Jason Barker - Medical Cannabis Patient & Organizer with LECUA Patient’s Coalition Of New Mexico 
LECUAPatientsCoalitionNM@gmail.com
dukecitywellness.blogspot.com
Tuesday, February 28th 2017
New Mexico State Department of Health
Medical Cannabis Advisory Board
Medical Cannabis Program
PO Box 26110
Santa Fe, NM, 87502-6110
Medical Cannabis Program
PO Box 26110
Santa Fe, NM, 87502-6110
Petition: Requesting The Inclusion Of A New Medical Condition: Rheumatoid Arthritis (RA) To Include:
There are more than 100 different forms of arthritis and related diseases. The most common types include osteoarthritis (OA), rheumatoid arthritis (RA), psoriatic arthritis (PsA), fibromyalgia and gout.
There are more than 100 different forms of arthritis and related diseases. The most common types include osteoarthritis (OA), rheumatoid arthritis (RA), psoriatic arthritis (PsA), fibromyalgia and gout.
Table of Contents
Pg. 1 Cover Page
Pg. 2 Petition Introduction
Pg. 3 Petition Purpose and Background
Pg. 12 Relief Requested In Petition
Pg. 13 - 15 References
Printing Provided By:
Petition Introduction: Requesting The Inclusion Of A New Medical Condition: Rheumatoid Arthritis (RA)
New Mexico’s medical cannabis history started in 1978, after public hearings the legislature enacted H.B. 329, the nation’s first law recognizing the medical value of cannabis. The New Mexico’s medical cannabis program (MCP) is the only program in the U.S. that places sole responsibility for regulation on the state’s Department of Health. Doctors must comply with state requirements for patients to be considered for applying to the medical cannabis program.
In the Lynn and Erin Compassionate Use Act, (2007) the law states; The Secretary of Health shall establish an advisory board consisting of eight practitioners representing the fields of neurology, pain management, medical oncology, psychiatry, infectious disease, family medicine and gynecology. The practitioners shall be nationally board-certified in their area of specialty and knowledgeable about the medical use of cannabis. The members shall be chosen for appointment by the Secretary from a list proposed by the New Mexico Medical Society. A quorum of the advisory board shall consist of three members. The advisory board shall:
A. review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis;
B. accept and review petitions to add medical conditions, medical treatments or diseases to the list of debilitating medical conditions that qualify for the medical use of cannabis;
C. convene at least twice per year to conduct public hearings and to evaluate petitions, which shall be maintained as confidential personal health information, to add medical conditions, medical treatments or diseases to the list of debilitating medical conditions that qualify for the medical use of cannabis;
D. issue recommendations concerning rules to be promulgated for the issuance of the registry identification cards; and
E. recommend quantities of cannabis that are necessary to constitute an adequate supply for qualified patients and primary caregivers.
First, do no harm. As an important step in becoming a doctor, medical students must take the Hippocratic Oath. And one of the promises within that oath is “first, do no harm”.
A. review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis;
B. accept and review petitions to add medical conditions, medical treatments or diseases to the list of debilitating medical conditions that qualify for the medical use of cannabis;
C. convene at least twice per year to conduct public hearings and to evaluate petitions, which shall be maintained as confidential personal health information, to add medical conditions, medical treatments or diseases to the list of debilitating medical conditions that qualify for the medical use of cannabis;
D. issue recommendations concerning rules to be promulgated for the issuance of the registry identification cards; and
E. recommend quantities of cannabis that are necessary to constitute an adequate supply for qualified patients and primary caregivers.
First, do no harm. As an important step in becoming a doctor, medical students must take the Hippocratic Oath. And one of the promises within that oath is “first, do no harm”.
We have a sound law in the Lynn and Erin Compassionate Use Act, as Section 2 reads; PURPOSE OF ACT.--The purpose of the Lynn and Erin Compassionate Use Act is to allow the beneficial use of medical cannabis in a regulated system for alleviating symptoms caused by debilitating medical conditions and their medical treatments.
“ARTICLE 2B. LYNN AND ERIN COMPASSIONATE USE ACT
N.M. Stat. Ann. § 26-2B-2 (2009)
§ 26-2B-2. Purpose of act
The purpose of the Lynn and Erin Compassionate Use Act [26-2B-1 NMSA 1978] is to allow the beneficial use of medical cannabis in a regulated system for alleviating symptoms caused by debilitating medical conditions and their medical treatments.
HISTORY: Laws 2007, ch. 210, § 2.
EFFECTIVE DATES. --Laws 2007, ch. 210, § 12 makes the act effective July 1, 2007.”
Mosby’s Medical Dictionary states that “medical treatment” means; the management and care of a patient to combat disease or disorder. Medical treatment includes: Using prescription medications, or use of a non-prescription drug at prescription strength; and or treatment of disease by hygienic and pharmacologic remedies, as distinguished from invasive surgical procedures. Treatment may be pharmacologic, using drugs; surgical, involving operative procedures; or supportive, building the patient's strength. It may be specific for the disorder, or symptomatic to relieve symptoms without effecting a cure.(Mosby's Medical Dictionary, 9th edition.)
What is a chronic medical condition?
A chronic disease is one lasting 3 months or more, by the definition of the U.S. National Center for Health Statistics. Chronic diseases generally cannot be prevented by vaccines or cured by medication, nor do they just disappear. Harvard Medical Dictionary defines chronic as: Any condition that lasts a long time or recurs over time; chronic pain as: Pain that persists after an injury has healed or a disease is over; and chronic pain syndrome as : Long-term, severe pain that doesn't spring from an injury or illness, that interferes with daily life, and is often accompanied by other problems, such as depression, irritability, and anxiety.
A chronic disease is one lasting 3 months or more, by the definition of the U.S. National Center for Health Statistics. Chronic diseases generally cannot be prevented by vaccines or cured by medication, nor do they just disappear. Harvard Medical Dictionary defines chronic as: Any condition that lasts a long time or recurs over time; chronic pain as: Pain that persists after an injury has healed or a disease is over; and chronic pain syndrome as : Long-term, severe pain that doesn't spring from an injury or illness, that interferes with daily life, and is often accompanied by other problems, such as depression, irritability, and anxiety.
What is the meaning of debilitating?
Something that's debilitating seriously affects someone or something's strength or ability to carry on with regular activities, like a debilitating illness. Debilitating comes from the Latin word debilis, meaning "weak." That's why you'll often see the adjective used to describe illness, despite the negative reference.
Something that's debilitating seriously affects someone or something's strength or ability to carry on with regular activities, like a debilitating illness. Debilitating comes from the Latin word debilis, meaning "weak." That's why you'll often see the adjective used to describe illness, despite the negative reference.
Petition Purpose and Background
The purpose of this Medical Treatment Petition: Requesting The Inclusion Of A New Medical Condition: Rheumatoid Arthritis (RA).
This petition for the Medical Treatment that pertains to: Requesting The Inclusion Of A New Medical Condition: Rheumatoid Arthritis (RA) is being provided to the state Department of Health Medical Cannabis Program so the advisory board can review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis with the Lynn and Erin Compassionate Use Act.
Who Should Qualify for Medical Cannabis Use?
