The practice of smoking cannabis has probably been around since pre-historic times. There is strong evidence that the plant was extensively cultivated about 6,000 years ago in North Eastern Asia, primarily used for its fiber. Records of medicinal use and physiological effects are found in the earliest pharmacopoeia in existence, attributed to Emperor Shen Nung (2,000 BC). Cannabis most likely diffused from Asia to Persia, India, and other parts of the Middle East before entering Africa and Western Europe. Muslim and Persian trade routes probably introduced cannabis or dagga to Africa during the first few centuries AD. Interestingly, cannabis smoking wasn’t documented in Jamaica until about 1807, after the British empire brought in slaves from India and Africa.
Researchers recently found the 2,700 year-old grave of a shaman that contained about 789 grams of cannabis flower tops. They speculate that the cannabis was used for ritual or medicinal properties. This was a rare find, but archaeologists also have found other evidence of ancient cannabis smoking. Ornate “smoking bowls” have been found at other sites. These vary greatly in design, intricacy, and often contain ancient cannabis resin. Such bowls have been found throughout Africa. It is also thought that tobacco smoking spread quickly in Europe because humans were already familiar with smoking cannabis.
Methods for smoking cannabis have been developed over thousands of years. Early implements worked similarly to the so called Persian “hubble bubble” or hookah. Ancient societies made waterpipes from gourds, animal horns, earthernwares, and even straight out of the ground using a “smoking bowl” and a tube or reed. The modern age offers something new: vaporizer technology. Vaporizers are the result of thousands of years of humans exploring new and better methods for the use of cannabis.
Since the advent of vaporizers the inadequacies of smoking have become more apparent. Vaporizers basically pass ‘hot air’ over the plant material to make a mist or steam. In addition to reducing the exposure to smoke, vaporizers are a more efficient delivery system for cannabinoids.
Take the example of a cannabis cigarette or joint which contains 1 gram (1,000mg) of cannabis with 5 percent CBD (cannabidiol) by weight, or about 50mg of CBD. Upon lighting the cigarette, cannabinoids begin to be destroyed by burning and lost through side stream smoke. Vaporizers can reduce much of this flame-related cannabinoid loss. From that 50mg, some 11.5mg will be delivered to the body through smoking. Research has shown that vaporizers can recover up to 99.5 percent of cannabinoids. However, some loss cannot be prevented, as only some of the CBD is absorbed by the lungs and the rest is exhaled. It is unlikely that cigarettes, vaporizers, or hookahs can change the amount absorbed through the lungs. Scientists aren’t sure how much is exhaled but some estimate it at 30 to 80 percent.
As cannabis re-enters mainstream medicine, vaporizers are beginning to be accepted in hospitals and have been used in recent clinical trials exploring the medical benefits of cannabis. Finding efficient non-smoking alternatives to deliver cannabinoids may be key to gaining widespread acceptance in modern medicine.
Sources: Li, Hui-Lin. The Origin and use of cannabis in Eastern Asia: Their linguistic-cultural implications. Cannabis and Culture, 1975, pgs 51-62.
Jones, Lovinger. The Marijuana Question. 1985, Supplement A pg 463.
Pomahacova et al. Cannabis Smoke Condensate III: The cannabinoid content of vaporised Cannabis Sativa. Inhalation Toxicology 2009, 1-5, iFirst.
Russo et al. Phytochemical and genetic analysis of ancient cannabis from central Asia. Journal of Experimental Botany, Vol. 59, No. 15, pp. 4171–4182, 2008
The original version of this article first appeared in the Lab Bench Science Column of the West Coast Leaf NewsPaper on June 4th 2010.
The Lab Bench
By Jahan Marcu
A research team from the School of Medicine at Temple University, Philadelphia, presented their preliminary cannabinoid and bone data at a scientific meeting in Anaheim, CA in April. Our results add to a growing body of scientific evidence, suggesting a prominent role for the endocannabinoid system in bone development. For the last year, researchers have been trying to reproduce and build upon previous work on cannabinoids and bone, specifically, by characterizing the effects of removing the CB1 and CB2 receptors from mice.
Few labs have published new discoveries regarding cannabis and bone. However, those that have are surprising so far. Some findings are so profound that the upcoming International Cannabinoid Research Society (ICRS) meeting will have a special symposium to discuss the bone data produced by just a few laboratories.
