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CBD Your Treat Can Anxiety? How



  • CBD Your Treat Can Anxiety? How
  • Cannabidiol as a Potential Treatment for Anxiety Disorders
  • How Can CBD Help Anxiety?
  • For people with anxiety, CBD oil is touted as an all-natural way to find relief. Find out whether this marijuana compound can help ease your. Since THC is the most intense psychoactive part of cannabis, it can really aggravate anxiety in some people. But, because CBD balances THC. Unfortunately, the medical system's solution to anxiety falls short for many supplementing your treatment with CBD oil or CBD vape pens.

    CBD Your Treat Can Anxiety? How

    Over the last decades, converging epidemiological, clinical and preclinical data have pointed to a key implication of cannabis and its endogenous system in the regulation of anxiety. In the following sections, we will present a brief synopsis on cannabinoids and the available classes of related agents, with a specific focus on their anxiolytic potential, and the scientific challenges that should be overcome to fully establish the applicability of such drugs in the therapy of anxiety disorders.

    The three species included in the Cannabis genus or sub-species, depending on the taxonomic classification; see [ 3 ], for a detailed discussion on the issue , sativa, indica and ruderalis , feature at least 85 unique terpenophenolic compounds, collectively named phytocannabinoids [ 4 ].

    The main classes of phytocannabinoids are outlined in Figure 1. Quantitative analyses of cannabis constituents are usually performed by chromatographic techniques generally Gas Chromatography, but also Thin-Layer Chromatography, or High-Performance Liquid Chromatography , often coupled with Mass Spectrometry. A detailed description of the instrumental methods used for classification and source tracing of Cannabis products including DNA identification for forensic and intelligence purposes is beyond the scope of this review, but can be found in [ 5 - 7 ].

    The main psychoactive constituent of Cannabis, THC is a highly lipophilic alkaloid produced mainly in the leaves, flowers and glandular trichomes of the plant. Most of the pharmacological effects elicited by hemp products, including emotional and cognitive changes, analgesia, hypothermia and appetite stimulation, are considered to be reflective of the action of THC as a partial agonist of cannabinoid CB 1 and CB 2 receptors see below. Additionally, THC has been shown to act as an acetylcholinesterase inhibitor [ 8 - 10 ].

    In contrast with THC, CBD is not psychotropic, but has nevertheless been shown to play a role in the modulation of behavioral effects of cannabis [ 11 ]. In fact, the THC: CBD ratio is the main criterion to define different cannabis chemotypes [ 12 ] and has been posited to contribute to the variability in neurobehavioral outcomes of marijuana or hashish consumption [ 13 , 14 ].

    Interestingly, most cannabis strains encountered in the illegal markets generally have elevated amounts of THC [ 15 ]. Additionally, CBD has been shown to exert some of its actions through other receptors, including the vanilloid receptor VR 1 and the serotonin receptor 5-HT 1A for a general overview of the topic, see [ 11 ].

    In addition to phytocannabinoids, several classes of synthetic CB receptor agonists have been developed; among these families, the best characterized are the synthetic analogs of THC - such as the biciclic compounds CP 47,, CP 55,, CP 55, and the benxopyrans HU and nabilone Fig.

    Of these agents, only nabilone has been approved for clinical use as an antiemetic treatment and an adjunct analgesic for neuropathic pain [ 25 ]. Unlike THC, which is a partial agonist of CB 1 receptors, these agents are full, high-potency CB 1 receptor activators [ 26 , 27 ], thereby eliciting greater psychotropic effects than THC as CB 1 receptors are the key mediators of the psychotropic actions of cannabis.

    For more details, see text. Following the identification of THC in the s [ 28 ], extensive research was devoted to the identification of its biological targets and endogenous counterparts. In line with their metabotropic nature, CB receptors mediate their intracellular response through a number of changes affecting signaling cascades, such as inhibition of adenylyl cyclase, activation of G-protein-activated inwardly rectifying potassium channels GIRKs and phosphorylation of extracellular signal-related kinases ERKs [ 35 , 36 ].

    The distribution pattern of CB 1 and CB 2 receptors is strikingly divergent, indicating diverse physiological functions: CB 1 is the most abundant metabotropic receptor in the brain, and is primarily distributed in the synaptic terminals of neurons across all the major structures that regulate emotional responsiveness, perception and memory, including prefrontal cortex, amygdala, septo-hippocampal system, striatum, thalamus, brainstem nuclei etc.