According to Americans For Safe Access Policy Studies & Research:
Background: The most fundamental aspect of medical cannabis laws is the relationship between a patient and their physician. It is often only the physician and the patient that possess information about a patient’s health condition. However, many public officials and others who oppose medical cannabis laws often make assumptions about people’s health. The media have even fomented such inappropriate assumptions by naming a category of patients “Young Able Bodied Males,” condemning certain patients by visual assessment alone.
According to Americans For Safe Access Policy Studies & Research:
Background: The most fundamental aspect of medical cannabis laws is the relationship between a patient and their physician. It is often only the physician and the patient that possess information about a patient’s health condition. However, many public officials and others who oppose medical cannabis laws often make assumptions about people’s health. The media have even fomented such inappropriate assumptions by naming a category of patients “Young Able Bodied Males,” condemning certain patients by visual assessment alone.
Findings: The health care information discussed between a patient and physician is considered private and protected under federal HIPAA laws. It is typically the purview of state medical boards to assess whether a physician has inappropriately recommended cannabis to someone who should not be qualified. Studies have shown in some medical cannabis states that the majority of patients suffer from chronic pain, an ailment that is not obviously detectable by another person. Nevertheless, police will often harass and arrest patients based on the assumption that someone is faking their illness.
Position: Medical professionals should have an unrestricted ability to recommend cannabis therapeutics and that should not be impacted by law enforcement’s perceptions.
Position: Medical professionals should have an unrestricted ability to recommend cannabis therapeutics and that should not be impacted by law enforcement’s perceptions.
“Qualifying medical condition” shall mean any condition for which treatment with medical cannabis would be beneficial, as determined by a patient's qualified medical professional, including but not limited to cancer, glaucoma, positive status for human immunodeficiency virus, acquired immune deficiency syndrome (AIDS), hepatitis C, amyotrophic lateral sclerosis (ALS), Crohn’s disease, Parkinson’s disease, post-traumatic stress disorder, arthritis, chronic pain, neuropathic and other intractable chronic pain, and multiple sclerosis.
“Qualifying patient” shall mean a person who has a written recommendation from a qualified medical professional for the medical use of cannabis.
Rheumatoid Arthritis (RA)
While arthritis involves the painful inflammation of one’s joints, Rheumatoid Arthritis is an autoimmune disease (a condition in which the individual’s own immune system attacks itself) characterized by chronic and systemic inflammation throughout several parts of the sufferer’s skeletal system and body. It is a severely disabling ailment that often comes with chronic pain. The ailment is not restricted to just one’s joints, but may also affect one’s skin, eyes, lungs, heart, blood, and or nerves.
The exact cause of Rheumatoid Arthritis is unknown, although genetics, diet, hormonal, and environmental factors are all believed to contribute to its development in sufferers. The disease affects everyone differently and it may develop gradually or quickly. Current medical advances do, however, offer a number of treatments and therapies aimed at tackling the symptoms of RA as well as with helping the disease go into remission.
Using Cannabis to Treat Rheumatoid Arthritis
Cannabis is a complex medicinal plant that may actually be used to treat a variety of debilitating symptoms caused by a surprisingly large number of ailments. Its usefulness as a non-lethal medicine (you cannot die from an overdose of cannabis) cannot be overstated and its versatility in terms of how it can be consumed and as to how it can be useful for so many illnesses is something to be excited about. However, it is important to remember that consulting with your primary care physician should be your first priority when considering incorporating cannabis into one’s medical regiment and that cannabis is to be used as an adjunct therapy and not a replacement. It is also your responsibility to communicate with your doctor as to how your use of cannabis has affected your health and of your progress with utilizing medical cannabis.
With that said, studies have shown that cannabis may be quite useful for treating individuals suffering from Rheumatoid Arthritis for the following reasons: reducing joint pain and swelling; suppression of joint destruction; and with helping to prevent progression/worsening of the disease.
Study: Cannabis Helps Manage Rheumatoid Arthritis Symptoms
Cannabis has been used to help treat the inflammatory symptoms of rheumatoid arthritis for years. Despite anecdotal success, past research offers little insight into the mechanism involved in treating the condition with cannabis.
A recent study to be published in Rheumatology does just that, suggesting that the benefits could be attributed to activation of the CB2 receptor.
Researchers Investigate Potential Cannabinoid Treatment
Before diving into the study, it’s helpful to know that fibroblast-like synoviocytes (FLS)are the type of cells most often associated with Rheumatoid Arthritis. They become constantly engaged in inflammatory mechanisms, which causes cartilage damage, joint destruction, and deformation over time.
As we know, there are currently two widely-acknowledged cannabinoid receptors. Some suggest that more could exist, but not all are in agreement. Nonetheless, activation of the CB2 receptor in particular has shown promise in treating a number of inflammatory conditions.
“Activation of the CB2 receptor – which occurs when one consumes cannabis – could be a potential therapeutic target of rheumatoid arthritis.”
A team of researchers from China sought to determine whether a similar mechanism could be beneficial for rheumatoid arthritis. In doing so, they investigated the potential effects of CB2 receptor activation in FLS-cell types.
According to their results, rheumatoid arthritis cell-types showed an increased amount of CB2 receptor expression. Further, activating the CB2 receptors seems to have inhibited the proliferation of the FLS cells associated with rheumatoid arthritis.
Medical Cannabis and Rheumatoid Arthritis
In conclusion, the Chinese team of researchers determined that activation of the CB2 receptor – which occurs when one consumes cannabis – could be a potential therapeutic target of for those suffering from rheumatoid arthritis.
Of course, the idea of applying cannabis extracts to the skin is nothing new. Cannabis infused topicals are a common method of treatment for joint pain, because they allow patients to target the areas in need of the most relief.
MEDICAL CANNABIS AND RHEUMATOID ARTHRITIS
More than 31 million Americans suffer from arthritis. There are two main types of arthritis: rheumatoid arthritis and osteoarthritis. Both affect the joints, causing pain and swelling, and limiting movement.
Rheumatoid arthritis (RA) is caused by a malfunction of the immune system. Instead of fighting off intruders such as bacteria or viruses, the body attacks the synovial membranes, which facilitate the movement of joints, eventually destroying cartilage and eroding bones. Rheumatoid arthritis is most common among the aged, whose immune systems are no longer as robust or efficient as they were when younger.
Osteoarthritis (OA), or arthritis of the bones, is also found primarily among the elderly, where cartilage has been worn away through many years of use. Arthritis may also manifest as chronic inflammation of the joints as the result of injuries. OA is the most common form of arthritis, affecting more than 10 million people worldwide. Currently, no drugs are available to treat or modify this disease, and treatment is primarily focused around the use of pain killers, which often have limited benefits and hazardous side effects.