Research shows that bone cells have cannabinoid receptors and produce endocannabinoids. Bone cells express a lot of CB2 receptors and nerves that traverse our bones produce CB1 receptors. The `anti-cannabinoid’ receptor, GPR55, is also expressed in bone.
These receptors appear to work together to regulate bone health. Some clinical evidence supports the role of cannabinoids in various diseases. The Clinical Endocannabinoid Deficiency (Russo 2004) is thought to underlie many treatment- resistant conditions such as irritable bowel syndrome, fibromyalgia, and chronic pain. Recently, CB1 receptor mutations were linked to migraines, bi-polar disorder, and major depression (Monteleone 2010).
Now CB2 receptor mutations may be linked to lower human bone density and hand-bone strength. Research from Japan and France shows that mutations correlate to osteoporosis in post-menopausal women. The two studies looked at 2,626 elderly adults with and without osteoporosis. A study out in Russia analyzed the hand-bone strength of 574 adults and found that those with CB2 receptor muta- tions had weaker hand-bone strength (Yamada 2007, Karsak 2005, 2009). These all suggest that a less functional receptor is related to poor bone health.
Researchers have been studying how the body responds to traumatic brain injuries (TBI). When TBI occurs in a mouse, endocannabinoids are made and new bone is formed. Thus, cannabinoids may enhance the healing of bones in some instances such as fractures.
Genetically modified mice without the cannabinoid receptors have a deregulated skeleton. Depending on genetic makeup, the animals make too much or too little bone. So, research has shown that cannabinoids can both increase and decrease bone mass. However, all mice without cannabinoid receptors eventually develop severe osteoporosis (Bab 2008).
Plant cannabinoids such as CBDV, CBG, CBN, THC, and THCV may increase the number of bone stem cells in rats (Scutt 2007). Conversely, Anandamide has been shown to increase bone turnover by acti- vating osteoclasts, the cells that remodel or dissolve bone. CBD can inhibit osteoclasts. The infamous diet drug Rimonabandt, or SR141716A, is thought to prevent bone loss in mice by activating GPR55, not the CB1 receptor. Additionally, derivatives like WIN55,212 and some JWH compounds appear to severely inhibit osteoclasts from remodeling bone. Researchers have already speculated that cannabinoids represent a new generation of drugs that could treat a variety of bone diseases. For more information check out this recent review of the scientific literature, which discusses the role of the endocannabinoid system in bone disease and pathology.
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Disclaimer: These views are strictly the views of the author and not those of Temple University or its units.
This blog is not intended to diagnose or treat any disease.
Each year thousands of articles are published about cannabis and cannabinoids.
Because of this promising research, scientists and doctors around the world are taking interest in cannabinoids. Part of the excitement comes from established data showing that cannabinoid receptors may be the most abundant protein in the human brain, and humans also produce a natural, THC-like compound, anandamide. In the first few months of 2010 a wide range of relevant research articles have already been published. Among the highlights: Researchers at the University of Leiden analyzed cannabis smoke and vapor by comparing their effects at the cannabinoid type 1 receptor (CB1R) (1). Both smoke and vapor activate the cannabinoid receptor equally, but vaporization is more efficient because fewer compounds are destroyed or degraded. However, what was shown for the first time was that terpenoids, the fragrant molecules such as myrcene, are a major component of the smoke and vapor.
The authors believe compounds such as myrcene may contribute to therapeutic benefits of medical cannabis.
Guinea pig studies suggest that the cannabinoid type 2 receptor (CB2R) may be helpful in preventing asthma (3). The development of asthma is linked to the activation of C-fibers, and researchers did find that CB2R activation, but not CB1R, could prevent the activation of C-fibers.Activating CB2R could be important in attenuating HIV-associated inflammation, which ultimately leads to destruction of parts of the body such as neurons, resulting in changes in cognitive and motor functions.
When HIV infects a cell, it releases viral proteins that create inflammation and attract healthy immune cells. One such viral protein called tat causes immune cells to arrive at the site of infection and usually become infected by HIV. Tat appears to be inhibited by cannabinods that activate the CB2R. THC and CP55,940 were both able to inhibit tat-mediated attraction and thus suppress this aspect of HIV/AIDS (4).