    CB 1 receptors are typically located on presynaptic terminals [ 42 , 43 ], but they have also been identified in postsynaptic locations [ 44 , 45 ]. In general, CB 1 activation has been shown to inhibit the neurotransmission of other mediators, including glycine, acetylcholine, norepinephrine and serotonin [ 50 ], but the underpinnings of these phenomena have not been completely elucidated.

    Additionally, CB 1 receptors have been implicated in short- and long-term synaptic depression, in relation to phasic or tonic endocannabinoid release for a review on these topics, see [ 51 ]. The function of CB 1 receptors may vary depending on the specific interactions that they entertain with other molecular targets. The key role of CB 1 receptors as mediators of neurochemical homeostasis in the brain is maintained through a complex regulation of their expression. For example, these receptors are subjected to a rapid internalization via clathrin-coated pits following their binding with full agonists; on the other hand, the receptors are also recycled, with a process that requires endosomal acidification and dephosphorilation [ 54 ].

    While CB 2 receptors are abundantly expressed in most peripheral organs and particularly in immune cells, where they regulate cytokine secretion and modulate cell trafficking [ 55 ], their distribution in the brain appears to be sparse and particularly confined to microglial cells; nevertheless, recent evidence has revealed the presence of CB 2 receptors in several areas of the brain [ 56 - 58 ].

    Interestingly, a number of studies suggest that neuronal CB 2 receptors may be mainly located in postsynaptic terminals [ 58 , 59 ]; nevertheless, the functional role of these targets in the brain remains largely elusive and awaits further characterization.

    The existence of cannabinoid receptors other than CB 1 and CB 2 has been postulated based on ample experimental evidence [ 60 - 62 ]. Interestingly, a number of investigations have pointed to GPR55 as a novel putative cannabinoid receptor [ 63 , 64 ]; nevertheless, evidence on the specificity of this receptor for endocannabinoid is still inconclusive [ 65 ].

    Both anandamide and 2-AG are derivatives of arachidonic acid, an unsaturated C20 fatty acid with 4 double bonds, which also serves as the precursor for synthesis of other eicosanoids, including prostaglandins and leukotriens. Anandamide is found in picomolar concentrations and acts as a high-affinity partial agonist for both CB 1 and CB 2 receptors.

    It is synthesized on demand by enzymatic hydrolysis of the membrane phospholipid N-arachidonoyl phosphatidylethanolamine NAPE , a process catalyzed by several phospholipases [ 66 - 68 ]. Following release and activation of CB receptors, anandamide is rapidly removed from the synaptic cleft by a carrier-mediated system [ 69 - 72 ] and subsequently hydrolyzed by the membrane enzyme fatty acid amide hydrolase FAAH [ 73 - 75 ].

    Both these compounds do not activate CB1 receptors [ 76 ], although they may reduce or slow down anandamide degradation by competing with it for FAAH activity. In comparison with anandamide, 2-AG is much more abundant occurring in nanomolar concentrations across most tissues and acts as a full agonist of both CB receptors.

    It is produced from 1,2diacylglycerol DAG by diacylglycerol lipase DAGL [ 77 ] and degraded mainly by the cytosolic serine hydrolase monoacylglycerol lipase MAGL [ 78 ], although other enzymes are known to contribute to this process [ 79 ].

    The divergent neurochemical profiles of anandamide and 2-AG underscore their different physiological roles. Although our current understanding of the different functions entertained by each endocannabinoid is still rudimentary, the development of FAAH and MAGL inhibitors [ 80 , 81 ] has been instrumental to elucidate the implication of each mediator in synaptic and neurochemical regulation.

    While 2-AG is known as the retrograde mediator of DSI [ 82 , 83 ] and DSE [ 84 - 87 ], a number of studies suggest that anandamide may serve as an activity-dependent regulator of monoaminergic transmission [ 88 - 90 ]. Recent evidence points to a potential biological antagonism between anandamide and 2-AG [ 91 , 92 ]; on the other hand, emerging evidence points to a similar role of anandamide and 2-AG in the regulation of anxiety albeit in relation to different receptors and pain [ 93 ].