An important aspect of arthritis pathology relates to maintaining healthy bone. As people age, bones undergo extensive remodeling, which can lead to destruction or functional degradation of synovial joints. Drugs which can not only modulate pain from arthritis but also protect bones are of great importance. Cannabis and cannabinoids represent a promising treatment which can reduce arthritic pain and inflammation and positively modulate bone growth and maintenance. It has already been demonstrated that cannabinoids can effectively treat some types of arthritic pain, but recent evidence suggests that the cannabinoids are also important for bone growth and maintenance throughout life.[27-32]
The importance of cannabinoids in bone health has been established in transgenic mice that are missing either the CB1 or CB2 receptor. These mice develop osteoporosis much more quickly than normal or wild mice. Research has recently shown that mice missing both cannabinoid receptors have extremely weak bones, a condition that underlies osteoporosis and osteoarthritis pathology.[33-35]
Based on genetic screening techniques, a correlation between cannabinoids and bone is emerging in humans as well. Three studies in three distinct ethnic groups have demonstrated that mutations in the type 2 cannabinoid receptor correlate to bone diseases. One study even showed that hand bone strength weakness is very well correlated with dysfunctional/mutant CB2 receptors.
Arthritis of any type can be an extremely painful and debilitating condition that presents challenges for pain management. The use of cannabis as a treatment for musclo-skeletal pain in western medicine dates to the 1700s.[36,37] Evidence from recent research suggests that cannabis-based therapies are effective in the treatment of arthritis and the other rheumatic and degenerative hip, joint and connective tissue disorders. Since these are frequently extremely painful conditions, the well-documented analgesic properties of cannabis make it useful in treating the pain associated with arthritis, both on its own and as an adjunct therapy that substantially enhances the efficacy of opioid painkillers.
Cannabis has also been shown to have powerful immune-modulation and anti-inflammatory properties,[38-41] suggesting that it could play a role not just in symptom management but treatment of arthritis. In fact, one of the earliest records of medical use of cannabis, a Chinese text dating from ca. 2000 BC, notes that cannabis "undoes rheumatism," suggesting its anti-inflammatory and immune modulating effects were known even then.[42]
Modern research on cannabidiol (CBD), one of the non-psychoactive cannabinoid components of cannabis, has found that it suppresses the immune response in mice and rats that is responsible for a disease resembling arthritis, protecting them from severe damage to their joints and markedly improving their condition.[43,44]
Human studies have repeatedly shown cannabis to be an effective treatment for rheumatoid arthritis, and it is one of the enumerated conditions for which many states allow legal medical use. Cannabis has a demonstrated ability to improve mobility and reduce morning stiffness and inflammation. Research has also shown that patients are able to reduce their usage of potentially harmful Non-Steroidal Anti-Inflammatory drugs (NSAIDs) when using cannabis as an adjunct therapy.[45,46]
Medical researchers at Hebrew University in Jerusalem found that when cannabidiol is metabolized, one result is the creation of a compound with potent anti-inflammatory action comparable to the drug indomethacin, but without the considerable gastrointestinal side effects associated with that drug.[47]
In addition, when the body metabolizes tetrahydrocannabinol (THC), one of the primary cannabinoid components of cannabis, it produces a number of related chemicals. At least one of these metabolites has anti-inflammatory and pain-relieving effects. By modifying this metabolite, researchers have produced a synthetic carboxylic acid known as CT-3 (also called dimethylheptyl-THC-11 oic acid or DMH-11C ), which is more powerful than the natural metabolite itself, and thus can be given in smaller doses. Animal tests found CT-3 effective against both chronic and acute inflammation, and it also prevented destruction of joint tissue from chronic inflammation.
The remarkable 5,000-year safety record of cannabis - there has never been a recorded death from an overdose - and the fact that a metabolite with the desired anti-inflammatory effect is produced in the body when cannabis is used, indicates that the development of targeted, safe, and effective anti-inflammatory drugs in this class are possible.[48] CT3 has also demonstrated considerable analgesic effects in animals. In some cases, the dose-dependent effect of THC was equivalent to morphine, but with a much greater duration of action and far less toxicity.[49,50]
In contrast to the NSAIDs commonly prescribed arthritis sufferers, CT3 did not cause ulcers at therapeutically effective doses. Moreover, it does not depress respiration, produce dependence, induce body weight loss, or cause mutations, as many commonly prescribed drugs do. Studies on its mechanism of action are currently underway, with cytokine synthesis one of the pathways being studied.[51}
Cannabis may also help combat rheumatoid arthritis through its well-recognized immune-modulation properties.[52] Rheumatoid arthritis is characterized by ysregulation of the immune system in response to an initial infection or trauma. Over-activity of the immune system's B-cells causes antibodies to attack and destroy the synovial tissues located in the joint.
The immunomodulatory properties of a group of fats found in cannabis, known as sterols and sterolins, have been used as natural alternatives to conventional rheumatoid arthritis treatments that employ highly toxic drugs to either suppress the entire immune response of the body or to palliate pain and the inflammatory process without correcting the underlying immune dysfunction.
Cytokines play a role in either fuelling or suppressing the inflammation that causes damage in rheumatoid arthritis and some other diseases. The release of selected cytokines is impaired by cannabis, but the findings differ by cell type, experimental conditions, and especially the concentration of the cannabinoids examined.[53-56] A sterol/sterolin combination has been experimentally demonstrated to reduce the secretion of the pro-inflammatory cytokines controlled by the TH2 helper cells and to increase the number of TH helper cells that regulate the secretion of antibodies from the B cells. This selective activation and inhibition of the immune system results is an effective control of the dysfunctional autoimmune response.
Similarly, ajulemic acid (another non-psychoactive cannabinoid) has been found to reduce joint tissue damage in rats with adjuvant arthritis.[57] Tests on human tissue done in vitro showed a 50% suppression of one of the body's chemicals (interleukin-1beta) central to the progression of inflammation and joint tissue injury in patients with rheumatoid arthritis.[58]
Conventional Arthritis Medications
Over 100 medications are listed by the Arthritis Foundation website for use with arthritis or other related conditions, such as fibromyalgia, psoriasis, osteoporosis and gout. These medicines include aspirin, ibuprofen and other oral and topical analgesics that dull pain. The most commonly used analgesic, acetaminophen (aspirin-free Anacin, Excedrin, Panadol, Tylenol) is usually not associated with side effects, though long-term use of acetaminophen is thought to be one of the common causes of end-stage renal disease.. To effectively control arthritis, aspirin must be taken in large, continuous doses (1000-5400 mg daily), which can cause stomach pain or damage; it is believed to cause more than 1,000 deaths annually in the United States. For that reason, some doctors prescribe one of several chemical variations referred to as nonacetylated salicylates, such as CMT, Tricosal, and Trilisate, which can cause deafness or ringing in the ears in large doses.
Much stronger analgesics are also prescribed for arthritis, sometimes along with acetaminophen. These are: codeine (Dolacet, Hydrocet, Lorcet, Lortab); morphine (Avinza, Oramorph); oxycodone (Vicodin, Oxycontin, Roxicodone); propoxyphene (Percocet, Darvon, Darvocet) and tramadol (Ultram, Ultracet). These medicines can cause psychological and physical dependence, as well as constipation, dizziness, lightheadedness, mood changes, nausea, sedation, shortness of breath and vomiting. Taking high doses or mixing with alcohol can slow down breathing, a potentially fatal condition.
