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Found 12 results

  1. Cannabinoids for Fibromyalgia Syndrome FibroAction has got an article discussing a recent journal article from Fibromyalgia Syndrome (Fibro) expert, Dr Roland Staud MD, and EB Koo, an undergraduate student at the University of Florida, discussing whether cannabinoids are a new treatment option for Fibromyalgia Syndrome. This is in light of the study by Skrabek et al, who carried out what was apparently the first randomized, controlled trial to assess the benefit of nabilone, a synthetic cannabinoid, on pain reduction and quality of life improvement in patients with Fibro. FibroAction is a new organisation, basd in the UK, which aims to make accurate, up-to-date information about Fibromyalgia Syndrome (Fibro) readily available, as well as raise awareness of the condition. My link Cannabinoids for Fibromyalgia Syndrome An article has been e-published ahead of print in the journal Nature Clinical Practice. Rheumatology by Fibromyalgia Syndrome expert, Dr Roland Staud MD, and EB Koo, an undergraduate student at the University of Florida, discussing whether cannabinoids are a new treatment option for Fibromyalgia Syndrome. [1] Dr Staud, author of 'Fibromyalgia for Dummies', is Professor of Medicine at the College of Medicine and Director of the Center for Musculoskeletal Pain Research at the University of Florida. The article discusses cannabinoids as a treatment option for Fibromyalgia Syndrome in light of the study by Skrabek et al, discussed in an article in the February issue of the Journal of Pain. [2] Skrabek et al carried out what was apparently the first randomized, controlled trial to assess the benefit of nabilone, a synthetic cannabinoid, on pain reduction and quality of life improvement in patients with Fibromyalgia Syndrome. [2] The randomized, double-blind, placebo-controlled trial was carried out on 40 patients with Fibromyalgia Syndrome. The primary outcome measure, visual analog scale (VAS) for pain, and the secondary outcome measures, number of tender points, the average tender point pain threshold, and the Fibromyalgia Impact Questionnaire (FIQ), were evaluated at 2 and 4 weeks into the trial and then again after a 4-week washout period. [2] Skrabek et al's trial found that there were significant decreases in the VAS (-2.04, P < .02), FIQ (-12.07, P < .02), and anxiety (-1.67, P < .02) in the nabilone treated group at 4 weeks, and that after the 4-week wash-out period, all benefits were lost, with the nabilone treated group returning to their baseline levels of pain and quality of life. There were no significant improvements in the placebo group. The treatment group experienced more side effects per person at 2 and 4 weeks (1.58, P < .02 and 1.54, P < .05), respectively, and although nabilone was not associated with serious adverse effects, some patients did experience drowsiness, dry mouth, vertigo and ataxia. [2] Skrabek et al said that: "Nabilone appears to be a beneficial, well-tolerated treatment option for fibromyalgia patients, with significant benefits in pain relief and functional improvement. ... As nabilone improved symptoms and was well-tolerated, it may be a useful adjunct for pain management in fibromyalgia." Nabilone, a synthetic cannabinoid, is used to treat chemotherapy-induced nausea and vomiting in patients who do not respond well to other anti-emetics. However, it has also been studied for use in treating cancer pain and neuropathic pain. Cannabinoids are chemicals that are structurally similar to cannabis or THC (the main psychoactive substance found in cannabis), or that bind to cannabinoid receptors. References: Staud R, Koo EB. Are cannabinoids a new treatment option for pain in patients with fibromyalgia? Nat Clin Pract Rheumatol. 2008 Jun 3. [Epub ahead of print]. Skrabek RQ, Galimova L, Ethans K, Perry D. Nabilone for the treatment of pain in fibromyalgia. J Pain. 2008 Feb;9(2):164-73. Epub 2007 Nov 5. Fibromyalgia and Alternative Treatments From acupuncture to chiropractic, from massage to meditation, alternative treatments are in great demand. That's especially true for people with pain-related illnesses such as fibromyalgia. Alternative medicine, including herbal therapy and homeopathy, is a form of "drug-free" doctoring that views the mind and body as a fully integrated system. For people with fibromyalgia, some alternative treatments work well. That's because holistic therapies influence your total being. In that way, they may allow you to reduce your medications and increase your normal activities. Study findings show that standard acupuncture may be effective in treating some people with fibromyalgia. Both biofeedback and electroacupuncture have also been used for relief of fibromyalgia symptoms. However, before you try alternative treatments, talk with your doctor. Check to see what limitations might apply to you. Working with your doctor, you can find an acceptable way to blend conventional medicine with alternative treatments or natural remedies. When you do, you may be able to increase restful sleep and reduce your fibromyalgia pain. Can acupuncture treat fibromyalgia? With acupuncture, a practitioner inserts one or more dry needles into the skin and underlying tissues at specific points. Gently twisting or otherwise manipulating the needles causes a measurable release of endorphins into the bloodstream. Endorphins are the body's natural opioids. In addition, according to acupuncture practitioners, energy blocks are removed. Removing them is said to restore the flow of energy along the meridians, which are specific energy channels. Studies show that acupuncture may alter brain chemistry. It appears to do this by changing the release of neurotransmitters. These neurotransmitters stimulate or inhibit nerve impulses in the brain that relay information about external stimuli and sensations such as pain. In this way, the patient's pain tolerance is increased. One acupuncture treatment in some patients may last weeks to help alleviate chronic pain. What is electroacupuncture? Electroacupuncture is another way of stimulating the acupuncture points. It uses a needle hooked up to small wires connected to very slight electrical currents. Heat - moxibustion -- and massage - acupressure -- can also be used during this electroacupuncture process. Laser acupuncture is yet another offshoot of this alternative therapy. It may occasionally be effective for the treatment of carpal tunnel syndrome. While it uses the same points, there are no needles involved. There are precautions to take if you want to try acupuncture. First, make sure you find a licensed acupuncturist who has a lot of experience. Also, make sure the acupuncturist uses only disposable needles. There are multiple styles of acupuncture. The style used depends on where the practitioner studied. For instance, Chinese acupuncture depends on larger bore needles and the practitioner may be more aggressive with moving them. Japanese acupuncture uses thinner bore needles with a relatively gentle approach. You'll need to find the style that suits your fibromyalgia needs. My link Marijuana Ingredient May Cut Fibromyalgia Pain Preliminary Study Shows Less Pain, Better Quality of Life in Fibromyalgia Patients Taking Nabilone By Miranda Hitti WebMD Health NewsReviewed by Brunilda Nazario, MDFeb. 19, 2008 -- Nabilone, a pain drug based on marijuana's active ingredient, may ease fibromyalgia pain. So say Canadian researchers, based on a preliminary, short-term study. The study included 40 fibromyalgia patients. First, they did three things: Rate the intensity of their fibromyalgia pain. The rating scale ranged from 0 (no pain) to 10 (the worst pain imaginable). Their average rating was about 6. Rate their quality of life. The rating scale ranged from 0 to 100, with higher scores indicating worse quality of life. Their average rating was 66. Get a check of their tender points -- parts of the body that are often sensitive in fibromyalgia patients. The researchers then split the patients into two groups. For a month, one group of patients took nabilone daily. The other group took a placebo pill. The patients didn't know which pill they were taking. After a month of nabilone treatment, fibromyalgia pain was less intense and quality of life had improved. No such changes were seen with the placebo. Nabilone treatment didn't affect the patients' number of tender points. And it didn't cure fibromyalgia pain -- when patients stopped taking nabilone, their fibromyalgia pain returned to its former intensity. Nabilone was well tolerated, but side effects were more commonly reported in the nabilone group. Those side effects -- which included drowsiness, dry mouth, vertigo, and movement problems -- were "generally mild," write the researchers. Longer studies are needed to track the long-term effects, note the University of Manitoba's Ryan Quinlan Skrabek, MD, and colleagues. Their study appears in the February edition of The Journal of Pain. source: http://www.webmd.com/fibromyalgia/news/200...?src=RSS_PUBLIC Pot Drug May Cut Fibromyalgia Pain Preliminary Study Shows Less Pain, Better Quality of Life in Fibromyalgia Patients Taking Nabilone By Miranda Hitti WebMD Health News Reviewed By Brunilda Nazario, MD Feb. 19, 2008 -- Nabilone, a pain drug based on marijuana's active ingredient, may ease fibromyalgia pain. So say Canadian researchers, based on a preliminary, short-term study. The study included 40 fibromyalgia patients. First, they did three things: Rate the intensity of their fibromyalgia pain. The rating scale ranged from 0 (no pain) to 10 (the worst pain imaginable). Their average rating was about 6. Rate their quality of life. The rating scale ranged from 0 to 100, with higher scores indicating worse quality of life. Their average rating was 66. Get a check of their tender points -- parts of the body that are often sensitive in fibromyalgia patients. The researchers then split the patients into two groups. For a month, one group of patients took nabilone daily. The other group took a placebo pill. The patients didn't know which pill they were taking. After a month of nabilone treatment, fibromyalgia pain was less intense and quality of life had improved. No such changes were seen with the placebo. Nabilone treatment didn't affect the patients' number of tender points. And it didn't cure fibromyalgia pain -- when patients stopped taking nabilone, their fibromyalgia pain returned to its former intensity. Nabilone was well tolerated, but side effects were more commonly reported in the nabilone group. Those side effects -- which included drowsiness, dry mouth, vertigo, and movement problems -- were "generally mild," write the researchers. Longer studies are needed to track the long-term effects, note the University of Manitoba's Ryan Quinlan Skrabek, MD, and colleagues. Their study appears in the February edition of The Journal of Pain. SOURCES: Skrabek, R. The Journal of Pain, February 2008; vol 9: pp 164-173. © 2008 WebMD Inc. All rights reserved. source: http://www.rxlist.co...rticlekey=87306 Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Russo EB. Source GW Pharmaceuticals, 2235 Wylie Avenue, Missoula, MT 59802, USA. erusso@montanadsl.net Abstract OBJECTIVES: This study examines the concept of clinical endocannabinoid deficiency (CECD), and the prospect that it could underlie the pathophysiology of migraine, fibromyalgia, irritable bowel syndrome, and other functional conditions alleviated by clinical cannabis. METHODS: Available literature was reviewed, and literature searches pursued via the National Library of Medicine database and other resources. RESULTS: Migraine has numerous relationships to endocannabinoid function. Anandamide (AEA) potentiates 5-HT1A and inhibits 5-HT2A receptors supporting therapeutic efficacy in acute and preventive migraine treatment. Cannabinoids also demonstrate dopamine-blocking and anti-inflammatory effects. AEA is tonically active in the periaqueductal gray matter, a migraine generator. THC modulates glutamatergic neurotransmission via NMDA receptors. Fibromyalgia is now conceived as a central sensitization state with secondary hyperalgesia. Cannabinoids have similarly demonstrated the ability to block spinal, peripheral and gastrointestinal mechanisms that promote pain in headache, fibromyalgia, IBS and related disorders. The past and potential clinical utility of cannabis-based medicines in their treatment is discussed, as are further suggestions for experimental investigation of CECD via CSF examination and neuro-imaging. CONCLUSION: Migraine, fibromyalgia, IBS and related conditions display common clinical, biochemical and pathophysiological patterns that suggest an underlying clinical endocannabinoid deficiency that may be suitably treated with cannabinoid medicines. Republished from Neuro Endocrinol Lett. 2004 Feb-Apr;25(1-2):31-9. Fibromyalgia (FM) is a chronic pain syndrome of unknown etiology. The disease is characterized by widespread musculoskeletal pain, fatigue and multiple tender points in the neck, spine, shoulders and hips. An estimated 3 to 6 million Americans are afflicted by fibromyalgia, which is often poorly controlled by standard pain medications. Fibromyalgia patients frequently self-report using cannabis therapeutically to treat symptoms of the disease,[1-2] and physicians – in instances where it is legal for them do so – often recommend the use of cannabis to treat musculoskeletal disorders.[3-4] To date however, there are few clinical trials assessing the use of cannabinoids to treat the disease. Previous clinical and preclinical trials have shown that both naturally occurring and endogenous cannabinoids hold analgesic qualities,[9-12] particularly in the treatment of pain resistant to conventional pain therapies. (Please see the 'Chronic Pain' section of this book for further details.) As a result, some experts have suggested that cannabinoids are potentially applicable for the treatment of chronic pain conditions such as fibromyalgia,[13] and have theorized that the disease may be associated with an underlying clinical deficiency of the endocannabinoid system.[14] REFERENCES [1] Swift et al. 2005. Survey of Australians using cannabis for medical purposes. Harm Reduction Journal 4: 2-18. [2] Ware et al. 2005. The medicinal use of cannabis in the UK: results of a nationwide survey. International Journal of Clinical Practice 59: 291-295. [3] Dale Gieringer. 2001. Medical use of cannabis: experience in California. In: Grotenhermen and Russo (Eds). Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. New York: Haworth Press: 153-170. [4] Gorter et al. 2005. Medical use of cannabis in the Netherlands. Neurology 64: 917-919. [5] Schley et al. 2006. Delta-9-THC based monotherapy in fibromyalgia patients on experimentally induced pain, axon reflex flare, and pain relief. Current Medical Research and Opinion 22: 1269-1276. [6] Skrabek et al. 2008. Nabilone for the treatment of pain in fibromyalgia. The Journal of Pain 9: 164-173. <a href="http://norml.org/library/item/fibromyalgia#b7">[7] Ware et al. 2010. The effects of nabilone on sleep in fibromyalgia: results of a randomized controlled trial. Anesthesia and Analgesia 110: 604-610. [8] Fiz et al. 2011. Cannabis use in patients with fibromyalgia: Effect on symptoms relief and health-related quality of life. PLoS One 6. [9] Burns and Ineck. 2006. Cannabinoid analgesia as a potential new therapeutic option in the treatment of chronic pain. The Annals of Pharmacotherapy 40: 251-260. [10] David Secko. 2005. Analgesia through endogenous cannabinoids. CMAJ 173. [11] Wallace et al. 2007. Dose-dependent effects of smoked cannabis on capsaicin-induced pain and hyperalgesia in healthy volunteers. Anesthesiology 107:785-96. [12] Cox et al. 2007. Synergy between delta9-tetrahydrocannabinol and morphine in the arthritic rat. European Journal of Pharmacology 567: 125-130. [13] Lynch and Campbell. 2011. op. cit. [14] Ethan Russo. 2004. Clinical endocannabinoid deficiency (CECD): Can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Neuroendocrinology Letters 25: 31-39. My link
  2. 10 Health Benefits That Legitimize Legalization source "There are no deaths from cannabis use. Anywhere. You can't find one," said Dr. Lester Grinspoon, professor emeritus at Harvard Medical School. Believe it: In 10,000 years of known use of cannabis, there's never been a single death attributed to marijuana. "I've heard you have to smoke something like 15,000 joints in 20 minutes to get a toxic amount of delta-9 tetrahydrocannibinol," said Dr. Paul Hornby, a biochemist and human pathologist who also happens to be one of the leading authorities on cannabis research. "I challenge anybody to do that." Alzheimer's disease - In 2006, the Scripps Research Institute in California discovered that delta-9-tetrahydrocannabinol (THC), the active ingredient in marijuana, can prevent an enzyme called acetylcholinesterase from accelerating the formation of "Alzheimer's plaques" in the brain, as well as protein clumps that can inhibit cognition and memory, more effectively than commercially marketed drugs. Epilepsy - A study performed by researchers at Virginia Commonwealth University discovered that ingredients found in natural marijuana "play a critical role in controlling spontaneous seizures in epilepsy." Dr. Robert J. DeLorenzo, professor of neurology at the VCU School of Medicine, added that "Although marijuana is illegal in the United States, individuals both here and abroad report that marijuana has been therapeutic for them in the treatment of a variety of ailments, including epilepsy." Multiple sclerosis- It's long been believed that smoking pot helps MS patients, and a study published as recently as May provided yet another clinical trial as evidence of marijuana's impact on multiple sclerosis patients with muscle spasticity. Even though the drug has been known to cause dizziness and fatigue in some users, most MS patients report marijuana not only helps ease the pain in their arms and legs when they painfully contract, but also helps them just "feel good." How many prescription drugs can say their side effects include "happiness"? Hepatitis C - A 2006 study performed by researchers at the University of California at San Francisco found that marijuana helps improve the effectiveness of drug therapy for hepatitis C, an infection that roughly 3 million Americans contract each year. Hepatitis C medications often have severe side effects like loss of appetite, depression, nausea, muscle aches and extreme fatigue. Patients that smoked marijuana every day or two found that not only did they complete the therapy, but that the marijuana even made it more effective in achieving a "sustained virological response," which is the gold standard in therapy, meaning there was no sign of the virus left in their bodies. Cachexia Aids (Hiv) & Aids Wasting Parkinson’S Disease Read more Marijuana: Why Is It Illegal Again? This is too big of a question to answer in just one single article, but looking at cannabis through the lens of its medical properties, there seem to be few, if any, reasons to keep marijuana off the market. It doesn't kill, and while it may not be as effective as other treatments, it doesn't seem to get in the way much. When Mikuriya was asked if there was a product out there today - anything - that has as many benefits as medical marijuana, he said simply: "No." Medical marijuana may be beneficial for everyone's health, but it's not very healthy for the pockets of the pharmaceutical companies. And unfortunately for Americans in need of a cheap, all-natural alternative medicine, the pharmaceutical industry is the biggest industry in America with powerful connections in high places. And they don't like marijuana. At all. "It's unlimited," Hornby said of marijuana. "Grow more, get more medicine. Pharmaceutical companies don't want you growing your own medicine." The idea of legalizing a cheap, all-natural medicine that grows out of the dirt is a threat to the pharmaceutical industry's bottom line.
