WE SUPPORT THE MEDICINAL USE OF CANNABIS
FOR INFECTED BLOOD VICTIMS
Current evidence suggests that cannabis has the potential of offering therapeutic benefits to patients with HCV and other liver diseases (Mallat, et al., 2011) including HIV/AIDS. From the earliest days of the HIV epidemic, cannabis has been used to treat many of the complications of disease, ranging from the symptoms of HIV wasting syndrome to side effects associated with antiretroviral drug use. While newer generation drugs for both HIV and HCV have greatly reduced the incidence and severity of many of the symptoms, cannabis is still popularly embraced by patients as a means to alleviate the myriad of ongoing symptoms that can accompany these conditions. Some studies indicate that cannabis may afford long-term benefits by effectively slowing or even preventing disease progression in these conditions.
The Content is not intended to be a substitute for professional medical advice, diagnosis, or treatment.
Dr. Donald Abrams Tells Us How Medical Marijuana Helps AIDS Patients – Pt 1
Dr. Donald Abrams Tells Us How Medical Marijuana Helps AIDS Patients - Pt 2
There is growing evidence that glucose metabolism in the liver is in part under the control of the endocannabinoid system (ECS) which is also supported by its presence in this organ. The ECS consists of its cannabinoid receptors (CBRs) and enzymes that are responsible for endocannabinoid production and metabolism. ECS is known to be differentially influenced by the hepatic glucose metabolism and insulin resistance, e.g., cannabinoid receptor type 1(CB1) antagonist can improve the glucose tolerance and insulin resistance. Interestingly, our own study shows that expression patterns of CBRs are influenced by the light/dark cycle, which is of significant physiological and clinical interest.
Although the mortality rates of cirrhosis are underestimated, its socioeconomic burden has demonstrated a significant global impact. Cirrhosis is defined by the disruption of normal liver architecture after years of chronic insult by different etiologies. Treatment modalities are
recommended primarily in decompensated cirrhosis and specifically tailored to the different manifestations of hepatic decompensation. Antifibrogenic therapies are within an active area of investigation.The endocannabinoid system has been shown to play a role in liver disease,and cirrhosis specifically, with intriguing possible therapeutic benefits.
REDUCED INCIDENCE AND BETTER LIVER DISEASE OUTCOMES AMONG CHRONIC HCV INFECTED PATIENTS WHO CONSUME CANNABIS.
Authors reported that subjects who consumed cannabis "had decreased prevalence of liver cirrhosis" and had "lower total health care cost ($39,642 versus $45,566) compared to non-cannabis users." They concluded, "Our findings suggest that cannabis use is associated with decreased incidence of liver cirrhosis."
INCREASED CONSUMPTION OF COFFEE AND MARIJUANA MAY SHARPLY REDUCE THE RISK FOR EARLY DEATH FROM HEPATITIS C INFECTION, RESEARCHERS HAVE FOUND.
The study of more than 1,200 patients with HIV and HCV found that those who drank the most coffee and used marijuana regularly or daily had more than a 60% lower risk for death from the infection over a five-year period.
HIV-INFECTED CANNABIS USERS HAVE LOWER CIRCULATING CD16 MONOCYTES AND IP-10 LEVELS COMPARED TO NON-USING HIV PATIENTS
A chemical found in marijuana, known as tetrahydrocannabinol, or THC, has been found to potentially slow the process in which mental decline can occur in up to 50 percent of HIV patients, says a new study.
We report here for the first time in vitro studies to demonstrate the antiviral activity of CBD against HCV. CBD was shown to have activity against HCV in vitro but not against HBV. A review of the literature seems to suggest that CBD may also have activity in vivo based on its interaction with the CB2 receptor and as such using a host mechanism to indirectly slow the pathogenic process of the HBV virus. Based on these findings, CBD as such has potential to be further developed as a treatment for viral hepatitis, especially as a combination therapy with the currently existing therapies. Further studies are in progress to further validate and assess the activity in vivo.
CANNABIS USE AND REDUCED RISK OF INSULIN RESISTANCE IN HIV-HCV INFECTED PATIENTS: A LONGITUDINAL ANALYSIS
Cannabis use is associated with a lower IR risk in HIV–HCV-coinfected patients. The benefits of cannabis-based pharmacotherapies for patients concerned with increased risk of IR and diabetes need to be evaluated in clinical research and practice.
Overall, marijuana use did not predict fibrosis stage, inflammation grade or steatosis. Sustained virological response and marijuana use data were available for 359 of the 550 cohort participants; a total of 211 (58.8%) achieved a sustained virological response. Marijuana use was not associated with premature interruption of therapy for side effects, the likelihood of completing a full course of therapy or sustained virological response.
MARIJUANA SMOKING DOES NOT ACCELERATE PROGRESSION OF LIVER DISEASE IN HIV–HEPATITIS C COINFECTION: A LONGITUDINAL COHORT ANALYSIS
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 results.
ANTI-TUMORAL ACTION OF CANNABINOIDS ON HEPATOCELLULAR CARCINOMA: ROLE OF AMPK-DEPENDENT ACTIVATION OF AUTOPHAGY
This study, investigated the effects of cannabinoids – a novel family of potential anticancer agents – on the growth of HCC. We found that Δ9-tetrahydrocannabinol (Δ9-THC, the main active component of Cannabis sativa) and JWH-015 (a cannabinoid receptor 2 (CB2) cannabinoid receptor-selective agonist) reduced the viability of the human HCC cell lines HepG2 (human hepatocellular liver carcinoma cell line) and HuH-7 (hepatocellular carcinoma cells), an effect that relied on the stimulation of CB2 receptor. We also found that Δ9-THC- and JWH-015-induced autophagy relies on tribbles homolog 3 (TRB3) upregulation, and subsequent inhibition of the serine–threonine kinase Akt/mammalian target of rapamycin C1 axis and adenosine monophosphate-activated kinase (AMPK) stimulation. Pharmacological and genetic inhibition of AMPK upstream kinases supported that calmodulin-activated kinase kinase β was responsible for cannabinoid-induced AMPK activation and autophagy. In vivo studies revealed that Δ9-THC and JWH-015 reduced the growth of HCC subcutaneous xenografts, an effect that was not evident when autophagy was genetically of pharmacologically inhibited in those tumors. Moreover, cannabinoids were also able to inhibit tumor growth and ascites in an orthotopic model of HCC xenograft. Our findings may contribute to the design of new therapeutic strategies for the management of HCC.