Analgesics don't treat the inflammation that can cause severe arthritis pain. For inflammation, steroids, NSAIDs and newer COX-2 inhibitors are prescribed. Corticosteroids (Cortisone), prednisone and related medications can cause bruising, cataracts, elevated blood sugar, hypertension, increased appetite, indigestion, insomnia, mood swings, muscle weakness, nervousness or restlessness, osteoporosis, susceptibility to infection and thin skin.
Twenty NSAIDs are available with a doctor's prescription, with three of those also available over the counter. They are diclofenac (Arthrotec, Cataflam, Voltaren); diflunisal (Dolobid); etodolac (Lodine); fenoprofen calcium (Nalfon); flurbiprofen (Ansaid); ibuprofen (Advil, Motrin IB, Nuprin); indomethacin (Indocin); ketoprofen (Orudis); meclofenamate sodium (Meclomen); mefenamic acid (Ponstel); meloxicam (Mobic); nabumetone (Relafen); naproxen (Naprosyn, Naprelan); naproxen sodium (Anaprox, Aleve);oxaprozin (Daypro); piroxicam (Feldene); sulindac (Clinoril); and olmetin sodium (Tolectin).
Side effects of NSAIDs include abdominal or stomach cramps, edema (swelling of the feet), pain or discomfort, diarrhea, dizziness, drowsiness or lightheadedness, headache, heartburn or indigestion, nausea or vomiting, gastric ulcers, stomach irritation, bleeding, fluid retention, and decreased kidney function. This is because NSAIDs act on arthritis by inhibiting prostaglandins, which protect the stomach lining, promote clotting of the blood, regulate salt and fluid balance, and maintain blood flow to the kidneys. The gastrointestinal complications of NSAIDS are the most commonly reported serious adverse drug reaction, though NSAIDs are reported to cause more than 10,000 deaths and 100,000 hospitalizations annually.
The newer group of arthritis drugs is known as cyclo-oxygenase-2 inhibitors (COX-2), which include Celebrex, Bextra and Vioxx. These medications have the same side effects as NSAIDS, except they are less likely to cause bleeding stomach ulcers and increase susceptibility to bruising or bleeding.
Non-selective NSAIDS have been associated with an increased risk of congestive heart failure. Less is known or has been concluded about the cardiovascular effects f COX-2 inhibitors, though a retrospective analysis of the risk of hospital admission for heart failure done by the Institute for Clinical Evaluative Sciences in Toronto, Canada suggests some may have serious side effects. The study of 130,000 older patients found that those using Vioxx had an 80% increased risk of hospital admission for congestive heart failure. Those using non-selective NSAIDS had a 40% increased risk, and those using Celebrex had the same rate of heart failure as people who had never used NSAIDS.
Antipyretic and anti-inflammatory effects of NSAIDs can mask the signs and symptoms of infection. Their use can interfere with the pharmacologic control of hypertension and cardiac failure in patients who take beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, or diuretics. Long-term use may damage chondrocyte (cartilage) function.
About 60% of patients will respond to any single NSAID. Approximately 10% of rheumatoid arthritis patients will not respond to any NSAID. Biologic response modifiers such as adalimumab (Humira); etanercept (Enbrel); infliximab (Remicade), and anakinra (Kineret) are prescribed to either inhibit or the supplement the immune system components called cytokines. Rare reports of lupus (with such symptoms as rash, fever and pleurisy) have been linked to treatment with adalimumab, etanercept and infliximab. Lupus symptoms resolve when the medication is stopped. Multiple sclerosis has rarely developed in patients receiving biologic response modifiers. Seizures have been reported with etanercept.
Cannabis: By comparison, the side effects associated with cannabis are typically mild and are classified as "low risk." Euphoric mood changes are among the most frequent side effects. Cannabinoids can exacerbate schizophrenic psychosis in predisposed persons. Cannabinoids impede cognitive and psychomotor performance, resulting in temporary impairment. Chronic use can lead to the development of tolerance. Tachycardia and hypotension are frequently documented as adverse events in the cardiovascular system. A few cases of myocardial ischemia have been reported in young and previously healthy patients. Inhaling the smoke of cannabis cigarettes induces side effects on the respiratory system. Cannabinoids are contraindicated for patients with a history of cardiac ischemia. In summary, a low risk profile is evident from the literature available. Serious complications are very rare and are not usually reported during the use of cannabinoids for medical indications. (See References II)
More than 31 million Americans suffer from arthritis. There are two main types of arthritis: rheumatoid arthritis and osteoarthritis. Both affect the joints, causing pain and swelling, and limiting movement.
Rheumatoid arthritis (RA) is caused by a malfunction of the immune system. Instead of fighting off intruders such as bacteria or viruses, the body attacks the synovial membranes, which facilitate the movement of joints, eventually destroying cartilage and eroding bones. Rheumatoid arthritis is most common among the aged, whose immune systems are no longer as robust or efficient as they were when younger.
Osteoarthritis (OA), or arthritis of the bones, is also found primarily among the elderly, where cartilage has been worn away through many years of use. Arthritis may also manifest as chronic inflammation of the joints as the result of injuries. OA is the most common form of arthritis, affecting more than 10 million people worldwide. Currently, no drugs are available to treat or modify this disease, and treatment is primarily focused around the use of pain killers, which often have limited benefits and hazardous side effects.
An important aspect of arthritis pathology relates to maintaining healthy bone. As people age, bones undergo extensive remodeling, which can lead to destruction or functional degradation of synovial joints. Drugs which can not only modulate pain from arthritis but also protect bones are of great importance. Cannabis and cannabinoids represent a promising treatment which can reduce arthritic pain and inflammation and positively modulate bone growth and maintenance. It has already been demonstrated that cannabinoids can effectively treat some types of arthritic pain, but recent evidence suggests that the cannabinoids are also important for bone growth and maintenance throughout life.[27-32]
The importance of cannabinoids in bone health has been established in transgenic mice that are missing either the CB1 or CB2 receptor. These mice develop osteoporosis much more quickly than normal or wild mice. Research has recently shown that mice missing both cannabinoid receptors have extremely weak bones, a condition that underlies osteoporosis and osteoarthritis pathology.[33-35]
Based on genetic screening techniques, a correlation between cannabinoids and bone is emerging in humans as well. Three studies in three distinct ethnic groups have demonstrated that mutations in the type 2 cannabinoid receptor correlate to bone diseases. One study even showed that hand bone strength weakness is very well correlated with dysfunctional/mutant CB2 receptors.
Arthritis of any type can be an extremely painful and debilitating condition that presents challenges for pain management. The use of cannabis as a treatment for musclo-skeletal pain in western medicine dates to the 1700s.[36,37] Evidence from recent research suggests that cannabis-based therapies are effective in the treatment of arthritis and the other rheumatic and degenerative hip, joint and connective tissue disorders. Since these are frequently extremely painful conditions, the well-documented analgesic properties of cannabis make it useful in treating the pain associated with arthritis, both on its own and as an adjunct therapy that substantially enhances the efficacy of opioid painkillers.