  3. Started by Desiderata Aug 11 2011 04:42 PM This crazy ride started in October 2000. I had a freak accident at work that compressed my vertebrae, rupturing two discs (L4, L5, S1) and nicked the myelin off of a nerve root near my spine.This set off some muscle spasms that still have not gone away. We tried epidurals, facet blocks, trigger point injections, physical therapy, massage and way too many muscle relaxers and pain meds. The pain not only did not go away, but got worse as time went by. In 2002, after a facet block that nicked the same bare spot on my central wiring, we could not stop the pain and spasms. It was so bad that you could actually see the bruises appearing on my spine and butt cheek. It literally felt like a combination of an axe, a burning knife and vice clenching down on my spine. After a few emergency calls to the neuro/pain doc, and some very powerful pain meds, he finally told my daughter to try whatever we had to help me stop screaming. All she had was some decent weed. She actually asked him if it would be alright. 'Try it', he said, or bring her to the ER for some morphine. A few hits and I felt the calm coming. Then the melting in my lower back. I woke up fourteen hours later with nearly no pain and a dilemma. Do I risk my job and use cannabis for the pain? I couldn't. That's when we decided that a low dose of Oxycontin would help manage the pain so I could continue working. 10mg, twice a day for starters. About a year later, I was up to 30mg, twice a day. In 2005, I was up to 40mg, three times a day. I was a zombie. The pain simply didn't matter. Oh, it was there, but I didn't care. About anything. The dosing fluctuated for a few more years, but never went to zero. In 2008, I had some simple surgery that allowed my doctors to get some pictures. My liver was 250% larger than it should be, inflamed and pale. My doctor confronted me with the issue of my 'alcohol' consumption. Problem is, I don't drink. Let me take that back. I do have a Jameson on the rocks for my birthday! I don't drink a fifth of anything in a day. He was puzzled. I wasn't. I told him it was probably the Oxy, but he offered no help. I even asked if I could be put in rehab just to get off the stuff. No help from my healthcare network. Last spring, the spasms in my lower back got so bad that they tore and locked the hamstring on my left leg. The trip to the ER was interesting. Everybody was ready to help me until I told them I was on Oxy. At first, they were ready to take an x-ray, but after that they tried to tell me to go home and 'dose up'. I pointed out an obvious problem. My leg was LOCKED. Bent at the knee, and would not move, not to mention the pain when we tried. They gave me two doses of Demerol and my leg finally relaxed enough for an x-ray. That was fine. They sent me home with no answers and still in pain. My pain doc put me on some more steroids, this time the daily dose, not the five day. That didn't work, but made me sick as ever. I knew I'd need to nearly overdose on the oxy to get some relief. Or.......smoke myself stupid with the stash I had. It worked. Better than I ever thought it could. I became more intent on finding a way to get the real medicine I needed. While I was doing that, my doctor had more bad news for me. My blood tests showed a severe elevation in my liver enzymes. Again, I thought it was the oxy. After more blood work, one to eliminate the diagnosis of Lupus, my doctor began to realize that I may have MS, especially since I did have an injury to the myelin so close to my spinal cord. This made me more intent on getting what I needed. I was able to get some of what I needed, but it drained my budget and fed the street dealers. That's when I decided to get brave and start my indoor garden. My son, Asuz, aka Ace, got all of that started for me. While waiting for my grow, I was gifted some roots to make balm. That was my first non-smoking experience I had with cannabis. The warmth when applied to my skin was one thing. The sensation that I can only describe as a pure and powerful healing moved deeper and deeper. The day after my first use, I think half of my joints, especially my hips and knees, went back into place. Much of the pain was gone. That was a gift that went beyond the physical. Then I got brave. Really brave for a timid, paranoid pot head. I called Pete. With even more courage, Ace and I went to Pete's in March. I met a man and wife with hearts so full of love, compassion and care that it nearly overwhelmed me. Especially when Punta told me that we'd be making some oil the next day! That was the day that changed so much. Those sweet little brownies transformed me from a painful mess to a kid again, running up and down the stairs with a playful husky! I didn't even realize it until Ace pointed it out. Maybe that was a 'Desi moment', not sure! I was at Pete's house, and well, 'nuf said! I was able to make my own batch of oil soon after that with just trim from our grow. To date, I have not taken an oxycontin since June 13, 2011. I still have three 10mg tabs in my medicine drawer. They are my trophy. I will say that I've been tempted to take one and haven't. Hence, the victory! I have not had a seizure since June 20th. My mind is so much clearer, it actually feels like I have more of my mind back. My skin is clearer, it looks like I've gotten five years back in my face. I'm more coordinated and less clumsy. I don't stutter like I did and I'm less confused. I am having some problems managing the pain, but it's different. I am able to move more, stretch out things that have been tightened for years. That can cause it's own discomfort. I may still be suffering from some withdraw symptoms, since those can last for six months to a year. I still take the anti-seizure medication, but I don't think I need it. I'm tapering off the blood pressure medication, because it can bring my blood pressure down too low. Maybe those will be gone soon, too. All from just a few drops of a perfect medicine. I've conquered one of the ugliest demons in my life. Thank you Cannabis I couldn't have done it without you. Posted 29 March 2012 - 06:46 AM I've had some March Madness here in my corner. Truly testing the power of the plant. On Sunday, the 18th, something started a spasm in my back that seemed to set off every nerve in my spine and literally twist me right round. I ended up in the hospital getting a full body MRI. No news other than my spine won't rest. They sent me home on Altram because I didn't want Oxy. For some reason in the next few days, I started feeling sick, weak, fatigued, but with a few spurts of energy. I was seeing my chiropractors and things started loosening up. Then Thursday, March 22, I woke up coughing up blood. I thought maybe it was from an old tooth extraction I had trouble with all last year, but I don't know. I ended up in the hospital on IV antibiotics and breathing treatments. For four days, they couldn't tell me what was wrong, and my pain got worse and worse. I needed my medicine for that pain, and I had Ace bring it to me. Day two wasn't so bad, but by the next day, just having the oil and balm wasn't enough. Add to that thought that I don't have health insurance and this hospital bill was growing. Like a fool, I signed myself out AMA (Against Medical Advice). They gave me a prescription for the antibiotic and I picked it up and went home. That was Sunday, March 25. It felt great to take a shower, toke a bowl and go to bed. Monday felt like a wonderful day. Back to my canna routine and feeling better. I actually fell asleep without any trouble. However, I woke up to what felt like my jaw exploding. I've felt that before with an abscess, and I'm hoping that's all it is. A good hefty dose of my canna root balm and NN2 calmed the ache. I have to say that this is making me paranoid now, since I've had these crazy symptoms since I've had that full body MRI a week ago. Could that have put my body over the edge? Could there be something that had been masked by the years of Oxy that is just becoming obvious? Right now I'm waiting for my daughter to pick me up to see my primary doc so we can expedite some insurance. I'm terrified. If it wasn't for the extra potent canna root and oil, I would be having a total mental breakdown right now. I am praying that it's just an infection from my teeth, a spasm in my shoulder and a pinched nerve in my lumbar/sacral region, and that I'm just a hypochondriac! I miss you guys, and I hope I'll have more energy to come back to the GP fold and play very soon. I need all the prayers and blessings I can gather right now, and I know I can count on all of you here for that. I'm sorry to drop this like a bomb, but I needed to get this off my mind before my baby girl showed up, and this is the only way I knew I could do it. Because I know I'm putting it in hands that can handle it here. Peace and Healing, Posted 28 September 2011 - 09:59 AM I have a deluge of links here, haven't read them all, but i was running out of room trying to keep up! http://forums.cannab...&Number=1224067 http://www.altmeds.c...bis/description http://www.unodc.org..._1_page003.html http://books.google....oultice&f=false http://books.google....oultice&f=false http://billingsmedic....com/rules.aspx http://www.cannabis.za.net/uses.html Posted 30 August 2011 - 08:37 PM I'm still free of the Oxy. I did find out however, that if I miss taking my oil for even a half day, I can feel it! The temptation to take something stronger is always there, and those three pills will always be there because I won't take them. I've just made another batch of oil, so I should be good for a while. I should set a timer for the Oil like I did for the Oxy! Posted 05 October 2011 - 07:51 AM I'm experimenting today. Since I've gotten low on oil, and I have plenty of root balm, I'm trying the root balm. I just took some at 8:30, so we'll see what happens. Knowing this plant, it can only be goodness! ** It's been about two hours since I ingested the same amount of root balm as I would have oil. I am feeling some pain relief and some muscles relaxing. The biggest thing I've noticed is the way my fatigue seems to be fading. I'll give it another hour and see if I need more. I may not. Update: It's becoming more clear to me that the more I cast off the shame of my past addictions and openly admit to them, the more pride I can take in how I use and share my MMJ. That way, the more others see how I've gotten better, the less they see me as a pot head or a stoner. It's a win, win card for MMJ. I still celebrate the days that have become better. Those that have known me and not seen me for a while are shocked when they do! I'm much more alert, I look better and I can actually carry on an intelligent conversation! I couldn't have done it without cannabis, and I know that because I tried for years. Right now the hardest thing for me to do is come to terms with the limitations I still have. They're in my way, but some are here to stay. However, I will make them as feel as unwelcome as possible! Until then, I'll take the good with the bit of bad, it's much better now that the good is winning. Update: Sent Today, 07:59 PM 10:00 pm It's been nearly a year! Things still hurt, but move much better. I'm standing up straighter, my skin and eyes look alive again, and my mind is open again. Smoking it still seems to work better on seizures, but the oil and balm are priceless in this victory. I'll be back to post more. The lawnmower gave me a workout today! Peace and healing! Desiderata
  4. Gordon Wiltsie / Getty ImagesA compound found in marijuana can treat schizophrenia as effectively as antipsychotic medications, with far fewer side effects, according to a preliminary clinical trial. Researchers led by Markus Leweke of the University of Cologne in Germany studied 39 people with schizophrenia who were hospitalized for a psychotic episode. Nineteen patients were treated with amisulpride, an antipsychotic medication that is not approved in the U.S., but is comparable to other medications that are. The rest of the patients were given cannabidiol (CBD), a substance found in marijuana that is thought to be responsible for some of its mellowing or anxiety-reducing effects. Unlike the main ingredient in marijuana, THC, which can produce psychotic reactions and may worsen schizophrenia, CBD has antipsychotic effects, according to previous research in both animals and humans. Neither the patients nor the scientists knew who was getting which drug. At the end of the four-week trial, both groups showed significant clinical improvement in their schizophrenic symptoms, and there was no difference between those getting CBD or amisulpride. (MORE: The Complex Link Between Marijuana and Schizophrenia) “The results were amazing,” says Daniel Piomelli, professor of pharmacology at the University of California-Irvine and a co-author of the study. “Not only was [CBD] as effective as standard antipsychotics, but it was also essentially free of the typical side effects seen with antipsychotic drugs.” Antipsychotic medications can potentially cause devastating and sometimes permanent movement disorders; they can also reduce users’ motivation and pleasure. The new generation of antipsychotic drugs also often leads to weight gain and can increase diabetes risk. These side effects have long been known to be a major obstacle to treatment. In the German study, published online in March by the journal Translational Psychiatry, weight gain and movement problems were seen in patients taking amisulpride, but not CBD. “These exciting findings should stimulate a great deal of research,” says Dr. John Krystal, chair of psychiatry at Yale University School of Medicine, who was not associated with the research. He notes that CBD not only had fewer side effects, but also seemed to work better on schizophrenia’s so-called “negative symptoms,” which are notoriously hard to treat. Negative symptoms include social withdrawal, blunting of pleasure and lack of motivation, which commonly occur in schizophrenia. Since current antipsychotic medications can themselves cause the same problems, however, it wasn’t clear whether CBD was better than amisulpride at treating these symptoms, or whether CBD simply caused fewer side effects to begin with. (MORE: Stoned Driving Nearly Doubles the Risk of Fatal Car Crash) Nevertheless, the new research helps elucidate the intricate complexities of the brain’s natural cannabinoid system and how CBD may work to alleviate symptoms of schizophrenia. Years ago, Piomelli and his colleagues discovered that people with schizophrenia have elevated levels of anandamide — a neurotransmitter that activates the same receptor activated by THC — in their cerebrospinal fluid, suggesting that they also had higher levels of it in the brain. The difference was huge: anandamide levels were nine times higher in schizophrenic people than in mentally healthy controls, Piomelli says. The researchers theorized that these radically high levels would correlate with hallucinations and delusions: the more anandamide bathing patients’ brains, the worse their disease would be. The thinking was, in essence, that people with schizophrenia are constantly high on their own natural THC. But what the researchers actually found was the