    Other lipids have been indicated as putative endocannabinoids, including 2-arachidonoylglycerylether noladin ether [ 95 ] and O-arachidonoylethanolamine virodhamine [ 96 ] Fig. Additionally, recent evidence has identified that CB receptors may be modulated by peptidic ligands, such as hemopressin and its derivatives [ 97 , 98 ]. The employment of cannabis for its medicinal, relaxing and mood-enhancing properties has been documented across most ancient civilizations.

    Originally introduced in Chinese pharmacopoeia during the third millennium BCE [ 99 , ], cannabis became a popular remedy throughout Asia and Europe in the following centuries [ 99 , ]. The inclusion of cannabis in the medical treatises by Dioscorides and Galen secured the herb a stable reputation in the Roman Empire and the Arabic world [ ]. Until the early 20 th century, the plant remained a valuable therapy for a large number of diseases [ ]; however, growing concerns about the psychoactive and narcotic effects of cannabis led to a progressive restriction and ultimate ban of its usage in the United States and several European countries [ , ].

    Despite its illicit status, cannabis remains one of the most popular recreational drugs, particular among adolescents and young adults, in view of its mood-enhancing and euphoriant characteristics [ - ]. Most psychological and behavioral effects of marijuana and other hemp products are induced by THC through activation of CB 1 brain receptors. In fact, although THC and most synthetic cannabinoids are known to activate both CB 1 and CB 2 receptors, their actions on anxiety-like behaviors and emotional regulation are efficiently countered by selective CB 1 receptor antagonists, such as rimonabant see next section [ ].

    The studies on the psychological effects of cannabis and THC have unfolded a highly complex and often contradictory scenario, fostering a long-standing debate on the potential harms and benefits of its products.

    An important aspect of this discussion particularly in consideration of its legal aspects and the potential therapeutic applications of hemp derivatives , revolves around the distinction between use and misuse of cannabis. In particular, whereas the abuse and dependence liability of cannabis is generally well-recognized [ , ], the definition of these phenomena has been heavily criticized as reflective of political agendas rather than scientific bases.

    For instance, the diagnosis of substance abuse, according to the criteria listed by the DSM—IV TR, is based on the manifestation of at least one of four symptoms: The applicability of some of these standards to marijuana and other cannabis derivatives, however, has been questioned [ 99 ], also in view of their lower potential to induce physical harm in comparison with other legal substances, such as alcohol and tobacco [ ]. While the controversies surrounding cannabis are far from subdued and are often permeated and masked by conflicting ideological credos , standardized studies on cannabinoids have highlighted that the psychological and behavioral outcomes of this substance are highly variable and range from relaxation, euthymia and heightened sociability to panic, paranoid ideation and psychosis [ - ].

    The latter interpretation is supported by the observation that anxiety-spectrum disturbances and traumas in early developmental stages are a strong predictor for later cannabis use disorders [ - ]; furthermore, several lines of evidence suggest that the anxiolytic effects of THC may partially account for the high prevalence of cannabis use in patients affected by PTSD [ - ] and OCD [ ].

    Accordingly, recent clinical studies have shown that THC elicits therapeutic effects in OCD [ ] and trichotillomania, an impulse-control disorder characterized by compulsive hair-pulling [ ]. Nevertheless, prospective analyses show that cannabis use and dependence increase the risk for development of panic disorder [ ], suggesting that the effect of cannabis may vary with respect to the nosological entities within the spectrum of anxiety disorders.

    Of note, chronic consumption of cannabis has been hypothesized to exacerbate depressive or anxious manifestations, and reduce the therapeutic efficacy of anxiolytic agents [ , - ]; an interesting theoretical implication of this finding is that long-term exposure to cannabinoid agents may lead to profound alterations of synaptic plasticity and neurochemical homeostasis and alter the pathophysiological trajectory of anxiety and mood disorders.

    Thus, while cannabis may be initially used as a self-therapy for certain anxiety disorders, the prolonged exposure to this substance in vulnerable individuals may in turn alter or aggravate the clinical course of these conditions and render the patients refractory to standard treatments.

    The ability of cannabis to either exacerbate or attenuate emotional reactivity is highly influenced by numerous factors, including its chemotype, as well as the influence of genetic, developmental and contextual variables. Unfortunately, little is still known about the susceptibility factors that govern the behavioral outcomes of cannabis in patients affected by anxiety-spectrum disorders. Indeed, several components have been shown to play a role in this link, including genetic background, age, gender, environmental stress and concurrent use of other drugs; a detailed analysis of these determinants is outside the scope of the present work, but the interested reader should refer to [ ].

