Positive Health Online

As press reports frequently tell us, many people with chronic pain conditions, such as fibromyalgia, choose to use illegal substances, such as cannabis, for relief of their symptoms. When people use cannabis/marijuana as a means of easing – for example – their pain symptoms, the active cannabinoid substance, anandamide, works by mimicking endogenous (self-produced) anandamide, by binding to cannabinoid neuroreceptors, producing pain relieving effects.[1]

It therefore appears that our bodies can produce virtually identical chemicals to those contained in cannabis.

This requires that we have receptor sites that can be stimulated by such self-produced chemicals. It also seems that there exist some surprising ways to encourage self-production of these endocannabinoids – including moderate or aerobic exercise[2] and bodywork!

This offers a partial explanation for phenomena that in the past were ascribed to endorphin effects – such as ‘runner’s high’, and possibly to the wonderfully relaxed and euphoric feelings following good bodywork/ massage!

As John McPartland[3] explains: “The endocannabinoid (eCB) system, like the better-known endorphin system, consists of cell membrane receptors, endogenous ligands, and ligand-metabolizing enzymes. Two cannabinoid receptors are known: CB1 is principally located in the nervous system, whereas CB2 is primarily associated with the immune system. Two eCB ligands, anandamide (AEA) and 2-AG, are mimicked by cannabis plant compounds.”

The endocannabinoid system is fascinating, and is very important to our understanding of a number of issues relating to pleasure, pain, weight gain and the links between these topics and bodywork and exercise!

What Happens when this System is Blocked?

Because endocannabinoids stimulate appetite, attempts have been made by pharmaceutical companies to find drugs to completely block the eCB receptors – the logic being that if these were non-operating, appetite would be suppressed, and weight would decline.

This hypothesis is at least partially correct – however when eCB receptors are blocked by drugs (such as rimonabant), so that endocannabinoids cannot function, while appetite is indeed suppressed and weight loss induced, the side-effects can be devastating.

In 2007 the US Food and Drug Adminstration (FDA)[4] rejected the licensing of such a drug because subjects in rimonabant studies suffered depressed mood, anxiety, headache, nausea and diarrhoea, while latent multiple sclerosis and seizure disorders were triggered, and the risk for suicide doubled.

As McPartland notes3, genetically modified mice that have no ability to produce endocannabinoids “suffer increased morbidity and premature mortality, and show greater aggression, epilepsy, age-related neuron loss, anxiogenic-like and depressive-like behavior”.[5]

To summarize (because of space constraints):
•    Endocannabinoids are self-produced chemicals (e.g. anandemide or AEA, also known as Tetrahydrocannabinol or THC) that mimic the pain relieving and pleasure enhancing effects of cannabis;[6]
•    In 2004 Dietrich & McDaniel[7] demonstrated that pleasant feelings following physical activity/exercise were the result of the release of the naturally produced body chemical, the endocannabinoid, anandamide;
•    Darmani et al[8] have noted that anandemide is copiously produced in the body, not only in response to aerobic activity, but to pain and – it seems – as a response to bodywork such as massage, deep tissue work, high velocity (HVLA) manipulation and – according to McPartland[9] – 4VC (4th ventricular compression) as used in cranial treatment;
•    Cranial therapists and practitioners may find it of interest that McPartland reports that cerebral spinal fluid (CSF) is “awash with eCBs”, and that cells lining the ventricular system express endocannabinoids and eCB enzymes[10], which modulate the rhythmic production of CSF, and control eCB levels in the CSF;[11]
•    The endocannabinoid system influences embryological development, diminishes pain transmission and sensation, and also reduces inflammation[12] in myofascial tissue;
•    To emphasize: as part of its normal ‘metabolic housekeeping’, as well as in response to aerobic activity, and to bodywork of all sorts (as well as to pain), your body produces chemicals – not only endorphins as previously thought[13], but endocannabinoids, that make you feel good (euphoria), ease pain, reduce inflammation and enhance a healthy appetite;
•    It seems from research evidence that the endocannabinoid (eCB) system also balances sympathetic-parasympathetic tone, imparts anti-emetic and antihypertensive benefits, and favourably modulates stress in the HPA axis;[14]
•    Suppression of the endocannabinoid system pharmaceutically in order to reduce weight has been shown to have potentially disastrous results.

References

1.    McPartland JM, Pruitt PL. Side Effects of Pharmaceuticals not Elicited by Comparable Herbal Medicines: The Case of Tetrahydrocannabinol and Marijuana. Altern Ther Health Med. 5(4):57-62. 1999.
2.    Sparling P et al. Exercise Activates the Endocannabinoid System. Neuroreport. 14(17): 2209-2211. 2003.
3.    McPartland J. Expression of the Endocannabinoid System in Fibroblasts and Myofascial Tissues. Journal of Bodywork and Movement Therapies. 12(2). 2008.
4.    Food and Drug Administration FDA Briefing Document: New Drug Application. 21-888. Zimulti (Rimonabant). Food and Drug Administration, Washington, DC. Available at: www.fda.gov/ohrms/dockets/AC/07/briefing/ 2007-4306b1-fda-backgrounder.pdf  2007.
5.    Martin M, Ledent C, Parmentier M et al. Involvement of CB1 Cannabinoid Receptors in Emotional Behaviour. Psychopharmacology (Berl). 159: 379-387. 2002.
6.    McPartland J Simons D  Myofascial Trigger Points: Translating Molecular Theory into Manual Therapy. Journal of Manual & Manipulative Therapy. 14(4): 150-157. 2006.
7.    Dietrich A, McDaniel, W. Endocannabinoids and Exercise. British Journal of Sports Medicine. 38(5): 536-541. 2004.
8.    Darmani N et al. Involvement of the Cannabimimetic Compound, N-Palmitoyl-Ethanolamine, in Inflammatory and Neuropathic Conditions. Jnl. Neuropharm. 48(8): 1154-1163. 2005.
9.    McPartland J et al. Cannabimimetic Effects of Osteopathic Manipulative Treatment. J Amer Osteopathic Assoc. 105: 283-291. 2005.
10.    Curtis MA, Faull RL, Glass M. A Novel Population of Progenitor Cells Expressing Cannabinoid Receptors in the Subependymal Layer of the Adult Normal and Huntington’s Disease Human Brain. Journal of Chemical Neuroanatomy. 31: 210-215. 2006.
11.    Ashton JC, Appleton I, Darlington CL, Smith PF. Cannabinoid CB1 Receptor Protein Expression in the Rat Choroid Plexus: A Possible Involvement of Cannabinoids in the Regulation of Cerebrospinal Fluid. Neuroscience Letters. 364: 40-42. 2004.
12.    Ashton JC. Cannabinoids for the Treatment of Inflammation. Current Opinion in Investigational Drugs. 8: 373-384. 2007.
13.    Hou C-R, Tsai L-C, Cheng K-F. Immediate Effects of Various Physical Therapeutic Modalities on Cervical Myofascial Pain and Trigger-Point Sensitivity. Archives of Physical and Medical Rehabilitation. 83: 1406-1414. 2002.
14.    Pertwee RG. The Therapeutic Potential of Drugs that Target Cannabinoid Receptors or Modulate the Tissue Levels or Actions of Endocannabinoids. AAPS Journal. 7: E625-E654. 2005.