opposite. “What you get is not a positive correlation, but a negative one. The higher the levels of anandamide, the lower the symptoms,” Piomelli says. It didn’t seem to make much sense at first, but research in both animals and humans now shows that anandamide is a natural stress reliever and antipsychotic. Piomelli thinks that the high levels seen in people with schizophrenia aren’t the cause of the problem, but the result of the brain’s attempts to solve it. (MORE: Study: Smoking Marijuana Not Linked with Lung Damage) The new study confirmed that as CBD relieved patients’ symptoms, anandamide levels rose in concert. “It looks like anandamide is a signaling molecule that has evolved to help us cope with stress,” Piomelli says. “In the brain, everything it does seems to be related to ways of relieving stress. It can relieve anxiety and reduce the stress response. It is involved in stress-induced analgesia [when you stop feeling pain while fighting or fleeing]. These are all mechanisms to help us prevent [negative outcomes related to stress],” says Piomelli. “If Dr. Piomelli is right, then the brain is exquisitely sensitive to changes in anandamide levels,” says Krystal. This raises another question, however. THC itself mimics anandamide. If high levels of anandamide are helpful for schizophrenia, why does marijuana smoking intensify psychotic states? Here’s where it gets complex. THC mimics not only anandamide, but also another cannabinoid, 2-AG, which fits the same receptors and is far more common. “There is 200 times more 2-AG than anandamide in the brain,” Piomelli says. “At the end of the day, the complexity is such that 2-AG has a whole cluster of effects. Anandamide has completely different effects, sometimes even opposite effects. That is why with THC you get a big mess.” (MORE: Marijuana May Both Trigger and Suppress Psychosis) Complicating matters further, when chronic marijuana smokers build up a tolerance to THC, it may down-regulate the entire system, making it harder for anandamide to have its positive effects. This may be why some studies find that people with schizophrenia who smoke marijuana get worse. So, where does CBD fit in? It doesn’t attach to a receptor like THC, or fool the brain into thinking that it’s getting extra anandamide or 2-AG. “What CBD seems to be doing is preventing anandamide from being destroyed,” says Piomelli. That allows the substance to exert its stress-reducing and antipsychotic effects on the brain longer, without the negative effects of THC. If replicated, the results suggest that CBD may be at least as effective as existing drugs for the treatment of schizophrenia, without the severe side effects that make patients reluctant to take medication. The catch: “The real problem with CBD is that it’s hard to develop for a variety of silly reasons,” says Piomelli. Because it comes from marijuana, there are obvious political issues surrounding its use. Extracting it from the plant is also expensive. But the biggest barrier may be that CBD is a natural compound, and therefore can’t be patented the way new drugs are. That means that despite the possibility that it could outsell their current blockbuster antipsychotic drugs, pharmaceutical companies aren’t likely to develop it — a particularly striking fact when you consider that every major manufacturer of new generation antipsychotics in the U.S. has so far paid out hundreds of millions or billions of dollars in fines for mismarketing these drugs. Yet they still reaped huge profits. (MORE: The Case Against the Ban on ‘Bath Salts’ and Fake Marijuana) Piomelli and others are working to develop synthetic versions of CBD that would avoid such hurdles. “We have one and are hoping to move forward in the near future,” he says. For people with schizophrenia and their families, of course, it is likely to be infuriating that non-scientific issues like marijuana policy and patenting problems could stand in the way of a treatment that could potentially be so restorative. While it’s possible that these study results may not hold up or that researchers could discover problems related to long-term use of CBD, it’s hard to imagine that they could be any worse than what patients already experience. Maia Szalavitz is a health writer for TIME.com. Find her on Twitter at @maiasz. You can also continue the discussion on TIME Healthland’s Facebook page and on Twitter at @TIMEHealthland. Read more: http://healthland.time.com/2012/05/30/marijuana-compound-treats-schizophrenia-with-few-side-effects-clinical-trial/#ixzz1wblOwaHI
  5. 10) MARIJUANA USE HAS NO EFFECT ON MORTALITY: A massive study of California HMO members funded by the National Institute on Drug Abuse (NIDA) found marijuana use caused no significant increase in mortality. Tobacco use was associated with increased risk of death. Sidney, S et al. Marijuana Use and Mortality. Source American Journal of Public Health. Vol. 87 No. 4, April 1997. p. 585-590. Sept. 2002. 9) HEAVY MARIJUANA USE AS A YOUNG ADULT WON’T RUIN YOUR LIFE: Veterans Affairs scientists looked at whether heavy marijuana use as a young adult caused long-term problems later, studying identical twins in which one twin had been a heavy marijuana user for a year or longer but had stopped at least one month before the study, while the second twin had used marijuana no more than five times ever. Marijuana use had no significant impact on physical or mental health care utilization, health-related quality of life, or current socio-demographic characteristics. Source Eisen SE et al. Does Marijuana Use Have Residual Adverse Effects on Self-Reported Health Measures, Socio-Demographics or Quality of Life? A Monozygotic Co-Twin Control Study in Men. Addiction. Vol. 97 No. 9. p.1083-1086. Sept. 1997 8) THE "GATEWAY EFFECT" MAY BE A MIRAGE: Marijuana is often called a "gateway drug" by supporters of prohibition, who point to statistical "associations" indicating that persons who use marijuana are more likely to eventually try hard drugs than those who never use marijuana — implying that marijuana use somehow causes hard drug use. But a model developed by RAND Corp. researcher Andrew Morral demonstrates that these associations can be explained "without requiring a gateway effect." More likely, this federally funded study suggests, some people simply have an underlying propensity to try drugs, and start with what’s most readily available.Source Morral AR, McCaffrey D and Paddock S. Reassessing the Marijuana Gateway Effect. Addiction. December 2002. p. 1493-1504. 7) PROHIBITION DOESN’T WORK (PART I): The White House had the National Research Council examine the data being gathered about drug use and the effects of U.S. drug policies. NRC concluded, "the nation possesses little information about the effectiveness of current drug policy, especially of drug law enforcement." And what data exist show "little apparent relationship between severity of sanctions prescribed for drug use and prevalence or frequency of use." In other words, there is no proof that prohibition — the cornerstone of U.S. drug policy for a century — reduces drug use.Source National Research Council. Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us. National Academy Press, 2001. p. 193. 6) PROHIBITION DOESN’T WORK (PART II: DOES PROHIBITION CAUSE THE "GATEWAY EFFECT"?): U.S. and Dutch researchers, supported in part by NIDA, compared marijuana users in San Francisco, where non-medical use remains illegal, to Amsterdam, where adults may possess and purchase small amounts of marijuana from regulated businesses. Looking at such parameters as frequency and quantity of use and age at onset of use, they found no differences except one: Lifetime use of hard drugs was significantly lower in Amsterdam, with its "tolerant" marijuana policies. For example, lifetime crack cocaine use was 4.5 times higher in San Francisco than Amsterdam.Source Reinarman, C, Cohen, PDA, and Kaal, HL. The Limited Relevance of Drug Policy: Cannabis in Amsterdam and San Francisco. American Journal of Public Health. Vol. 94, No. 5. May 2004. p. 836-842. 5) OOPS, MARIJUANA MAY PREVENT CANCER (PART I): Federal researchers implanted several types of cancer, including leukemia and lung cancers, in mice, then treated them with cannabinoids (unique, active components found in marijuana). THC and other cannabinoids shrank tumors and increased the mice’s lifespans. Source Munson, AE et al. Antineoplastic Activity of Cannabinoids. Journal of the National Cancer Institute. Sept. 1975. p. 597-602. 4) OOPS, MARIJUANA MAY PREVENT CANCER, (PART II): In a 1994 study the government tried to suppress, federal researchers gave mice and rats massive doses of THC, looking for cancers or other signs of toxicity. The rodents given THC lived longer and had fewer cancers, "in a dose-dependent manner" (i.e. the more THC they got, the fewer tumors). Source NTP Technical Report On The Toxicology And Carcinogenesis Studies Of 1-Trans- Delta-9-Tetrahydrocannabinol, CAS No. 1972-08-3, In F344/N Rats And B6C3F(1) Mice, Gavage Studies. See also, "Medical Marijuana: Unpublished Federal Study Found THC-Treated Rats Lived Longer, Had Less Cancer," AIDS Treatment News no. 263, Jan. 17, 1997. 3) OOPS, MARIJUANA MAY PREVENT CANCER (PART III): Researchers at the Kaiser-Permanente HMO, funded by NIDA, followed 65,000 patients for nearly a decade, comparing cancer rates among non-smokers, tobacco smokers, and marijuana smokers. Tobacco smokers had massively higher rates of lung cancer and other cancers. Marijuana smokers who didn’t also use tobacco had no increase in risk of tobacco-related cancers or of cancer risk overall. In fact their rates of lung and most other cancers were slightly lower than non-smokers, though the difference did not reach statistical significance. Source Sidney, S. et al. Marijuana Use and Cancer Incidence (California, United States). Cancer Causes and Control. Vol. 8. Sept. 1997, p. 722-728. 2) OOPS, MARIJUANA MAY PREVENT CANCER (PART IV): Donald Tashkin, a UCLA researcher whose work is funded by NIDA, did a case-control study comparing 1,200 patients with lung, head and neck cancers to a matched group with no cancer. Even the heaviest marijuana smokers had no increased risk of cancer, and had somewhat lower cancer risk than non-smokers (tobacco smokers had a 20-fold increased lung cancer risk). Source Tashkin D. Marijuana Use and Lung Cancer: Results of a Case-Control Study. American Thoracic Society International Conference. May 23, 2006. 1) MARIJUANA DOES HAVE MEDICAL VALUE: In response to passage of California’s medical marijuana law, the White House had the Institute of Medicine (IOM) review the data on marijuana’s medical benefits and risks. The IOM concluded, "Nausea, appetite loss, pain and anxiety are all afflictions of wasting, and all can be mitigated by marijuana." While noting potential risks of smoking, the report added, "we acknowledge that there is no clear alternative for people suffering from chronic conditions that might be relieved by smoking marijuana, such as pain or AIDS wasting." The government’s refusal to acknowledge this finding caused co-author John A. Benson to tell the New York Times that the government "loves to ignore our report … they would rather it never happened." Source Joy, JE, Watson, SJ, and Benson, JA. Marijuana and Medicine: Assessing the Science Base. National Academy Press. 1999. p. 159. See also, Harris, G. FDA Dismisses Medical Benefit From Marijuana. New York Times. Apr. 21, 2006 http://www.freerepub...m/1694937/posts Marijuana cures cancer and many other diseases/disorders http://www.youtube.com/watch?v=har8I0Lqsd4
  6. Fascinating documentary exposes cancer industry's death agenda: Cut Poison Burn (NaturalNews) As free as many Americans might think they are, there are certain glaring aspects of American life for which individuals are not free to make their own choices, and cancer treatment is one of them. In the sobering documentary Cut Poison Burn, filmmaker Wayne Chesler brings to light the sinister nature of the multi-billion dollar cancer industry, its suppression of any real pursuit of a cure, and its stranglehold on medicine that restricts individuals from choosing their own personalized, alternative forms of treatment. Learn more: http://www.naturalnews.com/035926_cancer_industry_poison_documentary.html#ixzz1vWvzbGQr Cancer is big business for drug companies and the federal government Thomas is not the only victim of the cancer industry, of course -- millions of Americans, including many children, have died on the altar of Big Pharma's cancer machine, and many more will follow unless the People wake up and take their freedoms back. And in order to wake people up to the truth, they need to hear and see the truth as it is plainly laid out in films like Cut Poison Burn. Be sure to watch the official trailer for Cut Poison Burn at the following link, where you can also purchase a DVD or downloadable copy of the film: http://cutpoisonburn.com/ Learn more: http://www.naturalnews.com/035926_cancer_industry_poison_documentary.html#ixzz1vWvv0Tqe
