Posts Tagged ‘cannabis study’

Four More Bullsh*t Marijuana Myths Busted Using the Fed’s Own Numbers

marijuana, facts, NORML, prohibition, states, report,

My apologies for getting this little nugget out to you guys late but you know how it is when you’re trying to pay attention and…well, you know how it is. Nevertheless, guess what I’ve got!?!

The Federal government’s annual report highlighting substance abuse. Now that may not sound interesting when I put it like that but if you look through the 300+ pages like Paul Armentano of NORML did right here. You’ll find even more myth busting information by comparing the data but in the meantime, here’s the breakdown.

Four More Bullsh*t  Mary Jane Myths BUSTED!!!

  • Myth: Marijuana use is prevalent in low income and urban areas thereby justifying the “War on Drug” and aggressive treatment and surveillance of poorer (read: Black and Latino) neighborhoods.

…..combating numerous drug warrior myths and stereotypes (such as the notion that high rates of illicit drug use — yes, the New England states lead in this broader category too — are typically relegated to poorer, urban, more racially diverse areas).

  • Myth: Marijuana use is neither determined nor undermined by state drug laws. People use marijuana if and when they choose to and not because states make marijuana possession laws harder.

…..it should be noted that despite the prevalence of medical marijuana states in these rankings, the authors of the report acknowledge that there is no evidence that the implementation of medi-pot laws is increasing the use of cannabis or other illicit drugs.

  • Myth: Establishing medical marijuana laws do not directly affect an increase in casual marijuana use.

They also call into question the notion that marijuana use among the general population is in any way influenced by the legal status of marijuana.

  • Myth: The Northeast loves them some Mary Jane. Nearly every state in the region made it’s way into the top spots for marijuana use.

The totals in the category ‘marijuana use in the past year among persons age 18 to 25‘ is even more New England-centric, with every northeast state (Connecticut, Massachusetts, Maine, New Hampshire, Rhode Island, and Vermont) all included in the top percentile (along with Alaska, Colorado, New York, and Oregon). In the category, ‘marijuana use in the past month among persons age 26 or older‘ Massachusetts, Maine, New Hampshire, Rhode Island, and Vermont top the list (along with Alaska, Colorado, Hawaii, and Oregon).

So, according this report by the United States government marijuana use is not the big bad monster that they make it out to be. With social concerns and morals aside, I wonder if a level-headed person would read this and ask themselves what the implication of this data means.

At the very least, our government has inflated the seriousness of marijuana’s affects on society. The decision to do so may have caused a  focus of limited state resources on treating a problem that may not have been a priority compared to other social issues.

At the very worst, this data shows a how an entire class of people (poor/brown) have been manufactured into a criminal class justifying the pursuit, expense and time required by the state to prosecute them when their marijuana use maybe less prevalent than in other (upper-class/white) areas. So if the real intent of the state is to pursue those that use illicit drugs the their polices effort to lock up offenders would correlate with drug use. This one theory begs the question of the states willingness to exploit their own criminal justice system to violate the rights of citizens to fund private industries that benefit from such discretion, specifically, the courts, the prisons and the legal industry.

Don’t be intimidated by false marijuana myths, educate yourself and stop the stupid with real data made by the same people that we’re fighting. Shout out to Norml for doing the hard part, now all you have to do is repeat it. Almost like cheating on a test but not. Until next time, people

- http://www.hailmaryjane.com

Marijuana Growers’ Kids In Better Health According To Canadian Study

Canada grow roomBy Steve Elliott of Toke of the Town

A new study from Canada flies in the face of stereotypes regarding the offspring of marijuana-growing parents. Children from homes where cannabis is grown were healthy and drug-free, according to the study — in fact, healthier than other children — leading to questions about why such kids are often removed from their homes.

The research from the Motherisk Program at Toronto’s Hospital for Sick Children indicates the automatic removal of kids from marijuana-growing parents can be worse for the children than allowing them to stay at home, according to Gideon Koren, a University of Toronto professor and the program’s director, reports CBC News.

“After examining 75 of the kids over several years, we came to very clear conclusions that a vast majority of these kids are doing well,” Koren said. “Well fed, well kept, doing well in school and developing well.”

