International Cannabis & Hemp Expo Coming To Oakland!

International Cannabis & Hemp Expo 3

CANNABIS EXPO INNOVATOR “TAKING IT TO THE STREETS”

OF OAKLAND PRESENTING LANDMARK EVENT

Saturday & Sunday, September 3^rd and 4^th

Oakland, Ca. – Cannabis activist and CEO of the International Cannabis & Hemp Expo (INTCHE) Kim Cue is proud to announce that the 2011 expo will be held out in the open on the streets of downtown Oakland on Saturday and Sunday, September 3^rd and 4^th from 12pm-8pm.  The area between 14^th St., Clay St. and San Pablo Ave including Ogawa Park will be blocked off for this celebration of education, awareness, and advancement of the cannabis movement.  Located directly in front of City Hall will be the designated  “215 Area” for patients to medicate. INTCHE was the first event to have an approved onsite medicating area for patients, and it was the first to bring the cannabis community together with the hemp industry to educate the general public on the 2 related plants and their individual benefits to the populace.  Since the debut of the first INTCHE, many other producers have created events to try to capitalize on the emerging industry – but without a solid agenda of professionalism, education and advancement of the political movement for patients of medical cannabis.

The agenda for the 2-day event includes speaker’s panels debating current cannabis and hemp issues.  One of those will be a discussion of the upcoming 2012 initiative to put legalization on the ballot in California.  This topic holds significance because Colorado and Washington State have already put plans in motion to put it on the 2012 ballot as well.  Historically initiatives have a greater chance of passing in presidential election years and when they have 60% support going into the race.  Colorado is already at 80% approval.   Passage of legalization propositions in any or all of these states will force a showdown with the Feds over States’ rights.  The Gallup National Poll in October of 2010 showed 46% of Americans now would vote for full legalization, and that number continues to grow.

In addition to the panels there will be over 300 vendors with information about how to obtain a recommendation for medical use, new products, growing techniques, locations of dispensaries, etc.  There will be live entertainment and a complimentary hash bar in the 215 Area.  A variety of food and nonalcoholic beverages will be available at the event.  Surrounding restaurants and bars outside the event will be open for business.

Judges who have purchased the $300 VIP ticket will receive a SWAG Bag with over 320 samples the week prior to the event.  This will include 120 strains of cannabis, 40 hashes, 40 oils, 40 waxes, and a variety of edibles.  The VIP ticket includes 2 days all access, a catered buffet including an array of cannabis infused foods, live entertainment on a private stage in the tented VIP area, a celebrity meet and greet, vapor lounge, and 2 hash bars. A limited number of these tickets are being offered.  Over 50% of these have already been sold.   These tickets are only available at:  Angels Care in San Jose, Sonoma Patients Group in Santa Rosa, and 7 Stars in El Sobrante.  Judges will cast their ballot at the event and winners will be announced at 4:20pm on Sunday.

Up to date information and advance ticket sales are available at www.intcheevents.org.

Cured: A Cannabis Story (Video)

Cannabis Compound A Promising Treatment For Liver Fibrosis

he administration of the non-psychotropic cannabinoid CBD (cannabidiol) induces selective apoptosis in hepatic stellate cells (HSCs), according to preclinical findings reported in the journal Cell Death and Disease. The activation of HSCs is considered to be a key cellular event underlying hepatic fibrogenesis (excessive tissue build up), a condition that can result in liver failure.

Authors reported: “In this study, we find that CBD selectively kills activated HSCs. … We provide a molecular basis of action for CBD and identify CBD as a novel potential therapeutic agent for liver fibrosis.”

They concluded, “These promising findings warrant future investigation evaluating the anti-fibrotic effect of CBD in vivo. The prospect of CBD as a new anti-fibrotic compound is rendered more appealing by the fact that CBD is a non-psychoactive small drug-like molecule already approved for clinical use in many countries.”

Liver fibrosis is the tenth leading cause of death in the United States.

Previous studies have consistently reported that cannabinoids can selectively promote cell suicide in various malignant cell lines, including breast cancer, lung cancer, and glioma.

For more information, please contact Paul Armentano, NORML Deputy Director, at: paul@norml.org. Full text of the study, “Cannabidiol causes activated hepatic stellate cell death through a mechanism of endoplasmic reticulum stress-induced apoptosis,” appears in Cell Death and Disease.

OCD Can Be Treated With Medical Marijuana

Obsessive–compulsive disorder (OCD) is basically an anxiety disorder characterized by intrusive thoughts that produce apprehension, fear, uneasiness or worry by repetitive behaviors aimed at reducing the associated anxiety. Unnecessary repetition of activities such as washing, cleaning, and hoarding during the day or being preoccupied with thoughts of coitus, violence, and religious ideologies as well as disgust of specific numbers are the main hints of a person suffering from OCD.

Treatment

OCD is a treatable disease. With adequate therapy and correct counseling by experienced psychiatrist and physicians, the intensity of the disease can be decreased in little time. Effective treatments for obsessive-compulsive disorder are now easily available, and fresh researches are yielding new and improved therapies that can help people with OCD and other anxiety disorders lead productive, fulfilling lives.

Some doctors even say that Medical Marijuana (Cannabis) can also help in eliminating the disease. Dr. Breen of Southern California insisted that he has been successful in treating two patients with OCD via medical Marijuana. He shared, “Today I had two patients who have been successfully treating their symptoms of obsessive compulsive disorder with medical marijuana. One was a 46-year-old man whose symptoms are primarily having ‘to check things all the time.’ He explained having to walk back to his car all the time to check his door locks etc. The second was an 18-year-old male who had the compulsion to try and touch the ceiling in a room. In both cases their symptoms were disruptive to their daily lives.

Amazingly both had been using cannabis with god results to control their symptoms.”

Moreover, Dr. Bennett, a pediatric psychologist at New York-Presbyterian Hospital/Weill Cornell Medical Center, observed that OCD, in its earlier stages, is more easily removed than in its later stages. He maintained that children and adolescent suffering from OCD must be given more attention to help them get rid of the anxiety and stress of OCD.

“Anxiety is a normal part of growing up, but when it interferes with school, friendships or family life, we recommend parents seek treatment for their child. If a family is going to extreme measures to accommodate their child’s anxiety, or if their child has a problem with involuntary movements or vocalizations, we can offer help,” says Dr. Bennett.

Worth Repeating: Government Has Patent For Cannabinoids Since 2003

Photo: The Julius Axelrod Papers

Dr. Julius Axelrod, pictured above, conducted some of the original research which culminated in the United States government getting a patent on all cannabinoids in 2003.

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Welcome to Room 420, where your instructor is Mr. Ron Marczyk and your subjects are wellness, disease prevention, self actualization, and chillin’.

Worth Repeating

​By Ron Marczyk, R.N.

Health Education Teacher (Retired)

The United States federal government holds a “medical patent” for all cannabinoids — a patent which it has held since 2003.

Let’s take a look at the rationale behind this patent, and highlight the good news it actually contains for disease prevention, medical treatment and for cannabis legalization.

This patent was the outcome from research conducted by:

• Dr. Aiden J. Hampson, a neuropharmacologist at the National Institute for Mental Health (NIMH) in Bethesda, Maryland

• Dr. Julius Axelrod (1912-2004), Professor Emeritus, National Institutes of Health, pharmacologist and neuroscientist who shared the 1970 Nobel Prize in Physiology and Medicine

• Dr. Maurizio Grimaldi, professor of neurology/neuropsychopharmacology and toxicology, NIMH

Here’s how it all went down in 1998.