    Aside from the influence of vulnerability factors, the available evidence indicates that cannabis, THC and other CB 1 receptor agonists exercise a bidirectional influence on anxiety responses as a function of the dosage. The majority of users report that consumption of modest amounts of cannabis and CB 1 receptor agonists results in euphoria, relaxation, heightened perception, sociability and creativity, moderate to high doses have been reported to elicit phobia, agitation, panic, dysphoria, psychotic manifestations and cognitive impairments [ - , , - ].

    In line with these premises, early studies showed a robust anxiolytic efficacy of low-dose nabilone in comparison with placebo [ , ]. The biphasic effects of cannabinoids on anxiety-related responses have been extensively documented in rodents. The bidirectional action of CB 1 receptors on anxiety responses may be related to the modulatory role of these targets on GABA and glutamate release across amygdala and other forebrain areas [ 41 , , ].

    As these two major neurotransmitters affect anxiety in an opposite fashion, different doses of cannabinoids and synthetic CB 1 receptor agonists may indeed produce highly divergent effects, in relation to their ability to affect the homeostasis and the balance of GABA and glutamate for a review on these issues, see [ ].

    Furthermore, CB 1 receptors have been shown to play critical roles in the regulation of most neurochemical substrates of anxiety, including the neurotransmitters serotonin, norepinephrine and acetylcholine, as well as stress hormones, colecystokynin and opioid peptides [ 50 , ].

    In line with this concept, the infusion in the periaqueductal grey of arachidonylchloroethylamide ACEA , an anandamide synthetic analog with high CB 1 receptor selectivity, elicited anxiolytic-like effects in rats in an elevated plus maze, with a bell-shaped dose-response curve [ ], the highest doses being associated to no significant behavioral change.

    Novel categories of compounds have been patented for potential efficacy as selective CB 1 receptor modulators, including sulfonyl-benzamides [ ] and tetrasubstituted imidazole derivatives [ ].

    To the best of our knowledge, however, no findings on the action of these compounds in anxiety regulation have been reported to date. The majority of preclinical studies found that these compounds are anxiogenic at high doses [ , , , ] and ineffective at low doses [ , ]. The anxiogenic properties of CB 1 antagonists, were unequivocally confirmed by clinical data on the psychiatric side effects of rimonabant.

    The significant increase in anxiety, depression and suicidality in patients under treatment with rimonabant [ - ], in particular, led to the withdrawal of the drug from the European market in October, As a consequence, several pharmaceutical companies announced the interruption of their clinical research on CB 1 receptor antagonists, including taranabant from Merck and otenabant from Pfizer , both in Phase 3 of development.

    Some of the anxiogenic properties of rimonabant and analogs have been speculated to be due to their activity as inverse agonists; as a result, the therapeutic use of newly-developed neutral CB 1 antagonists has been proposed, with the hypothesis that these compounds would not elicit the untoward psychological effects observed with rimonabant and its analogs [ , ]; this idea is supported by recent findings, showing that unlike CB 1 receptor inverse agonists, the neutral antagonists of this targets fail to facilitate the acquisition or consolidation of fear [ ].

    Few studies have actually evaluated the role of CB 2 receptor in anxiety and stress response. Some of these investigations indicated that the suppression of CB 2 receptor in the brain, through intracerebroventricular injection of antisense nucleotide sequences, elicited anxiolytic effects in rodents [ ]. In contrast, Garcia-Gutierrez and Manzanares [ ] recently described that the overexpression of CB 2 receptors reduced anxiogenic-related behaviors in the light-dark box and elevated plus maze.

    These premises point to the possibility that CB 2 receptor ligands may also play a role in the modulation of anxiety disorders. This hypothesis, however, awaits further examination with proper pharmacological tools.

    Several lines of preclinical work have shown that CBD reduces the effects of THC on several behavioral functions [ - ]. In line with these data, CBD has been found to reduce the anxiety and improve the sensation of well being induced by an acute, high THC dose in healthy volunteers [ ]. In contrast with these data, a number of studies have shown that CBD pretreatment potentiated the behavioral effects induced by THC [ - ].

