What is the biological function and therapeutic relevance of the endocannabinoid system in our body?8/13/2020 Over the last three decades, we have been accumulating abundant knowledge about cannabinoids and the endocannabinoid system and, more specifically, about their possible therapeutic applications. However, it is obvious that there are still many questions to be resolved in this area. This article constitutes a personal (and therefore subjective and rebuttable) reflection on a question that, in my opinion, would be crucial to understand in order to rationalize and, thereby, optimize the therapeutic action of live resin: what are the biological function and therapeutic relevance of the endocannabinoid system in our body?
Cannabinoid CB 1 and CB 2 receptors are present not only in our species ( Homo sapiens ) but also, at least, in all vertebrates and some of the invertebrates analyzed so far. In fact, these receptors are thought to have arisen in the evolution of animals (although not plants) a very long time ago, most likely nearly 600 million years ago. A first question that can be asked is: are cannabinoid receptors necessary for an organism to live? The most plausible answer is “no”, since, using genetic engineering techniques, various animals lacking cannabinoid receptors have been obtained in the laboratory and these animals are viable. Examples of this are a mammal (the mouse, Mus musculus ), an amphibian (the frog Xenopus laevis ), a fish (the zebrafish, Danio rerio ) and a worm (the nematode Caenorhabditis elegans). Now, are cannabinoid receptors Cannabis Oil for an organism to “live well”? In this case, the answer seems to be “yes”. Although not necessary for life, cannabinoid receptors are necessary for the correct functioning and physiological balance of an organism (what we know as “homeostasis”) to be maintained. In fact, the neurons and other cells of our organism hardly produce endocannabinoids in basal operating conditions, starting to generate them “on-demand” when they are significantly over-activated. Thus, the endocannabinoid system is usually considered as a “silent” system whose functioning is started in situations in which the homeostasis of the organism is altered and, therefore, whose performance is aimed at restoring that lost body balance. Without the endocannabinoid system, we could, therefore “survive” but not “live well”. In Vincenzo di Marzo’s words, the endocannabinoid system seems to have emerged in evolution to help us relax, feed, rest, forget (the superfluous or traumatic), and in general, protect us from numerous pathological changes. We have, however, to learn many precise details about the functioning of the endocannabinoid system in our body. For example, we do not know even in the brain of the mouse, let alone the human brain, in which specific places (for example, in which neuronal synapses) and by what precise mechanisms the endocannabinoids anandamide and / or 2-arachidonylglycerol are produced. We do not yet have Canna Clique analytical methods to measure the minute amounts of endocannabinoids that are generated at particular synapses (we are only able to do so in large portions of brain necropsies), much less in real-time and in the human brain. And when we talk about that in this or that physiological or pathological situation, the levels of endocannabinoids in humans rise or fall, It is also important to note that the endocannabinoid system is very ubiquitous and is expressed in many cell types throughout all moments of our lives, from the embryo to aging. The levels of its elements (cannabinoid receptors, endocannabinoids, enzyme systems that metabolize endocannabinoids) change in many diseases, especially in some that (a) are difficult to diagnose and treat, (b) involve comorbidity (that is, more than one they appear simultaneously in the same patient) and (c) is characterized by sensitization of the central nervous system (that is, some normal physiological responses are exacerbated in such a way that the patient perceives them as painful or, in general, harmful to health). Examples of these situations are fibromyalgia. There is some evidence that cannabinoids could alleviate, in some patients at least, the symptoms associated with these diseases, perhaps allowing the “normalization” of a biological hypoactivity of the endocannabinoid system inherent in them. However, from my point of view, we still sometimes move in the field of association and not of the cause-effect relationship, as well as the extrapolation to large populations of patients of some preclinical evidence (read, “if it works in mice, it will work in patients ") or anecdotal clinics (read,” if it seems to work in any patient, it will work in all “). In any case, this concept of “clinical endocannabinoid deficiency” (usually abbreviated as CECD of the English clinical endocannabinoid deficiency ), coined by Ethan Russo, it is an extraordinarily interesting challenge for the cannabinoid-clinical scientist on future research. In my opinion, a “great revolution” in the world of medicinal Cannabis would come from accurately identifying a disease whose primary etiology was the alteration of some element of the endocannabinoid system and, therefore, whose progression (and not only the palliation of its symptoms) it could be attenuated by a specifically (endo) cannabinoid treatment (which, together, we could call a “cannabipathy”). Another pathophysiological issue not yet resolved is that of the so-called “biphasic effects” of cannabinoids, already described by Raphael Mechoulam and other researchers several decades ago. For example, “low” doses of THC (and “low” quotes because they will vary between individuals) can decrease anxiety, inhibit vomiting, increase intake, and lessen seizures, while “high” doses of THC (again in quotation marks) can increase anxiety, induce vomiting, reduce intake, and cause seizures. CBD appears to be significantly less likely than THC to produce these biphasic effects in patients, although there is evidence that it can exert them in some specific situations in mice (for example, What could be the biphasic effects of THC? A hypothesis, based on seminal studies conducted with genetically modified mice by the laboratories of Beat Lutz and Giovanni Marsicano, proposes that THC, at “low” doses, would preferentially activate the CB 1 receptor located in excitatory-type neurons (which produce a neurotransmitter called glutamate), whereas, at “high” doses, it would preferentially activate the CB 1 receptor located in inhibitor-type neurons (which produce a neurotransmitter called γ-aminobutyric acid, -generally abbreviated as GABA, from the English gamma-aminobutyric acid -). Obviously, both processes would produce opposite effects. Other hypotheses propose differential modulation models of CB 1 receptor function depending not only on the dose of the alaskan thunder fuck strain but also on the time of exposure to the cannabinoid or the type of cannabinoid molecule under study. The future will probably provide precise answers to this complex process, which should allow us to better understand and thus perfect the therapeutic action of cannabinoids.
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