of my bungalow in Oakland, California, I can hear the rush-hour traffic, but I’ve already changed into my Big Lebowski–style robe and slippers. I tap the ground flakes into a canister that I attach to another piece, this one with a bag on the end, and set both on the vaporizer. I flip the switch, and the bag slowly inflates with plumes of white smoke. Once it’s fully clouded, I attach a mouthpiece to the canister, put this to my lips, and press. On the inhale, the cannabinoids taste like sunned grass. My prescription for anxiety disorder didn’t always begin and end with an herb. But I’ve run through enough pharmaceutical drugs to know that pot dulls my panic better than any pill.”

Read more;

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Medicinal cannabis: is delta9-tetrahydrocannabinol necessary for all its effects?


  “Cannabis is under clinical investigation to assess its potential for medicinal use, but the question arises as to whether there is any advantage in using cannabis extracts compared with isolated Delta9-trans-tetrahydrocannabinol (Delta9THC), the major psychoactive component. We have compared the effect of a standardized cannabis extract (SCE) with pure Delta9THC, at matched concentrations of Delta9THC, and also with a Delta9THC-free extract (Delta9THC-free SCE), using two cannabinoid-sensitive models, a mouse model of multiple sclerosis (MS), and an in-vitro rat brain slice model of epilepsy. Whilst SCE inhibited spasticity in the mouse model of MS to a comparable level, it caused a more rapid onset of muscle relaxation, and a reduction in the time to maximum effect compared with Delta9THC alone. The Delta9THC-free extract or cannabidiol (CBD) caused no inhibition of spasticity. However, in the in-vitro epilepsy model, in which sustained epileptiform seizures were induced by the muscarinic receptor agonist oxotremorine-M in immature rat piriform cortical brain slices, SCE was a more potent and again more rapidly-acting anticonvulsant than isolated Delta9THC, but in this model, the Delta9THC-free extract also exhibited anticonvulsant activity. Cannabidiol did not inhibit seizures, nor did it modulate the activity of Delta9THC in this model. Therefore, as far as some actions of cannabis were concerned (e.g. antispasticity), Delta9THC was the active constituent, which might be modified by the presence of other components. However, for other effects (e.g. anticonvulsant properties) Delta9THC, although active, might not be necessary for the observed effect. Above all, these results demonstrated that not all of the therapeutic actions of cannabis herb might be due to the Delta9THC content.”

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Analgesic and antiinflammatory activity of constituents of Cannabis sativa L.


“Two extracts of Cannabis sativa herb, one being cannabinoid-free (ethanol) and the other containing the cannabinoids (petroleum), were shown to inhibit PBQ-induced writhing in mouse when given orally and also to antagonize tetradecanoylphorbol acetate (TPA)-induced erythema of mouse skin when applied topically. With the exception of cannabinol (CBN) and delta 1-tetrahydrocannabinol (delta 1-THC), the cannabinoids and olivetol (their biosynthetic precursor) demonstrated activity in the PBQ test exhibiting their maximal effect at doses of about 100 micrograms/kg. delta 1-THC only became maximally effective in doses of 10 mg/kg. This higher dose corresponded to that which induced catalepsy and is indicative of a central action. CNB demonstrated little activity and even at doses in excess of 10 mg/kg could only produce a 40% inhibition of PBQ-induced writhing. Cannabinoid (CBD) was the most effective of the cannabinoids at doses of 100 micrograms/kg. Doses of cannabinoids that were effective in the analgesic test orally were used topically to antagonize TPA-induced erythema of skin. The fact that delta 1-THC and CBN were the least effective in this test suggests a structural relationship between analgesic activity and antiinflammatory activity among the cannabinoids related to their peripheral actions and separate from the central effects of delta 1-THC.”

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Cannabinoids in clinical practice.


