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Home >> Research >> Symptons/Conditions >> Treating Hep C

The Lifevine Foundation
2442 NW Market St. #508
Seattle, WA 98107
206-551-5559


Practicing Physicians
Medical Professionals
State of Washington

 

Dear Concerned Physician,

The patient presenting this letter to you has been diagnosed with Hepatitis C. The Lifevine Foundation is a non-profit public education and legal assistance provider for medical marijuana patients and their physicians. We urge you to consider the following information when determining whether this patient will potentially benefit from the use of cannabis.

Patients with even mild cases of Hepatitis C often experience nonspecific and intermittent symptoms such as nausea and vomiting, poor appetite, fatigue, depression, muscle and joint pains, weight loss, and mild right-upper-quadrant discomfort or tenderness. These symptoms may become more pronounced and chronic as the disease progresses.

As you are probably aware, drug therapy for Hepatitis C usually consists of the use of combination therapy with alpha interferon and ribavirin in those patients where such therapy is indicated. Common side effects of treatment (occurring in more than 10 percent of patients) include: nausea and vomiting, depression, irritability, weight loss, fatigue, muscle aches, headaches, and low-grade fever. Substance abuse relapse is often a common result of the therapy due to the psychological side effects. Flare-ups of pre-existing auto-immune diseases such as rheumatoid arthritis, ulcerative colitis and Crohn's Disease are common. Marijuana can mitigate the majority of these side effects as well as offering effective help to those patients where alpha-interferon treatment is not indicated.

Marijuana (Cannabis) is a powerful antiemetic2, 15, 18 that has been shown to be particularly effective controlling nausea and stimulating the appetites of immune surpressed patients such as those with HIV or undergoing chemotherapy. Cannabis has anti-depressant and anti-anxiety properties. It is an anti-inflammatory 3, 4, 6, 9, 10, 14, 18, 19 and immuno-modulating, 7, 8, 11, 12, agent that can help minimize portal 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. Cannabis has the added advantage of easing, or even completely eliminating, the muscle pains and cramping 1, 2, 5, 17, 18, 21 that patients often experience. Marijuana is an effective analgesic.2, 3, 9, 14,15, 16, 20, 21 Cannabis has also been demonstrated as effective with rheumatoid arthritis, MS, and Crohn's. 4, 7, 8, 20, it can aid in the prevention of inflammation associated with flare-ups of these conditions should they be present in your patient. Recent studies published this year (2002) have shown that cannabinoid receptors throughout the digestive tract act to reduce immune-reactivity and to surpress the vagal drive of the digestive system, slowing the digestive process, allowing more nutrients to be absorbed at a slower rate, thus putting less stress on the liver 1

The Washington State Medical Quality Assurance Board has included Hepatitis C as a debilitating medical condition that could potentially benefit from the use of medical marijuana. Please review the following reference data. The minimal side effects of cannabis will be discussed following the data.

Published Reference Data (Studies relevant to Hepatitis C, short synopsis - complete articles are available. Other references are located following the conclusion of this report.)

1. Adami, Frati, Bertini, Kulkarni-Narla, Brown, de Caro, Coruzzi, and Soldani, "Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach" British Journal of Pharmacology Vol. 135, 2002, The study found cannabinoid receptors throughout the gastrointestinal organs of rats. "Immunoreactivity to the CB1 receptor was co-localized with that of the cholinergic marker choline acetyltransferase in neural elements innervating smooth muscle, mucosa and submucosal blood vessels of rat stomach fundus, corpus and antrum. These results indicate that gastric antisecretory effects of cannabinoids in the rat are mediated by suppression of vagal drive to the stomach through activation of CB1 receptors, located on pre- and postganglionic cholinergic pathways."

2. Baron and Folan, "Ulcerative Colitis and Marijuana", Annals of Internal Medicine, Vol. 112, No.6, p 47, 1990, "The symptoms of ulcerative colitis were repeatedly relieved by smoked cannabis."

3. Beltramo and Piomelli, "Functional role of high-affinity anandamide transport as revealed by selective inhibition." Science, Vol.277, No. 5329, pp1094, 1997, "Cannabinoid and non-cannabinoid compounds in marijuana reduce pain and inflammation."