Patent No. U.S. 6,630,507 B1 (Source [PDF])

Assignee: The United States of America as represented by the Department of Health and Human Services (Washington, D.C.)

Graphic: rm3.us

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Patent Title: Cannabinoids act as antioxidants and neuroprotectants

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Field of the Invention (what it’s going to do)

The present invention concerns pharmaceutical compounds and compositions that are useful as tissue protectants, such as neuroprotectants and cardioprotectants. The compounds and compositions may be used, for example, in the treatment of acute ischemic neurological insults or chronic neurodegenerative diseases.

Definitions in this patent: Cannabinoid

“As used herein, a ‘cannabinoid’ is a chemical compound (such as cannabinol, THC or cannabidiol) that is found in the plant species Cannabis sativa (marijuana), and metabolites and synthetic analogues thereof that may or may not have psychoactive properties.”

Claims Found In Patent:

Claim #1: A method of treating diseases caused by oxidative stress, comprising administering a therapeutically effective amount of a cannabinoid to a subject who has a disease caused by oxidative stress.

Claim #15: A method of treating an ischemic or neurodegenerative disease in the central nervous system of a subject, comprising administering to the subject a therapeutically effective amount of a cannabinoid.

Claim #24: (A method of treating) wherein the ischemic or neurodegenerative disease is an ischemic infarct, Alzheimer’s disease, Parkinson’s disease, and human immunodeficiency virus dementia, Down’s syndrome, or heard disease.

If you read my last past, “Cannabis May Help Combat Aging of the Brain,” you’ll remember I presented current (2005-2009) evidence for cannabis and neuroprotection.

Well, apparently the U.S. government was way ahead of the curve on this one. Thank you, President Clinton, for filing this patent (April 29, 1999). Yo!

Maybe you didn’t inhale, but you may have legalized cannabis as a medicine through a back door during your presidency!

The “Assignee” on the patent is the United States of America. This means the people who are its citizens, who fund the government with their taxes, and are represented by it, and who in effect employ it to act as our agent protecting our welfare. The government works for us, and exists to serve us. We, the American people, are the ultimate owners of this patent that it holds for us.

In order to produce the maximum benefit for the most people, in the shortest time, we would like our patent to produce “fast tracked” cannabis-based medicines to treat the following medical conditions.

If you look at the chart below at the 10 o’clock position , “neuroprotection” is just the first benefit of this wonderful plant. We just scratched the surface of its full potential.

Graphic: TRENDS In Pharmacological Sciences

Pharmacological actions of non-psychotropic cannabinoids (with the indication of the proposed mechanisms of action). Abbreviations: D 9 -THC, D 9 -tetrahydrocannabinol; D 8 -THC, D 8 -tetrahydrocannabinol; CBN, cannabinol; CBD, cannabidiol; D 9 -THCV, D 9 -tetrahydrocannabivarin; CBC, cannabichromene; CBG, cannabigerol; D 9 -THCA, D 9 -tetrahydrocannabinolic acid; CBDA, cannabidiolic acid; TRPV1, transient receptor potential vanilloid type 1; PPARg, peroxisome proliferator-activated receptor g; ROS, reactive oxygen species; 5-HT1A, 5-hydroxytryptamine receptor subtype 1A; FAAH, fatty acid amide hydrolase. (+), direct or indirect activation; “, increase; #, decrease.

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And again, thank you for standing up for the people of this country first, not corporations. Thank you so much for looking out for our interests and securing the rights to this medicine so that it may be used by us, the American people.

That was eight years ago.

It makes one wonder what the U.​S. government was thinking when, this past March, it made the National Cancer Institute scrub its newly created cannabis web section to delete the phrase:

“In the practice of integrative oncology, the health care provider may recommend medical cannabis not only for symptom management but also for its possible direct anti-tumor effect.”

This, mind you, is after receiving a patent specifically on the point that cannabinoids are powerful anti-oxidative medicines that fight oxidative stress diseases. One of the main causes of cancer is oxidative stress disease.

“Many forms of cancer are thought to be the result of reactions between free radicals and DNA, resulting in mutations that can adversely affect the cell cycle and potentially lead to malignancy.”

Cancer patients need unrestricted access to cannabis products. The drug is self-regulating; if you use “too much,” you fall asleep.

This patent makes the case that cannabinoids should definitely be part of an integrative medical treatment plan for cancer and a multitude of other conditions as per the above statement.

All cannabinoids act as potent free-radical scavengers. Interesting fact: the patent claims that THC is equal to cannabidiol as an anti-oxidant in strength.

Only problem: it is “psychotoxic,” to use the patent’s terminology.

Translation: it gets you high.

Example of an Oxidative Disease

Skin immediately after exposure to 30 percent hydrogen peroxide

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Hydrogen peroxide‘s actions come from the fact that it oxidizes tissue.

This is how hydrogen peroxide gets that bloodstain out of your white shirt; it dissolves the cells by stealing electrons from proteins. Oxidation is to human DNA as rust is to an iron bridge, and as paint protects it from oxygen, cannabinoids are the “paint” that protect your DNA from destruction.

The cannabis plant originated in the mountains at high altitudes in Kurdistan. To protect itself from harmful ultraviolet radiation at in the thin air, the plant developed a chemical defense to protect itself. It evolutionarily selected for cannabinoids, antioxidants which counter this high intensity, less filtered form of sunlight radiation.

Now imagine this chemical reaction happening in your brain, just ripping apart neurons which are your individual brain cells. That is what neuroinflammation is. The good news is that cannabinoids shut down this reaction in the human body.

​Who would benefit from U.S. Patent #6,630,507 B1?

“Oxidative associated diseases include, without limitation, free radical associated diseases, such as ischemia, ischemic reperfusion injury, inflammatory diseases, systemic lupus erythematosis, myocardial ischemia or infarction, cerebrovascular accidents (such as thromboembolic or hermorrhagic stroke) that can lead to ischemia or an infarct in the brain, operative ischemia, traumatic hemorrhage (for example a hypovolemic stroke that can lead to CNS hypoxia or anoxia), spinal cord trauma, Down’s syndrome, Crohn’s disease, autoimmune diseases (e.g., rheumatoid arthritis or diabetes), cataract formation, uveitis, emphysema, gastric ulcers, oxygen toxicity, and neoplasia (cancer tumors).”

And radiation sickness, which I’m sure we will find in the Japanese population for years to come.

The government’s public mantra has always been that marijuana is not a medicine in any form, as in Schedule I, which means (a) the drug or other substance has a high potential for abuse; (b) it has no currently accepted medical use in treatment in the United States  (Remember U.S. Patent 6,630,507 B1?); and (c) there is a lack of accepted safety for use of the drug or other substance under medical supervision.

While spending billions of dollars to promote its anti-drug meme behind the scenes, it was simultaneously trying to prove to the Patent Office that cannabinoids are powerful anti-oxidative medicines that fight oxidative stress diseases in everyone.

So the crazy Catch 22 is that the U.S. government is now claiming cannabis is medicine, but is also saying it isn’t medicine and that it needs to be against the law.

How can any sane person explain this cognitive dissonance — this bipolar reefer insanity on the part of the government?

This patent contradicts the very definition of “Schedule I.”