The cannabinoid receptors are also abundant in the gut. A lot of work has studied the therapeutic role of cannabinoids to treat diseases of the intestines such as infections, irritable bowel syndrome, abdominal pain, etc. Cannabinoids help control the two main functions of the gut: digestion and host defense. The collective research on this subject was reviewed and the authors suggest that academia and industry should fully develop cannabinoids as a treatment for diseases of the gastro- intestinal tract (2).
Nearly every week positive research on cannabis and cannabinoids is published by labs around the world. Despite the promising implications, the work of these pioneering scientists often goes unnoticed in media and the ‘science sections’ of national newspapers. Furthermore, medical schools do not provide any classes on cannabinoids, which forces patients to stay up-todate with the research on their own, in order to better inform their doctors of potential benefits of cannabis.
These examples offer a glimpse of a blossoming research field. By discussing cannabis research with doctors, other patients, friends and family you can prevent more studies from remaining unnoticed, underreported, or misunderstood.
1) Fischedick et al. Cannabinoid Receptor 1 Binding Activity and Quantitative Analysis of Cannabis sativa L. Smoke and Vapor. Chem. Pharm. Bull. 58(2) 201—207 (2010) 2) Izzo et al. Cannabinoids and the gut: New developments and emerging concepts. Pharmacol Ther (2010). 3) Fukuda et al. The Cann. Receptor Agonist WIN 55,212-2 Inhibits Antigen-Induced Plasma Extravasation in Guinea Pig Airways. Int Arch Allergy Immunol 12;152(3):295-300 (2010) 4) Raborn et al. Cann. Inhibtion of Macrophage Migration To the TAT protein of HIV-1 is linked to the CB2 canabinoid receptor. JPET (2010).
Synthetic cannabinoids found in streets of Europe and Japan
A team in Japan analyzed 46 herbal preparations sold on the black market and found that 44 of them contained synthetic cannabinoids.
Previously, “Spice” and other herbal preparations were found to contain synthetic cannabinoids in the UK and some parts of Europe. Surprisingly high amounts of alpha-tocopherol, or vitamin E, were also found in many of the samples.
The three main synthetic cannabinoids found varied greatly in their concentrations: cannabicyclohexanol (1.1 to 16.9 milligram/ gram), JWH-018 (2.0 to 35.9 milligram/ gram), and oleamide (7.6 to 210.9 mg/g). The authors call for more research into these synthetic cannabinoids, as well as continued analysis of herbal products.
They conclude, “Monitoring and surveillance analyses are a first-step in the regulation of abused compounds.”
Source:
N. Uchiyama, et al., Chem analysis of synthetic cannabinoids as designer drugs in herbal products, Forensic Sci. Int. (2010
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Thanks,
Jahan
Acetaminophen and cannabinoid receptor interactions were the focus of a research article published in the journal of Neuropharmacology in late December 2009. The research demonstrates that the effects of Acetaminophen on pain are mediated through the CB1 receptor. Acetaminophen has previously been shown to elevate the levels of endocannabinoids in the body. Thus increasing the amount of activated cannabinoid receptors, leading to pain relief and anti-inflammatory effects.
The study investigated the effects of acetaminophen in combination with different pain killers. The authors found that a combination of acetaminophen with gabapentin or morphine produced synergistic pain killing effects in rats. The results may have clinical significance because the effect was observed in rats that are a model of spinal cord injury. Interestingly, this synergistic pain relief disappeared when the rats were given AM251. AM251 blocks the Cannabinoid Type 1 Receptor (CB1R) thus inhibiting CB1R activation.
Given the notable toxicity of acetaminophen, cannabinoids might be a reasonable supplement to accompany current treatments for pain.
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Jahan
The Journal of Molecular Psychiatry recently published an LTE from a group of researchers who demonstrated that chronic low doses of the cannabinoid WIN55212, resulted in new brain cells or neurons in the hippocampus of old rats. As we age, our ability to make new cells decreases, this may be the cause of many age related disorders. A class of drugs that can restore neurons may be a potential cure for diseases such as Parkinson’s, depression, etc.
