HEPATITIS C - 12 MARIJUANA RESEARCH PAPERS
Hepatitis C - Medical Marijuana Research Papers Worldwide - 2000- 2017
The overwhelming consensus opinion of independent clinical research is that marijuana most definitely helps treat Hepatitis C.
Therapists should recognize that CBD, the non-psychoactive component along with D9-THC (the psychoactive component) work together along with several terpenes to deliver a myriad of effects, which vary from individual to individual. This multiple cannabinoid / terpene interaction are know as the entourage effect. The entourage effect was discovered more than forty years ago, however, many researchers don't know of, or recognize this basic premise of the science of cannabis medicine.
Negative studies tend to be funded - almost exclusively by governmental agencies or pharmaceutical corporations that have no interest in positive findings toward the efficacy of cannabis. Furthermore, this polarized research group's findings invariably oppose that of independent worldwide clinical researchers.
Negative studies tend to focus on loose statistical methods and data collected from non-clinical situations.
For example, there are several research reports that marijuana is a risk factor in liver fibrosis. Upon examination of the methods, researchers, funding and study type (clinical or nonclinical), distilling down fact from fiction, we could find little of substance apart from hearsay as a basis for these claims.
1 72% OF 170 OF HEPATITIS SUFFERERS WERE MUCH IMPROVED WITH MARIJUANA
1 Findings of a standardized survey on the medicinal use of marijuana products in the German-speaking area. Schnelle et-al year 1999. Forschende Komplementärmedizin - Germany 3: 28 to 36.
1 Findings of a Standardized Survey on the Medical Use of cannabis Products in the German-Speaking Area The plant marijuana sativa has a long history of medical use in the treatment of pain and spasms, the promotion of sleep, and the suppression of nausea and vomiting. However, in the early 70s marijuana was classified in the Narcotic Acts in countries all over the world as having no therapeutic benefit; therefore, it cannot be prescribed by physicians or dispensed by pharmacists.
1 In the light of this paradoxical paradigm, an increasing quantity of patient practices self-prescription with marijuana based medicines for relieving a variety of symptoms. An anonymous standardized survey of the medicinal use of marijuana and marijuana products of victims in Germany, Austria and Switzerland was conducted by the Association for marijuana as Medicine - Cologne, Germany.
1 During the period of about about one year 170 subjects participated in this survey; questionnaires of 128 subjects could be included into the study-evaluation. 68 percent of these subjects were males, 32 percent women, with a total average age of 37.5 - ± 9.6- years. The most frequently mentioned indications for medicinal marijuana use were depression - 12.0 percent- multiple sclerosis - 10.8 percent- HIV-infection - 9.0 percent- migraine - 6.6 percent- asthma - 6.0 percent- back pain - 5.4 percent- hepatitis C - 4.8 percent- sleeping disorders - 4.8 percent- epilepsy - 3.6 percent- spasticity - 3.6 percent- headache - 3.6 percent- alcoholism - 3.0 percent- glaucoma - 3.0 percent- nausea - 3.0 percent- disk prolapse - 2.4 percent, and spinal cord injury - 2.4 percent.
1 The majority of subjects employed natural marijuana products such as marijuana, hashish and an alcoholic tincture; in just 5 instances dronabinol (synthetic D9-THC) - Marinol- r- was taken by prescription.
1 About half of the 128 subjects of the survey - 52.4 percent had employed marijuana as a recreational drug before the onset of their sickness. To this day 14.3 percent took marijuana by mouth), 49.2 percent by inhalation and in 36.5 percent of instances both application modes were employed. 72.2 percent of the subjects stated the symptoms of their sickness to have ''much improved'' after marijuana ingestion, 23.4 percent stated to have ''slightly improved'', 4.8 percent experienced ''no change'' and 1.6 percent reported that their symptoms got ''worse''.
1 Being asked for the satisfaction with their therapeutic use of marijuana 60.8 percent stated to be ''very satisfied'', 24.0 percent ''satisfied'', 11.2 percent ''partly satisfied'' and 4.0 percent were ''not satisfied''. 70.8 percent experienced no side effects, 26.4 percent reported ''moderate'' and 3.3 percent ''strong'' side effects. 84.1 percent of subjects have not felt any need for dose increase during the last 3 months, 11.0 percent had to increase their marijuana dose ''moderately'' and 4.8 percent ''strongly'' in order to maintain the therapeutic effects.
1 Thus, this survey demonstrates a successful use of marijuana products for the treatment of a multitude of various illnesses and symptoms. This use was usually accompanied only by slight and in general acceptable side effects. Because the patient group responding to this survey is presumably highly selected, no conclusions can be drawn about the quantity of wanted and unwanted effects of the medicinal use of the hemp plant for particular indications.