And does the government’s patent also hold the cure for cancer and neurodegenerative diseases, and many other oxidative stress-related disorders?

Point to remember: this patent is making medical claims for cannabidiol only. THC is cannabidiol’s therapeutic partner, and they work together best in a synergistic fashion, which can be described as “cannabinergic.”

The patent acknowledges that all cannabinoids are therapeutic, but claims very high doses are needed to get the effect. This is an untested negative assumption about marijuana’s ability to change consciousness that has been an ideologically driven bias against cannabis since 1937.

This therapeutic dose would produce unwanted side effects if THC was used in this amount. The high from THC is described as “psychotoxic” in the patent. This is true if THC is not used with cannabidiol, as it is found in the whole plant.

Dr. Julius Axelrod

​From U.S. Patent #6,630,507 B1:

“As referred to herein, the term ‘psychoactivity’ means ‘cannabinoid receptor mediated psychoactivity.’ Such effects include euphoria, lightheadedness, reduced motor coordination, and memory impairment. Psychoactivity is not meant to include non-cannabinoid receptor mediated effects such as the anxiolytic effect of CBD.”

Translation: Euphoria, literally, to “bear well,” is medically recognized as a positive mental, emotional state defined as a profound sense of well-being or wellness.

Lightheadedness, reduced motor coordination, and memory impairment, of course, can be bad. These last three apply to alcohol, high blood pressure meds, and many psychiatric meds in general.

Anxiolytic (anti-anxiety) is good.

Question: How does one separate “anxiety-free” from “experiencing joy and happiness”?

Why do we live in a Buzz-Kill Nation?

I have discovered that suffering and pain and very overrated, and don’t build character.

Did your last root canal surgery make you a better person? It only works if others in your peer group witness it and reward it within the group.

Pain and suffering damage the immune system.

Joy and happiness and giggling and laughing boost the immune response. When you laugh, your immune system laughs with you, and a laughing immune system is a good thing to have when you are fighting cancer or any serious illness.

Reduction of laughter frequency is a symptom of a diseased state.

Doesn’t the idea of making nature against the law seem a bit paranoid?

Mirthful laughter has a positive effect on stress and natural killer cell activity.

From U.S. Patent #6,630,507 B1:

“THC is another of the cannabinoids that has been shown to be neuroprotective in cell cultures, but this protection was believed to be mediated by interaction at the cannabinoid receptor, and so would be accompanied by undesired psychotropic side effects.”

Here’s what happens when THC is used without its partner, cannabidiol.

Intravenous THC and Cannabidiol Experiment

What anti-marijuana researchers do is isolate and give pure THC only to test subjects, which in large amounts can cause psychosis-like symptoms. Then they claim marijuana causes psychotic behavior.

Both THC and cannabidiol are both equal in strength as antioxidants. But THC gets you high, which disqualifies it as medicine.

A medicine that makes you laugh is bad?

The patent made it sound like getting high — or should I say having a marijuana-induced “peak experience,” which leads in time to varying degrees of self-actualization — is a bad thing.

The “high” is therapeutic in its own right, being that cannabis is an entheogen drug and not an intoxicant. It can’t be included in the intoxicant category due to the fact that it is not toxic, and has never caused a recorded death directly from its use.

The change in consciousness induced by the THC/cannabidiol combo is anxiolytic, anti-depressive, and antipsychotic in nature. A cancer diagnosis with harsh chemo and radiation produces intense periods of anxiety and depression through the long course of treatment.

So let me get this part straight: the serious untoward side effects of cannabis are red eyes, lightheadedness, intense bouts of uncontrollable enlightened laughter, intense hunger followed by periods of deep mystical introspection, followed by deep sound sleep.

In short, happy, hungry and sleepy.

Cannabis is not an intoxicant. It is an entheogenic substance. Think altruism, group bonding and cooperation, nonviolence and sharing. Think Woodstock!

“Splendid by Law! Declaring Law, truth speaking, truthful in thy works, enouncing faith, King Soma! … O [Soma] Pavāmana, place me in that deathless, undecaying world wherein the light of heaven is set, and everlasting lustre shines … Make me immortal in that realm where happiness and transports, where joy and felicities combine.” ~ from the Rig Veda, the “Creator of the Gods.”

Cannabis is like yoga for your mind. But only different — and oh, the places you’ll go!

I believe if you live long enough, through many decades, absorbing the tragedies of the human condition, you have a high probability of developing a type of “generalized life PTSD.” It’s part of the psychological profile of aging, and it can’t be helped.

Life wears you down over time.

Cannabis is just a milder, non-toxic form of MDMA, which is helping some of our combat vets who return home with PTSD.

Many who are lucky enough to survive cancer go on to develop a “cancer PTSD” syndrome that will always be there.

So what are free radicals?

“Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.

The antioxidants give an electron to the free radical so its outer shell is complete. If not, the free radicals degrade your DNA by plucking electrons from its structure. This damages the correct code for making new proteins that cells use to rebuild; this process is called “oxidation stress,” which means your cellular DNA is under attack by highly reactive chemicals.

What causes this oxidation?

• X-rays and all forms of radiation, even sunlight.

• Cancer treatment: chemotherapy, radiation treatment. From the patent: “The invention includes methods for using cannabinoids in subjects who have been exposed to oxidant inducing agents such as cancer chemotherapy, radiation, and other sources of oxidative stress.”

• Chemicals in our water and air that are toxic to cells. We live in a close bio-system; anything we dump down the drain winds up in the food chain, in the water we drink, and in the air we breathe.

It’s the sum total of every chemical and radiation assault against your DNA at the cellular level, inside the nucleus of your cells, that you don’t see. This damage causes mutations in cells that lead to abnormal cell growth and cancer.

​This is why cannabinoids may slow the aging process.

This may be why cannabis smokers have a lower rate of lung cancer and head and neck cancer than the non-smoking population.

Cannabinoids protect the cells from oxidation. Marijuana saves lives!

Think of cannabis as a super free-radical-fighting vegetable. Get at least one serving of this green phytochemical per day to maintain good health!

Perhaps the FDA should consider adding cannabis to its new Food Pyramid. ☺

Thank you, Julius Axelrod (1912-2004), for all your hard work. Perhaps someone will name a medicine strain of cannabis for you.

http://www.theweedblog.com

Marijuana Compound Helps Treat HIV In Animal Testing

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The long-term administration of delta-9-THC, the primary psychoactive compound in marijuana, is associated with decreased mortality in monkeys infected with the simian immunodeficiency virus (SIV), a primate model of HIV (human immunodeficiency virus) disease, according to in vivo experimental trial data published in the June issue of the journal AIDS Research and Human Retroviruses.

Investigators at the Louisiana State University Health Sciences Center assessed the impact of chronic intramuscular THC administration compared to placebo on immune and metabolic indicators of SIV disease during the initial six-month phase of infection.

Researchers reported, “Contrary to what we expected, … delta-9-THC treatment clearly did not increase disease progression, and indeed resulted in generalized attenuation of classic markers of SIV disease.” Authors also reported that THC administration was associated with “decreased early mortality from SIV infection” and “retention of body mass.”

Investigators concluded, “These results indicate that chronic delta-9-THC does not increase viral load or aggravate morbidity and may actually ameliorate SIV disease progression.”

Clinical trials have previously documented that the short-term inhalation of cannabis does not adversely impact viral loads in HIV patients, and may even improve immune function.