4. BW Healthwire, January 1998, "Pre-clinical studies show CT-3 reduces chronic and acute inflammation and reduces destruction of joints." Atlantic Pharmaceuticals was evaluating CT-3, a cannabinoid derivative. The company reported "In recent studies, the agent was found to reduce inflammation and prevent the destruction of joint tissue."

5. Egli, Elsohly, Henn and Spiess. International Journal of Clinical Pharmacology, Vol. 34, No. 10, pp46-452, 1988, "The effect of orally and rectally administered delta-9-tetrahydrocannabinol on spasticity" "THC was shown to relieve muscle spasms in human patients."

6. Formukong, Evans, and Evans "Analgesic and anti-inflammatory activity of constituents of cannabis sativa l" Inflammation, Vol. 12 No. 4, pp361-371, 1988, "Cannabidol is more effective than aspirin in reducing inflammation" (Cannabidol or CBD, is one of the scores of cannibinoids found in marijuana other than THC)

7. Friedman, H.; Klein, T.W.; Newton, C.; and Daaka, Y., "Marijuana receptors and immunomodulation." Advances in Experimental Medicine and Biology 373: pp103-113, 1995, "The study suggested that the immunosuppressive effects of cannabinoids might be useful clinically; for example, in treating multiple sclerosis.

8. Grotenhermen Dr. Franjo, IACM-Bulletin of 25 June 2000, (IACM): "We know from animal studies that THC inhibits the production of Th-1 cytokines such as IL-1, IL-2, and IFN-gamma and stimulates the production of Th-2 cytokines such as IL-4, IL-10, and TGF-beta. This would give reason for a causal therapeutic use of THC in certain autoimmune diseases that appear to be Th-1 mediated such as Crohn's disease, a form of chronic intestinal inflammation, and rheumatoid arthritis."

9. Holdcroft, et al., "Pain relief with oral cannabinoids in familial Mediterranean fever" Anesthesia, Vol. 52, No. 5, May 1997. This research paper done at Hammersmith Hospital in London confirmed cannabis' analgesic effects in the first UK clinical trial. The paper states "Cannabinoids have analgesic and possibly anti-inflammatory properties but their clinical use has been restricted by legislation"

10. Hollister L.E, "Health Aspects of Marijuana" Pharmacological Review, Vol. 38, No. 1, 1986, "Constituents of marijuana; CBC, olivitol, and cannoflavin all have marked anti-inflammatory properties."

11. Hollister L.E, "Marijuana and immunity" Journal of Psychoactive Drugs Vol.20 (1:): 3-8, January-March, 1988, Cannabinoids found in marijuana are effective immunomodulators.

12. Kaminsky N. E., "Evidence for a cannabinoid receptor in immunomodulation by cannabinoid compounds" Advances in Experimental Medicine and Biology, Vol. 335, 115-120, 1993, Identifies the receptors and process that allows marijuana to be an effective immunomodulator

13. Kaminsky N. E. Journal of Neuroimmunology, 1998, "These [cannabinoids] might be useful as immune modulators, perhaps to be used as anti-inflammatory agents"

14. Maurer, Henn, Dietrich and Hoffmann "Delta-9-tetrahydrocannibinol shows anti-spastic and analgesic effects in a single case double-blind trial" European Archive of Psychiatry and Neurological Science, Vol. 240 No. 1 pp1-4 1990, The trial compared Codeine, THC, and a placebo. The study found codeine and THC had comparable analgesic effects but only THC had a significant beneficial effect on spasticity and inflammation."

15. National Academy of Science, Institute of Medicine, "Marijuana and Medicine; Assessing the Science Base " Executive Summary, 1999, "Conclusion: Scientific data indicate the potential therapeutic value of cannabinoid drugs, primarily THC, for pain relief, control of nausea and vomiting, and appetite stimulation;"

16. Noyes and Barnes, Comprehensive Psychiatry, Vol. 15, No. 6, pp 413s-416s, 1974, "There are indications that the active ingredients in marijuana may be an effective analgesic that is efficacious in functional pain"

17. Petro and Ellenberger, "Treatment of human spasticity with delta-9-tetrahrdrocannibinol" Journal of Clinical Pharmacology, Vol. 21, 1981, "THC can relieve a broad range of muscle spasms in humans and animals"

18. Pharmos Corporation Press Release, May 21 1998, Researchers reported that experimental treatment of rats suffering from ulcerative colitis with Dexanabinol (synthetic cannabidiol-CBD) "significantly reduced the anorexia and the colonic inflammation associated with this condition compared with untreated rats."