  7. A.D.A.M. Medical Encyclopedia. Sciatica Neuropathy - sciatic nerve; Sciatic nerve dysfunctionLast reviewed: June 4, 2011. Sciatica refers to pain, weakness, numbness, or tingling in the leg. It is caused by injury to or pressure on the sciatic nerve. Sciatica is a symptom of another medical problem, not a medical condition on its own. Causes, incidence, and risk factors Sciatica occurs when there is pressure or damage to the sciatic nerve. This nerve starts in the lower spine and runs down the back of each leg. This nerve controls the muscles of the back of the knee and lower leg and provides sensation to the back of the thigh, part of the lower leg, and the sole of the foot. Common causes of sciatica include: Slipped disk Piriformis syndrome (a pain disorder involving the narrow muscle in the buttocks) Pelvic injury or fracture Tumors Symptoms Sciatica pain can vary widely. It may feel like a mild tingling, dull ache, or a burning sensation. In some cases, the pain is severe enough to make a person unable to move. The pain most often occurs on one side. Some people have sharp pain in one part of the leg or hip and numbness in other parts. The pain or numbness may also be felt on the back of the calf or on the sole of the foot. The affected leg may feel weak. The pain often starts slowly. Sciatica pain may get worse: After standing or sitting At night When sneezing, coughing, or laughing When bending backwards or walking more than a few yards, especially if caused by spinal stenosis Signs and tests Treatment Because sciatica is a symptom of another medical condition, the underlying cause should be identified and treated. In some cases, no treatment is required and recovery occurs on its own. Conservative treatment is best in many cases. Your doctor may recommend the following steps to calm your symptoms and reduce inflammation. Apply heat or ice to the painful area. Try ice for the first 48 - 72 hours, then use heat after that. Take over-the-counter pain relievers such as ibuprofen (Advil, Motrin IB) or acetaminophen (Tylenol). Bed rest is not recommended. Reduce your activity for the first couple of days. Then, slowly start your usual activities after that. Avoid heavy lifting or twisting of your back for the first 6 weeks after the pain begins. You should start exercising again after 2-3 weeks. This should include exercises to strengthen your abdomen and improve flexibility of your spine. Complications Spinal stenosis Pseudo-claudication; Central spinal stenosis; Foraminal spinal stenosisLast reviewed: June 4, 2011. Spinal stenosis is narrowing of the spinal column that causes pressure on the spinal cord, or narrowing of the openings (called neural foramina) where spinal nerves leave the spinal column. Causes, incidence, and risk factors Spinal stenosis usually occurs as a person ages and the disks become drier and start to shrink. At the same time, the bones and ligaments of the spine swell or grow larger due to arthritis or long-term swelling (inflammation). Spinal stenosis may also be caused by: Arthritis of the spine, usually in middle-aged or elderly people Bone diseases, such as Paget's disease of bone and achondroplasia Defect or growth in the spine that was present from birth (congenital defect) Herniated or slipped disk, which often happened in the past Injury that causes pressure on the nerve roots or the spinal cord Tumors in the spine Treatment When your back pain does not go away, or it gets more painful at times, learning to take care of your back at home and prevent repeat episodes of your back pain can help you avoid surgery. Your doctor and other health professionals will help you manage your pain and keep you as active as possible. Your doctor may refer you for physical therapy. The physical therapist will help you try to reduce your pain using stretches. The therapist will show you how to do exercises that make your neck muscles stronger. You may also see a massage therapist, and someone who performs acupuncture. Sometimes a few visits will help your back or neck pain. Cold packs and heat therapy may help your pain during flare-ups. A number of different medications can help with your back pain. See also: Medicines for chronic pain A type of talk therapy called cognitive behavioral therapy may be helpful if the pain is having a serious impact on your life. This technique helps you better understand your pain and teaches you how to manage back pain. SURGERY If the pain does not respond to these treatments, or you lose movement or feeling, you may need surgery. Surgery is done to relieve pressure on the nerves or spinal cord. You and your doctor can decide when you need to have surgery for these symptoms. Spinal stenosis symptoms often become worse over time, but this may happen very slowly. People who had long-term back pain before their surgery are likely to still have some pain afterwards. Spinal fusion probably will not take away all the pain and other symptoms. Even when using MRI scans or other tests, it is hard for your surgeon to always predict whether you will improve and how much relief surgery will provide. For more information about how surgery is done and who is most likely to benefit, see also: Foraminotomy Laminectomy Spinal fusion CANNABIS AND TREATMENTS Of course, whenever a physician tells a victim of sciatica to leave the bed occasionally and to move around a bit, that advice does not reduce the victim’s pain. The physician must thus suggest a medication that can cause the inflammation to subside and can reduce the amount of pain suffered by the mildly mobile patient. Medical marijuana appears to “fill the bill” in terms of seeing to the patient’s comfort as he or she passes through the period of “watchful waiting.” In fact, the choices available a victim of sciatica, i.e. either bedrest or watchful waiting point out the absence of a better treatment. In fact, they highlight the advantage linked to medical marijuana. That substance not only causes the pain to subside but helps to prevent the development of depression. That unhealthy mental state can take hold of the mind if a person is allowed to perform only a few restricted activities. Until fifteen years ago, total bed rest was the primary treatment for sciatica. However, a study done more than one decade ago showed that recovery could be achieved through use of a strategy called “watchful waiting.” When a doctor prescribes this approach, he or she calls for a pattern of greatly reduced movement but not continued confinement to a bed. There are numerous studies that researchers and scientists have conducted that have proven data that the properties in medical marijuana are a safe and effective treatment as an anti-inflammatory and to reduce pain, without causing side effects. Marijuana Has Anti-Inflammatory That Won't Get You High Richard A. Lovett for National Geographic News June 24, 2008 A compound in marijuana may be a potent anti-inflammatory agent that won't get people high, scientists say. The finding could be a boon to sufferers of arthritis, cirrhosis, and other diseases. Existing drugs can be less effective for some people and can carry side effects, from stomach ulcers to increased risk of heart attacks. Marijuana supporters have long argued that the plant's active ingredients, known as cannabinoids, are safe and effective treatments for pain, nausea, and other ailments. The most active cannabinoid—delta-9-tetrahydrocannabinol, or THC—is known to have anti-inflammatory properties. But it is also responsible for the plant's psychotropic effects. Now researchers say that another cannabinoid, called beta-caryophyllene, or (E)-BCP, helps combat inflammation without affecting the brain. (E)-BCP is already part of many people's daily diets, the researchers note. Foods that are particularly high in the compound include black pepper, oregano, basil, lime, cinnamon, carrots, and celery. Essential oils from cannabis plants—whose leaves and flowers are used to make the marijuana drug—contain up to 35 percent (E)-BCP. But even after decades of cannabis research, scientists hadn't previously known that the compound had anti-inflammatory properties. "This is because the focus was on the classical cannabinoids [rather than (E)-BCP]," said lead study author Jürg Gertsch of the Swiss Federal Institute of Technology. My link Science Daily ScienceDaily (July 20, 2008) — Cannabis has long been accredited with anti-inflammatory properties. ETH Zurich researchers, however, have now discovered that it is not only the familiar psychoactive substances that are responsible for this; a compound we take in every day in vegetable nutriment also plays a significant role. People not only rate cannabis sativa L. highly because of its intoxicating effects; it has also long been used as a medicinal plant. Although the plant has been scrutinized for years, surprising new aspects keep cropping up. For example, researchers from ETH Zurich and Bonn University examined a component in the plant’s essential oil that until then had largely been ignored and found it to have remarkable phar- macological effects. The findings open up interesting perspectives, especially for the prevention and treatment of inflammations. Completely different molecule structure The hemp plant contains over 450 different substances, only three of which are responsible for its intoxicating effect. They activate the two receptors in the body CB1 and CB2. Whilst the CB1 receptor in the central nervous system influences perception, the CB2 receptor in the tissue plays a crucial role in inhibiting inflammation. If the receptor is activated, the cell releases fewer pro-inflammatory signal substances, or cytokines. The scientists have now discovered that the substance beta-carophyllene, which composes between 12 and 35 percent of the cannabis plant’s essential oil, activates the CB2 receptor selectively. Unlike the three psychoactive substances, however, beta-carophyllene does not latch onto the CB1 receptor and consequently does not trigger the intoxicating effect. “Due to the various effects of cannabis, we had suspected for quite some time that other substances could come into play besides the psychoactive ones”, explains Jürg Gertsch from the Institute of Pharmaceutical Sciences at ETH Zurich. “However, astonishingly we didn’t know what substances these were until now.” more Both the spice, cinnamon and the medicinal herb, cannabis, provide beneficial anti-inflammatory effects. At least some of these healthy effects are from stimulation of the same receptors in your endocannabinoid receptor system. Although useful and beneficial when protecting the body against bacterial intruders and other perils, inflammation becomes a medical problem if it becomes chronic. Diseases ending in “itis,” such as arthritis and gingivitis are just two of dozens of such maladies, laden with toxic effects to the tissues affected and destructive to the body in general. Indeed, chronic inflammation has become a key medical villain in the degenerative diseases that bedevil modern society. Such inflammation is now seen as a generator of atherosclerosis and is a potent cardiovascular risk factor. Cinnamon has long been recognized for health-enhancing properties, including providing anti-inflammatory effects. The spice’s component coumarin, in cinnamomum aromaticum thins the blood. Increasingly, cinnamon appears to be very useful in addressing insulin resistance and diabetes. At least some of the spice’s anti-inflammatory properties come from its another component shared with other spices, beta-caryophyllene. Cloves, black pepper, rosemary, hops and other spices all provide this component of essential oils. For further info contact Skunk pharm Research LLC (tell em Eddie sent ya) Stimulation of cannabinoid receptor 2 (CB2) suppresses microglial activation Background Activated microglial cells have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), multiple sclerosis (MS), and HIV dementia. It is well known that inflammatory mediators such as nitric oxide (NO), cytokines, and chemokines play an important role in microglial cell-associated neuron cell damage. Our previous studies have shown that CD40 signaling is involved in pathological activation of microglial cells. Many data reveal that cannabinoids mediate suppression of inflammation in vitro and in vivo through stimulation of cannabinoid receptor 2 (CB2). Methods In this study, we investigated the effects of a cannabinoid agonist on CD40 expression and function by cultured microglial cells activated by IFN-γ using RT-PCR, Western immunoblotting, flow cytometry, and anti-CB2 small interfering RNA (siRNA) analyses. Furthermore, we examined if the stimulation of CB2 could modulate the capacity of microglial cells to phagocytise Aβ1–42 peptide using a phagocytosis assay. Results We found that the selective stimulation of cannabinoid receptor CB2 by JWH-015 suppressed IFN-γ-induced CD40 expression. In addition, this CB2 agonist markedly inhibited IFN-γ-induced phosphorylation of JAK/STAT1. Further, this stimulation was also able to suppress microglial TNF-α and nitric oxide production induced either by IFN-γ or Aβ peptide challenge in the presence of CD40 ligation. Finally, we showed that CB2 activation by JWH-015 markedly attenuated CD40-mediated inhibition of microglial phagocytosis of Aβ1–42 peptide. Taken together, these results provide mechanistic insight into beneficial effects provided by cannabinoid receptor CB2 modulation in neurodegenerative diseases, particularly AD. more List of abbreviations Aβ : Amyloid-β peptide CD40: CD40 receptor CD40L: CD40 ligand CNS: Central nervous system HIV: Human immunodeficiency virus IFN-γ : Interferon-gamma JAK: Janus kinase MHC II: Major histocompatibility complex II STAT1: Signal transducer and activator of transcription 1 TNF-α : Tumor necrosis factor-alpha
  8. What cannabis actually does to your brain Archaeologists recently found a 2,700-year-old pot stash, so we know humans have been smoking weed for thousands of years. But it was only about 20 years ago that neuroscientists began to understand how it affects our brains. Meet the cannabinoid receptor In the 1980s and 90s, researchers identified cannabinoid receptors, long, ropy proteins that weave themselves into the surfaces of our cells and process THC. They also process other chemicals, many of them naturally occurring in our bodies. Once we'd discovered these receptors, we knew exactly where THC was being processed in our bodies and brains, as well as what physical systems it was affecting. My link A bit of the old timey wimey Cannabis also distorts your sense of time. THC affects your brain's dopamine system, creating a stimulant effect. People who are stoned often report feeling excited, anxious, or energetic as a result. Like other stimulants, this affects people's sense of time. Things seem to pass quickly because the brain's clock is sped up. At the same time, as we discussed earlier (if you can remember), the drug slows down your ability to remember things. That's because it interferes with the brain's acetylcholine system, which is part of what helps you store those memories in your hippocampus. You can see that system's pathway through the brain in red in the illustration at left. In an article io9 published last year about the neuroscience of time, we noted:
  9. Pharmaceutical Drugs Based on Cannabis Pharmaceutical drugs have been developed which either contain or have similar chemicals as those found in the marijuana (cannabis) plant. Some researchers have used their understanding of how the brain processes cannabinoids to develop drugs which follow the same pathways but work differently than marijuana. Pharmaceutical drugs based on marijuana are divided into four categories and listed below with the names, trade names, manufacturers, approval status, suggested medical use and cannabis-related properties. All drugs referenced are in pill form unless otherwise noted. Approved and launched in the UK on June 21, 2010, making it the first cannabis-based prescription medicine in the world. Licensed to Bayer in the UK and to Almirall in Europe. Approved to treat spasticity caused by multiple sclerosis in Spain (July 28, 2010), Canada (Aug. 31, 2010), Czech Republic (Apr. 15, 2011), Denmark (June 8, 2011), Germany (July 4, 2011), Sweden (Dec. 22, 2011), and Austria (Feb. 7, 2012). In the US, Phase III clinical trials started in late 2006 for treatment of pain in cancer patients. On Apr. 20, 2011, a US patent was granted for Sativex in cancer pain. GW Pharmaceuticals stated in a July 28, 2010 press release (700 KB) that it expects Sativex to be approved in other European countries (including France and Italy) in 2011. My link
