February 13, 2016

The CBD Research that Time Forgot

7/28/2011 – Time magazine made a flawed, sensationalistic attempt at covering cannibinoid research in a recent article. The piece details the effects of a synthetic cannabinoid (called JWH-133) and its ability to deter cocaine addiction in an animal model by activating the CB2 receptor in the brain. The implications of this study imply that cannabinoids could be potentially used as an “exit” drug for cocaine users. But Time confused the synthetic drug used in the study with a natural substance called cannabidiol or CBD.

Unfortunately, the seemingly good news about CB2 receptors and the treatment of cocaine addiction was over-shadowed by a plethora of inaccurate scientific information.

Here are the three main points that Time forgot:

  • CBD does not activate CB2 receptors at a reasonable concentration. This crucial information was published in 1996. In test tube experiments, CBD can only activate the CB2 receptor at a concentration unachievable through any known or conventional route of administration. If, for instance, a patient had an IV hooked up to a vat of nearly pure CBD, then there might be enough CBD to affect receptor dynamics and thus lead to the activation of CB2 receptors. In short, CBD may be able to treat cocaine addiction, but not by acting through cannabinoid receptors.
  • Time magazine glaringly overlooked the most relevant research done on the effects of actual CBD (not a synthetic cannibinoid like JWH-133) and cocaine addiction by Raphael Mechoulam, one of the most noted Cannabis researchers in history. Dr. Mechoulam is credited as the first scientist to isolate THC as the primary ingredient in Cannabis back in 1964 and he continues to produce groundbreaking cannabis research. His important 2004 study looked at CBD and cocaine addiction but the research cited by Time never even mentions CBD.

One of the most basic concepts in cannabinoid science is that THC activates CB1 and CB2 receptors, but CBD does not activate CB1 and CB2 receptors. To refute this fundamental understanding of cannabinoid receptors is an insult to the scientific community and ultimately does more harm than good. As a scientist, this type of research is extremely complex and all news organizations will need to do a better job when conveying information to the public.

Dr. Raphael Mechoulam - The scientist that Time forgot

Read more Science at Freedomisgreen.com

Jahan Marcu is currently investigating the pharmacology of cannabinoid receptors. He was working at the California Pacific Medical Center Research Institute when exciting discoveries were made showing enhanced anti-cancer effects with THC and CBD from the Cannabis plant. The findings were published in the Journal of Molecular Cancer Therapeutics. In 2009 he received the Billy Martin Award from the International Cannabinoid Research Society (ICRS). Jahan is currently the vice-chair the Medical and Scientific Advisory Board at Americans for Safe Access (ASA). Questions?   Contact    science@freedomisgreen.com

DISCLAIMER: The views and opinions expressed are those of the author and do not necessarily represent any University, business or affiliates. While the information provided in this blog is from published scientific studies it is not intended to diagnose or treat any disease.


  1. Warren Klofkorn says:

    The apparent inability of mainstream journalists to communicate accurately the essence of almost any scientific research continues to dumbfound me. This is NOT limited to cannabis-relate research, but coverage of this research certainly typifies the phenomenon.


  2. Sunil says:

    It may be tissue dependent, perhaps, Jahan? See:

    Br J Pharmacol. 2007 Mar;150(5):613-23. Epub 2007 Jan 22.

    Cannabidiol displays unexpectedly high potency as an antagonist of CB1 and CB2 receptor agonists in vitro.

    Thomas A, Baillie GL, Phillips AM, Razdan RK, Ross RA, Pertwee RG.

    School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK. a.thomas@ed.ac.uk


    BACKGROUND AND PURPOSE: A nonpsychoactive constituent of the cannabis plant, cannabidiol has been demonstrated to have low affinity for both cannabinoid CB1 and CB2 receptors. We have shown previously that cannabidiol can enhance electrically evoked contractions of the mouse vas deferens, suggestive of inverse agonism. We have also shown that cannabidiol can antagonize cannabinoid receptor agonists in this tissue with a greater potency than we would expect from its poor affinity for cannabinoid receptors. This study aimed to investigate whether these properties of cannabidiol extend to CB1 receptors expressed in mouse brain and to human CB2 receptors that have been transfected into CHO cells.

    EXPERIMENTAL APPROACH: The [35S]GTPS binding assay was used to determine both the efficacy of cannabidiol and the ability of cannabidiol to antagonize cannabinoid receptor agonists (CP55940 and R-(+)-WIN55212) at the mouse CB1 and the human CB2 receptor.

    KEY RESULTS: This paper reports firstly that cannabidiol displays inverse agonism at the human CB2 receptor. Secondly, we demonstrate that cannabidiol is a high potency antagonist of cannabinoid receptor agonists in mouse brain and in membranes from CHO cells transfected with human CB2 receptors.

    CONCLUSIONS AND IMPLICATIONS: This study has provided the first evidence that cannabidiol can display CB2 receptor inverse agonism, an action that appears to be responsible for its antagonism of CP55940 at the human CB2 receptor. The ability of cannabidiol to behave as a CB2 receptor inverse agonist may contribute to its documented anti-inflammatory properties.


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