19. Richardson, Kilo, & Hargreaves, "Cannabinoids Reduce Hyperalgesia and Inflammation via Interaction with Peripheral CB1 Receptors". Pain Vol. 75, 1 pp. 111-119, 1998, Conclusion is in title.

20. Society for Neuroscience Conference, symposium syllabus, Functional Role of Cannabinoid Receptors, Aug. '98, "Cannabinoids were shown to have a direct effect on the biochemical pain signals in the central nervous system, and to exhibit superior pain control to addictive opiate based narcotics. Cannabinoids prevented hyperalgia and were shown to be particularly effective in the treatment of arthritis and other inflammation induced pain.

21. Zeltser, R.; Seltzer, Z.; Eisen, A.; Feigenbaum, J.J.; and Mechoulam, R "Suppression of neuropathic pain behavior in rats by a non-psychotropic synthetic cannabinoid with NMDA receptor-blocking properties" Pain Vol. 47(1): 95-103, October. 1991, The study found cannabis surpressed neuropathic pain which complicates many CNS diseases. Cannabis was effective when few available therapies provided even partial relief.

Historical Data

*The oldest medical text known to man was written over 5,000 years ago. The Chinese Pen Ts'ao, prescribed cannabis for rheumatism and digestive disorders among other illnesses.

*The New English Dispensary of 1764 recommended hemp to reduce inflammation.

*In 1814, Nicholas Culpepper published his Complete Herbal, which included "allaying humors of the bowels" and "reducing inflammation" among the applications of cannabis.

*Surgeon William O'Shoughnessy in his 1839 paper titled On the preparation of the Indian Hemp found that cannabis relieved rheumatism, convulsions and muscle spasms.

*The 1854 United States Dispensatory listed many uses for cannabis including "reduction of inflammation", "relax muscle contractions", "treatment of digestive disorders" and as "an analgesic and sedative"

*Between 1840 and 1890 over 100 papers were published on the medical uses of cannabis.

*Sir William Osler, known as the "father of modern medicine", proclaimed cannabis the best treatment for migraine pain in his authoritative 1915 textbook.

*In 1937, when the Marijuana Tax Act was before Congress The American Medical Association protested vehemently, Dr William C. Woodward, the AMA's counsel, testified that the bill would deprive Americans of one of the most useful drugs known to medicine. He also complained that the only reason there hadn't been a larger public outcry was because the Act referred to the Mexican slang "marijuana" and not to cannabis, which everyone understood was a medicine

Side Effects

There has never been a reported death from overdose of marijuana 10, 15, 22, 23, 26 27. There has never been a death or permanent health effect reported from long-term heavy use of marijuana 10, 22, 23, 27. Side effects include; a slight increase in heart rate24, 25, slight hypotension24, 25, increased appetite 15, 24, and of course, a mild euphoric effect. There are "no deleterious effects on the normal cardiovascular system" as a result of these side effects according to a 1997 WHO report27,. An Australian National Drug Strategy report states "Tolerance to the cardiovascular effects develop within 7-10 days in persons receiving daily doses of THC" 24,.

The euphoria also is subject to the effects of tolerance. Any effects on coordination and cognition dissipate within 7-10 days of daily use15, 24. However marijuana's effects continue to aid with the patient's stress reduction and to alleviate the depression and other emotional problems that Hepatitis C patients often suffer from 10, 15, 28, 29, 30. Many patients find cannabis far superior to Valium, Serax, Elavil, or Sinequan; all are commonly prescribed to Hepatitis C sufferers. Please contact the Lifevine Foundation for published data regarding the anti-anxiety and anti-depressant properties of cannabis. Hepatitis C patients find the appetite stimulation10, 15, 31, an added benefit. It is likely that your patient has already tried marijuana for their symptoms and feels the perceived benefits outweigh any side effects they have experienced.