“In fact, the health problems found in this population were actually fewer than those in the general Canadian population,” according to a news release from the Hospital for Sick Children.

Children often enjoyed the lifestyle benefits of having high-income parents — even though that income is made illegally — and taking them away often “does a lot of damage,” Koren said.

“Taking a small child from his or her parents in a well-adapted environment causes fear, anxiety, confusion and sadness — everything that comes from separation,” he said.

When children are found in homes identified as marijuana-growing operations, they are usually removed, separating them from their parents and often placing them into foster care.

The Hospital for Sick Children examined 75 kids between 2006 and 2010 from Ontario’s York Region, just north of Toronto.

canada marijuanaSince 2006, child-welfare workers have learned more about the effects marijuana grow-ops have on children and have changed how they maintain the children’s safety, according to Patrick Lake, executive director of the York Region Children’s Aid Society.

“We have developed a more customize and comprehensive process to determine best response, on a case-by-case basis, while looking for ways to safely maintain children with their parents or relatives,” Lake said.

This was the first study done on the topic, and the findings mean authorities will now see these children differently, according to Koren.

“When police and children’s aid go into that situation, they have to look much more carefully on what happened to that child, and now blanket-wise moving kids out of their homes,” he said.

Article From Toke of the Town and republished with special permission.

Study: Marijuana Derivative Fights Cocaine Addiction In Mice

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​A marijuana component helps mitigate cocaine addiction in mice, according to a new study, lending further evidence to the notion that marijuana is an “exit” drug and could become the next big anti-addiction therapy.

The discovery by researchers in China and Maryland was announced in the July 2011 issue of Nature Neuroscience magazine, reports Stephen C. Webster at The Raw Story.
Cannabidiol (CBD), a medically useful component of marijuana that does not produce a “high,” effectively turns down a receptor in the brain that is stimulated by cocaine, the study found.
Scientists used a synthetic version of cannabidiol, called JWH-133, to see how mice given regular doses of cocaine might respond. The found the mice dramatically reduced their intravenous cocaine intake — by up to 60 percent — after being given JWH-133.
“It’s a very significant reduction,” said Zheng-Xiong Xi, the lead author of the study and a researcher at the National Institute on Drug Abuse (NIDA), reports Maia Szalavitz at Time.
“It’s extremely exciting,” said Antonello Bonci, scientific director for intramural research at NIDA.
After THC, CBD is the second most prevalent compound in marijuana. Researchers formerly believed that cannabidiol’s CB2 receptor wasn’t found in the brain and that therefore CBD had no psychoactive effects, but a growing body of evidence suggests otherwise.
Their demonstrated success of reducing cocaine consumption could lead to new drug replacement therapies for cocaine and crack addicts, helping them detox and overcome withdrawal symptoms. Having quit cocaine in 2004 with the aid of cannabis, I can personally attest to the effectiveness of this method.
Ethnographic research by Ric Curtis, chair of anthropology at John Jay College in New York, backs me up on that point. National surveys found that as crack cocaine use declined in the early 1990s, marijuana use rose — and Curtis found that many recovering crack addicts reported substituting marijuana for crack, finding it cheaper and less disruptive.
Marijuana, as a recreational drug, produces less dependence and withdrawal effects than even coffee. Cocaine, on the other hand, is much more intoxicating and reinforcing, making users more likely to use the drug again, and with increasing frequency.
JWH-133 is chemically related to JWH-018, which has been the subject of controversy because of its use in Spice, K2, Black Mamba and other herbal “incense” smoking blends which are supposed to produce marijuana-like highs.
While JWH-133 does not produce such effects, JWH-018 and similar chemicals do, leading the Drug Enforcement Administration (DEA) to recently place them on their list of controlled substances.
The International Narcotics Control Board, a prohibitionist agency set up by the United Nations, claimed recently that outlawing JWH-018 was a “positive step” in drug control efforts. It urged UN members to go farther and put blanket bans in place on new substances “to prevent the rise of new designer drugs.”
Unfortunately, if this policy is adopted, it would also apply to JWH-133 and effectively shut down  the most promising avenue of research in drug addiction treatment.