Cannabis has also been shown to have powerful immune-modulation and anti-inflammatory properties,[38-41] suggesting that it could play a role not just in symptom management but treatment of arthritis. In fact, one of the earliest records of medical use of cannabis, a Chinese text dating from ca. 2000 BC, notes that cannabis "undoes rheumatism," suggesting its anti-inflammatory and immune modulating effects were known even then.[42]
Modern research on cannabidiol (CBD), one of the non-psychoactive cannabinoid components of cannabis, has found that it suppresses the immune response in mice and rats that is responsible for a disease resembling arthritis, protecting them from severe damage to their joints and markedly improving their condition.[43,44]
Human studies have repeatedly shown cannabis to be an effective treatment for rheumatoid arthritis, and it is one of the enumerated conditions for which many states allow legal medical use. Cannabis has a demonstrated ability to improve mobility and reduce morning stiffness and inflammation. Research has also shown that patients are able to reduce their usage of potentially harmful Non-Steroidal Anti-Inflammatory drugs (NSAIDs) when using cannabis as an adjunct therapy.[45,46]
Medical researchers at Hebrew University in Jerusalem found that when cannabidiol is metabolized, one result is the creation of a compound with potent anti-inflammatory action comparable to the drug indomethacin, but without the considerable gastrointestinal side effects associated with that drug.[47]
In addition, when the body metabolizes tetrahydrocannabinol (THC), one of the primary cannabinoid components of cannabis, it produces a number of related chemicals. At least one of these metabolites has anti-inflammatory and pain-relieving effects. By modifying this metabolite, researchers have produced a synthetic carboxylic acid known as CT-3 (also called dimethylheptyl-THC-11 oic acid or DMH-11C ), which is more powerful than the natural metabolite itself, and thus can be given in smaller doses. Animal tests found CT-3 effective against both chronic and acute inflammation, and it also prevented destruction of joint tissue from chronic inflammation.
The remarkable 5,000-year safety record of cannabis - there has never been a recorded death from an overdose - and the fact that a metabolite with the desired anti-inflammatory effect is produced in the body when cannabis is used, indicates that the development of targeted, safe, and effective anti-inflammatory drugs in this class are possible.[48] CT3 has also demonstrated considerable analgesic effects in animals. In some cases, the dose-dependent effect of THC was equivalent to morphine, but with a much greater duration of action and far less toxicity.[49,50]
In contrast to the NSAIDs commonly prescribed arthritis sufferers, CT3 did not cause ulcers at therapeutically effective doses. Moreover, it does not depress respiration, produce dependence, induce body weight loss, or cause mutations, as many commonly prescribed drugs do. Studies on its mechanism of action are currently underway, with cytokine synthesis one of the pathways being studied.[51}
Cannabis may also help combat rheumatoid arthritis through its well-recognized immune-modulation properties.[52] Rheumatoid arthritis is characterized by ysregulation of the immune system in response to an initial infection or trauma. Over-activity of the immune system's B-cells causes antibodies to attack and destroy the synovial tissues located in the joint.
The immunomodulatory properties of a group of fats found in cannabis, known as sterols and sterolins, have been used as natural alternatives to conventional rheumatoid arthritis treatments that employ highly toxic drugs to either suppress the entire immune response of the body or to palliate pain and the inflammatory process without correcting the underlying immune dysfunction.
Cytokines play a role in either fuelling or suppressing the inflammation that causes damage in rheumatoid arthritis and some other diseases. The release of selected cytokines is impaired by cannabis, but the findings differ by cell type, experimental conditions, and especially the concentration of the cannabinoids examined.[53-56] A sterol/sterolin combination has been experimentally demonstrated to reduce the secretion of the pro-inflammatory cytokines controlled by the TH2 helper cells and to increase the number of TH helper cells that regulate the secretion of antibodies from the B cells. This selective activation and inhibition of the immune system results is an effective control of the dysfunctional autoimmune response.
Similarly, ajulemic acid (another non-psychoactive cannabinoid) has been found to reduce joint tissue damage in rats with adjuvant arthritis.[57] Tests on human tissue done in vitro showed a 50% suppression of one of the body's chemicals (interleukin-1beta) central to the progression of inflammation and joint tissue injury in patients with rheumatoid arthritis.[58]
Conventional Arthritis Medications
Over 100 medications are listed by the Arthritis Foundation website for use with arthritis or other related conditions, such as fibromyalgia, psoriasis, osteoporosis and gout. These medicines include aspirin, ibuprofen and other oral and topical analgesics that dull pain. The most commonly used analgesic, acetaminophen (aspirin-free Anacin, Excedrin, Panadol, Tylenol) is usually not associated with side effects, though long-term use of acetaminophen is thought to be one of the common causes of end-stage renal disease.. To effectively control arthritis, aspirin must be taken in large, continuous doses (1000-5400 mg daily), which can cause stomach pain or damage; it is believed to cause more than 1,000 deaths annually in the United States. For that reason, some doctors prescribe one of several chemical variations referred to as nonacetylated salicylates, such as CMT, Tricosal, and Trilisate, which can cause deafness or ringing in the ears in large doses.
Much stronger analgesics are also prescribed for arthritis, sometimes along with acetaminophen. These are: codeine (Dolacet, Hydrocet, Lorcet, Lortab); morphine (Avinza, Oramorph); oxycodone (Vicodin, Oxycontin, Roxicodone); propoxyphene (Percocet, Darvon, Darvocet) and tramadol (Ultram, Ultracet). These medicines can cause psychological and physical dependence, as well as constipation, dizziness, lightheadedness, mood changes, nausea, sedation, shortness of breath and vomiting. Taking high doses or mixing with alcohol can slow down breathing, a potentially fatal condition.
Analgesics don't treat the inflammation that can cause severe arthritis pain. For inflammation, steroids, NSAIDs and newer COX-2 inhibitors are prescribed. Corticosteroids (Cortisone), prednisone and related medications can cause bruising, cataracts, elevated blood sugar, hypertension, increased appetite, indigestion, insomnia, mood swings, muscle weakness, nervousness or restlessness, osteoporosis, susceptibility to infection and thin skin.
Twenty NSAIDs are available with a doctor's prescription, with three of those also available over the counter. They are diclofenac (Arthrotec, Cataflam, Voltaren); diflunisal (Dolobid); etodolac (Lodine); fenoprofen calcium (Nalfon); flurbiprofen (Ansaid); ibuprofen (Advil, Motrin IB, Nuprin); indomethacin (Indocin); ketoprofen (Orudis); meclofenamate sodium (Meclomen); mefenamic acid (Ponstel); meloxicam (Mobic); nabumetone (Relafen); naproxen (Naprosyn, Naprelan); naproxen sodium (Anaprox, Aleve);oxaprozin (Daypro); piroxicam (Feldene); sulindac (Clinoril); and olmetin sodium (Tolectin).
Side effects of NSAIDs include abdominal or stomach cramps, edema (swelling of the feet), pain or discomfort, diarrhea, dizziness, drowsiness or lightheadedness, headache, heartburn or indigestion, nausea or vomiting, gastric ulcers, stomach irritation, bleeding, fluid retention, and decreased kidney function. This is because NSAIDs act on arthritis by inhibiting prostaglandins, which protect the stomach lining, promote clotting of the blood, regulate salt and fluid balance, and maintain blood flow to the kidneys. The gastrointestinal complications of NSAIDS are the most commonly reported serious adverse drug reaction, though NSAIDs are reported to cause more than 10,000 deaths and 100,000 hospitalizations annually.