Risks

The most obvious risk of smoking marijuana, is, of course, the risk incurred smoking any vegetable material. There are several factors to consider when determining this risk. If your patient is not suffering from malabsorbtion due to their Hepatitis C and they are able to keep food digesting for two hours, the patient may choose to eat their cannabis and avoid all smoking risks. Other smoking methods such as vaporizers (which heat the cannabis to a temperature high enough to "vaporize" the cannabinoids on the surface of the marijuana without igniting the vegetable matter) may minimize the smoking risks.

The carcinogenic ingredients in both tobacco and cannabis are primarily the tars that reside in both plants - not the THC or other cannabinoids of cannabis. The main difference in the incidence of development of lung cancer is a matter of exposure to these tars, which is overwhelmingly greater with tobacco than with cannabis.

It takes 20 - 25 pack/years or more (1 pack/year = smoking 1 pack of cigarettes/day for 1 year.) for most tobacco-induced lung cancers to develop. 20 - 25 pack/years worth of cigarettes = 150,000 to 200,000 cigarettes. Of all those people who smoke 1 pack/day or more of tobacco cigarettes for all of their adult lives, only 1 in 5 (20%) will actually develop tobacco-induced lung cancer.

Most patients who use marijuana medicinally develop their illness in mid to late life, and start smoking marijuana medicinally only when their projected remaining life span is already relatively short. Light medical marijuana users - (1-2 joints/day) in one year would smoke 365 - 730 joints; In ten years - 3650 - 7300 joints. In order to reach the equivalent of 200,000 cigarettes it would take them 270 years, at which time 1/5 of them might develop a cancer.

Very heavy use of medicinal marijuana may amount to 10 joints/day. In one year they would smoke roughly 3,650 joints; in ten years- 36,500 joints It would take them 54 years to smoke the equivalent of 200,000 tobacco cigarettes, at which time 1/5 of them might develop a cancer. These figures assume large (1 gm) joints are being smoked - similar in size to a tobacco cigarette

Tobacco smoke is a bronchial constrictor known to penetrate the lung's smaller peripheral air passages and causes inflammation of the lung's absorbent microphages. Tobacco causes blockages which leads to emphysema. Dr. Donald Tashkin, a federally sponsored pulmonologist and professor of medicine at UCLA Medical School has determined that marijuana smoke acts as a bronchial dilator and surpresses inflammation of the lung's macrophages. In a 1997 UCLA study involving 394 participants32 Tashkin noted "Neither habitual long-term marijuana smokers nor intermittent marijuana smokers exhibited any significantly different rates of decline in lung function. No differences were noted between even quite heavy smoking and non-smoking of marijuana." In contrast, the tobacco-only smokers in the study experienced a rapid decline in lung function during the eight years this study ran. The study also found no connection between marijuana and tobacco smoking in those s ubjects who smoked both. The evidence from this exhaustive real-world study indicates that the pulmonary health of marijuana smokers is no different from that of the general population.

In an article in American Journal of Respiratory Cellular and Molecular Biology 2001 Mar; 24(3): 339-44 titled "Induction and regulation of the carcinogen-metabolizing enzyme CYP1A1 by marijuana smoke and delta (9) tetrahydrocannabinol" by the Roth et al, Division of Pulmonary and Critical Care Medicine, Department of Pathology and Laboratory Medicine, UCLA School of Medicine, "Induction of the carcinogen-metabolizing enzyme cytochrome P4501A1 (CYP1A1) is a key step in the development of tobacco-related cancers." They determined THC had a significant inhibitory effect on the cancer-causing enzyme's induction into the body.

Other tests conducted by Dr. Tashkin at UCLA have found a slightly higher risk of bronchitis and other upper respiratory infections in marijuana smokers33. This risk may be mitigated by the use of vaporizers or by the use of ice or water-cooled pipes

Other risks include physical or psychological dependence. These risks are far lower than with any other psychotropic drug15. The addictive properties of marijuana are less than caffeine, ephedrine, or benzodiazepines (like Valium).15 Marijuana is similar to chocolate in it's potential for dependency34. Unlike alcohol, nicotine, opiates, barbiturates, amphetamines, cocaine or chocolate, marijuana does not effect the dopamine receptors of the brain35, 36. There is no physical withdrawal10, 15, 26, 27,36. Unlike steroids and other pharmaceuticals, one can cease use immediately; there is no need to "taper down" dosages.

