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The Bogus History of CBD for Hepatitis-C

George Bennet PURE CBD Leave a Comment

It Began With a Satirical Web Site Describing Hepatitis-C Cures Via CBD

In June of 2014 a satirical web site claiming to be the Wyoming Institute of Technology (which does not actually exist) wrote an unfortunately believable joke article titled MARIJUANA CAN CURE HEPATITIS C, WIT RESEARCH SHOWS.  Thankfully the article has been removed from the satirical web site.  But misinformation on the internet takes on a life of its own: the article can still be found, spreading its damaging misinformation in places like this.  Even the American Journal of Medicine felt compelled to point out another “Wit” hoax which claimed that 92% of murderers have autism.The Misinformation Spreads

With this background it is inevitable that with the release of every legitimate study  showing that CBD seems to have properties which can lead to reduced liver inflammation and fibrosis, helping disorders such as autoimmune hepatitis writers will immediately link to those studies and claim (incorrectly) that they apply to Hepatitis-C, and then tout CBD as a cure.

Take for example this incorrect statement dated 28 September 2015 from MedicalMarijuannaInc: “Previous studies had actually implicated cannabis in the progression of cirrhosis, fibrosis, and other liver diseases (Fischer, et al., 2006). However, more recent research has found no link to marijuana smoking and the progression of liver disease (Brunet, et al., 2013).”

The 2013 Brunet article here is titled “Marijuana Smoking Does Not Accelerate Progression of Liver Disease in HIV–Hepatitis C Coinfection: A Longitudinal Cohort Analysis”.  So the misleading article quoted above should have said “… no link to marijuana smoking and the progression of liver disease in a group of people who were also infected with HIV“.  Even as corrected this has no relevancy to CBD based treatment since marijuana includes many cannabinoids.  THC for example has a strong affinity for the CB1 receptor which has been shown to be pro-inflammatory, fibrosis and steatosis.

Another example of a study which could easily to one to an incorrect conclusion is Cannabis use improves retention and virological outcomes in patients treated for hepatitis  from The European Journal of Gastroenterology and Hepatology.  In reality this study has nothing to do with the effects of cannabinoids on liver disease, rather the point is simply that marijuana smokers tend to adhere to their nausea creating interferon and ribivirin treatment better than non-cannabis users.

The Role of Cannabinoid Receptors on Disease Progression is Complex

Taken from Cannabinoids in Liver Diseases,  a 26 Feb 2016 article in The American Association for the Study of Liver Diseases journal by Eleonora Patsenker Ph.D. and Felix Stickel M.D., Ph.D., Table 1 shows some of the conclusions concerning the effects of various cannabinoid receptor agonists and antagonists.

Another good description is found in The Endocannabinoid System and Liver Diseases, published in The Journal of Neuroendocrinlogy, 17 April 2008 by P. Caraceni, M. Dominicali and M Bernardi.

While CBD has proven anti-inflammatory effects which may be very helpful for autoimmune hepatitis it may be that those same anti-inflammatory effects hinder the body’s fight against an infection like HCV.  No one knows until there is adequate research as to whether that is the case.

The Plot Thickens

In the Feb. 12 2017 edition of The Jamaican Observer the headline J’can scientists close to creating affordable hepatitis C drug from ganja led to a storm of web articles once again touting CBD as a valid HCV cure.  This is based on a study published in Pharmacognosy Research on Feb. 8, 2017, Potential of cannabidiol for the treatment of viral hepatitis.  It would take an appropriately qualified scientist to evaluate the validity of this study and what it means in reference to treating HCV with CBD.  However even a non-scientist can take note of such things as: clear commercial involvement – lots of conflict of interest here, no animal studies, just cell cultures, one-of-a-kind conclusions – no other confirming studies.  Clearly the “close to creating affordable hepatitis C drug” is hyperbole.

The Takeaway

While it is interesting to read about research studies and to listen to the latest “science news” report on television one has to remember that it is all taken out of context.  This is why what we are constantly told that “science” has just discovered is usually very contradictory from report to report.  Therefore it is best to consult qualified medical personnel rather than making your medical decisions based on some random article on the internet (yes, even this one).  For valid information on nutritional approaches to health and disease management carefully chosen science-based sources should be found, such as Dr. Fuhrman’s, which has great online communities and “Ask the Doctor” forums.


Table 1. Cannabinoid Receptor Agonists/Antagonists Applied in Animal Models and Human Studies of CLD
Compound Disease Effects
  1. Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGT, gamma-glutamyl transferase; HDL, high-density lipoprotein; NASH, nonalcoholic steatohepatitis; T2D, type 2 diabetes; TG, triglyceride.
Animal experiments
CB1 antagonists SR141716 (rimonabant), CB1−/− mice Cirrhosis, high-fat diet, biliary fibrosis, alcoholic hepatitis, I/R Improved fibrosis, steatosis, ascites, hypotension, portal pressure, cardiac contractility, fatty acids oxidation, insulin and leptin sensitivity, I/R-related tissue damage, increased adiponectin
New, peripherally restricted AM6545, JD5037, TM38837, VD60 Improved liver damage, reduced obesity and leptin resistance
CB2 agonists JWH-133, HU-308, HU-910 Acute liver injury, alcoholic liver disease, I/R, autoimmune hepatitis, biliary fibrosis, cirrhosis Suppressed histopathological and apoptotic liver damage, reduced inflammation, oxidative stress, fibrosis and bacterial translocation
Metabolic liver disease/high-fat diet Induced insulin resistance and steatosis
HU-444 (new, peripherally restricted) Suppressed hepatic inflammation and fibrogenesis
Human studies
CB1 and CB2 agonism Exogenous cannabinoids (THC, cannabis smoking) HCV/HIV Promoted fibrosis progression rate, steatosis severity, glucose intolerance (?), lowered insulin resistance risk
CB1- and CB2-independent, GPR55 antagonist Exogenous cannabinoid (cannabidiol) Hepatic encephalopathy Improved cognitive and motor function, neuroinflammation
CB1 antagonists Rimonabant Obesity, metabolic syndrome, NASH, T2D Reduced the prevalence of metabolic syndrome, body weight, TG, waist circumference, ALT, AST, GGT; increased HDL cholesterol


By George Bennet,
freelance journalist

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