For more information, please contact Paul Armentano, NORML Deputy Director, at: paul@norml.org. Full text of the study, “Cannabinoid administration attenuates the progression of simian immunodeficiency virus,” is available online here:http://www.liebertonline.com/doi/pdf/10.1089/aid.2010.0218. Additional studies documenting the disease modifying potential of marijuana is available in the NORML handbook, Emerging Clinical Applications For Cannabis & Cannabinoids: Fourth Edition, available online at: http://norml.org/index.cfm?Group_ID=7002.

From Norml.org

Medical Marijuana And Cachexia

You won’t have to research medical conditions treatable with medical marijuana for very long before you come across the term cachexia; if you’re not sure what this term means, you’re not alone so here we’ll explain exactly what cachexia is and how cannabis can help to alleviate it.

What is Cachexia?

This definition from the National Cancer Institute:

cachexia (ka-KEK-see-a)

Loss of body weight and muscle mass, and weakness that may occur in patients with cancer, AIDS, or other chronic diseases.

Cachexia invariably occurs with anorexia:

anorexia (a-nuh-REK-see-uh)

An abnormal loss of the appetite for food. Anorexia can be caused by cancer, AIDS, a mental disorder (i.e., anorexia nervosa), or other diseases.

What Causes Cachexia?

Although it depends very much on what type of cancer a patient has, it’s estimated that 50% to 80% of all cancer patients will develop cachexia, usually during the final stages of pancreatic, lung, and prostate cancers. The condition appears to result from the immune system’s response to the tumor.

Another major cause of cachexia is HIV/AIDS infection.

Cachexia Treatments

In most cases the standard for advanced cachexia is intravenous feeding, together with administration of an appetite stimulant drug – Megace. The problem with Megace is that the weight gain it stimulates is in the form of fat; the weight loss through the cachexia is lean tissue – muscles, heart tissue and the like.

Marijuana and Cachexia

Most people know about the way weed stimulates the appetite – the infamous munchies. The munchies is caused by the action of THC on the body and there have been a number of studies confirming that patients who use medical marijuana experience a reduction in rate of weight loss together with an increase in appetite. Sadly, research has also failed to show any advantage of taking THC and Megace in combination – they do not augment each other’s effects.

Chemotherapy Induced Nausea and Marijuana

It has been shown in various studies that, when used in the treatment of chemotherapy-induced nausea and vomiting, THC is more quickly absorbed from marijuana smoke than from any oral preparation. The only problem appears to be one of dose measurement; however, with experience, chemotherapy patients will learn to manage their weed dosage.

Courtesy of the Medical Marijuana Blog

Worth Repeating: Over 50 Studies Show Cannabis is Medicine

Graphic: The Truth Source

​Welcome to Room 420, where your instructor is Mr. Ron Marczyk and your subjects are wellness, disease prevention, self actualization, and chillin’.

Worth Repeating

​By Ron Marczyk, R.N.

Health Education Teacher (Retired)

The quote below, from a news release, is a political statement that is based on incomplete and biased science. Remember, once science is politicized, it is no longer science.

“No sound scientific studies supported medical use of marijuana for treatment in the United States, and no animal or human data supported the safety or efficacy of marijuana for general medical use.”

Not true! An overwhelming number of studies exist to firmly support cannabis as all-purpose medicine and very possibly a strong candidate as a cure for cancer as was originally reported by the National Cancer Institute.

There has never been a single documented primary human fatality from overdosing on cannabis in its natural form in any amount. How’s that for safety!

In addition, cannabis can be vaporized or eaten in sweets, which takes the smoking issue off the table!  And as counter-intuitive as its sounds, evidence exists that cannabis offers a mild protective effect against cancer.

Photo: THC Finder

​ I would like to bring attention to the 50+ empirical studies (footnoted below) that may have been overlooked by the FDA in their ”thoroughly analyzed search of all the relevant medical, scientific data” on medical cannabis.

“In 2001, the Food and Drug Administration (FDA) and the Drug Enforcement Administration thoroughly analyzed the relevant medical, scientific, and abuse data and concluded that marijuana continues to meet the criteria for placement in schedule I of the Controlled Substances Act. The Food and Drug Administration reiterated this determination in April 2006, stating in a news release:

“Marijuana is listed in Schedule I of the Controlled Substances Act (CSA), the most restrictive schedule. The Drug Enforcement Administration (DEA), which administers the CSA, continues to support that placement and FDA concurred because marijuana met the three criteria for placement in Schedule I under 21 U.S.C. 812(b)(1) (e.g., marijuana has a high potential for abuse, has no currently accepted medical use in treatment in the United States, and has a lack of accepted safety for use under medical supervision).

“Furthermore, there is currently sound evidence that smoked marijuana is harmful. A past evaluation by several Department of Health and Human Services (HHS) agencies, including the Food and Drug Administration (FDA), Substance Abuse and Mental Health Services Administration (SAMHSA) and National Institute for Drug Abuse (NIDA), concluded that no sound scientific studies supported medical use of marijuana for treatment in the United States, and no animal or human data supported the safety or efficacy of marijuana for general medical use. There are alternative FDA-approved medications in existence for treatment of many of the proposed uses of smoked marijuana.” (Source: justice.gov)

Empirically Based Evidence Supporting Medical Cannabis

Cannabinoids As Cancer Hope

by Paul Armentano

NORML Foundation/Senior Policy Analyst

“Cannabinoids possess … anticancer activity [and may] possibly represent a new class of anti-cancer drugs that retard cancer growth, inhibit angiogenesis (the formation of new blood vessels) and the metastatic spreading of cancer cells.” So concludes a comprehensive review published in the October 2005 issue of the scientific journal Mini-Reviews in Medicinal Chemistry.

Not familiar with the emerging body of research touting cannabis’ ability to stave the spread of certain types of cancers? You’re not alone.

For over 30 years, US politicians and bureaucrats have systematically turned a blind eye to scientific research indicating that marijuana may play a role in cancer prevention — a finding that was first documented in 1974. That year, a research team at the Medical College of Virginia (acting at the behest of the federal government) discovered that cannabis inhibited malignant tumor cell growth in culture and in mice. According to the study’s results, reported nationally in an Aug. 18, 1974, Washington Post newspaper feature, administration of marijuana’s primary cannabinoid 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.”

Despite these favorable preclinical findings, US government officials dismissed the study (which was eventually published in the Journal of the National Cancer Institute in 1975), and refused to fund any follow-up research until conducting a similar — though secret — clinical trial in the mid-1990s. That study, conducted by the US National Toxicology Program to the tune of $2 million concluded that mice and rats administered high doses of THC over long periods experienced greater protection against malignant tumors than untreated controls.

Rather than publicize their findings, government researchers once again shelved the results, which only came to light after a draft copy of its findings were leaked in 1997 to a medical journal, which in turn forwarded the story to the national media.

Nevertheless, in the decade since the completion of the National Toxicology trial, the U.S. government has yet to encourage or fund additional, follow up studies examining the cannabinoids’ potential to protect against the spread cancerous tumors.

Fortunately, scientists overseas have generously picked up where US researchers so abruptly left off. In 1998, a research team at Madrid’s Complutense University discovered that THC can selectively induce apoptosis (program cell death) in brain tumor cells without negatively impacting the surrounding healthy cells. Then in 2000, they reported in the journal Nature Medicine that injections of synthetic THC eradicated malignant gliomas (brain tumors) in one-third of treated rats, and prolonged life in another third by six weeks.