2 MODEST MARIJUANA USE IMPROVES VIRUS - HEP-C SYMPTOMS VIRUS - HEP-C
2 marijuana use improves retention & virological outcomes in test subjects treated for hepatitis C. Sylvestre et-al year 2006. European Journal of Gastroenterology & Hepatology. 18: 1057 to 1063.
2 Despite the widespread use of polypharmacy, the management of hepatitis C virus - HCV treatment-related side-effects is often incomplete, and many test subjects turn to marijuana for symptom relief. Unfortunately, there are few data about marijuana use on treatment outcomes, leaving clinicians without the data needed to inform recommendations.
2 Methods: To define the impact of marijuana use during HCV treatment, we conducted a prospective observational study of standard interferon and ribavirin treatment in 71 recovering substance users, of whom 22 - 31 percent employed marijuana and 49 - 69 percent did not.
2 Our findings suggest that modest marijuana use may offer symptomatic and virological benefit to some test subjects undergoing HCV treatment by helping them maintain adherence to the challenging medication regimen.
3 CANNABIS INGREDIENTS A BASIS FOR PRESENT AND FUTURE HEP-C THERAPY
3 The endocannabinoid (body's own) system in chronic liver disease - PDF. Zamora-Valdes et-al year 2005. Annals of Hepatology 4: 248 to 254.
3 Recently, endocannabinoids (body's own) was implicated in the hemodynamic alterations occurring in cirrhosis. These changes appear to be regulated via specific cannabinoid receptors - CB1 on splanchnic and hepatic (liver) vascular endothelium (blood vessel lining) . Plasma levels of endocannabinoids (body's own) also seem to be elevated in hepatitis, and are involved in apoptosis of hepatocytes by a membrane mechanism not related to a specific receptor.
3 Other trials and studies suggest a therapeutic role for phyto-cannabinoids in dialing down the inflammation of experimental hepatitis. In an animal-rodent model of acute hepatic (liver) failure, both endocannabinoids (body's own) and the antagonist to the Cannabinoid-CB1 receptor was found to have a therapeutic action on neurological and cognitive (brain) function.
3 Conclusions: Endocannabinoids (body's own) 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.
4 CANNABINOIDS ARE INVOLVED IN THE LIVER DISEASE PROCESS
4 Endocannabinoids (body's own) & liver disease – review. Gabbey et-al year 2005. Liver International 25: 921 to 926.
4 Recently, endocannabinoids (body's own) was implicated in the hemodynamic alterations occurring in cirrhosis. These changes appear to be regulated via specific cannabinoid receptors - CB1 on splanchnic and hepatic (liver) vascular endothelium (blood vessel lining) . Plasma levels of endocannabinoids (body's own) also seem to be elevated in hepatitis, and are involved in apoptosis of hepatocytes by a membrane mechanism not related to a specific receptor.
4 Other trials and studies suggest a therapeutic role for phyto-cannabinoids in dialing down the inflammation of experimental hepatitis. In an animal-rodent model of acute hepatic (liver) failure, both endocannabinoids (body's own) and the antagonist to the Cannabinoid-CB1 receptor was found to have a therapeutic action on neurological and cognitive (brain) function.
4 Endocannabinoids (body's own) 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.
5 CANNABIS IS AN ANTI-INFLAMMATORY - HELPS HEP-C - MECHANISM OF ACTION PROPOSED
5 A novel synthetic cannabinoid derivative inhibits inflammatory liver damage via negative cytokine regulation. Lavon et-al year 2003. Molecular Pharmacology 64: 1334 to 1344.
5 In conclusion, we propose that PRS-211,092 reduces liver injury through early induction of IL-6 and IL-10 followed by an increase in SOCS proteins, which in turn down-regulate pro-inflammatory cytokine and chemokine signaling. This is the first time, to our knowledge, that evidence has been presented for the induction of SOCS-1 and 3 by any natural or synthetic cannabinoid. Because there are indications that d9-THC and endocannabinoids such as anandamide have immunomodulatory properties - Berdyshev, year 2000.
5 We suggest that the negative feedback control of cytokine signaling by the SOCS may be a generic feature of phyto-cannabinoids. In contrast to PRS-211,092, which partially inhibits proinflammatory cytokine expression, FK506, the typically employed immunosuppressant, completely shuts down the autoimmune response after Con A challenge - Figs. 2 and 4. Thus, unlike FK506, PRS-211,092 down-modulates inflammation, but maintains an active auto-immune defense system.
5 In summary, the protective property of PRS-211,092 on autoimmune-regulated hepatitis through cytokine modulation suggests that this compound and its congeners may provide the basis for developing immunomodulatory drugs for treating hepatitis, as well as for other short- and long-term inflammatory diseases.
