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Official websites use. Share sensitive information only on official, secure websites. Corresponding author. E-mail address: Marta. Di Forti. This is an open access article distributed under the Creative Commons Attribution License 4. The spread of laws legalising cannabis for medicinal or recreational use has been accompanied by more relaxed attitudes towards cannabis. Data from the United States show that in states that have legalised cannabis, prevalence of daily, weekly, and monthly cannabis use was CBD does not induce euphoria but may exert anxiolytic, antiepileptic, anti-inflammatory, and analgesic properties Figure 1. This diagram graphically illustrated first, the differential and in fact opposite psychiatric and cognitive effects of THC and of CBD, and second, how both compounds derive from the same precursor. Therefore if, for instance, a Cannabis sativa plant is genetically driven to the production of high quantity of THC, it will only be capable to synthesise small quantities of CBD. Nevertheless, discontinuation of long-term frequent cannabis use can induce anger, decreased appetite, irritability, nervousness, restlessness, and sleep difficulties, 13 , 79 suggesting that the alleviation of abstinence symptoms contributes to the maintenance of daily cannabis use. Cross-sectional and prospective studies demonstrate a causal link between cannabis use and psychotic disorder, with greater risk for cannabis users, compared to nonusers. A meta-analysis by Large et al. Another study showed that if subjects had used high-potency cannabis daily, their illness onset was, on average, 6 years earlier 31 compared to never users. Boydell et al. The first, clear evidence of the impact of cannabis use on rates of psychotic disorder comes from the EUGEI study. Further independent evidence comes from Portugal that has registered a steady increase in the rate of hospital admissions for psychotic disorders with comorbid CUD. The self-medication hypothesis suggests that patients with psychotic disorders use cannabis to seek relief from their symptoms. More recently, Mendelian randomization investigated the relationship between cannabis use and randomly assorted genetic variants that are associated with psychosis, which were used as proxy for psychosis itself. Mendelian randomization studies have suggested that cannabis use initiation is partly explained by common genetic variants associated with risk of schizophrenia, thus proposing a direction of causality from schizophrenia genes to cannabis use ie, reverse causality rather than from cannabis use to schizophrenia and other psychosis. On the contrary, heavy cannabis use increased the risk for psychotic disorders independent of the individual's schizophrenia PRS. A meta-analysis indicates that patients with a psychotic disorder who continue to use cannabis after their illness onset experience a worse clinical and functional outcome than those who stop. Some evidence begin to suggest that individuals at ultra-high risk for psychosis have higher rates of CUDs 14 and, conversely, patients with CUDs are more likely to transition to psychosis. This is often considered a limitation. Nevertheless, although biological measures can provide valid and reliable measures of current use, they cannot provide data on use over time. Indeed, studies that analysed both self-reported information and laboratory data indicated that cannabis users are reliable in reporting how frequently they use and the type they used. Administration of cannabis and THC has shown to precipitate, with a dose—response relationship, the onset of transient positive psychotic symptoms eg, ideas of reference, paranoid delusions, hallucinations, depersonalization, or derealization and, to a less extent, negative symptoms eg, blunted affect in healthy volunteers and to temporary exacerbated psychotic symptoms in schizophrenia patients. The Dunedin study was the first to indicate adolescents as a group particularly vulnerable to the psychotogenic effect of cannabis use. Subjects with a family history of psychotic disorders have a greater sensitivity to the psychotogenic effect of cannabis 66 and if they develop a cannabis-induced psychotic disorder, they are more likely to transition to schizophrenia. Another potentially vulnerable population might be represented by individuals exposed to childhood adversity, which may enhance the psychotogenic effect of cannabis, through sensitization. Several studies observed that the joined effect of early trauma and cannabis use on psychosis was greater than their independent effect, 54 , 62 , 63 , 70 but the findings were not fully consistent. Two meta-analyses 47 , described a modest residual cannabis-related impairment in measures of both overall and specific cognitive functions after 12 hours to 25 days of abstinence, with no residual cognitive impairment after 25 days of abstinence. In young adults, chronic cannabis use most commonly affects immediate recall and verbal reasoning 12 , 38 , but not spatial working memory; however, the latter is affected in adolescents, 55 suggestive of a differential effect on the developing brain. Both in adolescents and adult users, attention is impaired during cannabis intoxication and persists for several weeks. Regular cannabis use is associated with lack of motivation for naturally rewarding activities, which is a core feature of depressive disorders. Evidence for a weaker association between cannabis use and anxiety disorders comes from a meta-analysis, estimating ORs from 1. All prescribed and recreational drugs have adverse effects, even those coming from plants, fruits, and flowers as we have learnt from the use of tobacco, alcohol, and opium. Cannabis is not an exception Tables 1 and 2. Therefore, at a time of changes in the laws concerning cannabis use, it is of clinical and public health importance to provide evidence-based and clear information on what we know concerning 1 the acute and persistent adverse effects and 2 how to screen for those individuals more susceptible to experience them when cannabis is used recreationally or medicinally. This table illustrates the findings from meta-analyses that report an association between several mental health outcomes, cognition, and cannabis use. Summary of the mental health and cognitive acute and persistent adverse effects associated with cannabis use. Di Forti reports personal fees from Janssen, outside the submitted work. The remaining authors have no conflict of interest to declare. Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. As a library, NLM provides access to scientific literature. Find articles by Lucia Sideli. Find articles by Giulia Trotta. Find articles by Edoardo Spinazzola. Find articles by Caterina La Cascia. Find articles by Marta Di Forti. Published by Wolters Kluwer Health, Inc. Open in a new tab. Summary of meta-analyses reporting adverse effects associated with cannabis use. Family history of psychosis 2. High polygenic risk score for schizophrenia 3. Dose—response relationship with THC content high-potency cannabis and daily use 2. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel. Marconi et al. High levels of cannabis use increase the risk of psychotic outcomes with a dose—response relationship. Large et al. Relationship between cannabis use and earlier onset of psychotic illness. Schoeler et al. Continued cannabis use after onset of psychosis predicts adverse outcome than for nonusers. Gibbs et al. Association between cannabis use and both the exacerbation of manic symptoms in those with previously diagnosed bipolar disorder and new-onset manic symptoms. Gobbi et al. Cannabis consumption in adolescence is associated with increased risk of developing depression in young adulthood. Lev-Ran et al. Heavy cannabis use may be associated with an increased risk for developing depressive disorders. Twomey et al. Cannabis use is no more than a minor risk factor for the development of elevated anxiety symptoms in the general population. Grant et al. There might be decrements in the ability to learn and remember new information in chronic users, whereas other cognitive abilities are unaffected. Schreiner et al. A small negative residual effect of cannabis use on overall cognitive performance, no evidence of lasting residual effect.

Cannabinoid biosynthesis: How are CBD and THC produced?

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One of the greatest pleasures of knowledge is to discover that it never ends. The topic we will discuss today in the blog is the synthesis or biosynthesis of cannabinoids. And why is the study of how cannabinoids are produced important? Well, for many things actually. Cannabinoid biosynthesis is an area of great research interest in the cannabis industry and medicine, as these compounds have a wide range of potential therapeutic properties. Understanding the processes for producing cannabinoids can help improve the production of specific cannabinoids for use in medical treatments. Cannabis plants produce chemical compounds known as phytocannabinoids through a biological process called cannabinoid biosynthesis. This process occurs in the trichomes of cannabis. The biochemical pathway by which the cannabinoids we know are produced is long and involves: non-cannabinoids, cannabinoids and enzymes. Furthermore, as a curiosity, in the cannabis plant, the upstream steps of cannabinoid biosynthesis converge with the pathway of the terpenes. The marijuana plant produces cannabinoids in acid form, and these, when heated, change to their neutral form by a process called decarboxylation. Upon heating, a chemical process called decarboxylation occurs, where these compounds change to their neutral form \[1\]. This neutral form of cannabinoids is the one that interacts the most with our endocannabinoid system \[2\]. For this reason, to obtain the effect of cannabis we smoke, vape, infuse or cook the plant. The synthesis of cannabinoids within the plant occurs thanks to proteins called enzymes. To simplify, we could say that enzymes are a type of protein that performs a function, does something. In this case, the enzymes of cannabinoid synthesis act as an architect that modifies or transforms one molecule into another. In reality, these changes occur in many ways: sometimes by trimming the chemical molecule, but sometimes by folding it, or by gluing a chemical group, and so on. Well, this is not always the case: as we shall see, these enzymes have a lot to say. So, CBGA is the mother that gives birth to these cannabinoids. In the figure I show the last two of the many steps that occur within the plant in the biosynthesis of cannabinoids:. Wondering what the ancestor of cannabinoids is? If CBGA is the mother cannabinoid, the great-grandmother of all cannabinoids is palmitic acid. Like the endocannabinoids phytocannabinoids are synthesized from fatty acids. As you can see in the figure, there are many different enzymes involved in cannabinoid synthesis. These proteins perform a task, in this case synthases, as they catalyze cause, provoke a reaction, which gives rise to the various cannabinoids. The enzyme CBGAS cannabigerolic acid synthase converts olivetolic acid OLA; derived from palmitic acid and geranyl diphosphate into cannabigerolic acid. Chemical readers will tell me if I am translating these names properly from English to Spanish. This structural difference translates into differences in their biological effects. The enzymes involved in cannabinoid synthesis can produce up to eight different compounds in vitro, including the compound in the other \[8\]. And, apparently, also in the plant in vivo these enzymes are not very specific \[8\], although many studies are needed to confirm what, and in what amounts, these enzymes are producing in the plant. And according to my hypothesis, yet to be confirmed, the most neglected of all is CBCA synthase, but this is also another story for later. Moreover, as these three enzymes use CBGA as a precursor