  10. Psychological Conditions Questions: Does marijuana use cause lasting schizophrenia, psychosis, or other mental disorders? Is medical marijuana an effective treatment for depression, bipolar disorders, anxiety, and similar mood disorders? Does marijuana cause depression or other mood disorders? John McGrath, MBBS, MD, PhD, Psychiatrist at the Queensland Centre for Mental Health Research, et al., stated the following in their May 2010 article titled "Association Between Cannabis Use and Psychosis-Related Outcomes Using Sibling Pair Analysis in a Cohort of Young Adults," published in Archives of General Psychiatry: "Longer duration since first cannabis use was associated with multiple psychosis-related outcomes in young adults... the longer the duration since first cannabis use, the higher the risk of psychosis-related outcomes... Compared with those who had never used cannabis, young adults who had 6 or more years since first use of cannabis (i.e., who commenced use when around 15 years or younger) were twice as likely to develop a noneffective psychosis... This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults." Cannabis and mental health Addictions: your views wanted: We are interested in finding out if patients being treated for drug and/or alcohol problems have experienced any changes in their treatment in the past year. About this leaflet Two million people in the UK smoke cannabis. Half of all 16 to 29 year olds have tried it at least once. In spite of government warnings about health risks, many people see it as a harmless substance that helps you to relax and ‘chill’ – a drug that, unlike alcohol and cigarettes, might even be good for your physical and mental health. On the other hand, recent research has suggested that it can be a major cause of psychotic illnesses in those who are genetically vulnerable. This leaflet looks at the research on the effects of cannabis use and mental health and is for anyone who is concerned about the issue. We hope that this will help people to make informed choices about using – or not using – cannabis. What is cannabis? Cannabis sativa and cannabis indica are members of the nettle family that have grown wild throughout the world for centuries. Both plants have been used for a variety of purposes including hemp to make rope and textiles, as a medical herb and as the popular recreational drug. The plant is used as: The resin – a brown/black lump, known as bhang, ganja, hashish, resin etc; Herbal cannabis – made up of the dried flowering tops and variable amounts of dried leaves - known as grass, marijuana, spliff, weed etc. Skunk refers to a range of stronger types of cannabis, grown for their higher concentration of active substances. The name refers to the pungent smell they give off while growing. They can be grown either under grow-lights or in a greenhouse, often using hydroponic (growing in nutrient rich liquids rather than soil) techniques. There are hundreds of other varieties of cannabis with exotic names such as AK-47 or Destroyer. Street cannabis can come in a wide variety of strengths, so it is often not possible to judge exactly what is being used in any one particular session. How is it used? Most commonly, the resin or the dried leaves are mixed with tobacco and smoked as a ‘spliff’ or ‘joint’. The smoke is inhaled strongly and held in the lungs for a number of seconds. It can also be smoked in a pipe, a water pipe, or collected in a container before inhaling it - a 'bucket'. It can be brewed as tea or cooked in cakes. More than half of its psychologically active chemical ingredients are absorbed into the blood when smoked. These compounds tend to build up in fatty tissues throughout the body, so it takes a long time to be excreted in the urine. This is why cannabis can be detected in urine up to 56 days after it has last been used. My link Andrew Johns, MB, Consultant in Forensic Psychiatry at the Maudsley Hospital in London, noted in a Feb. 2001 article, "Psychiatric Effects of Cannabis," published in the British Journal of Psychiatry: "There is good evidence that taking cannabis leads to acute adverse mental effects in a high proportion of regular users. Many of these effects are dose-related, but adverse symptoms may be aggravated by constitutional factors including youthfulness, personality attributes and vulnerability to serious mental illness.... An appreciable proportion of cannabis users report short-lived adverse effects, including psychotic states following heavy consumption, and regular users are at risk of dependence... The untoward mental effects of cannabis may be classified: Psychological responses such as panic, anxiety, depression or psychosis. These effects may be described as 'toxic' in that they generally relate to excess consumption of the drug. Effects of cannabis on ore-existing mental illness and cannabis as a risk-factor for mental illness. Dependency or withdrawal effects." Paul Armentano, Senior Policy Analyst at the National Organization for the Reform of Marijuana Laws (NORML), stated in an Aug. 2, 2007 press release titled "NORML Responds to New Rash of Pot and Mental Health Claims": "Despite the enormous popularity of cannabis in the 1960s and 1970s in numerous Western cultures, rates of psychotic disorders haven't increased since then in any of these societies. Individuals suffering from mental illness such as schizophrenia tend to use all intoxicants - particularly alcohol and tobacco - at greater rates than the general population. Not surprisingly, many of these individuals also use cannabis." Aug. 2, 2007 - Paul Armentano What are its effects? My link Pleasant A ‘high’ - a sense of relaxation, happiness, sleepiness, colours appear more intense, music sounds better. Unpleasant Around 1 in 10 cannabis users have unpleasant experiences, including confusion, hallucinations, anxiety and paranoia. The same person may have either pleasant or unpleasant effects depending on their mood and circumstances. These feelings are usually only temporary – although as the drug can stay in the system for some weeks, the effect can be more long-lasting than users realise. Long-term use can have a depressant effect, reducing motivation. Education and learning There have also been suggestions that cannabis may interfere with a person's capacity to: concentrate organise information use information This effect seems to last several weeks after use, which can cause particular problems for students. However, a large study in New Zealand followed up 1265 children for 25 years. It found that cannabis use in adolescence was linked to poor school performance, but that there was no direct connection between the two. It looked as though it was simply because cannabis use encouraged a way of life that didn't help with schoolwork. Work It seems to have a similar effect on people at work. There is no evidence that cannabis causes specific health hazards. But users are more likely to leave work without permission, spend work time on personal matters or simply daydream. Cannabis users themselves report that drug use has interfered with their work and social life. Of course, some areas of work are more demanding than others. A review of the research on the effect of cannabis on pilots revealed that those who had used cannabis made far more mistakes, both major and minor, than when they had not smoked cannabis. As you can imagine, the pilots were tested in flight simulators, not actually flying... The worst effects were in the first four hours, although they persisted for at least 24 hours, even when the pilot had no sense at all of being 'high'. It concluded "Most of us, with this evidence, would not want to fly with a pilot who had smoked cannabis within the last day or so". What about driving? In New Zealand, researchers found that those who smoked regularly, and had smoked before driving, were more likely to be injured in a car crash. A recent study in France looked at over 10,000 drivers who were involved in fatal car crashes. Even when the influence of alcohol was taken into account, cannabis users were more than twice as likely to be the cause of a fatal crash than to be one of the victims. So - perhaps most of us would also not want to be driven by somebody who had smoked cannabis in the last day or so. Mental health problems There is growing evidence that people with serious mental illness, including depression and psychosis, are more likely to use cannabis or have used it for long periods of time in the past. Regular use of the drug has appeared to double the risk of developing a psychotic episode or long-term schizophrenia. However, does cannabis cause depression and schizophrenia or do people with these disorders use it as a medication? Over the past few years, research has strongly suggested that there is a clear link between early cannabis use and later mental health problems in those with a genetic vulnerability - and that there is a particular issue with the use of cannabis by adolescents. Depression A study following 1600 Australian school-children, aged 14 to 15 for seven years, found that while children who use cannabis regularly have a significantly higher risk of depression, the opposite was not the case - children who already suffered from depression were not more likely than anyone else to use cannabis. However, adolescents who used cannabis daily were five times more likely to develop depression and anxiety in later life. Schizophrenia Three major studies followed large numbers of people over several years, and showed that those people who use cannabis have a higher than average risk of developing schizophrenia. If you start smoking it before the age of 15, you are 4 times more likely to develop a psychotic disorder by the time you are 26. They found no evidence of self-medication. It seemed that, the more cannabis someone used, the more likely they were to develop symptoms. Why should teenagers be particularly vulnerable to the use of cannabis? No one knows for certain, but it may be something to do with brain development. The brain is still developing in the teenage years – up to the age of around 20, in fact. A massive process of ‘neural pruning’ is going on. This is rather like streamlining a tangled jumble of circuits so they can work more effectively. Any experience, or substance, that affects this process has the potential to produce long-term psychological effects. Recent research in Europe, and in the UK, has suggested that people who have a family background of mental illness – and so probably have a genetic vulnerability anyway - are more likely to develop schizophrenia if they use cannabis as well. Physical health problems The main risk to physical health from cannabis is probably from the tobacco that is is often smoked with. Is there such a thing as ‘cannabis psychosis’? Recent research in Denmark suggests that yes, there is. It is a short-lived psychotic disorder that seems to be brought on by cannabis use but which subsides fairly quickly once the individual has stopped using it. It's quite unusual though – in the whole of Denmark they found only around 100 new cases per year. However, they also found that: Three quarters had a different psychotic disorder diagnosed within the next year. Nearly half still had a psychotic disorder 3 years later. So, it also seems probable that nearly half of those diagnosed as having cannabis psychosis are actually showing the first signs of a more long-lasting psychotic disorder, such as schizophrenia. It may be this group of people who are particularly vulnerable to the effects of cannabis, and so should probably avoid it in the future. Is cannabis addictive? It has some of the features of addictive drugs such as: tolerance – having to take more and more to get the same effect withdrawal symptoms. These have been shown in heavy users and include: - craving - decreased appetite - sleep difficulty - weight loss - aggression and/or anger - irritability - restlessness - strange dreams. These symptoms of withdrawal produce about the same amount of discomfort as withdrawing from tobacco. For regular, long-term users: 3 out of 4 experience cravings; half become irritable; 7 out of 10 switch to tobacco in an attempt to stay off cannabis. The irritability, anxiety and problems with sleeping usually appear 10 hours after the last joint, and peak at around one week after the last use of the drug. The Institute of Medicine published in its Mar. 1999 report titled "Marijuana and Medicine: Assessing the Science Base": "Although euphoria is the more common reaction to smoking marijuana, adverse mood reactions can occur. Such reactions occur most frequently in inexperienced users after large doses of smoked or oral marijuana. They usually disappear within hours and respond well to reassurance and a supportive environment." Compulsive use The user feels they have to have it and spends much of their life seeking, buying and using it. They cannot stop even when other important parts of their life (family, school, work) suffer. You are most likely to become dependent on cannabis if you use it every day. Where can I get more help and information? Talk to Frank is an excellent website. You can order free information leaflets for different age groups, read real life stories of other people's experience with drugs and get reliable, factual information. Helpline: 0800 77 66 00 Use the search facility to get the contact details of organisations offering practical help and support in your area. Film Exchange on Alcohol and Drugs (FEAD): an online resource from leading figures in the alcohol and drugs field. References Reclassification of cannabis Further consideration of the classification of cannabis under the Misuse of Drugs Act 1971 (2005) Advisory Council on the Misuse of Drugs. Home Office: London. Cannabis use and mental health in young people: cohort study (2002) George C Patton et al. British Medical Journal, 325:1195-1198. Cannabis and educational achievement (2003) Fergusson DM, Horwood LJ & Beautrais AL. Addiction 98(12):1681-92. Cannabinoids and the human uterus during pregnancy (2004) Dennedy MC et al. American Journal of Obstetrics and Gynaecology. 190(1), 2–9. Bandolier: <a href="http://www.medicine..../cannfly.html"> Cannabis and flying Cannabis intoxication and fatal road crashes in France: population based case control study (2005) Laumon B et al. British Medical Journal, 331, 1371-1377. Marijuana abstinence effects in marijuana smokers maintained in their home environment (2001) Budney AJ et al. Archives of General Psychiatry, 58, 917-924. Marijuana use and car crash injury (2005) Blows S et al. Addiction, 100, 5, 605. Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study (2002) Zammit S, Allebeck P, Andreasson S, Lundberg I, Lewis G. British Medical Journal 2002; 325: 1199-1201. Cannabis use and psychosis: A longitudinal population-based study (2002) Van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. American Journal of Epidemiology; 156: 319-327. Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study (2002) Arseneault L, Cannon M, Poulton R, Murray R, Caspi A, Moffit TE. British Medical Journal; 325: 1212-1213. Cannabis use and mental health in young people: cohort study (2002) Patton GC, Coffey C, Carlin JB, Degenhardt L, Lynskey M, Hall W. British Medical Journal; 325: 1195-1198. A longitudinal study of cannabis use and mental health from adolescence to early adulthood (2000) McGee R, Williams S, Poulton R, Moffitt T. Addiction; 95: 491-503 Mental health of teenagers who use cannabis (2002) Rey JM et al. British Journal of Psychiatry, 180, 216-221. Prospective cohort study of cannabis use, predisposition for psychosis and psychotic symptoms in young people. Henquet C et al British Medical Journal, 330, 11-14. Tests of causal linkages between cannabis use and psychotic symptoms (2005) Fergusson DM, Horwood LJ and Ridder EM Addiction, 100 (3). Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders: follow-up study of 535 incident cases (2005) Arendt M et al British Journal of Psychiatry, 187: 510 - 515.