    These actions may signify the ability of CBD to inhibit cytochrome Pmediated drug metabolism [ , ], which may increase THC blood and brain concentrations [ , ]. Of note, the anxiolytic action of CBD also appears to be bidirectional, as only low to moderate doses, but not high doses, have been associated with exert anxiolytic effects [ , ]. The anxiolytic action of CBD do not appear to be mediated by benzodiazepine receptors [ ], but rather by 5-HT 1A serotonin receptors in the bed nucleus of the stria terminalis [ ], a critical component of the amygdaloid complex involved in the regulation of stress response.

    Accordingly, CBD has been shown to reduce amygdalar responses to fearful stimuli [ ]; this mechanism may be essential for the anxiolytic effects of this compound in social phobia [ ]. Furthermore, CBD has been shown to elicit antipanic effects through the activation of 5-HT 1A receptors in the dorsal periaqueductal gray, a critical area for the modulation of emotional reactivity to stress [ , ].

    The systemic administration of the endocannabinoid transport blocker AM Fig. The same compound was shown to attenuate marble burying a paradigm for compulsivity testing in mice, suggesting that this compound may have some potential efficacy for OCD [ ].

    Interestingly, the anxiolytic effects of AM were shown to be contributed by both CB 1 and 5-HT 1A receptors [ , ], in a fashion similar to the potent CB 1 receptor agonist CP 55, [ ]. Additionally, AM has been suggested to act as a FAAH inhibitor [ ], although evidence in this respect is controversial [ 72 ]. Chemical structures of endocannabinoid degradation inactivators. Although the possibility of targeting the endocannabinoid carrier for the development of anxiolytic compounds is appealing and has been targeted by a patent proposing these compounds as a pharmacological support for psychotherapy [ ], the elusive molecular identity of the transporter itself has greatly limited the studies.

    Furthermore, preliminary data indicate that AM elicits reward in animals and is self-administered by squirrel monkeys [ , ], raising the possibility that endocannabinoid transport blockers may be addictive.

    In addition to its anxiolytic-like properties, URB was found to exert also antidepressant-like effects in several animal models with high face and predictive validity, such as the forced swim, tail suspension and chronic mild stress paradigms [ 89 , , , ].

    The anxiolytic action of FAAH inhibitors has been suggested to depend on the enhancement of anandamide in the dorsolateral periaqueductal gray [ ]; interestingly, however, only low doses of URB in the prefrontal cortex were found to elicit anxiolytic-like effects, through CB 1 receptor activation.

    However, higher doses ceased to elicit anxiolysis, in view of their interaction with TPRV1 vanilloid receptors [ ]. Furthermore, the anxiolytic and antidepressant actions of FAAH inhibitors were observed only under conditions of high environmental aversiveness, but not under normal conditions [ , , ]. Importantly, the psychotropic effects of FAAH inhibitors are partially distinct from those associated with cannabinoids, in that they appear to fail to reproduce the hedonic and interoceptive states produced by CB receptor agonists [ 89 ] and to induce self-administration in squirrel monkeys [ ].

    Taken together, these data suggest that FAAH inhibitors may be promising tools in the therapy of anxiety and mood disorders with a safer profile than cannabinoid direct agonists. This idea has been recently endorsed by several authors in recent articles and patents, featuring novel categories of highly selective and potent FAAH inhibitors [ - ] [ ]. However, it should be noted that recent data have recently shown that URB induce a number of side effects in rats, including social withdrawal, working memory deficits [ ] and impairments in auditory discrimination and reversal of olfactory discrimination [ ].

    The role of 2-AG in emotional regulation has been difficult to ascertain until the recent development of highly selective monoacylglycerol lipase MAGL inhibitors [ 35 , ]. Several lines of evidence have suggested that 2-AG plays a pivotal role in the pathophysiology of anxiety and defensive behaviors. Recent evidence has shown that this compound exerts anxiolytic-like effects in the elevated plus maze and in marble buyring, at doses that do not affect locomotor activity [ 93 , , ].

    Similarly to the effects described for FAAH inhibitors see above , the anxiolytic effects of this compound were observed in highly aversive or anxiogenic contextual settings [ ]. The neurobiological role of 2-AG in anxiety is still poorly understood, although several studies have shown that environmental stressors alter its biosynthesis and degradation in key brain structures controlling emotional regulation, including periaqueductal grey, amygdala and hippocampus [ , ].

    Interestingly, recent evidence has shown that the anxiolytic properties of JZL appear to be mediated by CB 2 , rather than CB 1 receptors [ 93 ], pointing to a potential implication of this receptor in the role of 2-AG in anxiety regulation. In light of the limitations of our current pharmacological armamentarium for anxiety disorders, the ability of cannabinoids to modulate emotional responses is extremely attractive for the development of novel anxiolytic agents [ ].