In 2003, researchers at the University of Milan in Naples, Italy, reported that non-psychoactive compounds in marijuana inhibited the growth of glioma cells in a dose dependent manner and selectively targeted and killed malignant cancer cells.

The following year, researchers reported in the journal of the American Association for Cancer Research that marijuana’s constituents inhibited the spread of brain cancer in human tumor biopsies. In a related development, a research team from the University of South Florida further noted that THC can also selectively inhibit the activation and replication of gamma herpes viruses. The viruses, which can lie dormant for years within white blood cells before becoming active and spreading to other cells, are thought to increase one’s chances of developing cancers such as Karposis Sarcoma, Burkitts lymphoma, and Hodgkins disease.

More recently, investigators published pre-clinical findings demonstrating that cannabinoids may play a role in inhibiting cell growth of colectoral cancer, skin carcinoma, breast cancer, and prostate cancer, among other conditions. When investigators compared the efficacy of natural cannabinoids to that of a synthetic agonist, THC proved far more beneficial – selectively decreasing the proliferation of malignant cells and inducing apoptosis more rapidly than its synthetic alternative while simultaneously leaving healthy cells unscathed.

Nevertheless, US politicians have been little swayed by these results, and remain steadfastly opposed to the notion of sponsoring – or even acknowledging – this growing body clinical research, preferring instead to promote the unfounded notion that cannabis use causes cancer. Until this bias changes, expect the bulk of research investigating the use of cannabinoids as anticancer agents to remain overseas and, regrettably, overlooked in the public discourse.”

Thanks, Paul.

The following current research studies all provide overwhelming evidence that THC holds the promise of being a non-toxic multipurpose chemotherapy agent that may have anti-tumor action on many different types of cancer.

THC and synthetic cannabinoids both have similar action on CB1/2 receptors, and seem to work best in combination, just as ingesting cannabis as a whole plant produces its wide spectrum healing effects, such as relieving vomiting, being able eat, having no physical pain and being able to sleep. This is how the body heals itself.

Medical cannabis is a family of unique cannabinoids  that also have antiemetic effects, appetite stimulation, pain relief, and improved sleep, as reported by the National Cancer Institute:   http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page5

These four medically proven cancer treatment effects of cannabis on their own totally disprove the FDA statement, but with an anti-tumor effect added, as also reported by NCI, this plant becomes a “Swiss survival knife”of medicines.  Imagine that – one drug that treats five different medical conditions at once!

A quick search of Wikipedia yields the following five studies:

“Investigators at Madrid’s Complutense University, School of Biology, first reported that THC induced apoptosis (programmed cell death) in glioma cells in culture”[1a]

“Investigators followed up their initial findings, reporting that the administration of both THC and the synthetic cannabinoid agonist WIN55-212-2 induced a considerable regression of malignant gliomas in animals” [2b]

“Researchers again confirmed cannabinoids’ ability to inhibit tumor growth in animals in 2003″[3c]

“Most Recently investigators at the University of California, Pacific Medical Center reported that cannabinoids possess synergistic anti-cancer properties — finding that the administration of a combination of the plant’s constituents is superior to the administration of isolated compounds alone”[4d]

“Consequently, many experts now believe that cannabinoids may represent a new class of anticancer drugs that retard cancer growth, inhibit angiogenesis and the metastic spreading of cancer cells [5e] and have recommended that at least one cannabinoid, cannabidiol, now be utilized in cancer therapy.”

​

Gliomas/Brain Cancer

by Paul Armentano

NORML Foundation/Senior Policy Analyst

Gliomas (tumors in the brain) are especially aggressive malignant forms of cancer, often resulting in the death of affected patients within one to two years following diagnosis. There is no cure for gliomas and most available treatments provide only minor symptomatic relief.

A review of the modern scientific literature reveals numerous preclinical studies and one pilot clinical study demonstrating cannabinoids’ ability to act as anti-neoplastic agents, particularly on glioma cell lines.

Writing in the September 1998 issue of the journal FEBS Letters, investigators at Madrid’s Complutense University, School of Biology, first reported that delta-9-THC induced apoptosis (programmed cell death) in glioma cells in culture.[1] Investigators followed up their initial findings in 2000, reporting that the administration of both THC and the synthetic cannabinoid agonist WIN 55,212-2 ”induced a considerable regression of malignant gliomas” in animals.[2] Researchers again confirmed cannabinoids’ ability to inhibit tumor growth in animals in 2003.[3]

That same year, Italian investigators at the University of Milan, Department of Pharmacology, Chemotherapy and Toxicology, reported that the non-psychoactive cannabinoid, cannabidiol (CBD), inhibited the growth of various human glioma cell lines in vivo and in vitro in a dose dependent manner. Writing in the November 2003 issue of the Journal of Pharmacology and Experimental Therapeutics Fast Forward, researchers concluded, “Non-psychoactive CBD … produce[s] a significant anti-tumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an anti neoplastic agent.”[4]

In 2004, Guzman and colleagues reported that cannabinoids inhibited glioma tumor growth in animals and in human glioblastoma multiforme (GBM) tumor samples by altering blood vessel morphology (e.g., VEGF pathways). Writing in the August 2004 issue of Cancer Research, investigators concluded, “The present laboratory and clinical findings provide a novel pharmacological target for cannabinoid-based therapies.”[5]

Five Other Studies Found on pub.Med. Relating to Gliomas

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

J Clin Invest. 2009 May;119(5):1359-72     Department of Biochemistry and Molecular Biology, Complutense University, Madrid, Spain.

FINDINGS:

Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that delta(9)-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy.

The finding of this study describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.

From this study:

Graphic: J. Clin. Invest.

In the image above, the blue is just staining for the nucleus, and it shows where the nucleus is and that there are cells there. The green is staining for the LC3 with or without treatment (shown on the top) in the presence of small inhibitors made of RNA (siC, sip8, siTRB3)-(shown on the side of each panel). The red is control for those inhibitors used (random siRNA) that just shows that the inhibitors that they used targeted the intended genes.

​

2. Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor

Cancer Res. 2001 Aug 1;61(15):5784-9. Dept of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.

FINDINGS:

The development of new therapeutic strategies is essential for the management of gliomas, one of the most malignant forms of cancer. We have shown previously that the growth of the rat glioma C6 cell line is inhibited by psychoactive cannabinoids.  These compounds act on the brain and some other organs through the widely expressed CB(1) receptor. By contrast, the other cannabinoid receptor subtype, the CB(2) receptor, shows a much more restricted distribution and is absent from normal brain. Cannabinoid receptor expression was subsequently examined in biopsies from human astrocytomas.

A full 70 percent (26 of 37) of the human astrocytomas analyzed expressed significant levels of cannabinoid receptors. Of interest, the extent of CB(2) receptor expression was directly related with tumor malignancy.

3. Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation

Nat Med. 2000 Mar;6(3):313-9.  Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040-Madrid, Spain.

FINDINGS:

Delta 9-Tetrahydrocannabinol, the main active component of marijuana, induces apoptosis of transformed neural cells in culture. Here, we show that intratumoral administration of Delta9-tetrahydrocannabinol and the synthetic cannabinoid agonist WIN-55,212-2 induced a considerable regression of malignant gliomas in Wistar rats and in mice deficient in recombination activating gene.