  11. Hepatitis C Is marijuana an effective treatment for the symptoms of hepatitis C? General Reference (not clearly pro or con) The US National Institute of Health stated on its website (accessed Sep. 29, 2006): "Hepatitis C is an inflammation of the liver caused by infection with the hepatitis C virus (HCV).[...] There are approximately 4 million people in the United States who are infected with hepatitis C (about 1 in 70 to 100 people). Other hepatitis virus infections include hepatitis A and hepatitis B. Each viral hepatitis infection is caused by a different virus. Many people who are infected with the hepatitis C do not have symptoms. Hepatitis C is often detected during blood tests for a routine physical or other medical procedure. If the infection has been present for many years, the liver may be permanently scarred -- a condition called cirrhosis. In many cases, there may be no symptoms of the disease until cirrhosis has developed. The following symptoms could occur with hepatitis C infection: Jaundice, Abdominal pain (right upper abdomen), Fatigue, Loss of appetite, Nausea, Vomiting, Low-grade fever, Pale or clay-colored stools, Dark urine, Generalized itching, Ascites, Bleeding varices (dilated veins in the esophagus)." More on Pro's and Con's PRO (yes) CON (no) Diana L. Sylvestre, MD, Assistant Clinical Professor in the Department of Medicine at the University of California, San Francisco, et al. stated in the Oct. 2006 article "Cannabis Use Improves Retention and Virological Outcomes in Patients Treated for Hepatitis C," published in the European Journal of Gastroenterology & Hepatology: "Our results suggest that modest cannabis use may offer symptomatic and virological benefit to some patients undergoing HCV treatment by helping them maintain adherence to the challenging medication regimen." More Medical Marijuana and Hepatitis C What Is Hepatitis C ? Hepatitis C is an often chronic infection of the liver caused by the hepatitis C virus (HCV), which can result in cirrhosis of the liver. Hepatitus C is responsible for most of the liver transplants conducted each year. Medical Marijuana and Hepatitis C Hepatitis C is a liver disease that affects 300 million people worldwide. Based on current statistics for hepatitis C, it is estimated that 8,000 to 10,000 people die each year from chronic liver disease caused by this condition. Hepatitis C is typically treated with interferon medication, but many patients are unable to complete the full treatment regimen due to the severe side effects it can induce, such as fatigue, insomnia, loss of appetite, nausea, muscle and joint pain, and depression. Because of these side effects, many patients are forced to reduce their doses or discontinue treatment altogether—both of which deter interferon’s effectiveness against the Hepatitis C virus. There is strong scientific and anecdotal evidence that medical marijuana is a safe, effective medicine that helps patients with Hepatitis C endure the side effects of treatment—thereby helping patients complete the full treatment regimen. Many marijuana states include Hepatitis C on their list of qualifying conditions. Additionally, marijuana side effects are typically mild and are classified as "low risk," with euphoric mood changes among the most frequent side effects. Hepatitis C - The Silent Killer Can Medical Cannabis Help? Jay R. Cavanaugh, PhD Hepatitis C (HCV) is a blood borne pathogen that presently infects some four to eight million Americans making it the leading blood borne virus in America. HCV is the primary cause of liver cancer and cirrhosis and kills over 10,000 Americans each year. Hepatitis C is the leading factor in patients who require liver transplant. Some 80% of those who contract HCV will go on to develop chronic infection and 20% of these will develop cirrhosis, liver cancer, or liver failure. A slim 20% of those infected will eliminate the virus from their body on their own. Patients can contract Hepatitis C from using shared needles, accidental needle stick injuries, blood transfusions (prior to 1990), and to a minor degree from unprotected sex. HCV can be transmitted from an infected tattoo needle, dental instruments, or tools used in commercial nail care. Anything that assists the transfer of HCV infected blood from one person to another can be a vector. The blood of a patient with HCV can be highly contagious and precautions should be taken to not come in contact with it. Hepatitis C usually produces no early symptoms. The disease can go unrecognized for decades. This is why HCV is termed a "silent killer". During the decades of quiescence the virus can continue to slowly destroy liver cells without the patient having any idea this is happening. The following groups are considered "high risk" and should be tested for the virus: IV drug users who have shared needles Sexual partners of HCV patients Family members of HCV patients Individuals receiving a blood transfusion prior to 1990 Patients who undergo dialysis Individuals with tattoos or who have their nails frequently done Individuals who have suffered a needle stick incident Patients who have been diagnosed with any liver disease Symptoms: While patients are generally unaware of HCV infection for many years, some 80% may eventually develop symptoms which can include: Fatigue and malaise Loss of appetite Weight loss Jaundice Joint pain and headache Fluid retention in the abdomen (ascites) Nausea and vomiting Itching Diagnosis: Diagnosis begins with a simple history and blood test. The history looks at risk factors and symptoms. The blood test is generally to measure both liver enzymes (produced when the liver is damaged) and to detect antibodies to the Hepatitis C virus and/or to quantify the amount of virus present in the blood stream. The amount of virus is called the "titer" and is determined using the polymerase chain reaction (PCR) with HCV "primers". Additional blood tests can determine the specific strain of virus present (some strains are more pathogenic than others). A physical examination will be conducted that includes probing the liver for enlargement and looking for other possible factors such as swelling in the legs and feet and jaundice. Prior to the initiation of treatment, it is common practice to conduct additional tests to more closely ascertain the status of the liver and the need for treatment. A liver scan using radioactive isotopes and X-ray can highlight liver structures and blood flow. A CAT scan may be conducted to look for tumors or blockage. The definitive diagnostic procedure is a liver biopsy where small samples of the liver are extracted through an office surgical procedure and examined for pathology. A liver biopsy taken from different quadrants of the liver can reveal hepatocarcinoma (liver cancer), fatty deposits, and cirrhosis (scarring). Why is the liver important? The liver is the largest internal organ. It is within the liver that medications and toxins are neutralized, metabolized, and eliminated (with the help of the kidneys). The liver is the site of sugar storage (glycogen) and plays a vital role in maintaining normal blood sugar along with the pancreas. The body’s fluid balance and blood clotting are largely controlled by the liver as is the processing of proteins. Bile produced in the liver aides in the digestion of food. Most noticeable is the role of the liver in energy production which is why fatigue is so common in liver disease. Treatment for Hepatitis C: Current therapy focuses on the subcutaneous administration of a combination of Interferon alpha (an immunomodulator) and the anti-viral drug Ribavirin. Depending upon the type of Interferon used, dosing can be one to three times a week for six to 18 months. Approximately 50% of those treated respond although it is not yet known how long the response might last. Combination drug therapy is usually not attempted when there is no sign of liver damage as determined by histopathology following biopsy. Drug therapy is also contraindicated when patients have long standing problems with depression or heart disease. The major side effects of the therapy include flu like symptoms, joint pain, nausea, anemia and depression. The decision to undergo combination therapy is a very serious one and should be done only under the supervision of a qualified and experienced physician. HCV patients with liver impairment must avoid hepatotoxins, particularly alcohol and acetaminophen (Tylenol). Alcohol is a key toxin that damages the liver. Normal healthy adults are advised to drink no more than two drinks a day for men and one for women. With liver disease that recommendation drops to zero. Yet, many in the general population and the HCV population are heavy drinkers. Cannabis can be an effective harm reduction agent for those with alcohol problems along with therapy and self help. Long term Complications of Hepatitis C: Cirrhosis - As liver cells are destroyed by virally induced inflammation, they can be replaced by scar tissue (hence the name) which does not function to conduct normal liver functions. Cirrhosis is chronic and progressive. Cirrhosis occurs in approximately 20% of all HCV cases and may lead to cancer. The course of cirrhosis is variable but usually includes fluid build up in the abdomen (ascites), portal hypertension, and esophageal varices (swollen blood vessels). Treatment is limited to alleviating symptoms. Fluid may be periodically drained and medicines provided to reduce hypertension and fluid imbalances. Cirrhosis can cause uncontrolled bleeding, coma, and death. Hepatocellular carcinoma (liver cancer) - Constant cell death and division caused by HCV can lead to tumors in 1-5% of all patients. Liver cancer is curable only in its earliest stages if it is contained within the liver in an area approachable by surgery. In other cases various treatments can be used including cryotherapy (freezing) and ethanol ablation. Chemotherapy, at present, is not usually effective with liver tumor. Liver cancer is generally terminal with treatment limited to symptomatic relief and improving the quality and length of life. Liver failure and transplantation - As HCV destroys liver tissue; liver function can be increasingly compromised leading to failure. As the liver fails toxins can circulate that harm other organs and effect perception and behavior. Medications are not metabolized normally and have an increased risk of side effects and adverse reaction. Essential clotting factors may not be produced leading to uncontrolled internal bleeding. Complete failure results in coma and death. Patients with cirrhosis, cancer, and/or liver failure can sometimes be helped by a liver transplant. Hard to come by, transplants are usually restricted to those cases where they may materially help. Patients who continue to abuse alcohol or drugs are often excluded from transplant waiting lists as are those whose cancer has spread beyond the liver. Others excluded are surgical risks (usually those with cardiac disease) and those with compromised immune systems. Patients survive transplantation in nearly 80% of trials although continued use of immunosuppressants is needed. Can medical cannabis help? The short answer is yes. The primary role of cannabis is to stimulate appetite, reduce nausea and vomiting, and treat joint pain. This role is applicable to HCV patients undergoing chemotherapy, those with cancer or cirrhosis, and those with joint pain and headache. Cannabis is far less toxic than other medications that might be prescribed for these conditions and where liver impairment is concerned, it is vital to avoid toxicity. Cannabis may help alleviate the depression often produced by chronic illness and by combination drug therapy. Additionally, cannabis based food products may provide needed extra nutrition without taxing the liver. Using cannabis in place of alcohol is an established harm reduction technique particularly important when liver disease is present. Perhaps more important but still unknown is the possibility that some of the chemical components of cannabis (the Cannabinoids) may actually reduce liver inflammation and slow the progression of both cirrhosis and Hepatocellular carcinoma. The cannabinoids have been shown to be powerful anti-inflammatories and anti-oxidants. They have also been shown to have anti-neoplastic activity, at least in gliomas (a form of brain cancer). Cannabinoids both slow programmed cell death (apoptosis) in normal cells while accelerating apoptosis in cancer cells. Since cannabis is nontoxic it might as well be tried, particularly in patients who have chronic progressive disease that is likely to result in death. It is important to point out that whole cannabis (whether smoked, vaporized, elixir, or in food products) is preferable to Marinol. The prescription drug Marinol contains only one cannabinoid (THC) and lacks the other healing properties of the whole herb and its extracts. Dosing is up to the physician and patient. Usually patients "self-titrate" or use only what they feel they need for symptomatic relief. This may be a mistake as the protective effects of cannabis are best achieved with a steady state minimal blood level of Cannabinoids. It is recommended that a base line level of Cannabinoids be maintained with regular doses of oral cannabis products and the smoked or vaporized form of cannabis used for acute symptomatic relief. source: http://www.letfreedo...hepatitis_c.htm (Marijuana/Hash) Endocannabinoids and liver disease - review Liver International Volume 25 Issue 5 Page 921 - October 2005 Ezra Gabbay1,2, Yosefa Avraham1, Yaron Ilan2, Eran Israeli and Elliot M. Berry1 1Department of Metabolism and Human Nutrition, Hadassah-Hebrew University Medical School, 2The Liver Unit, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Abstract: Aims: Endocannabinoids are endogenous compounds that bind to the same receptors as tetrahydrocannabinol, the active component in marijuana and hashish. They have been found to have many physiological and patho-physiological functions, including mood alteration, control of feeding and appetite, motor and co-ordination activities, analgesia, immune modulation and gut motility. In this review we aim to elucidate current knowledge as to their role in liver physiology and disease. Methods: The major findings published to date concerning endocannabinoids and liver disease are described, and their implications with regard to understanding disease mechanisms, and the development of new treatments is considered. Results: Recently, endocannabinoids have been implicated in the hemodynamic alterations occurring in cirrhosis. These changes appear to be mediated via specific cannabinoid receptors (CB1) on splanchnic and hepatic vascular endothelium. Plasma levels of endocannabinoids also seem to be elevated in hepatitis, and are involved in apoptosis of hepatocytes by a membrane mechanism not related to a specific receptor. Other studies suggest a beneficial role for cannabinoids in reducing the inflammation of experimental hepatitis. In an animal model of acute hepatic failure, both endocannabinoids and the antagonist to the CB1 receptor have been found to have a beneficial effect on neurological and cognitive function. Conclusions: Endocannabinoids appear to be involved in several aspects of acute and chronic liver disease, including vascular changes, modulation of inflammatory process and neurological function, Further research may provide new insights into the pathophysiology of liver disease, as well as a basis for novel treatment modalities. ARTICLE TEXT Cannabis has been used for psychoactive and recreational purposes as well as in traditional medicine, long before the advent of modern medicine and scientific research (1, 2). The active component of cannabis, tetra-hydro-cannabinol (THC) was discovered in 1964 (3). This finding led to the discovery of two specific receptors to cannabinoids. The cannabinoid receptor antagonist (CB1) receptor was found initially in the brain (4) and subsequently in the gut and vascular endothelium (5-7). The CB2 receptor was isolated primarily in the immune system (8). Both receptors are coupled to G-proteins and act via adenylate cyclase and calcium channels (4). The first endogenous ligand for these receptors was found in 1992, and designated as Anandamide (from the Sanskrit 'Ananda'-bliss) (9). This compound is an amide of arachidonic acid and ethanolamine, and is a member of the fatty acid amide (FAA) family. Following this breakthrough, several other ligands were reported, e.g. 2-arachidonyl-glycerol (2-AG), noladine and oleamide (10-13). Specific antagonists to each subtype of cannabinoid receptors were also found: SR141716A for the CB1 receptor and SR 14452 for the CB2 receptor (14, 15). Cannabinoids have been studied extensively in recent years and have been found to have important functions in many physiological and pathophysiolocal processes. They have been found throughout the CNS, and effect many neurological and psychological phenomena such as mood, appetite, emesis control, memory, spatial coordination muscle tone and analgesia (5, 16-29). These effects are mediated primarily through the CB1 receptor. Outside the CNS, cannabinoids exert immunomodulatory and anti-inflammatory effects via CB2 receptors found in lymphocytes, monocytes and neutrophils (30-34). Other effects include vasodilation of splanchnic vessels via receptors on the surface of endothelial cells (7, 35), and inhibition of gut motility by anadamide released from nerve ends (10, 16). In this review, we examine the implications of basic-science and clinical research of cannabinoids' role in hepatic physiology and disease. Endocannabinoids and liver disease Portal hypertension, a complication of cirrhosis, is caused by both increased resistance to flow in the portal