    At the same time, great concern arises from the protean role of cannabinoids on the regulation of these responses, as well as their misuse liability and other side effects. The identification of operational strategies for the employment of cannabinoids in the therapy of anxiety disorders is therefore a fundamental goal in psychiatry research.

    As outlined above, clinical evidence strongly suggests that acute administration of low doses of CB 1 receptor agonists results in anxiolytic effects, while excessive activation of these targets elicits opposite outcomes, following a reverse U-shaped dose-response pattern. This concept indicates a potential evolution in the search for direct CB agonists, in sharp contrast with the previous trend aimed at the identification of high-affinity CB receptor activators. However, recent preliminary clinical studies have shown that this formulation did not significantly reduce anxiety in fact, it was reported to induce a mild, yet not significant increase of this symptom [ , ], and that CBD did not appear to elicit a significant opposition to the effect of dronabinol [ ], plausibly indicating that a higher concentration of this ingredient or lower relative amount of THC may be necessary to elicit anxiolytic effects.

    A third, highly promising avenue for the development of cannabinoid-based anxiolytic therapies may be afforded by FAAH inhibitors. Unlike endocannabinoid transport blockers and direct CB receptor agonists, these compounds exhibit a number of highly desirable properties for anxiolytic agents: The neurobiological bases of this phenomenon are not completely understood, and may be related to the involvement of other FAAH substrates, such as OEA or PEA; however, recent investigations suggest that the lack of 2-AG enhancement ensuing FAAH inactivation may contribute to the lack of reinforcing properties of URB [ ], potentially suggesting a different role of anandamide and 2-AG in the modulation of reward; this idea is actually consistent with the recent finding that 2-AG is induces self-administration in monkeys [ ].

    A key problem concerning the potential application of cannabinoid-related agents and cannabinoids is the relatively little information about their long-term effects following chronic administration. Indeed, the subjective effects of cannabis have been shown to be typically different in chronic users as compared to occasional marijuana smokers [ , ].

    Prolonged consumption of cannabis has been shown to induce affective sequelae, including alexithymia and avolition [ , - ]. Interestingly, tolerance has been shown to the effects of THC [ , ], while no information is available on endocannabinoid-related agents. Long-term administration of cannabinoids has been shown to result in a number of neuroplastic adaptive processes, including CB receptor down-regulation [ , ].

    Some of these phenomena may indeed be critical in shaping the different emotional responsiveness to cannabis throughout life and reflect a potential pathophysiological loop which may compound the severity of pre-existing anxiety and affective disorders.

    Finally, another important step for the employment of cannabinoid-based anxiolytic therapies will be the analysis of the vulnerability factors implicated in the differential responses and long-term sequelae induced by cannabis consumption.

    For example, numerous meta-analyses and longitudinal studies have established that cannabis consumption in adolescence is conducive to an increased risk for psychotic disorders [ - ]. This association is particularly significant in the presence of other genetic factors, such as the Val Met allelic variant of the gene encoding Catechol-O-methyltransferase COMT [ , ], one of the main enzymes for the degradation of the neurotransmitter dopamine. Interestingly, it has been shown that the synergistic effect of COMT haplotype and cannabis in adolescence is more robust in conjunction with predisposing environmental variables, such as the exposure to urbanicity and psychosocial stress [ ].

    Another gene that may modulate the behavioral responsiveness to cannabinoids is Nrg1 , which encodes for the synaptic protein neuregulin 1. Indeed, the heterozygous deletion of this gene ablates the development of tolerance to the anxiogenic effects of CB receptor agonists [ , ]. These findings suggest that the employment of a pharmacogenetic approach may be a critical screening instrument to identify which patients may be treated with cannabis for medical purposes without risks of neuropsychiatric side effects.

    Notably, the role of genes in the mental sequelae of cannabis may also be contributed by epigenetic factors, in consideration of the recent finding that THC induces expression of histone deacetylase 3 [ ]. While studies on the biological determinants of different responses to cannabis are still at their preliminary stages, advances in this area may be essential to allow a personalized approach for the employment of cannabinoid-based therapies in anxiety and mood disorders.