The newer group of arthritis drugs is known as cyclo-oxygenase-2 inhibitors (COX-2), which include Celebrex, Bextra and Vioxx. These medications have the same side effects as NSAIDS, except they are less likely to cause bleeding stomach ulcers and increase susceptibility to bruising or bleeding.
Non-selective NSAIDS have been associated with an increased risk of congestive heart failure. Less is known or has been concluded about the cardiovascular effects f COX-2 inhibitors, though a retrospective analysis of the risk of hospital admission for heart failure done by the Institute for Clinical Evaluative Sciences in Toronto, Canada suggests some may have serious side effects. The study of 130,000 older patients found that those using Vioxx had an 80% increased risk of hospital admission for congestive heart failure. Those using non-selective NSAIDS had a 40% increased risk, and those using Celebrex had the same rate of heart failure as people who had never used NSAIDS.
Antipyretic and anti-inflammatory effects of NSAIDs can mask the signs and symptoms of infection. Their use can interfere with the pharmacologic control of hypertension and cardiac failure in patients who take beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, or diuretics. Long-term use may damage chondrocyte (cartilage) function.
About 60% of patients will respond to any single NSAID. Approximately 10% of rheumatoid arthritis patients will not respond to any NSAID. Biologic response modifiers such as adalimumab (Humira); etanercept (Enbrel); infliximab (Remicade), and anakinra (Kineret) are prescribed to either inhibit or the supplement the immune system components called cytokines. Rare reports of lupus (with such symptoms as rash, fever and pleurisy) have been linked to treatment with adalimumab, etanercept and infliximab. Lupus symptoms resolve when the medication is stopped. Multiple sclerosis has rarely developed in patients receiving biologic response modifiers. Seizures have been reported with etanercept.
Cannabis: By comparison, the side effects associated with cannabis are typically mild and are classified as "low risk." Euphoric mood changes are among the most frequent side effects. Cannabinoids can exacerbate schizophrenic psychosis in predisposed persons. Cannabinoids impede cognitive and psychomotor performance, resulting in temporary impairment. Chronic use can lead to the development of tolerance. Tachycardia and hypotension are frequently documented as adverse events in the cardiovascular system. A few cases of myocardial ischemia have been reported in young and previously healthy patients. Inhaling the smoke of cannabis cigarettes induces side effects on the respiratory system. Cannabinoids are contraindicated for patients with a history of cardiac ischemia. In summary, a low risk profile is evident from the literature available. Serious complications are very rare and are not usually reported during the use of cannabinoids for medical indications. (See References II)
Beneficial Cannabinoids and Terpenoids Useful for Treating Rheumatoid Arthritis
The cannabis plant offers a plethora of therapeutic benefits and contains cannabinoids and terpenoid compounds that are useful for treating the painful symptoms of RA. Many of the current studies and research surrounding cannabis as a treatment for Rheumatoid Arthritis are focused on the anti-inflammatory properties of Cannabidiol (CBD) and on the usefulness of Tetrahydrocannabinol (THC) as an effective pain-reliever.
it was stated that, “Taken together, these data show that CBD, through its combined immunosuppressive and anti-inflammatory actions, has a potent anti-arthritic effect in CIA (collagen-induced arthritis).”
With that said, the following list also denotes which cannabinoids and terpenoids work synergistically with each other for possible therapeutic benefit. It may be beneficial to seek out strains that contain these cannabinoids and terpenoids.
Expert Opinions
“There’s no question that cannabinoids have the potential to have an impact on the disease.” – Mary-Ann Fitzcharles, MD (2011)
“We don’t know how the drug affects the disease process, but it does seem to have a positive analgesic effect on RA [rheumatoid arthritis].” – Kathryn Cunningham, PhD (2011)
“The results from the first controlled study of CBM [cannabis-based medicine] in rheumatoid arthritis are encouraging, with overall improvements in pain on movement and at rest, improvement in the quality of sleep and improvement in the overall condition of the patients’ arthritis.” – Ronald Jubb, MD (2005)
“It’s not going to cure the disease, but it will do a lot to alleviate the pain and suffering of people with rheumatoid arthritis. Cannabis is probably less harmful than other available painkillers.” – Arthritis Research Campaign (2004)
“The spinal cord is loaded with cannabinoid receptors. These cannabinoid compounds apparently reduce swelling from inflammation… But more than that, they kill the pain from inflammation specifically. They work on the peripheral nerves that carry pain from your joint into the spinal cord.” – J. Michael Walker, PhD (2000)
“There’s no question that cannabinoids have the potential to have an impact on the disease.” – Mary-Ann Fitzcharles, MD (2011)
“We don’t know how the drug affects the disease process, but it does seem to have a positive analgesic effect on RA [rheumatoid arthritis].” – Kathryn Cunningham, PhD (2011)
“The results from the first controlled study of CBM [cannabis-based medicine] in rheumatoid arthritis are encouraging, with overall improvements in pain on movement and at rest, improvement in the quality of sleep and improvement in the overall condition of the patients’ arthritis.” – Ronald Jubb, MD (2005)
“It’s not going to cure the disease, but it will do a lot to alleviate the pain and suffering of people with rheumatoid arthritis. Cannabis is probably less harmful than other available painkillers.” – Arthritis Research Campaign (2004)
“The spinal cord is loaded with cannabinoid receptors. These cannabinoid compounds apparently reduce swelling from inflammation… But more than that, they kill the pain from inflammation specifically. They work on the peripheral nerves that carry pain from your joint into the spinal cord.” – J. Michael Walker, PhD (2000)
Rheumatoid arthritis, cannabis based medicine eases pain and suppresses disease
Arthritis & Medical Cannabis Related Clinical Information
- http://www.ncbi.nlm.nih.gov/pubmed/15857325
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430692/
- http://www.pnas.org/content/103/3/696.abstract
- http://www.ncbi.nlm.nih.gov/pubmed/16536902
- http://www.ncbi.nlm.nih.gov/pubmed/18416822
- http://rheumatology.oxfordjournals.org/content/45/1/50.long
- Preliminary assessment of the efficacy, tolerability and safety of a cannabis-based medicine (Sativex) in the treatment of pain caused by rheumatoid arthritis [http://www.ncbi.nlm.nih.gov/pubmed/16282192]
- Involvement of the endocannabinoid system in osteoarthritis pain [http://www.ncbi.nlm.nih.gov/pubmed/24494687]
- The abnormal cannabidiol analogue O-1602 reduces nociception in a rat model of acute arthritis via the putative cannabinoid receptor GPR55 [http://www.ncbi.nlm.nih.gov/pubmed/21683763]
Rules, Regulations, & Policy Solution For the Petition: Requesting The Inclusion Of A New Medical Condition: Rheumatoid Arthritis (RA)
The approval of this petition: Requesting The Inclusion Of A New Medical Condition: Rheumatoid Arthritis (RA), that is being provided to the state Department of Health Medical Cannabis Program so the advisory board can review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis with the Lynn and Erin Compassionate Use Act. The approval of this petition would bring the Department of Health in compliance with the intent of the law and uphold the spirit of the Lynn and Erin Compassionate Use Act, 2007. Fulfilling both;“ Section 2. PURPOSE OF ACT.--The purpose of the Lynn and Erin Compassionate Use Act is to allow the beneficial use of medical cannabis in a regulated system for alleviating symptoms caused by debilitating medical conditions and their medical treatments” And Section 6. ADVISORY BOARD CREATED--DUTIES: The advisory board shall: A. review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis.” New Mexico’s medical cannabis history started in 1978. After public hearings the legislature enacted H.B. 329, the nation’s first law recognizing the medical value of cannabis...the first law.