Cannabinoid treatment did not produce any substantial neurotoxic effect in the conditions used. Experiments with two subclones of C6 glioma cells in culture showed that cannabinoids signal apoptosis by a pathway involving cannabinoid receptors, sustained ceramide accumulation and Raf1/extracellular signal-regulated kinase activation. These results may provide the basis for a new therapeutic approach for the treatment of malignant gliomas.

4.  Hypothesis: cannabinoid therapy for the treatment of gliomas?

Neuropharmacology. 2004 Sept.

Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Avenida Complutense, sn, 28040 Madrid, Spain.

http://www.ncbi.nlm.nih.gov/pubmed/15275820

Abstract

Gliomas, in particular glioblastoma multiforme or grade IV astrocytoma, are the most frequent class of malignant primary brain tumours and one of the most aggressive forms of cancer. Current therapeutic strategies for the treatment of glioblastoma multiforme are usually ineffective or just palliative. During the last few years, several studies have shown that cannabinoids – the active components of the plant Cannabis sativa and their derivatives –slow the growth of different types of tumours, including gliomas, in laboratory animals.

Remarkably, cannabinoids kill glioma cells selectively and can protect non-transformed glial cells from death. These and other findings reviewed here might set the basis for a potential use of cannabinoids in the management of gliomas.

5.  A pilot clinical study of delta 9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme (Human Study)

British Journal of Cancer 2006   Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid 28040, Spain

FINDINGS:

Delta 9-Tetrahydrocannabinol (THC) and other cannabinoids inhibit tumour growth and angiogenesis in animal models, so their potential application as antitumoral drugs has been suggested. However, the antitumoral effect of cannabinoids has never been tested in humans. Here we report the first clinical study aimed at assessing cannabinoid antitumoral action, specifically a pilot phase I trial in which nine patients with recurrent glioblastoma multiforme were administered THC intratumorally.

The patients had previously failed standard therapy (surgery and radiotherapy) and had clear evidence of tumour progression. The primary end point of the study was to determine the safety of intracranial THC administration. We also evaluated THC action on the length of survival and various tumour-cell parameters. A dose escalation regimen for THC administration was assessed. Cannabinoid delivery was safe and could be achieved without overt psychoactive effects. Median survival of the cohort from the beginning of cannabinoid administration was 24 weeks (95% confidence interval: 15-33). 9-Tetrahydrocannabinol inhibited tumour-cell proliferation in vitro and decreased tumour-cell Ki67 immunostaining when administered to two patients. The fair safety profile of THC, together with its possible antiproliferative action on tumour cells reported here and in other studies, may set the basis for future trials aimed at evaluating the potential antitumoral activity of cannabinoids.

CANCER IN GENERAL 

From Paul Armentano at NORML:

In addition to cannabinoids’ ability to moderate glioma cells, separate studies demonstrate that cannabinoids and endocannabinoids can also inhibit the proliferation of other various cancer cell lines, including breast carcinoma,[11-15] prostate carcinoma,[16-18] colorectal carcinoma,[19] gastric adenocarcinoma,[20] skin carcinoma,[21] leukemia cells,[22-23]neuroblastoma,[24] lung carcinoma,[25-26] uterus carcinoma,[27] thyroid epithelioma,[28] pancreatic adenocarcinoma,[29-30], cervical carcinoma,[31] oral cancer,[32] biliary tract cancer (cholangiocarcinoma)[33] and lymphoma.[34-35]

Studies also indicate that the administration of cannabinoids, in conjunction with conventional anti-cancer therapies, can enhance the effectiveness of standard cancer treatments.[36] Most recently, investigators at the University of California, Pacific Medical Center reported that cannabinoids possess synergistic anti-cancer properties — finding that the administration of a combination of the plant’s constituents is superior to the administration of isolated compounds alone.[37]

Consequently, many experts now believe that cannabinoids “may represent a new class of anticancer drugs that retard cancer growth, inhibit angiogenesis and the metastatic spreading of cancer cells.”[38-39]

Studies found on Pub. Med.

1.  The stress-regulated protein p8 mediates cannabinoid-induced apoptosis of tumor cells.

Cancer Cell. 2006 Apr;9(4):301-12.

Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.

http://www.ncbi.nlm.nih.gov/pubmed/16616335

FINDINGS: One of the most exciting areas of current research in the cannabinoid field is the study of the potential application of these compounds as antitumoral drugs. Here, we describe the signaling pathway that mediates cannabinoid-induced apoptosis of tumor cells. By using a wide array of experimental approaches, we identify the stress-regulated protein p8 as an essential mediator of cannabinoid antitumoral action. Activation of this pathway may constitute a potential therapeutic strategy for inhibiting tumor growth.

2. Cannabis-derived substances in cancer therapy–an emerging anti-inflammatory role for the cannabinoids

Curr Clin Pharmacol. 2010 Nov 1;5(4):281-7.

Division of Cellular and Molecular Medicine (Oncology), St George’s University of London, London, UK. w.liu@sgul.ac.uk

FINDINGS:

• Cannabinoids, the active components of the cannabis plant, have some clinical merit both as an anti-emetic and appetite stimulant in patients. Recently, interest in developing cannabinoids as therapies has increased following reports that they possess anti-tumour properties.

• Research into cannabinoids as anti-cancer agents is in its infancy, and has mainly focused on the pro-apoptotic effects of this class of agent. Impressive anti-cancer activities have been reported; actions that are mediated in large part by disruptions to ubiquitous signalling pathways such as ERK and PI3-K.

• However, recent developments have highlighted a putative role for cannabinoids as anti-inflammatory agents. Chronic inflammation has been associated with neoplasia for sometime, and as a consequence, reducing inflammation as a way of impacting cancer presents a new role for these compounds. This article reviews the ever-changing relationship between cannabinoids and cancer, and updates our understanding of this class of agent. Furthermore, the relationship between chronic inflammation and cancer, and how cannabinoids can impact this relationship will be described.

3.  Cannabinoids for cancer treatment: progress and promise

Neuropharmacology. 2004 Sept

Chemoprevention Program, Paul P. Carbone Comprehensive Cancer Center and Dept of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin 53706, USA.

FINDINGS:

Cannabinoids are a class of pharmacologic compounds that offer potential applications as antitumor drugs, based on the ability of some members of this class to limit inflammation, cell proliferation, and cell survival. In particular, emerging evidence suggests that agonists of cannabinoid receptors expressed by tumor cells may offer a novel strategy to treat cancer. Here, we review recent work that raises interest in the development and exploration of potent, nontoxic, and nonhabit forming cannabinoids for cancer therapy.

4.  Use of cannabinoid receptor agonists in cancer therapy as palliative and curative agents

Best Pract Res Clin Endocrinol Metab. 2009 Feb.

Department of Pharmaceutical Sciences, University of Salerno, Italy.

FINDINGS:

Cannabinoids (the active components of Cannabis sativa) and their derivatives have received renewed interest in recent years due to their diverse pharmacological activities. In particular, cannabinoids offer potential applications as anti-tumour drugs, based on the ability of some members of this class of compounds to limit cell proliferation and to induce tumour-selective cell death.

Although synthetic cannabinoids may have pro-tumour effects in vivo due to their immunosuppressive properties, predominantly inhibitory effects on tumour growth and migration, angiogenesis, metastasis, and also inflammation have been described. Emerging evidence suggests that agonists of cannabinoid receptors expressed by tumour cells may offer a novel strategy to treat cancer. In this chapter we review the more recent results generating interest in the field of cannabinoids and cancer, and provide novel suggestions for the development, exploration and use of cannabinoid agonists for cancer therapy, not only as palliative but also as curative drugs.