vein, and, at a later stage, by increased flow in the mesenteric vasculature. Systemic vasodilation further complicates this condition, causing a decrease in effective blood volume, hypotension, fluid and salt retention, worsening ascites and deterioration of renal function (36). Ascites is associated with increased plasma levels of the bacterial endotoxin lipopolysaccharide (LPS). In a study designed to assess the prognostic value of plasma endotoxin levels, it was found that plasma endotoxin levels increased progressively as liver function deteriorated. In short-term survival analysis, plasma endotoxin levels were significantly higher in non-survivors than in survivors. In long-term survival analysis, plasma endotoxin levels did not differ significantly between survivors and non-survivors, and was not an independent predictor of long-term survival. The authors concluded that in patients with cirrhosis, plasma endotoxin levels progressively increase as liver function deteriorates and may be useful in predicting short-term survival (37). LPS appears to contribute to the hemodynamic changes observed in cirrhosis, possibly mediated via enhanced nitric oxide (NO) production (38). LPS acts on macrophages, in a complex mechanism involving the CD14 protein expressed on their membranes, resulting in increased production of cytokines, including interleukin (IL) 1-beta and tumor necrosis factor-alpha (39, 40). Anandamide is found in macrophages (41). The finding that activation of peripheral CB1 receptors in rats by macrophage- and platelet-derived substances contributes to the hypotension in hemorrhagic shock (42) prompted the investigation of the possible role of endocannabinoids in endotoxin-induced shock. In that study, rat platelets were found to contain 2-AG. In vitro exposure of platelets to LPS markedly increases 2-AG levels. Prolonged hypotension and tachycardia were elicited in rats treated with LPS, as well as by macrophages plus platelets isolated from LPS-treated donor rats; rat macrophages or platelets preincubated in vitro with LPS had a similar effect. In all four cases, the hypotension but not the tachycardia was prevented by pretreatment of the recipient rat with the CB1 receptor antagonist SR141716A (3 mg/kg i.v.), which also inhibits the hypotensive response to anandamide or 2-AG. The hypotension elicited by LPS-treated macrophages or platelets remains unchanged in the absence of sympathetic tone or after blockade of NO synthetase. These findings indicate that platelets and macrophages generate different endogenous cannabinoids, and that both 2-AG and anandamide may be paracrine mediators of endotoxin-induced hypotension via activation of vascular CB1 receptors (43). These results led to further studies designed to explore the possible role of endocannabinoids in the hemodynamic changes in chronic liver disease. Hypotension in rats with biliary cirrhosis was improved by the CB1 receptor antagonist SR141716A. Similar results were also observed in rats with CCl4-induced cirrhosis, wherein SR141716A also reduced the elevated mesenteric blood flow and portal pressure. Monocytes from cirrhotic humans and rats elicited SR141716A-sensitive hypotension in normal recipient rats. Significantly elevated levels of anandamide were found in these cells. Compared with non-cirrhotic controls, in cirrhotic human livers there was a three-fold increase in CB1 receptors on isolated vascular endothelial cells indicating up-regulation of these receptors in chronic liver disease (44). In a similar study, arterial pressure, cardiac output, and total peripheral resistance were measured before and after the administration of SR141716A to cirrhotic rats with ascites, and to control rats. CB1 receptor blockade increased arterial pressure and peripheral resistance in cirrhotic animals, but not in healthy ones. A suspension of blood cells from cirrhotic rats induced hypotension in recipient rats. Monocyte levels of anandamide were significantly elevated in cirrhotic animals as compared to those in healthy controls. Here too, the conclusion was that in cirrhosis, monocytes increase their production of anandamide, and that this process contributes to hypotension and hemodynamic deterioration (45). It would thus seem that endocannabinoids are involved in the hemodynamic alterations of cirrhosis by acting as mediators between endotoxin/LPS and blood vessels. LPS acts on monocytes and platelets, thereby increasing production of anandamide and 2-AG, respectively. The endocannabinoids produced in response to LPS may then act on systemic and mesenteric vasculature, decreasing blood pressure and effective blood volume, increasing fluid and solute retention, thereby worsening ascites and contributing to renal dysfunction. The mechanism of vasodilation is at least partially mediated by the CB1 receptor, as demonstrated by the effects of SR141716A. However, a non-CB1 receptor mechanism cannot be ruled out as a contributor to these processes. One such mechanism may be via the vanniloid receptor and possibly by the subsequent release of CGRP that requires NO production, as demonstrated in endothelium-denuded aortic rings in rabbits (46). Given the central role of NO in the hemodynamics of cirrhosis, such a mechanism would seem plausible. The development of new chromatographic techniques has allowed for more accurate measurements of serum cannabinoids. Using this method, four-fold and three-fold increased levels of ANA and 2-AG, respectively, were found in the sera of patients with endotoxic shock compared to healthy subjects (47). In a subsequent study, the investigators demonstrated that compared to serum anandamide levels in healthy humans (4.0±0.79 nM), a significant increase was seen in acute non-severe hepatitis (8.8± 0.98 nM), with a further rise in severe acute hepatitis (15.8±10.25 nM). In chronic cirrhosis, anandamide levels were also elevated at 11.64±1.93 nM. In the acute hepatitis group, serum anandamide levels were found to correlate with the extent of tissue damage as indicated by serum ALT levels. Furthermore, tissue samples from the cirrhotic patients showed massive hepatocellular apoptosis and liver fibrosis. Since anandamide has been known to induce apoptosis, particularly of lymphocytes (48), the effect of anadamide on hepatocellular apoptosis was therefore assessed. Anandamide induced apoptosis of human heptaoma cells (HepG2) in a dose-dependent manner. This was preceded by G0/G1 cell cycle arrest, and the activation of pro-apoptotic signaling pathways such as p38mitogen-activated protein kinase. The mechanism of apoptosis was thought to be either CB receptor-mediated as in thymic lymphocytes (48) or vanilloid receptor (VR1) mediated, as seen in human neuroblastoma CHP100 and lymphoma U937 cells (49). As neither SR141716A nor SR144528 produced significant inhibition of apoptosis in VR1 knock-out mice, it was concluded that the principal mechanism of apoptosis was non-receptor mediated. Depletion of membrane cholesterol by MCD or treatment with HMG-coA-reductase inhibitors, did result in suppression of apoptosis, as did treatment with the antioxidant N-acetyl-cystein. Polymixin binding studies indicated that anadamide interacts with membrane cholesterol. Similar results were observed in normal rat hepatocytes. This indicated that the apoptotic effect of anandamide on liver cells is mediated through a direct effect on membrane cholesterol designated as lipid-lipid plasma membrane interaction and not through specific receptors. The effect seems to involve enhanced susceptibility to oxidative stress (50). The effects of endocannabinoids on neurological and cognitive aspects of hepatic encephalopathy (HE) were studied in an animal model of acute hepatic failure. The pathogenesis of HE is a complex process involving several mechanisms including functional changes in neurotransmitter systems such as the opiodergic (51, 52) and gamma amino butyric acid (GABA-ergic) (53-58) systems that are known to interact with the endocannabinergic system (16, 59). Fulminant hepatic failure (FHF) was induced by thioacetamide (TAA). Neurological performance (assessed by a fourteen point scale based on reflexes and task performance), activity (evaluated in an infra red maze), and cognitive function (performance in an eight arm maze) were measured after administration of the 2-AG SR141716A or both. Encephalopathic mice treated with SR141716A or 2-AG or both, showed improved neurological function, activity and cognitive function compared to untreated animals. SR141716A showed a dose-response pattern in the improvement of neurological function. CNS levels of 2-AG were found to be elevated in mice with TAA induced liver failure when compared to healthy mice. Administration of exogenous 2-AG resulted in decreased brain levels of endogenous 2-AG. The endocannabinoid system may therefore have a role in the pathogenesis of hepatic encephalopthy. The similar effect of 2-AG and SR141716A could be explained by two hypotheses: end-product inhibition of 2-AG and exertion of the effect through a non-CB1-receptor target (60). Other publications have shown that certain cannabinoid compounds decrease the extent of experimental hepatitis. The synthetic, non-psychotropic cannabinoid (PRS-211,092) decreased concanavalin A-induced liver injury in mice that was accompanied by promotion of early gene exp ression of IL-6 and IL-10, induction of early gene exp ression of the suppressors of cytokine signaling (SOCS-1 and 3), and inhibition of several pro-inflammatory mediators, including IL-2, monocyte chemoattractant protein-1 (MCP-1), IL-1beta, interferon-gamma, and tumor necrosis factor alpha. PRS-211,092 inhibited IL-2 production and nuclear factor of activated T cells activity in cultured T cells (61). A recently published study, examined the potential hepatotoxic effects of marijuana use in humans. A transversal study was conducted among 123 patients over 2 years in Sao-Paolo, Brazil. The patients were divided into three groups: 26 (21%) using only marijuana, 83 (67.5%) using marijuana and crack, and 14 (11.4%) consuming marijuana and alcohol. Among patients who reported using marijuana alone, hepatomegaly was observed in 57.7% and splenomegaly in 73.1%. These patients were found to have slightly elevated AST (42.3%), ALT (34.6%) and AP (53.8%). The prevalence of hepatomegaly, splenomegaly and hepatosplenomegaly was not different in the three groups. Patients who consumed both marijuana and alcohol had the highest levels of aminotransferases. These results suggest that chronic marijuana use, alone or in combination with alcohol or other drugs, may have hepatotoxic effects (62). The methodological issues involved, particularly the isolation of cannabis use from the use of other substances warrants caution as to the interpretation of these results. What are the therapeutic implications of these data for patients with liver disease? Very little clinical data are available as to the efficacy of endocannabinoids or their receptor antagonists in humans with hepatic disease. THC treatment for intractable cholestatic-related pruritus (ICRP) was evaluated in a report of three patients who had previously been treated with standard therapies for ICRP including: diphenhydramine, chlorpheniramine, cholestyramine, rifampicin, phenobarbital, doxepin, naltrexone, UV therapy, topical lotions and plasmapheresis. Patients were given 5 mg of delta-9-THC (Marinol) at bedtime. All three patients reported a decrease in pruritus, marked improvement in sleep, and were eventually able to return to work. Resolution of depression occurred in two of three. Side effects related to the drug included coordination disturbance in one patient. Marinol dosage was decreased to 2.5 mg in this patient with resolution of symptoms. The duration of antipruritic effect was approximately 4-6 h in all three patients suggesting that frequent dosing may be needed (63). One possible mechanism for the beneficial effect on cholestasis may be related to an increase in the threshold for nociception. This hypothesis was tested in rats with bile-duct-resection induced cholestasis and in sham-resected controls. Administration of the cannabinoid agonist WIN 55, 212-2 resulted in an increase in the tail-flick latency - an index of the nociception threshold - in both groups as compared to baseline. These results support the notion that the analgesic effect of cannabinoids may be of use in treating pruritus, a nociceptive stimulus, in patients with liver disease (64). Despite the scarcity of information, certain conclusions may be drawn from clinical experience in other fields. Cannabinoids such as THC, cannabis and nabilone have been tried in patients with multiple sclerosis with some success (28). The safety profile of these agents may also prove problematic. A review of cannabinoids in clinical practice found that some patients, particularly women and the elderly had panic or anxiety attacks. Psychosis is also a possible consequence of cannabis use that must be considered. The slow elimination time of cannabinoids from the body may impair task performance and driving (65). The development of new, non-psychotropic cannabinoids such as HU-320 (66) may enable the development of new therapeutic agents, while avoiding the legal and social issues that may be associated with the use of compounds derived from illicit drugs. SR141716A, the CB1 receptor antagonist is currently under investigation for treatment of obesity and for smoking cessation, given the cannabinoids' known effect in appetite stimulation and reward (1, 5, 16, 67). Preliminary results of the RIO-Europe trial, now in phase III show that this agent (labeled Rimonabant) was safe and effective in achieving weight reduction, improved lipid profile and amelioration of the metabolic syndrome compared to placebo (68, 69). In summary, endocannabinoids are relatively recently discovered compounds, that have many physiological and pathophysiological functions. Though much has been learned about their effects in the CNS, immune system and gut, relatively little is known about their role in liver physiology and disease. There is convincing evidence for their role in the hemodynamic compromise as seen in cirrhosis. The mechanism underlying this phenomenon appears to involve an increase in production of 2-AG and anandamide in platelets and macrophages, respectively, and a subsequent vasodilation, at least partially mediated by CB1 receptors on endothelial cells. Studies have revealed an increase in serum anandamide concentration in both acute and chronic liver disease in humans, as well as an apoptotic effect of anandamide on liver cells, via a direct interaction with membrane cholesterol. The endocannabiod system may also be involved in the pathogenesis of HE, as are several other neurotransmitter systems. Some epidemiological data supports the notion of a hepatotoxic effect for marijuana; however, methodological problems preclude conclusion in this context. Certain cannabinoids may improve hepatic inflammation and pruritus secondary to liver disease, but more data are needed to substantiate these propositions. The development of therapeutic modalities based on cannabinoids or their antagonists depends on their safety as well as efficacy. Synthetic, non-psychotropic cannabinoids may be better tolerated and reduce social and legal tensions that may impede the pharmacological use of substances derived from illicit drugs. source: http://www.natap.org...V/091905_01.htm A Novel Synthetic Cannabinoid Derivative Inhibits Inflammatory Liver Damage via Negative Cytokine Regulation Iris Lavon, Tatiana Sheinin, Sigal Meilin, Efrat Biton, Ayelet Weksler, Gilat Efroni, Avi Bar-Joseph, George Fink, and Ayelet Avraham Pharmos Limited, Kiryat Weizmann, Rehovot, Israel The therapeutic potential of cannabinoids has been described previously for several inflammatory diseases, but the molecular mechanisms underlying the anti-inflammatory properties of cannabinoids are not well understood. In this study, we investigated the mechanism of action of a novel synthetic cannabinoid, [(+)(6aS,10aS)-6,6-Dimethyl-3-(1,1-dimethylheptyl)-1-hydroxy-9-(1H-imidazol-2-ylsulfanylmethyl]-6a,7,10,10a-tetrahydro-6H-dibenzo[b,d]pyran (PRS-211,092) that has no psychotropic effects but exhibits immunomodulatory properties. Treatment with PRS-211,092 significantly decreased Concanavalin A-induced liver injury in mice that was accompanied by: 1) promotion of early gene exp ression of interleukin (IL)-6 and IL-10 that play a protective role in this model; 2) induction of early gene exp ression of the suppressors of cytokine signaling (SOCS-1 and 3), followed by 3) inhibition of several pro-inflammatory mediators, including IL-2, monocyte chemoattractant protein-1 (MCP-1), IL-1{beta}, interferon-{gamma}, and tumor necrosis factor {alpha}. Based on these results, we propose a mechanism by which PRS-211,092 stimulates the exp ression of IL-6, IL-10 and the SOCS proteins that, in turn, negatively regulates the exp ression of pro-inflammatory cytokines. Negative regulation by PRS-211,092 was further demonstrated in cultured T cells, where it inhibited IL-2 production and nuclear factor of activated T cells activity. These findings suggest that this cannabinoid derivative is an immunomodulator that could be developed as a potential drug for hepatitis as well as for other short- or long-term inflammatory diseases. source: http://molpharm.aspe...tract/64/6/1334 June 02, 2008 Marijuana Use Sparks Liver Transplant Controversy Despite its legality in 12 states, learn why medical marijuana use may render a person with Hepatitis C ineligible for a liver transplant. by Nicole Cutler, L.Ac. Hepatitis C is not only the leading cause of chronic liver disease in the United States, it is also the most common reason for liver