6 CBD MAY REPRESENT A TREATMENT FOR LIVER FIBROSIS
6 Daily marijuana smoking as a risk factor for progression of fibrosis in chronic hepatitis C. Hezode et-al year 2005. Hepatology 42: 63 to 71.
6 This study shows a strong link between daily marijuana consumption and fibrosis progression rate in test subjects with chronic hepatitis C. These findings support experimental data demonstrating the profibrogenic role of Cannabinoid-CB1 receptors, Daily marijuana consumption should be avoided in test subjects with chronic hepatitis C.
6 In multivariate analysis, fibrosis progression rate >0.08 U per year was independently related to a 4 times larger risk from daily marijuana smoking; alcohol intake 30 grams/day showed double the risk for faster fibrosis progression; age at contamination >24 years was associated with a 4 times larger risk for faster fibrosis progression; and activity A2 was associated with 7 times larger risk for faster fibrosis progression. Pharmacologic antagonists of Cannabinoid-CB1 receptors may represent a new approach in the treatment of liver fibrosis.
7 JAPANESE LED NEGATIVE STUDY - MARIJUANA IS RISKY
7 Influence of marijuana use on severity of hepatitis C disease. Ishida et-al year 2008 Clinical Gastroenterology & Hepatology 6: 69 to 75.
7 Daily marijuana use is strongly associated with moderate to severe fibrosis, and HCV-infected individuals should be counseled to reduce or abstain from marijuana use.
7 Although we identified a modest cross-sectional association between higher marijuana exposure and lower eGFR cys among young adults with preserved eGFR, our findings were largely null and did not demonstrate a longitudinal association between marijuana use and eGFR cys change, rapid eGFR cys decline, or prevalent albuminuria.
Editor's note: Positive findings were thrown out.
8 CANNABIS EFFECT ON CELL RECEPTORS IS ANTI INFLAMMATORY AND CBD CAN DIAL DOWN LIVER SCAR TISSUE
8 Role of phyto-cannabinoids in liver disease. Parfieniuk & Flisiak. year 2008. World Journal of Gastroenterology 14: 6109 to 6114.
8 Phyto-cannabinoids are a group of compounds acting primarily via Cannabinoid-CB1 and Cannabinoid-CB2 receptors. The expression of cannabinoid receptors in normal liver is low or absent. However, many reports have proven dial-up of the expression of Cannabinoid-CB1 and Cannabinoid-CB2 receptors in hepatic (liver) myofibroblasts and vascular endothelial (blood vessel lining) cells, as well as increased concentrationS of endocannabinoids in liver in the course of chronic progressive liver diseases.
8 It has been shown that Cannabinoid-CB1 receptor signalling exerts profibrogenic and proinflammatory effects in liver tissue, primarily due to the stimulation of hepatic (liver) stellate cells, whereas the activation of Cannabinoid-CB2 receptors inhibits or even reverses liver fibrogenesis. In the same way, Cannabinoid-CB1 receptor stimulation contributes to progression of liver steatosis.
8 In end-stage liver disease, the endocannabinoid system has been shown to contribute to hepatic (liver) encephalopathy and vascular effects, such as portal hypertension, splanchnic vasodilatation, relative peripheral hypotension and probably cirrhotic cardiomyopathy.
8 So far, available evidence is based on cellular cultures or animal-rodent models. Clinical data on the effects of phyto-cannabinoids in chronic liver diseases are limited. However, recent trials and trials, and studies have shown the contribution of marijuana smoking to the progression of liver fibrosis and steatosis. Moreover, controlling Cannabinoid-CB1 or Cannabinoid-CB2 signalling appears to be an attractive target in managing liver diseases.
9 MARIJUANA IS PLUS AND MINUS IN HEP-C PATIENTS
9 Marijuana smoking does not accelerate progression of liver disease in HIV-hepatitis C coinfection: a longitudinal cohort analysis. Brunet et-al year 2013. Clinical Infectious Diseases 57: 663 to 670.
9 At baseline, 53 percent had smoked marijuana in the past 6 months, consuming a median of 7 joints/week - IQR, 1-21; 40 percent smoked daily. There was no evidence that marijuana smoking accelerates progression to significant liver fibrosis - APRI ≥ 1.5 or cirrhosis - APRI ≥ 2; hazard ratio 1.02 and 0.99, respectively. Each ten additional joints/week smoked slightly increased the risk of progression to a clinical diagnosis of cirrhosis and ESLD combined. However, when exposure was lagged to 6-12 months before the diagnosis, marijuana was no longer associated with clinical disease progression.