    National Center for Biotechnology Information , U. Author manuscript; available in PMC Jun Simone Tambaro and Marco Bortolato. Author information Copyright and License information Disclaimer. See other articles in PMC that cite the published article. Abstract Rich evidence has shown that cannabis products exert a broad gamut of effects on emotional regulation.

    According to the current classification of anxiety disorders in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders DSM-IV [ 2 ], the main diagnostic entities in this category are: Table 1 Current pharmacological strategies for the treatment of anxiety disorders. Generalized anxiety disorder Benzodiazepines. Panic attack High-potency benzodiazepines. Post-traumatic stress disorder Selective serotonin reuptake inhibitors.

    Obsessive-compulsive disorder Tricyclic antidepressants. Open in a separate window. Table 2 Paradigms for testing of anxiety-like behaviors in rodents. Unconditioned anxiety Tests for social anxiety Maternal separation-induced ultrasonic vocalizations for pups.

    Tests based on antipredator defensive behavior Mouse defense test battery. Other tests Novelty-induced feeding suppression. Conditioned anxiety Tests on conditional fear Fear- conditioned freezing. Operant conflict test Geiller-Seifter test conditioned suppression of eating. Chemical structures of the major phytocannabinoids. Synthetic cannabinoids In addition to phytocannabinoids, several classes of synthetic CB receptor agonists have been developed; among these families, the best characterized are the synthetic analogs of THC - such as the biciclic compounds CP 47,, CP 55,, CP 55, and the benxopyrans HU and nabilone Fig.

    Chemical structures of the major endocannabinoids. Endocannabinoids Both anandamide and 2-AG are derivatives of arachidonic acid, an unsaturated C20 fatty acid with 4 double bonds, which also serves as the precursor for synthesis of other eicosanoids, including prostaglandins and leukotriens.

    CB 2 receptor ligands Few studies have actually evaluated the role of CB 2 receptor in anxiety and stress response. Endocannabinoid transport blockers The systemic administration of the endocannabinoid transport blocker AM Fig. MAGL inhibitors The role of 2-AG in emotional regulation has been difficult to ascertain until the recent development of highly selective monoacylglycerol lipase MAGL inhibitors [ 35 , ].

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    Oral nabilone capsules in the treatment of chemotherapy-induced nausea and vomiting and pain. Expert Opin Investig Drugs. Gaoni Y, Mecbonlam R. J Amer Chem Soc. Structure of a cannabinoid receptor and functional expression of the cloned cDNA. Molecular characterization of a peripheral receptor for cannabinoids. Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Identification of an endogenous 2-monoglyceride, present in canine gut, that binds to cannabinoid receptors.

    Biochem Biophys Res Commun. Involvement of Gi in the inhibition of adenylate cyclase by cannabimimetic drugs. Transmitter systems involved in neural plasticity underlying increased anxiety and defense--implications for understanding anxiety following traumatic stress.

    Demuth DG, Molleman A. Cannabinoid receptor localization in brain. Characterization and localization of cannabinoid receptors in rat brain: Charney DS, Deutch A. A functional neuroanatomy of anxiety and fear: Cannabinoid receptors in the human brain: The Journal of neuroscience: Role of endogenous cannabinoids in synaptic signaling. Distribution of cannabinoid receptors in the central and peripheral nervous system. Immunohistochemical distribution of cannabinoid CB1 receptors in the rat central nervous system.

    Pre- and postsynaptic localizations of the CB1 cannabinoid receptor in the dorsal horn of the rat spinal cord. Morishita W, Alger BE. Endogenous cannabinoids mediate retrograde signalling at hippocampal synapses. Endogenous cannabinoids mediate retrograde signals from depolarized postsynaptic neurons to presynaptic terminals. Metabotropic glutamate receptors drive the endocannabinoid system in hippocampus.

    Szabo B, Schlicker E. Effects of cannabinoids on neurotransmission. Endocannabinoid Signaling in Neural Plasticity. Pharmacology of Neurotransmitter Release. Cannabinoid receptors and their ligands: Walter L, Stella N. These pharmaceutical reuptake inhibitors only focus on one neurotransmitter, SSRIs, for example, focuses on increasing only serotonin in the brain. The issue with these drugs is that most cases of depression and anxiety are due to multiple neurotransmitter imbalances.