Upside Down Reasoning in Australia

Because they're in the southern hemisphere, you see.

Researchers based out of James Cook University in Queensland, Australia have been doing some research into cannabis use among the Aboriginal population in the far northern, tropical area of Cape York. The researchers reported their findings at the Tropical Medical Conference in Cairnes last weekend. The researchers stated, presumably with straight faces, that marijuana was causing a 50% rate of mental illness in the Aborigine community. This is like hitting someone with an axe and determining death was caused by their resultant fall to the ground.

The study, if one can call it that, is part of the Cape York Cannabis Project: “a part of the Weed it out initiative run by the Queensland Police Service and James Cook University, the aim of which is to promote Indigenous community action to reduce harms associated with heavy cannabis use in remote communities in the Cape York region.”

The basis of the scientific method is basically: 1. coming up with an idea, 2. testing that idea using experiments and observations and 3. comparing those results to your original idea in order to see if it is valid. On the other hand, there is propaganda: coming up with an idea and then selectively pulling or inventing information that backs your idea in order to make it believable. Which of these two do you think applies to a “study” funded by an anti-cannabis police initiative? The outcome and findings were never in question, thus the findings aren’t scientifically valid. The fact that the spurious results are even getting media attention does a disservice to humanity.

JCU Assoc. Prof. Alan Clough headed the “research” team along with associate Dr. India Bohanna. They determined that, since 50% of the population surveyed reported using marijuana, and 50% of the individuals were reported to have at least one symptom of mental illness, pot was causing the illness.

OH REALLY? So, let’s see: the Australian aborigines, the original inhabitants of the Australian continent, have (since the British colonized Oz in 1788) had their homeland effectively stolen, their culture brutally discouraged, been massacred, and had their children stolen from them, and have a life expectancy 17 years shorter than the average white Aussie, have a high incidence of mental illness because they use cannabis?

Image via

Mr. Clough and Ms. Bohanna were both paid to come up with that exact result, and I hope they were paid well to mortgage their professional reputations, because no one can take anything they publish seriously ever again after that preposterous claim.

Worth Repeating: Government Has Patent For Cannabinoids Since 2003

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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.
​​​
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.)
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Graphic: rm3.us

Patent Title: Cannabinoids act as antioxidants and neuroprotectants
Cannabinoids Patent Abstract.jpg

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.
Cannabinoid Uses.jpg
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.

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 hydrogen peroxide.jpg
Skin immediately after exposure to 30 percent hydrogen peroxide

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.
free radical damage to motor neurons.jpg

​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.
axelrod mug.jpg
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.
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.
normal oxygen atom.jpg
​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.

Worth Repeating: Over 50 Studies Show Cannabis is Medicine

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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.
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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
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.”
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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:
Glioma photo 1.jpeg
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.

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.
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.
Neuropharmacology. 2004 Sept.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Avenida Complutense, sn, 28040 Madrid, Spain.
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.

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.
Cancer Cell. 2006 Apr;9(4):301-12.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.
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.
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.
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.

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
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
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
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
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:10.1038/73171PMID 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:10.1080/10428190802239188PMID 18608861.

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

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

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

3] Guzman et al. 2003. Inhibition of tumor angiogenesis by cannabinoidsThe 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 cellsJournal of Neurooncology 74: 31-40.

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

8] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomasExpert 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 cellsActa Oncologica 12: 1-9.

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

[11] Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulationCancer 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 carcinomaJournal 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 proliferationProceedings 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 cancerCancer 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 mechanismFEBS 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-2Gut 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 linesBlood 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 mitochondriaMolecular 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 vivoOncogene 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 genesCancer Research 66: 6748-6755.

[30] Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and painInternational 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-1Journal of the National Cancer Institute 100: 59-69.

[32] Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cellsPharmacology 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 concentrationCancer 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 lymphomaMolecular 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 activationInternational 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 approachLeukemia and Lymphoma 49: 1800-1809.

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

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

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

2011-04-14_14-18-03_72.jpeg
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.



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