Clinical Endocannabinoid Deficiency: Devil in the Detail

The endocannabinoid system is  a network of receptors and function modulatory agents. Clinical endocannabinoid deficiency suggests a dysfunction in the system. This was first introduced in 2001 by one Dr Ethan Russo. The research was published in 2004 and later updated in 2016. This concept was based on the idea that brain disorders are associated with neurotransmitter issues. Like acetylcholine in Alzheimer’s and serotonin in depression. 

It is hypothesised that the endocannabinoid system can be dismayed in one or several of four ways. The first being an overabundance of enzymes that overload endocannabinoid function. The second in lack of or insufficient amounts of synthesised endocannabinoids. The third is a broken connection between the endocannabinoids and receptors. Then the fourth is insufficient number of receptors. 

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In his updated research, Dr Russo suggests a number of reasons for the above four. The CED could be genetic. That means it could be a familial thing. It could als be congenital. That means that it was present at birth. It could also be a progression of an existing disease. This means that another disease is causing the endocannabinoid deficiency. Consequently, bringing about  hot of other diseases. It could also be brought about by injury. 

Body of Evidence

Research has been ongoing for years. In an effort to find evidence to support the endocannabinoid deficiency theories. So far, it is promising. In fact, a member of the International Cannabinoid Research Society was quoted saying that manipulation of the endocannabinoid system could save more lives than surgery. This is quite a statement from a notable member of the medical field. 

Science has so far, conclusively, associated at east three conditions to endocannabinoid deficiency. 

  • Irritable Bowel Syndrome is a condition characterised by inflammation of the gastrointestinal tract. Research has revealed that propulsion, secretion and even inflammation of the tract is driven by the endocannabinoid system. IN fact, in the 19th  century cannabis was the first ever fully effective intervention for related symptoms.

Biopsies were done on IBS patients and other healthy volunteers. It was found that the IBS patient biopsies had an elevated TRPV-1 immunoreactive nerve fiber. THis was said to contribute to the hypersensitivity and pain suffered by IBS patients. Therapy to boost AEA (anandamide) levels or desensitise TRPV was administered. CBD  is a non-hostile agent in this respect. 

  • Migraines are the third most common disease in the world. Chronic migraines affect more than 2% of the global population. It is characterised by sensory homeostatic imbalance. Correcting such an imbalance is the chief purpose of the endocannabinoid system. 

An assay of cerebrospinal fluid was done in 15 chronic migraineurs in which it was found that AEA levels were elevated. AEA caused blood vessel dilation in the brain area associated with migraines. There was action to prevent release of Nitric oxide. It was hypothesized that repetitive administration of TRPV-1 agonist like CBD would desensitise the receptor and ease migraine pain. 

  • Fibromyalgia is a condition characterised by pain. Widespread neuropathic pain. Studies found that pharmacological therapy should involve NMDA blockage. See, fibromyalgia patients exhibit a higher level of glutamate. By blocking the NMDA receptor, pain stimuli can be disabled or at least toned down. The extreme pain is associated with endocannabinoid hypofunction of the spinal cord. Endocannabinoid stimulation has been found to reduce hyperalgesia. 
  • Motion sickness is a doozy. It is characterised by nausea and just general lethargy. The endocannabinoid system was found to be instrumental in the pathophysiology. SEven out of 21 adults with acute motion sickness were found to have reduced AEA and 2-AG in the blood. These are the chief endocannabinoids produced by the body. Tests were done before and after flight tests maneuvers. The conclusion was that manipulation of the ECS could be an effective pathway for therapy especially in cases where traditional therapies have been grossly unsuccessful. 
  • Multiple Sclerosis is a condition of the central nervous system in which synapses are interrupted. There is widespread miscommunication leading to a variety of symptoms. Just by being a condition of the central nervous system, MS is already associated with ECS dysfunction. Seeing as ECS is widely involved in synaptic activity. Animal models for MS revealed that the ECS has a role in MS. It was found that the endocannabinoid system was impaired, more especially in the secondary progressive cases. 
  • Huntington’s Disease is characterised by neurodegeneration which brings about a variety of physical, cognitive and emotional issues. In 2008, Huntington’s mice models revealed that there is certainly a causal endocannabinoid deficiency. A further analysis of postmortem brain was done which revealed loss of cannabinoid receptor 1 activity. Another study was done on living Huntington’s patients. It was found that they had a decreased receptor availability. Huntington’s may be inherited but the progression and physiopathology is definitely rooted on CED. 
  • After the 9-11 tragedy, survivors were examined. Those who exhibited signs of PTSD had reduced levels of 2-AG. This is somewhat strong evidence of clinical endocannabinoid deficiency in PTSD patients. The same explains the efficacy of CBD and other phytocannabinoids for the condition. 

Testing

Testing of clinical endocannabinoid deficiency is usually done by investigating several aspects of the ECS. For example, one may be tested for AEA levels. AEA is involved in expressing the tonal strength of the endocannabinoid system. 

A hundred years ago before science was so far advanced, testing for this deficiency and other aspects of the ECS was very complicated and often invasive. It involved breaching of the cranial shell to investigate the masses beneath. As time went by, science came up with new ways. The new way, involved a needle in the brain.

There has been further advancement and CED can now be tested through the human saliva. The general consensus on endocannabinoid testing by the salva is that it is reliable and quantifiable. However, a study in 2012 concluded that AEA levels correlated with obesity but not feeding status. This means that there will be a significant difference between people of different weight classes. More research is needed to conclusively name saliva a diagnostic tool for clinical endocannabinoid deficiency.

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