    Focusing on just one neurotransmitter does not make it likely that this drugs will exacerbate the disease. So, while these drugs may be effective for many patients, some do not respond favorably and actually seem to get worse with common side effects not to mention many are highly addictive. Could cannabidiol CBD , a non-psychoactive compound found in the cannabis plant provide a viable alternative to pharmaceutical anxiety and depression medications? These cannabinoids are all unique and interact with receptors in cells of the human body.

    While there are many different reasons people might be gravitating toward CBD, the center of its abilities is its highly anti-inflammatory properties. Chronic inflammation is the cause of almost all chronic diseases including cancer, digestive issues, heart disease, diabetes, autoimmune conditions, fibromyalgia, hormonal, and brain issues. This makes CBD a promising natural supplement for those suffering from underlying inflammatory issues, both mental and physical. CBD has gained much popularity in recent years because of the amount of interest among not only consumers but clinicians and scientist as well.

    With over 20, plus scientific articles on the cannabis plant , there is much reason to believe that the medical uses for this plant are here to stay. Numerous animal and human experimental, clinical and epidemiological studies suggest CBD has powerful anti-anxiety and anti-depression properties. It has been shown to be safe, well-tolerated and may be beneficial for disorders including:.

    Believe it or not, cannabinoids do not only interact well in the body, but they are also already present in the body! We have receptors on the edge of our cells that take cues and organize chemicals. The biggest class of receptors in the body are cannabinoid receptors, which are specifically designed to process cannabinoids. You read that right, we have receptors in our bodies for the same compounds found in the hemp plant.

    We actually have cannabinoids inside our bodies that modulate the way we make hormones, the way we run our immune system and neurotransmitters in the brain. These receptors finetune neurons that produce serotonin, dopamine, GABA, and glutamate. The dominant two receptors in our bodies are CB1 and CB2. CB1 is concentrated in the central nervous system but also found in other tissues as well, including liver, gut, uterus, prostate, adrenals, the cardiovascular system, and very high levels in several regions of the brain.

    CB2 is localized in the immune cells. CB2 is what controls inflammatory responses making it the more important one to pay attention to for therapeutic effects in general.

    CB1 receptors are found in different parts of the brain, including those concerned with cognition, sensory perception, memory, and emotion. It regulates every other neurotransmitter system including serotonin, dopamine, norepinephrine, and GABA. The endocannabinoid system ECS plays a very important role in the human body for our survival. This is due to its ability to play a critical role in maintaining the homeostasis of the human body meaning it is constantly working to bring about a state of balance to our bodies and minds , which includes the brain, endocrine, and immune system, to name a few.

    This whole system regulates important activities such as sleep, immune, gastrointestinal, central and peripheral nervous system, reproductive, digestive, mood, memory, appetite, and other cognitive and physical processes.

    Cannabinoids are chemical messengers of the ECS system and they modulate the way we make hormones, the way we run our neurotransmitters in the brain as well as our immune system. They are predominantly in the brain, the central nervous system, and the peripheral immune cells.

    CBD modulates what your endocannabinoids are doing and it increases the number of your endocannabinoids so when we take CBD oil , we are replenishing the endocannabinoid system with cannabidiol. CBD opens the channels and pathways in our brain and stimulates brain receptors to help regulate our system which definitely shows how good CBD for anxiety. This is what helps the body have an alkaline balance. When our bodies are inflamed we have higher levels of acidity thus making CBD powerfully anti-inflammatory for the body.

    Because it works directly with the very system that balances our bodies, it knows what to do in the body to bring you back into balance. CBD overall helps balance us emotionally, mentally and spiritually bringing our bodies back into the states we are meant to be in.

    Cannabidiol as a Potential Treatment for Anxiety Disorders

    This article is sponsored by TryTheCBD, encouraging you to feel life at its best. We are here to help, offering a 20% discount on products to students, students. CBD oil, hemp oil, cannabis oil, and many more) can be an effective treatment for mood disorders like anxiety and depression. In fact, a study published by Chemistry. CBD has proven to be an effective natural remedy for anxiety sufferers, thanks to the way it interacts with the body's endocannabinoid system.

    How Can CBD Help Anxiety?



    This article is sponsored by TryTheCBD, encouraging you to feel life at its best. We are here to help, offering a 20% discount on products to students, students.


    CBD oil, hemp oil, cannabis oil, and many more) can be an effective treatment for mood disorders like anxiety and depression. In fact, a study published by Chemistry.


    CBD has proven to be an effective natural remedy for anxiety sufferers, thanks to the way it interacts with the body's endocannabinoid system.

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