BREAST CANCER

Cannabinoids in the treatment of cancer

Cancer Lett. 2009 Nov 18;285(1):6-12. Epub 2009 May 12.Dept of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.

FINDINGS:

Cannabinoids, the active components of the hemp plant Cannabis sativa, along with their endogenous counterparts and synthetic derivatives, have elicited anti-cancer effects in many different in vitro and in vivo models of cancer. While the various cannabinoids have been examined in a variety of cancer models, recent studies have focused on the role of cannabinoid receptor agonists (both CB(1) and CB(2)) in the treatment of estrogen receptor-negative breast cancer. This review will summarize the anti-cancer properties of the cannabinoids, discuss their potential mechanisms of action, as well as explore controversies surrounding the results.

CERVICAL CANCER

Inhibition of cancer cell invasion by cannabinoids via increased expression of tissue inhibitor of matrix metalloproteinases-1

J Natl Cancer Inst. 2008 Jan 2;100(1):59-69. Epub 2007 Dec 25.

Institute of Toxicology and Pharmacology, University of Rostock, Schillingallee 70, Rostock D-18057, Germany.

BACKGROUND:

Cannabinoids, in addition to having palliative benefits in cancer therapy, have been associated with anticarcinogenic effects. Although the antiproliferative activities of cannabinoids have been intensively investigated, little is known about their effects on tumor invasion. we found that ..

FINDINGS:

Increased expression of TIMP-1 mediates an anti-invasive effect of cannabinoids. Cannabinoids may therefore offer a therapeutic option in the treatment of highly invasive cancers.

PROSTATE CANCER

Cannabinoid receptor as a novel target for the treatment of prostate cancer

Cancer Res. 2005 Mar 1;65(5):1635-41

Department of Dermatology, University of Wisconsin, Madison, Wisconsin 53706, USA.

FINDINGS:

Cannabinoids, the active components of Cannabis sativa  (marijuana) and their derivatives have received renewed interest in recent years due to their diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory effects and tumor regression.

Here we show that expression levels of both cannabinoid receptors, CB1 and CB2, are significantly higher in CA-human papillomavirus-10 (virally transformed cells derived from adenocarcinoma of human prostate tissue), and other human prostate cells LNCaP, DUI45, PC3, and CWR22Rnu1 than in human prostate epithelial and PZ-HPV-7 (virally transformed cells derived from normal human prostate tissue) cells. WIN-55,212-2 (mixed CB1/CB2 agonist) treatment with androgen-responsive LNCaP cells resulted in a dose- (1-10 micromol/L) and time-dependent (24-48 hours) inhibition of cell growth, blocking of CB1 and CB2 receptors by their antagonists SR141716 (CB1) and SR144528 (CB2) significantly prevented this effect. Extending this observation, we found that WIN-55,212-2 treatment with LNCaP resulted in a dose- (1-10 micromol/L) and time-dependent (24-72 hours) induction of apoptosis (a), decrease in protein and mRNA expression of androgen receptor (b), decrease in intracellular protein and mRNA expression of prostate-specific antigen (c), decrease in secreted prostate-specific antigen levels (d), and decrease in protein expression of proliferation cell nuclear antigen and vascular endothelial growth factor (e). Our results suggest that WIN-55,212-2 or other non-habit-forming cannabinoid receptor agonists could be developed as novel therapeutic agents for the treatment of prostate cancer.

COLORECTAL CANCER

The cannabinoid delta(9)-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells

Int J Cancer. 2007 Nov 15;121(10):2172-80.

Department of Cellular and Molecular Medicine, Cancer Research UK, Colorectal Tumour Biology Group, School of Medical Sciences, University of Bristol, University Walk, Bristol, United Kingdom.

FINDINGS:

Deregulation of cell survival pathways and resistance to apoptosis are widely accepted to be fundamental aspects of tumorigenesis. As in many tumours, the aberrant growth and survival of colorectal tumour cells is dependent upon a small number of highly activated signalling pathways, the inhibition of which elicits potent growth inhibitory or apoptotic responses in tumour cells. Accordingly, there is considerable interest in therapeutics that can modulate survival signalling pathways and target cancer cells for death.

There is emerging evidence that cannabinoids, especially Delta(9)-tetrahydrocannabinol (THC), may represent novel anticancer agents, due to their ability to regulate signalling pathways critical for cell growth and survival. Here, we report that CB1 and CB2 cannabinoid receptors are expressed in human colorectal adenoma and carcinoma cells, and show for the first time that THC induces apoptosis in colorectal cancer cells. These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy. 

FOOTNOTES

1a.       Guzman, C; et al.. “Delta-9-tetrahydrocannabinol induces apoptosis in C6 glioma cells”. FEBS Letters 436 (1): 6-10.doi:10.1016/S0014-5793(98)01085-0.        PMID 9771884.

 2b.    Guzman, I; et al.. “Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation.”. Nature Medicine 6 (3): 313-319. doi:10.1038/73171. PMID 10700234.

3c.    Liu, WM; et al. (2008). “Enhancing the in vitro cytoxic activity of Delta9-tetrahydracannabinol in leukemic cells through a combinatorial approach.”. Leukemia and Lymphoma 49 (9): 1800-1809. doi:10.1080/10428190802239188. PMID 18608861.

4d.      Marcu, J. P.; et al. (2010). “Cannabidiol enhances the inhibitory effects of delta9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival.”. Molecular Cancer Theraputics 9 (1): 180-189. doi:10.1158/1535-7163.MCT-09-0407. PMC 2806496.PMID 20053780. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2806496.

5d.   Natalya, Kogan. “Cannabinoids and cancer”. Mini-Reviews in Medicinal Chemistry 5 (10): 941-952.doi:10.2174/138955705774329555. PMID 16250836

[1] Guzman et al. 1998. Delta-9-tetrahydrocannabinol induces apoptosis in C6 glioma cells. FEBS Letters 436: 6-10.

[2] Guzman et al. 2000. Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation. Nature Medicine 6: 313-319.

3] Guzman et al. 2003. Inhibition of tumor angiogenesis by cannabinoids. The FASEB Journal 17: 529-531.

4] Massi et al. 2004. Antitumor effects of cannabidiol, a non-psychotropic cannabinoid, on human glioma cell lines.Journal of Pharmacology and Experimental Therapeutics Fast Forward 308: 838-845.

5] Guzman et al. 2004. Cannabinoids inhibit the vascular endothelial growth factor pathways in gliomas (PDF). Cancer Research 64: 5617-5623.

[6] Allister et al. 2005. Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells. Journal of Neurooncology 74: 31-40.

[7] Guzman et al. 2006. A pilot clinical study of delta-9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer (E-pub ahead of print).

8] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomas. Expert Reviews of Neurotherapeutics 8: 37-49

[9] Galanti et al. 2007. Delta9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells. Acta Oncologica 12: 1-9.

[10] Calatozzolo et al. 2007. Expression of cannabinoid receptors and neurotrophins in human gliomas. Neurological Sciences 28: 304-310.

[11] Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation. Cancer Research 66: 6615-6621.

[12] Di Marzo et al. 2006. Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. Journal of Pharmacology and Experimental Therapeutics Fast Forward 318: 1375-1387.