“Cannabis has a potential for clinical use often obscured by unreliable and purely anecdotal reports. The most important natural cannabinoid is the psychoactive tetrahydrocannabinol (delta9-THC); others include cannabidiol (CBD) and cannabigerol (CBG). Not all the observed effects can be ascribed to THC, and the other constituents may also modulate its action; for example CBD reduces anxiety induced by THC. A standardised extract of the herb may be therefore be more beneficial in practice and clinical trial protocols have been drawn up to assess this. The mechanism of action is still not fully understood, although cannabinoid receptors have been cloned and natural ligands identified. Cannabis is frequently used by patients with multiple sclerosis (MS) for muscle spasm and pain, and in an experimental model of MS low doses of cannabinoids alleviated tremor. Most of the controlled studies have been carried out with THC rather than cannabis herb and so do not mimic the usual clincal situation. Small clinical studies have confirmed the usefulness of THC as an analgesic; CBD and CBG also have analgesic and antiinflammatory effects, indicating that there is scope for developing drugs which do not have the psychoactive properties of THC. Patients taking the synthetic derivative nabilone for neurogenic pain actually preferred cannabis herb and reported that it relieved not only pain but the associated depression and anxiety. Cannabinoids are effective in chemotherapy-induced emesis and nabilone has been licensed for this use for several years. Currently, the synthetic cannabinoid HU211 is undergoing trials as a protective agent after brain trauma. Anecdotal reports of cannabis use include case studies in migraine and Tourette’s syndrome, and as a treatment for asthma and glaucoma. Apart from the smoking aspect, the safety profile of cannabis is fairly good. However, adverse reactions include panic or anxiety attacks, which are worse in the elderly and in women, and less likely in children. Although psychosis has been cited as a consequence of cannabis use, an examination of psychiatric hospital admissions found no evidence of this, however, it may exacerbate existing symptoms. The relatively slow elimination from the body of the cannabinoids has safety implications for cognitive tasks, especially driving and operating machinery; although driving impairment with cannabis is only moderate, there is a significant interaction with alcohol. Natural materials are highly variable and multiple components need to be standardised to ensure reproducible effects. Pure natural and synthetic compounds do not have these disadvantages but may not have the overall therapeutic effect of the herb.”

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Non-psychotropic plant cannabinoids: new therapeutic opportunities from an ancient herb.

“Delta(9)-tetrahydrocannabinol binds cannabinoid (CB(1) and CB(2)) receptors, which are activated by endogenous compounds (endocannabinoids) and are involved in a wide range of physiopathological processes (e.g. modulation of neurotransmitter release, regulation of pain perception, and of cardiovascular, gastrointestinal and liver functions).

The well-known psychotropic effects of Delta(9)-tetrahydrocannabinol, which are mediated by activation of brain CB(1) receptors, have greatly limited its clinical use. However, the plant Cannabis contains many cannabinoids with weak or no psychoactivity that, therapeutically, might be more promising than Delta(9)-tetrahydrocannabinol.

Here, we provide an overview of the recent pharmacological advances, novel mechanisms of action, and potential therapeutic applications of such non-psychotropic plant-derived cannabinoids. Special emphasis is given to cannabidiol,

the possible applications of which have recently emerged in inflammation, diabetes, cancer, affective and neurodegenerative diseases, and to Delta(9)-tetrahydrocannabivarin, a novel CB(1) antagonist which exerts potentially useful actions in the treatment of epilepsy and obesity.”

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Phytocannabinoids as novel therapeutic agents in CNS disorders.


“The Cannabis sativa herb contains over 100 phytocannabinoid (pCB) compounds and has been used for thousands of years for both recreational and medicinal purposes. In the past two decades, characterisation of the body’s endogenous cannabinoid (CB) (endocannabinoid, eCB) system (ECS) has highlighted activation of central CB(1) receptors by the major pCB, Δ(9)-tetrahydrocannabinol (Δ(9)-THC) as the primary mediator of the psychoactive, hyperphagic and some of the potentially therapeutic properties of ingested cannabis. Whilst Δ(9)-THC is the most prevalent and widely studied pCB, it is also the predominant psychotropic component of cannabis, a property that likely limits its widespread therapeutic use as an isolated agent. In this regard, research focus has recently widened to include other pCBs including cannabidiol (CBD), cannabigerol (CBG), Δ(9)tetrahydrocannabivarin (Δ(9)-THCV) and cannabidivarin (CBDV), some of which show potential as therapeutic agents in preclinical models of CNS disease. Moreover, it is becoming evident that these non-Δ(9)-THC pCBs act at a wide range of pharmacological targets, not solely limited to CB receptors. Disorders that could be targeted include epilepsy, neurodegenerative diseases, affective disorders and the central modulation of feeding behaviour. Here, we review pCB effects in preclinical models of CNS disease and, where available, clinical trial data that support therapeutic effects. Such developments may soon yield the first non-Δ(9)-THC pCB-based medicines.”

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