References
Understanding medical cannabis.Elemental Wellness Center, 2014 Jul.
Cannabinoids for treatment of chronic non-cancer pain; a systematic review of randomized trials.Lynch, Mary E., et al.
British Journal of Clinical Pharmacology, 2011 Nov, 72(5): 735-744.
Characterisation of the cannabinoid receptor system in synovial tissue and fluid in patients with osteoarthritis and rheumatoid arthritis.Richardson, Denise, et al.
Arthritis Research & Therapy, 2008, (online article).
Cannabis, pain, and sleep: lessons from therapeutic clinical trials of Sativex, a cannabis-based medicine.Russo, Ethan B, et al.
Chemistry & Biodiversity, 2007 Aug, 4(8): 1729-1743.
The use of a cannabis-based medicine (Sativex) in the treatment of pain caused by rheumatoid arthritis.Wright, S, et al.
Oxford Journals: Rheumatology, 2006 Jun, 45(6): 781 (correspondence).
Preliminary assessment of the efficacy, tolerability and safety of a cannabis-based medicine (Sativex) in the treatment of pain caused by rheumatoid arthritis.Blake, D.R, et al.
Oxford Journals: Rheumatology, 2006 Jan, 45(1): 50-52.
Arthritis and cannabinoids: HU-210 ad Win-55,212-2 prevent IL-1 α-induced matrix degradation in bovine articular chondrocytes in-vitro.Mbvundula, Estery C., et al.
Journal of Pharmacy and Pharmacology, 2006 Mar, 58(3): 351-358.
BIOforum Europe, 2005 Jul, (online article).
Cannabinoid-based drugs as anti-inflammatory therapeutics.Klein, Thomas W.
Nature Reviews Immunology, 2005 May, 5: 400-411.
Oral anti-inflammatory activiy of cannabidiol, a nonpsychoactive constituent of cannabis, in acute carrageenan-induced inflammation in the rat paw.Costa, Barbara, et al.
Naunyn-Schmiedberg’s Archives of Pharmacology, 2004 Mar, 369(3): 294-299.
The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis.Malfait, A. M., et al.
Proceedings of the National Academy of Sciences of the United States of America, 2000 Mar 10, 97(17): 9561-9566.
References II
27. Bab I and Zimmer A (2008). Cannabinoid receptors and the regulation of bone mass. Br J Pharmacol 153(2):182-188.
28. Buckley NE, et al (2000) .Immunomodulation by cannabinoids is absent in mice deficient for the cannabinoid CB(2) receptor. Eur J Pharmacol 396(2-3):141-149.
29. Idris AI, et al (2009). Cannabinoid receptor type 1 protects against age-related osteoporosis by regulating osteoblast and adipocyte differentiation in marrow stromal cells. Cell Metab 10(2):139-147.
30. Ofek O, et al (2006). Peripheral cannabinoid receptor, CB2, regulates bone mass. Proc Natl Acad Sci U S A 103(3):696-701.
31. Tam J, et al (2006). Involvement of neuronal cannabinoid receptor CB1 in regulation of bone mass and bone remodeling. Mol Pharmacol 70(3):786-792.
32. Tam J, et al (2008). The cannabinoid CB1 receptor regulates bone formation by modulating adrenergic signaling. Faseb J 22(1):285-294.
33. Huang QY, et al (2009). Multiple osteoporosis susceptibility genes on chromosome 1p36 in Chinese. Bone 44(5):984-988.
34. Karsak M, et al (2005). Cannabinoid receptor type 2 gene is associated with human osteoporosis. Hum Mol Genet 14(22):3389-3396.
35. Karsak M, et al (2009). The cannabinoid receptor type 2 (CNR2) gene is associated with hand bone strength phenotypes in an ethnically homogeneous family sample. Hum Genet.
36. Russo EB (2002). Role of cannabis and cannabinoids in pain management. In: Weiner RS, editor. Pain management: A practical guide for clinicians. 6th ed. Boca Raton, FL: CRC Press. p. 357-375.
37. Marcandier M (1764). Treatise on hemp. London: T. Becket and P.A. de Hondt.
38. Formukong E et al (1988). Analgesic and Antiinflammatory Activity of Constituents of Cannabis Sativa L. Inflammation 12: 361.
39. Barret ML et al (1985). Isolation from Cannabis sativa L. of Cannflavon - a novel inhibitor of prostaglandin production. Biochem. Pharmacol. 34: 2019
40. Burstein SH et al (1989). Antagonism to the actions of platelet activating factor by a nonpsychoactive cannabinoid. J Pharmacol. Exp. Therap. 251: 531-5
41. Sofia RD (1989). Antiedemic and analgesic properties of delta-9-THC compared with three other drugs. Eur. J. Pharamacol. 41: 705-9
42. Zurier RB et al (1998). Dimethylheptyl-THC-11 Oic Acid: A Nonpsychoactive Antiinflammatory Agent with a Cannabinoid Template Structure. ARTHRITIS AND RHEUMATISM January; volume 41, number 1, pages 163-170.
43. Costa B et al (2004). Oral anti-inflammatory activity of cannabidiol, a non-psychoactive constituent of cannabis, in acute carrageenan-induced inflammation in the rat paw. Naunyn Schmiedebergs Arch Pharmacol. Mar;369(3):294-9. Epub 2004 Feb 12.
44. Malfait AM et al (2000) .The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. Proc Natl Acad Sci U S A. Aug 15 97(17):9561-6.
45. James JS (1998). Marijuana, inflammation, and CT-3 (DMH-11C): cannabis leads to new class of antiinflammatory drugs. AIDS Treat News. Jan 23;(No 287):1, 5.
46. Straus SE (2000). Immunoactive cannabinoids: Therapeutic prospects for marijuana constituents. Proc Natl Acad Sci U S A. Aug 15 97(17):9563.
47. Shohami E (2001). Nature. Oct 4;413(6855):527-31.
48. Burstein SH (2000). Ajulemic acid (CT3): a potent analog of the acid metabolites of THC. Curr Pharm Des. Sep 6(13):1339-45.
49. Burstein SH et al (2004). Ajulemic acid: A novel cannabinoid produces analgesia without a "high". Life Sci. Aug 6;75(12):1513-22.
50. Devane WAet al1(1992). Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science.258:1946-1949.
51. Barg J et al (1995). Cannabinomimetic behavioral effects of andadenylate cyclase inhibition by two new endogenous anandamides. Eur J Pharmacol.;287:145-152.
52. Klein TW et al (1998). Cannabinoid receptors and immunity. Immunol Today. 797:225-233.
53. Daaka Y et al (1996). Cannabinoid receptor proteins are increased in jurkat, human T-cell line after mitogen activation. J Pharmacol Exp Ther. 276:776-783.
