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.
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.
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.
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.
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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