Conclusion

There is compelling evidence that cannabis is an effective antiemetic, anti-inflammatory, immune modulating, analgesic and anti spasmodic agent. These properties are indicated for patients suffering from Hepatitis C. Five thousand years of recorded medical of use, has shown no long-term consequences. Side effects from the use of medical marijuana are much milder than the side effects of the traditional drugs used to treat Hepatitis C. Many patients who use cannabis report they are able to continue the use of their prescription medications only when the side effect can be mitigated with cannabis. Marijuana also has recognized anti-anxiety, anti-depressant and stress reducing qualities which ease psychological symptoms and side effects as well as helping to prevent substance abuse relapse. Cannabis has the ability to stimulate appetite, which many Hepatitis C patients find beneficial. Patients without prescription insurance find the ability to grow their own medicine at li ttle or no cost to be an additional benefit.s

RCW 69.51A states that for a patient to qualify for use of medical marijuana, their physician must find that "It is their medical opinion that the potential benefits of the medical use of marijuana would likely outweigh the health risks for this patient." We urge you to sign the enclosed "Documentation of Medical Authorization to Possess Marijuana for Medical Purposes in Washington State." The Washington State Medical Association has prepared this document for use by our state's physicians. The link between stress and Hepatitis C is well established. Eliminating the stress induced by the fear of arrest by patients who currently use marijuana for their symptoms is yet one more benefit of the medical marijuana act.

 

Other Published reference data

22. Mechoulam R. 1986. The pharmacology of cannabis sativa. In Cannabinoids as Therapeutic Agents, ed. R Mechoulam, pp. 1Ð19. Boca Raton, FL: CRC

23. Zias J, Stark H, Sellgman J, Levy R, Werker E, et al. 1993. Early medical use of cannabis. Nature 363:215

24. Nelson, A critical review of the research literature concerning some biological and psychological effects of cannabis Advisory Committee on Illicit Drugs, Cannabis and the Law in Queensland: Criminal Justice Commision of Queenslans Australia 1993

25. Avakian, Hovath, Michael and Jacobs, Effects of marijuana on cardio-respiratory responses to submaximal exercise Clinical Pharmacological Therapeutics Vol. 6, pp771-781, 1979

26. National Commision on Marijuana and Drug Abuse Report, 1972

27. World Health Organization Project on Health Implications of Cannabis Use, 1997

28 Guimares, Anxioltic effect of cannabidol derivatives in the elevated plus-maze, General Pharmacology Vol. 25, pp 161-164 1994

29. Zuardi, et al, Action of cannabidol on the anxiety and other effects produced by delta-9 THC in normal subjects, Pschopharmacology Vol. 76 pp 245-250

30. Zuardi, et al, Effects of isapirone and cannabidol on human experimental anxiety, Journal of Pschopharmacology Vol. 7, pp 82-88

31. Nelson K, Walsh D, Deeter P, Sheehan F. 1994. A phase II study of delta-9-tetrahydrocannabinol for appetite stimulation in cancer-associated anorexia. J.Palliative Care 10:14Ð18

32. Tashkin et al, Effects of habitual use of marijuana and/or cocaine on the lung, Research findings on smoking abused substances, NIDA Monograph 99, 1990

33. Tashkin, Is frequent marijuana smoking hazardous to health?, Western Journal of Medicine Vol 158, No. 6, pp596-601 1993

34. Piomelli D. 1997. Functional role of high-affinity anandamide transport, as revealed by selective-inhibition. Science 277:1094Ð

35.Casteneda et al, 1991, THC does not effect striatal dopamine release:micro dialasis in freely moving rats.

36. Gifford, Gardner and Ashby The effects of intravenous administration of delta-9 tetrahydracannabinol on the activity of A-10 dopamine neurons recorded in vivo in anesthetized rats, Neuropsychopharmacology Vol. 36 No.2, pp.96-99 1997

 

 

 

 

Report by Bruce Buckner