compound, and it is the same compound where all three act, they could also be categorized as promiscuous enzymes. As you can see, our little enzymatic friends are out and about, promiscuous and careless, producing the compound of the one, or the other, or other compounds out there, a la topa tolondra which, if you go to Cali Colombia, I recommend you to go dancing at that discotheque. Something that I found quite interesting is the genetic structure of the gene that codes for the CBGA synthase enzyme. This gene has many exons, and therefore also introns \[6\]. Exons are the part of the gene that has the information to produce proteins, while introns have no information. Although both exons and introns are found in the DNA or genetic material of cannabis, forming part of the gene that produces CBGAS, when the enzyme or protein is produced, it only has the genetic information of the exons. What I find interesting about this genetic structure is that the introns are quite large , up to almost 11, nitrogen base pairs letters; \[6\] , and, although introns of this size have been reported, they are not that common. So, it is a gene with quite a few pieces , which is also interesting because several types of proteins can be produced, which hopefully will be studied scientifically in the near future. The gene encoding the CBGA synthase enzyme has an interesting structure with several exons and introns. Exons are the part of the gene that is translated into protein, and having several of these provides the possibility of forming different protein structures. This is another reason why CBGA is my favorite cannabinoid, because, although scientific studies are lacking to confirm this hypothesis, suddenly, the gene can produce different protein structures, thus being versatile, moldable, and giving, as we mothers are. Even so, these apparently have pharmacological properties and possible medicinal uses. These are produced in an alternate route using divarinolic acid instead of olivetolic acid, which we will discuss on another occasion. For many years, and in a clandestine way, the methods used to select which cannabinoids we want a plant to produce were through artificial selection , that is, selecting plants with the desired characteristics, based on aroma, potency, vigorousness…. Marijuana growers, informally, knew about cannabinoid biosynthesis long before scientists described these chemical reactions. Artificial selection has been used in many plants and other organisms. For example, in dogs, to obtain varieties, or different breeds cultivars, if we apply it to cannabis , with desired characteristics. But behind this ancient technique, there is cannabinoid chemistry. Genetically, cannabis plants very high in CBD have the gene that produces the enzyme THCA synthase truncated or defective The cannabinoid THC is not produced in the plant, or not as much because, remember, they are neglected enzymes , and other cannabinoids, such as CBD, are accumulated. In contrast, strains that are very high in THC, with very psychoactive effects, tend to have the gene for the CBDA synthase enzyme misfired. This is one of the reasons why the production of cannabinoids in cannabis plants can vary significantly depending on genetics, although aspects of cultivation lighting, irrigation, soil pH, temperature… also play a role. One might think that, if we want strains that do not produce a type of cannabinoid, we could silence the genes that produce the particular synthase enzyme. But this is not the case: As we have seen, these enzymes are neglected, and all of them, in theory, are capable of producing THC, and in practice we see that, when there are plants that produce high CBD, they usually also have THC, even if in small quantities. It is quite likely that those legislators who wrote the hemp and marijuana rules had no idea that these enzymes were on the rampage. Because had they known that cannabinoid enzymes were promiscuous and sloppy, perhaps they would have set the THC limit higher than 0. On a previous occasion I had told you about my deep anger and frustration due to these unjust and absurd regulations about the types of marijuana. If they see these ignorant legends out there, tell them that there is an evolutionary biologist and cannabis researcher out there strongly criticizing their uninformed, unconscious and selfish decisions. Gertsch, J. Proceedings of the National Academy of Sciences, Page, J. Stout, Cannabichromenic acid synthase from Cannabis sativa. Vergara, D. Trends in plant science, Innes, P. Vergara, Genomic description of critical upstream cannabinoid biosynthesis genes. Schranz, Origin and evolution of the cannabinoid oxidocyclase gene family. Genome Biology and Evolution, Zirpel, B. Kayser, and F. Journal of biotechnology, Smith, C. PLoS one, Cannabinoid biosynthesis describes the chemical reactions that occur in the cannabis plant by which cannabinoids originate. The process of cannabinoid biosynthesis involves a series of enzymatic steps that convert precursor chemicals into active cannabinoids. However, synthetic cannabinoids can also be produced. Madrid Store C. Argumosa, 25 , Madrid, Spain. CBD products are not medications and are intended for external use. Consult a specialist if you have symptoms of pain or illness before use. Cannactiva information and its products are not intended to diagnose, treat or prevent diseases. Age verification Please confirm that you are over 18 years old to continue. Index Toggle. Figure: Biosynthesis of cannabinoids and enzymes involved. Figure modified from references 3, 4, 5, and 6. Credit: Dr. Daniela Vergara. Hart, C. Neuropsychopharmacology, What is cannabinoid synthesis? Where does cannabinoid synthesis occur? Related entries. Products to test negative in drug tests: Do they work? Sativa vs Indica: Do you know the differences? Members of. Mi Cesta 0. There are no products in the cart! Continue shopping. Powered by Joinchat. Can we help you?

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