54. Kaminski NE (1996); Immune regulation by cannabinoid compounds through the inhibition of the cyclic AMP signaling cascade and altered gene expression. Biochem Pharmacol; 52(8):1133-40.
55. Di Marzo V (1998). 'Endocannabinoids' and other fatty acid derivatives with cannabimimetic properties: biochemistry and possible physiopathological relevance. Biochimica et Biophysica Acta.1392(2-3):153-75.
56. Smith PB et al (1994). The pharmacological activity of anandamide, a putative endogenous cannabinoid in mice. J Pharmacol Exp Ther. 270:219-227.
57. Burstein SH (2000). Ajulemic acid (CT3): a potent analog of the acid metabolites of THC. Curr Pharm Des. Sep;6(13):1339-45.
58. Zurier RB et al (2003). Suppression of human monocyte interleukin-1beta production by ajulemic acid, a nonpsychoactive cannabinoid. Biochem Pharmacol. Feb 15;65(4):649-55.
59. Hazekamp A et al (2006). Evaluation of a vaporizing device (Volcano(R)) for the pulmonary administration of tetrahydrocannabinol. J Pharm Sci 95 (6) Apr 24: 1308-1317.
28. Buckley NE, et al (2000) .Immunomodulation by cannabinoids is absent in mice deficient for the cannabinoid CB(2) receptor. Eur J Pharmacol 396(2-3):141-149.
29. Idris AI, et al (2009). Cannabinoid receptor type 1 protects against age-related osteoporosis by regulating osteoblast and adipocyte differentiation in marrow stromal cells. Cell Metab 10(2):139-147.
30. Ofek O, et al (2006). Peripheral cannabinoid receptor, CB2, regulates bone mass. Proc Natl Acad Sci U S A 103(3):696-701.
31. Tam J, et al (2006). Involvement of neuronal cannabinoid receptor CB1 in regulation of bone mass and bone remodeling. Mol Pharmacol 70(3):786-792.
32. Tam J, et al (2008). The cannabinoid CB1 receptor regulates bone formation by modulating adrenergic signaling. Faseb J 22(1):285-294.
33. Huang QY, et al (2009). Multiple osteoporosis susceptibility genes on chromosome 1p36 in Chinese. Bone 44(5):984-988.
34. Karsak M, et al (2005). Cannabinoid receptor type 2 gene is associated with human osteoporosis. Hum Mol Genet 14(22):3389-3396.
35. Karsak M, et al (2009). The cannabinoid receptor type 2 (CNR2) gene is associated with hand bone strength phenotypes in an ethnically homogeneous family sample. Hum Genet.
36. Russo EB (2002). Role of cannabis and cannabinoids in pain management. In: Weiner RS, editor. Pain management: A practical guide for clinicians. 6th ed. Boca Raton, FL: CRC Press. p. 357-375.
37. Marcandier M (1764). Treatise on hemp. London: T. Becket and P.A. de Hondt.
38. Formukong E et al (1988). Analgesic and Antiinflammatory Activity of Constituents of Cannabis Sativa L. Inflammation 12: 361.
39. Barret ML et al (1985). Isolation from Cannabis sativa L. of Cannflavon - a novel inhibitor of prostaglandin production. Biochem. Pharmacol. 34: 2019
40. Burstein SH et al (1989). Antagonism to the actions of platelet activating factor by a nonpsychoactive cannabinoid. J Pharmacol. Exp. Therap. 251: 531-5
41. Sofia RD (1989). Antiedemic and analgesic properties of delta-9-THC compared with three other drugs. Eur. J. Pharamacol. 41: 705-9
42. Zurier RB et al (1998). Dimethylheptyl-THC-11 Oic Acid: A Nonpsychoactive Antiinflammatory Agent with a Cannabinoid Template Structure. ARTHRITIS AND RHEUMATISM January; volume 41, number 1, pages 163-170.
43. Costa B et al (2004). Oral anti-inflammatory activity of cannabidiol, a non-psychoactive constituent of cannabis, in acute carrageenan-induced inflammation in the rat paw. Naunyn Schmiedebergs Arch Pharmacol. Mar;369(3):294-9. Epub 2004 Feb 12.
44. Malfait AM et al (2000) .The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. Proc Natl Acad Sci U S A. Aug 15 97(17):9561-6.
45. James JS (1998). Marijuana, inflammation, and CT-3 (DMH-11C): cannabis leads to new class of antiinflammatory drugs. AIDS Treat News. Jan 23;(No 287):1, 5.
46. Straus SE (2000). Immunoactive cannabinoids: Therapeutic prospects for marijuana constituents. Proc Natl Acad Sci U S A. Aug 15 97(17):9563.
47. Shohami E (2001). Nature. Oct 4;413(6855):527-31.
48. Burstein SH (2000). Ajulemic acid (CT3): a potent analog of the acid metabolites of THC. Curr Pharm Des. Sep 6(13):1339-45.
49. Burstein SH et al (2004). Ajulemic acid: A novel cannabinoid produces analgesia without a "high". Life Sci. Aug 6;75(12):1513-22.
50. Devane WAet al1(1992). Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science.258:1946-1949.
51. Barg J et al (1995). Cannabinomimetic behavioral effects of andadenylate cyclase inhibition by two new endogenous anandamides. Eur J Pharmacol.;287:145-152.
52. Klein TW et al (1998). Cannabinoid receptors and immunity. Immunol Today. 797:225-233.
53. Daaka Y et al (1996). Cannabinoid receptor proteins are increased in jurkat, human T-cell line after mitogen activation. J Pharmacol Exp Ther. 276:776-783.
54. Kaminski NE (1996); Immune regulation by cannabinoid compounds through the inhibition of the cyclic AMP signaling cascade and altered gene expression. Biochem Pharmacol; 52(8):1133-40.
55. Di Marzo V (1998). 'Endocannabinoids' and other fatty acid derivatives with cannabimimetic properties: biochemistry and possible physiopathological relevance. Biochimica et Biophysica Acta.1392(2-3):153-75.
56. Smith PB et al (1994). The pharmacological activity of anandamide, a putative endogenous cannabinoid in mice. J Pharmacol Exp Ther. 270:219-227.
57. Burstein SH (2000). Ajulemic acid (CT3): a potent analog of the acid metabolites of THC. Curr Pharm Des. Sep;6(13):1339-45.
58. Zurier RB et al (2003). Suppression of human monocyte interleukin-1beta production by ajulemic acid, a nonpsychoactive cannabinoid. Biochem Pharmacol. Feb 15;65(4):649-55.
59. Hazekamp A et al (2006). Evaluation of a vaporizing device (Volcano(R)) for the pulmonary administration of tetrahydrocannabinol. J Pharm Sci 95 (6) Apr 24: 1308-1317.
Lynn & Erin Compassionate Use Act Patient’s Coalition of New Mexico ~ A GrassRoots Movement!
UNITE-NETWORK-GROW-INFORM-KNOW-EDUCATE-ACTIVISM-VOTE-HEALTH-WELLNESS
(All Rights Reserved 04/20/2016)
No comments:
Post a Comment