9 In this prospective analysis, we found no evidence for an association between marijuana smoking and significant liver fibrosis progression in HIV/HCV coinfection. A slight increase in the hazard of cirrhosis and ESLD with higher intensity of marijuana smoking was attenuated after lagging marijuana exposure, suggesting that reverse causation due to self-medication could explain previous findings.
Editor's note: This paper reflects the immaturity of the medical community toward marijuana. Marijuana is not one thing, as the different strains afford vastly different quantities of different cannabinoids, some of which are receptor antagonists (block the activity) and others are agonists (bind to receptor), which can either increase or decrease the tendency toward fibrosis. Until the medical community understands these fundamentals, research studies will lack fundamental merit.
10 RESEARCHERS APPROACH STUDY WITH THE BELIEF THAT CANNABIS IS A NARCOTIC
10 Treatment for hepatitis C virus & marijuana use in illicit drug user patients: implications & questions. Fischer et-al year 2006. European Journal of Gastroenterology & Hepatology. 18: 1039 to 1042.
10 Illicit drug users are the primary risk group for HCV transmission, and will form the largest HCV treatment population for years to come. Sylvestre et al.’s study suggests that marijuana use may benefit treatment retention and outcomes in illicit drug users undergoing HCV treatment. In fact, there is substantial evidence that marijuana use may help address key challenges faced by
drug users in HCV treatment - e.g., nausea, depression, especially when such treatment occurs in the context of methadone maintenance treatment which may amplify these consequences.
10 While further research is required on the biological and clinical aspects of the benefits of marijuana use for HCV treatment, and the effectiveness of marijuana use for HCV treatment needs to be explored in
larger study populations, we advocate that in the interim, existing barriers to marijuana use are removed for drug users undergoing HCV treatment until the conclusive empirical basis for evidence-based guidance is available.
11 NEGATIVE STUDY - MIXTURE OF TOBACCO, BOOZE AND MARIJUANA STATS = ???
11 Daily marijuana use: a novel risk factor of steatosis severity in people with chronic hepatitis C. Hezode et-al year 2008. Gastroenterology 134: 432 to 439.
11 A total of 315 consecutive people with untreated CHC undergoing liver biopsy were included. Detailed histories of recent marijuana, alcohol, and tobacco use were recorded. Steatosis, activity, and fibrosis stage were assessed by 2 pathologists according to METAVIR. Marked steatosis was designated as >/=30 percent. Patients were categorized as marijuana nonusers - 63.5 percent, occasional marijuana smokers - 12.4 percent, or daily marijuana smokers - 24.1 percent.
11 Our findings identify daily marijuana smoking as a novel independent predictor of steatosis severity during CHC and strongly argue for a teratogenic role of the cannabinoid system. marijuana use should be discouraged in people with CHC.
** Christophe Hezode, MD is a definitely pro-pharmaceutical, anti-marijuana researcher.
12 CANNABIS IS IMPORTANT IN REGULATING LIVER FUNCTION - THERAPY OPTIONS SUGGESTED
12 Role of phyto-cannabinoids in the development of fatty liver - steatosis.Purohit et-al year year 2010. The AAPS Journal 12: 233 to 237.
12 Emerging evidence suggests that phyto-cannabinoids play an important role in the modulation of fatty liver, which appears to be regulated via activation of phyto-cannabinoid receptors. Teratogenic agents such as ethyl-alcohol and high-fat diet can dial-up the activity of cannabinoid 1 - Cannabinoid-CB1- receptors via increasing synthesis of endocannabinoids, 2-arachidonoylglycerol, and anandamide. Cannabinoid-CB1 receptors can also be dial-up by obesity.
12 Cannabinoid-CB1 receptor activation findings in upregulation of lipogenic transcription factor, sterol regulatory element-binding protein 1c and its target enzymes, acetyl-CoA carboxylase-1, and fatty acid synthase and concomitantly, downregulation of carnitine palmitoyltransferase-1. This leads to increased de novo fatty acid synthesis as well as decreased fatty acid oxidation, culminating into the development of fatty liver. High-fat diet, in addition to Cannabinoid-CB1 receptor activation, appears to activate Cannabinoid-CB2 receptors that may also contribute to fatty liver.
12 In non-alcoholic fatty liver disease, Cannabinoid-CB2 receptor activation is associated with the development of fatty liver. marijuana smoking can increase the severity of fatty liver in hepatitis C victims although the precise mechanism is unknown. As the mechanisms involved in endocannabinoid receptor signaling are being increasingly well understood and the biosynthetic regulatory elements elucidated, these present good opportunities for the pharmaceutical scientists to design drugs to treat liver diseases, including steatosis, based on the phyto-cannabinoids, endocannabinoids, and related templates.
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