The data was simply amazing–3 weeks of treatment resulted in noticeable effects! So this blog includes the figures from the publication, see below. On the left hand side, Figure A shows brain cells stained with red and green. Green, spindle like, staining indicates neuron growth. Pictures A and B show the typical neuron growth in developing brains. As you can see in pictures E and F, chronic administration of a non-psychotropic dose of WIN55212 restores neuron production in older rats, indicated by the green wisps. Note that this green stain is very low in old rats that did not receive the cannabinoid, pictures C and D.
The authors speculate, “Cannabinoid receptor stimulation therapy may thus provide clinical benefit for humans with age-associated memory impairment.”
Lots of molecules can activate cannabinoid receptors, so take your pick. More research is needed to determine which cannabinoids are the best option. None of the plant cannabinoids have not been explored for this effect. This not the first time cannabinoids have been linked to neurogenesis; HU-210 has also demonstrated similar effects.
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The San Jose Mercury News reported that Marijuana smoke will be added to the ever-growing list of cancer-causing materials covered by prop. 65 in CA.
Putting marijuana smoke in this category seems misplaced at best when diet colas, which contain everything from saccharine to questionably FDA-approved Nutrasweet and other chemically engineered sweeteners are not included. (Sorry if Nutrasweet or Diet Coke is on the list, but I couldn’t find it.)
It is particularly ironic that marijuana smoke will be the only smoke on the list, given the level of industrial air pollutants that are not included on the list.
It’s too bad the very studies used by OEHHA to make this decision were deeply flawed regarding the methods, leading to artificially high readings of hazardous compounds. Some of the leading cannabis researchers in the world published a three part study on cannabis smoke a few months ago. This study compared the techniques used to analyze cannabis smoke and they found huge flaws with current methods which produced exaggerated levels of side products. In some cases, the authors suggest that previous researchers left out essential information regarding their methods–making it impossible to repeat previous experiments or confirm the results! Despite credible reports which demonstrate that practically all previous research comparing cannabis and tobacco smoke is flawed and inaccurate, OEHHA went ahead and used bad science to support their politics.
A political decision like this, will undoubtedly cause confusion for years to come. After all the two main ingredients on the plant, THC and CBD, have notable anti-cancer properties. In fact, research which demonstrates that combining THC and CBD has synergistic or greater than additive anti-cancer properties, will be presented at the upcoming International Cannabinoid Research Society meeting (July 7th-11th in Chicago).
Prop 65 may cause future inconveniences for any cannabis patients who needs to be able to smoke in a public or private facilities, i.e. trying to ease their glaucoma before their eyes explode from the ocular pressure.
However, there remains two benefits to this decision:
1) Legitimacy
2) Deterrence to non-medical users
1) This is a step towards regulating cannabis. A simple regulatory mechanism such as requiring a warning label, may provide some legal protections for those who follow it. Therefore by listing the potential harms, as on every bottle of a pharmaceutical drug, it provides a bit of legitimacy because the consumer is protected or informed, and because it reinforces the reality that cannabis is a medical treatment.
2) Often I hear criticisms regarding access to medical cannabis, specifically with regard to who has access to it and who gets it. Additionally, some are concerned that people who fake illnesses to get pharmaceutical drugs will also con doctors who recommend medical cannabis. A cancer warning would deter any casual/recreational user from taking advantage of a system intended to serve the state’s seriously afflicted and chronically ill population.
What about the Science?
It has never been conclusively shown that smoking cannabis will cause, prevent, or treat cancer. What science has shown is that:
A) the active ingredients in cannabis, when isolated or in combination have anti-cancer properties.
So, there is no concrete proof that smoking cannabis will cause or fight cancer but the individual compounds in the smoke have anti-cancer and pro-cancer properties. Meaning the side products of cannabis smoke can cause cancer but the most abundant ingredients (cannabinoids) fight cancer. How they work together remains unclear, so it seems unfair to label cannabis smoke as a carcinogen because that’s only half the story.
I know neither politics nor science is about being “fair.” However, science is the pursuit of truth/facts. So in the interest of truth, let’s incorporate what is actually known about cannabis smoke into the Prop 65 warning:
“Cannabis Smoke contains compounds known to the State of California that may cause or treat cancer.”
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