[13] De Petrocellis et al. 1998. The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation. Proceedings of the National Academy of Sciences of the United States of America 95: 8375-8380.

[14] McAllister et al. 2007. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells.Molecular Cancer Therapeutics 6: 2921-2927.

[15] Cafferal et al. 2010. Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition.Molecular Cancer 9: 196.

[16] Sarfaraz et al. 2005. Cannabinoid receptors as a novel target for the treatment of prostate cancer. Cancer Research 65: 1635-1641.

[17] Mimeault et al. 2003. Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines.Prostate 56: 1-12.

[18] Ruiz et al. 1999. Delta-9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism. FEBS Letters 458: 400-404.

[19] Pastos et al. 2005. The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase-2. Gut 54: 1741-1750.

[20] Di Marzo et al. 2006. op. cit

[21] Casanova et al. Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. 2003. Journal of Clinical Investigation 111: 43-50.

[22] Powles et al. 2005. Cannabis-induced cytotoxicity in leukemic cell lines. Blood 105: 1214-1221

[23] Jia et al 2006. Delta-9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemic T cells in regulated by translocation of Bad to mitochondria. Molecular Cancer Research 4: 549-562.

[24] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.

[25] Ibid.

[26] Preet et al. 2008. Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 10: 339-346.

[27] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.

[28] Baek et al. 1998. Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research: 21: 353-356.

[29] Carracedo et al. 2006. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. Cancer Research 66: 6748-6755.

[30] Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and pain. International Journal of Cancer 122: 742-750.

[31] Ramer and Hinz. 2008. Inhibition of cancer cell invasion by cannabinoids via increased cell expression of tissue inhibitor of matrix metalloproteinases-1. Journal of the National Cancer Institute 100: 59-69.

[32] Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cells. Pharmacology 85: 328-335.

[33] Leelawat et al. 2010. The dual effects of delta(9)-tetrahydrocannabinol on cholangiocarcinoma cells: anti-invasion activity at low concentration and apoptosis induction at high concentration. Cancer Investigation 28: 357-363.

[34] Gustafsson et al. 2006. Cannabinoid receptor-mediated apoptosis induced by R(+)-methanandamide and Win55,212 is associated with ceramide accumulation and p38 activation in mantle cell lymphoma. Molecular Pharmacology 70: 1612-1620.

[35] Gustafsson et al. 2008. Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: Growth inhibition by receptor activation. International Journal of Cancer 123: 1025-1033.

[36] Liu et al. 2008. Enhancing the in vitro cytotoxic activity of Ä9-tetrahydrocannabinol in leukemic cells through a combinatorial approach. Leukemia and Lymphoma 49: 1800-1809.

[37] Marcu et al. 2010. Cannabidiol enhances the inhibitory effects of delta9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival. Molecular Cancer Therapeutics 9: 180-189.

[38] Natalya Kogan. 2005. Cannabinoids and cancer. Mini-Reviews in Medicinal Chemistry 5: 941-952.

[39] Sarafaraz et al. 2008. Cannabinoids for cancer treatment: progress and promise. Cancer Research 68: 339-342.

Photo: Ron Marczyk

Mr. Worth Repeating: former NYPD cop, former high school health teacher, the unstoppable Ron Marczyk, R.N., Toke of the Town columnist

​Editor’s note: Ron Marczyk is a retired high school health education teacher who taught Wellness and Disease Prevention, Drug and Sex Ed, and AIDS education to teens aged 13-17. He also taught a high school International Baccalaureate psychology course. He taught in a New York City public school as a Drug Prevention Specialist. He is a Registered Nurse with six years of ER/Critical Care experience in NYC hospitals, earned an M.S. in cardiac rehabilitation and exercise physiology, and worked as a New York City police officer for two years. Currently he is focused on how evolutionary psychology explains human behavior.

How To: Make Pot Tea

A simple recipe for pot tea along with an additional method for making weed wine.

You will need:

• 1-2 grams of good hash
• 1 fluid ounce of vodka
• a pot of tea

Directions:

THC is not soluble in water, so while steeping your cannabis leaves to make tea will produce flavor, the tea will have no effect. However, should you have some hash oil honey, adding a teaspoon or so to the boiling water is an easy fix. If you don’t have any hash oil honey, try gently heating a single shot of vodka and stirring in the hash until it fully dissolves, then adding it to a pot of brewed tea.

If you prefer your tea sweet, try adding a bit of condensed milk, as this will also act to absorb the THC.

The same vodka trick can also be used to infuse your favorite bottle of wine. Simply uncork the bottle, remove a shots worth of wine, replacing it with the still-warm vodka mixture, and then re-cork. Shake the bottle carefully to combine the two liquids and set aside for an off-day. We’d suggest labeling it.

Proposed Tracking Program Has SF Medical Marijuana Growers In Fear Feds Or Criminals Could Obtain Addresses

San Francisco officials want to keep a record of all suppliers of medical marijuana dispensaries, an idea that has some members of the pot community fuming.

“If there is a list, it’s available to the public, and it’s available to the feds,” said Kevin Reed, a member of The City’s Medical Cannabis Task Force and owner of the Green Cross, a medical cannabis delivery service.

Reed said most members of cannabis collectives and cooperatives grow small amounts of pot in their homes, warning that a city record of their names and addresses could be accessible by anyone — including federal law enforcement officials or criminals who rob grow operations.

Despite statements by the Obama administration that it would not go after medical marijuana dispensaries that comply with state laws, cannabis supporters say such raids have continued, and Reed remained wary about a public record of growers.

“It just goes against everything that we’re doing,” Reed said. “What we do is federally illegal. As long as The City is offering patients no protection, it’s just absurd.”

According to a written statement from the San Francisco Department of Public Health, officials announced at a May 20 task force meeting that they “anticipated maintaining a record of all sources/cultivators for each [dispensary].”

Public health officials would only answer questions about this proposal in writing, and a spokeswoman did not respond to a question about whether the list would be publicly available.

The statement noted that the department, which issues permits for medical cannabis dispensaries, is tasked with ensuring that the cannabis such dispensaries cultivate and distribute is in compliance with state and local laws.

There currently are 26 permitted dispensaries in The City, and nine more have applied for permits.

Dr. Rajiv Bhatia, the director of environmental health, said such dispensaries get their products from “diverse sources” and that the department needs to ensure those sources are legal. California law requires that marijuana distributed by medical cannabis collectives or co-operatives be cultivated only by their members, and not for profit.

“Over the past few years, there has been a proliferation of cultivation in many San Francisco neighborhoods,” Bhatia said. Some of these sites violate city planning and building codes, and create fire or hazardous materials dangers, according to his statement.

“The department’s overarching aim is to steer [medical cannabis dispensary] practices towards conformity with California and San Francisco law,” Bhatia said. “In this way, we reduced the likelihood for MCDs of community concerns and criminal prosecution.”

The idea is apparently just in its formative stages, however, and no decision has been made.
“We are open to alternative ways to ensure the safety and legality of cultivation,” Bhatia said. “We will be discussing this with the dispensary community.”

Community activist and task force member Stephanie Tucker called a public list “a deal-breaker.”

“DPH historically has always been very good at protecting safe access, and balancing that with public safety,” Tucker said. “Obviously, as a community, we have concerns about that information becoming public.

“We need to find a solution, a happy medium.”

http://www.theweedblog.com/proposed-tracking-program-has-sf-medical-marijuana-growers-in-fear-feds-or-criminals-could-obtain-addresses/