transplants in this country. Unfortunately, some with Hepatitis C are being denied access to liver transplants because of their use of a controversial type of symptom relief. Although transplantation is considered a last resort for liver disease, the number of people waiting for a new organ far outnumbers the supply. Since donated livers are in such high demand, a complex system of prioritizing who gets transplant surgery has evolved. Obviously, great deliberation is involved in deciphering transplant eligibility and recipient ranking. However, the ethics of this process has been called into question for those using medical marijuana. Occasionally used to ease Hepatitis C symptoms, patients legally using medical marijuana are at high risk of being denied a spot on the liver transplant recipient queue. UNOS The United Network for Organ Sharing (UNOS) is a non-profit, scientific and educational organization that administers the nation's only Organ Procurement and Transplantation Network. UNOS is responsible for organ matching and placement throughout the United States. According to the UNOS website, over 98,000 people are currently on an organ transplant waiting list. Many people wait for years for a new liver, often not surviving the wait. According to the Scientific Registry of Transplant Recipients, less than a third of those waiting for a liver actually receive one. The UNOS entrusts individual hospitals and transplant centers to develop their own criteria for transplant candidates. Some of these institutions automatically reject people who use "illicit substances" — including those legally prescribed medical marijuana. "Most transplant centers struggle with issues of how to deal with people who are known to use marijuana, whether or not it's with a doctor's prescription," said Dr. Robert Sade, director of the Institute of Human Values in Health Care at the Medical University of South Carolina. "Marijuana, unlike alcohol, has no direct effect on the liver. It is, however, a concern ... in that it's a potential indicator of an addictive personality." Medical Marijuana Marijuana has been used for medicinal purposes for approximately 4,000 years. Surviving texts from ancient India confirm that its psychoactive properties were recognized, and doctors used it for a variety of illnesses and ailments. These included a whole host of gastrointestinal disorders, nausea, low appetite, insomnia, headaches and as a pain reliever. People with Hepatitis C have reported using marijuana (cannabis) to treat both symptoms of the disease as well as the nausea associated with antiviral therapy. An observational study by investigators at the University of California at San Francisco (UCSF) found that Hepatitis C patients who used cannabis were significantly more likely to adhere to their treatment regimen than patients who didn't use it. Despite this support for medical marijuana, several trials reported an association between daily cannabis use and the development of liver fibrosis in Hepatitis C. Aside from the question of legality, experts disagree on the therapeutic use of cannabinoids for Hepatitis C treatment. The medical use of cannabis has been legalized in several countries including Canada, Belgium, Australia, the Netherlands, the United Kingdom, New Zealand and Spain. Since 1996, twelve U.S. states have legalized medical marijuana use: Alaska, California, Colorado, Hawaii, Maine, Montana, Nevada, New Mexico, Oregon, Rhode Island, Vermont and Washington. Doctors in these states can write a prescription for marijuana for a legitimate medical issue. However, the United States Supreme Court ruled that the federal government has the right to regulate and criminalize marijuana in these states, even for medical purposes. Sad Outcome in Washington The debate about medical marijuana’s impact on liver transplant eligibility jumped to center stage in May of 2008 when Washington state resident Timothy Garon passed away. To combat his Hepatitis C symptoms, Garon’s physician had authorized medical marijuana for alleviating his nausea and stomach pain and to stimulate his appetite. Legally authorized in Washington state since 1998, Garon’s attorney believes that his client’s medical marijuana use kept him off of the liver transplant list, a decision that ultimately cost Garon a chance for survival. No one tracks how many patients are denied transplants over medical marijuana use. Pro-marijuana groups have cited a handful of cases, including at least two patient deaths, in Oregon and California, since the mid- to late 1990s, when states began adopting medical marijuana laws. With the nation’s shortage of transplantable livers, some administrators may be using their moral judgment to decide who gets on an eligibility list. Thus, using medical marijuana to ease advanced Hepatitis C symptoms may put some people at a disadvantage. Until our nation’s lawmakers, physicians and administrators are all in agreement about the use of cannabis for certain illnesses, those in need of a liver transplant may wish to think ahead – and either choose a different medicine for symptom relief or consult with their chosen hospital about their view on medical marijuana as a factor in transplant eligibility. References: http://en.wikipedia.org , Medical Cannabis, Wikimedia Foundation Inc., 2008. http://norml.org , Hepatitis C, The National Organization for the Reform of Marijuana Laws, 2008. http://seattletimes.newsource.com , Is medical-marijuana use reason to deny someone an organ transplant?, Seattle Times Staff and Associated Press, The Seattle Times Company, May 2008. http://stopthedrugwar.com , Marinol Death Sentence: Oregon Man Denied Liver Transplant Because of Prescription -- He's Not the Only One, stopthedrugwar.com, 2008. Sylvestre, et al, Cannabis use improves retention and virological outcomes in patients treated for hepatitis C, European Journal of Gastroenterology & Hepatology, 2006. www.cbhd.org, Liver Transplants: How Do We Choose Who Should Live When Not All Can?, Gregory W. Rutecki, The Center for Bioethics and Human Dignity, 2008. www.drugwarfacts.org, Medical Marijuana, Common Sense for Drug Policy, 2008. www.unos.org, Who We Are, United Network for Organ Sharing, 2008. www.usatoday.com, Playing field for liver transplants is not level, studies find, Robert Davis, USA Today, 2008. SOURCE: http://www.hepatitis...uana_use_s.html Moderate Cannabis Use Associated with Improved Treatment Response in Hepatitis C Patients on Methadone By Liz Highleyman Interferon-based therapy for chronic hepatitis C virus (HCV) infection is often limited by side effects including flu-like symptoms, fatigue, insomnia, loss of appetite, nausea, muscle and joint pain, and depression, which can lead to poor adherence, dose reduction, or treatment discontinuation. Medicinal cannabis may relieve such side effects and help patients stay on treatment, according to a study published in the October 2006 European Journal of Gastroenterology and Hepatology. Several studies - as well as ample anecdotal evidence - have demonstrated that medical marijuana can reduce nausea, increase appetite, and improve wasting in people with HIV. Diana Sylvestre, MD, of the University of California at San Francisco and colleagues conducted a study to define the impact of cannabis use during HCV treatment. The prospective observational study included 71 patients at OASIS (Organization to Achieve Solutions in Substance Abuse), a community-based clinic providing medical and psychiatric treatment to substance users in Oakland, California. Patient Demographics Eligible participants were recovering substance users with HCV who had been on methadone maintenance therapy for at least 3 months. Patients with non-HCV-related liver disease or decompensated cirrhosis were excluded. Among the 30 patients with liver biopsy results, the mean Metavir inflammation grade was 2.4 and the mean fibrosis stage was 2.6. Subjects with untreated depression were first stabilized on antidepressants. Use of cannabis during the study was "neither endorsed nor prohibited." About one-third of participants used marijuana during hepatitis C treatment. "Regular" marijuana use was defined as every day or every other day for at least 4 weeks. Drug and alcohol use were assessed by self-report and random monthly urine testing. 22 patients (31%) reported cannabis use during ant-HCV treatment, while 49 (69%) did not. Baseline characteristics were generally similar between marijuana users and non-users. The median age was about 50 years in both groups. Compared with non-users, cannabis users were somewhat more likely to be male (68% vs 57%) and Caucasian (86% vs 69%), but less likely to have genotype 1 HCV (48% vs 61%). About 60% of participants reported a previous psychiatric diagnosis (usually depression); cannabis users and non-users had similar rates of psychiatric diagnosis and antidepressant use. 32% of cannabis users and 37% of non-users reported use of other illicit substances during HCV treatment (including heroin, cocaine, and methamphetamine), while 14% and 24%, respectively, reported alcohol consumption; these differences were not statistically significant. Participants were treated with conventional interferon alfa-2b (3 million units 3 times weekly) plus 1000-1200 mg daily ribavirin. Patients were initially treated for 48 weeks regardless of genotype, but the protocol was later amended to allow 24-week therapy for those with genotypes 2 or 3. Adherence to therapy was assessed by self-report, ribavirin pill counts, and returned empty interferon vials. Participants were considered adherent if they took 80% or more of prescribed interferon and ribavirin for at least 80% of the projected treatment course. Results In an intent-to-treat analysis, 37 patients (52%) achieved an end-of-treatment response (undetectable HCV RNA at the end of 24 or 48 weeks of therapy): - 14 cannabis users (64%); - 23 non-users (47%) (P = 0.21). Overall, 21 out of 71 participants (30%) achieved sustained virological response (SVR), or continued undetectable HCV RNA 6 months after the end of therapy: - 12 of 22 cannabis users (54%); - 9 of 49 non-users (18%) (P = 0.009). Post-treatment virological relapse rates were 14% for cannabis users and 61% for non-users (P = 0.009). End-of-treatment response rates were similar among occasional cannabis users (10 of 16; 62%) and regular users (4 of 6; 67%). 10 of 16 occasional users (62%) went on to achieve SVR, compared with 2 of 6 regular users (33%), but the difference was not statistically significant. Most patients (93%) reported at least one treatment-related side-effect, with similar rates among cannabis users and non-users. Overall, 17 of 71 patients (24%) discontinued therapy early: - 1 cannabis user (5%); - 16 cannabis non-users (33%) (P = 0.01). Overall, 48 patients were adherent (68%): - 19 cannabis users (86%); - 29 non-users (59%) (P = 0.03). There was no significant difference in adherence between occasional and regular cannabis users (87% vs 83%) 91% of cannabis users took at least 80% of prescribed interferon, compared with 76% of non-users. For ribavirin, the corresponding rates were 91% and 84%; these differences were not statistically significant. However, cannabis users were significantly more likely than non-users to remain on therapy for at least 80% of the projected treatment duration (95% vs 67%; P = 0.01). The average duration of HCV treatment was 38 weeks for cannabis users, compared with 33 weeks for non-users. Conclusion In conclusion, the authors wrote, "Our results suggest that modest cannabis use may offer symptomatic and virological benefit to some patients undergoing HCV treatment by helping them maintain adherence to the challenging medication regimen." Discussion In their discussion, the authors wrote that their results "suggest that the use of cannabis during HCV treatment can improve adherence by increasing the duration of time that patients remain on therapy; this translates to reduced rates of post-treatment virological relapse and improved SVR." "Although other potential mechanisms may contribute to its enhancement of treatment outcomes, such as altered immunological function and improved nutritional status," they added, "it appears that the moderate use of cannabis during HCV treatment does not lead to deleterious consequences." In this study, it appears that the treatment response benefit was primarily due to improved ability to stay on adequate doses of interferon and/or ribavirin. Sylvestre told HIV and Hepatitis.com that the researchers could not judge whether there was a direct antiviral effect. "It was probably more of a side-effect management effect than an antiviral effect, but we can't rule out the latter," she said. There remain concerns about the safety of marijuana use by individuals with chronic hepatitis C. Cannabinoid receptors are present on immune cells, and use of the drug may suppress immune function. In addition, there is some evidence that frequent marijuana use may contribute to liver fibrosis. As reported in the July 2005 issue of Hepatology, French researchers found that HCV positive individuals who smoked cannabis daily were more likely to have severe fibrosis and were at higher risk for rapid fibrosis progression than those who used marijuana only occasionally or not at all. However, the participants in that study were not receiving treatment for hepatitis C. Notably, in the current study, there was no direct dose-response relationship between the amount of cannabis consumed and the likelihood of sustained virological response. In fact, the patients who used the largest amounts of cannabis did not show as much benefit from hepatitis C therapy. The researchers did not perform pre- and post-treatment histological assessments using paired liver biopsies, and did not measure immune parameters. "The lack of dose response in our study argues against specific receptor or metabolism-related effects, and suggests instead that cannabis exerted its benefit by non-specific improvements in symptom management," the authors stated. "Interestingly, because the benefits of heavy cannabis use were less apparent, we cannot rule out the possibility that detrimental biological or immunological mechanisms may be relevant at higher levels of consumption. Obviously, further study is needed." Unfortunately, because cannabis is strictly controlled in the U.S. and the federal government considers the drug illegal even in states with medical marijuana laws, it is difficult to conduct randomized, controlled trials. Editorial In an accompanying editorial, a group of hepatitis C experts from Canada and Germany noted that people who use illicit drugs are the main risk group for new hepatitis C infections, and "will form the largest HCV treatment population for years to come." While past treatment guidelines advised against hepatitis C treatment for active substance users and those with a recent history of active use, this categorical recommendation is no longer in effect in the U.S. and Europe, since recent studies have shown that such patients can achieve good treatment outcomes as long as they are able to maintain adequate adherence. Treatment remains a challenge for this population, however, in part because substance users have a higher prevalence of depression and other psychiatric conditions, which are associated with an increased likelihood of neuropsychological side effects during interferon therapy. Sylvestre's study, the editorial authors wrote, "suggests that cannabis use may benefit treatment retention and outcomes in illicit drug users undergoing HCV treatment" and that "there is substantial evidence that cannabis use may help address key challenges faced by drug users in HCV treatment." Several recent studies have demonstrated the benefits of combining anti-HCV therapy with methadone maintenance, in effect offering "one-stop shopping." The authors suggested that the therapeutic effects of cannabis "may be of principal importance and benefit for the distinct needs of illicit drug users" on methadone maintenance, because methadone itself is associated with some of the same side effects as interferon (bone aches, loss of energy, depression). "Overall, cannabis use may thus even offer dual benefits, in facilitating adherence to both methadone maintenance therapy and HCV treatment in the HCV-infected drug user, and thus contribute to public health benefits related to both these interventions," they noted. "While further research is required on the biological and clinical aspects of the benefits of cannabis use for HCV treatment, and the effectiveness of cannabis use for HCV treatment needs to be explored in larger study populations," they concluded, "we advocate that in the interim existing barriers to cannabis use are removed for drug users undergoing HCV treatment until the conclusive empirical basis for evidence-based guidance is available." In particular, they suggested that medical marijuana laws and programs that specify its use for patients with specific conditions such as AIDS and cancer should also include people with hepatitis C. 9/15/06 References D L Sylvestre, B J Clements, Y Malibu. Cannabis use improves retention and virological outcomes in patients treated for hepatitis C. European Journal of Gastroenterology and Hepatology 18(10): 1057-1063. October 2006. B Fischer, J Reimer, M Firestone, and others. Treatment for hepatitis C virus and cannabis use in illicit drug user patients: implications and questions. European Journal of Gastroenterology and Hepatology 18(10): 1039-1042. October 2006. C Hezode, F Roudot-Thoraval, S Nguyen, and others. Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C. Hepatology 42(1): 63-71. July 2005. SOURCE: http://www.hivandhep...6/091506_a.html
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