FAAH inhibitor: The anxiolytic efficacy of CBD may be a result of its ability to act as an enzymatic inhibitor of FAAH (fatty acid amide hydroxylase).  FAAH is an enzyme responsible for metabolizing endocannabinoids such as anandamide, but when inhibited, these endocannabinoid concentrations are increased.  Increased concentrations of endocannabinoids such as anandamide and 2-AG, both of which bind to peripheral CB1/CB2 receptor sites.
Evidence from animal studies have begun to characterize the details of how CBD acts in the brain, and human studies of patients with and without anxiety disorders are starting to validate CBD’s efficacy as an anti-anxiety treatment. Given the huge social and financial costs of anxiety disorders in the U.S., CBD has the potential to play a significant role in treating a myriad of anxiety-related disorders.

Human trials are few and far between. The lone 2016 CBD and sleep-related study was restricted to a single adolescent suffering from PTSD and resulting insomnia. Although, the conclusions indicate the poor girl was sleeping better and on the road to recovery with a low sublingual spray dose of CBD. We must disclose that GW Pharmaceuticals founded the Cannabinoid Research Institute that carried out the research.
One of the biggest stumbling blocks to widespread use of CBD is price. High-quality tinctures from brands like Floyd’s of Leadville and PlusCBD cost $35 or more; the bottles contain enough tincture to last about a month if you’re using an eyedropper’s worth per day. Prevail’s 2-ounce topical salve, which the company says should last most users between 30 and 45 days, costs $133. A one-month supply of a daily gel typically costs $30 to $60.
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Cannabis has been used medicinally for centuries, as a sleep aid, a pain and nausea reducer, to relieve anxiety and other mood problems. In the mid-1960s, scientists identified the first cannabinoid. Since then, scientists have gone on to identify more than 80 individual cannabinoids and continue to investigate them for their potential symptom-relieving and disease-fighting abilities.
Certain individuals may be more prone to anxiety than others as a result of mu-opioid receptor expression and/or activation.  Research indicates that mu-opioid receptors participate in the modulation of anxiety based on the specific region of the brain in which they are stimulated.  What’s more, a report published in 2015 indicated that the neural circuitry associated with the DOR (delta opioid receptor) can induce OR inhibit anxiety.
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I assume this is also a side effect of the eased anxiety, but I seem to fall asleep within the 20- to 30-minute range rather than my normal 45 minutes to one hour (or longer). Not only do I seem to be skipping (or at least shortening) the whole tossing-and-turning phase of my sleep cycle, but I'm able to snap out of the overthinking mindset that often keeps me up at night. Of course, there's no telling whether a big life event would kindly disrupt this newfound bliss, but I'd like to think it's helped on day-to-day basis.
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Withdrawal: It is unclear as to whether there are any withdrawal symptoms ensuing following discontinuation of chronic CBD oil administration. It is apparent that there are marijuana withdrawal symptoms – it took years for these to receive legitimate scientific attention in the literature.  Though most would speculate that CBD is unlikely to cause discontinuation effects, withdrawal symptoms cannot be ruled out among long-term, chronic users.
You can rub CBD oil on your skin or drop it under your tongue; you can eat it as a sugarcoated gummy or drink it as a Goop-approved cocktail. There's evidence (some scientific, plenty anecdotal) that it helps with epileptic seizures, opioid addiction, PTSD, arthritis, anxiety, insomnia, nausea, chronic pain, and much more. If you believe the hype, CBD can do just about anything for your physical and mental health — and it won't get you high as a kite.

It also is distinct from THC which acts as a CB1/CB2 partial agonist, thereby stimulating the receptor sites.  If it acted the same as THC at the CB1/CB2 receptor sites, its therapeutic potential may be reduced.  Moreover, since cannabidiol acts as an inverse agonist at the CB1/CB2 receptor sites, it doesn’t induce psychological euphoria and/or pleasure associated with downstream dopaminergic enhancement in the mesolimbic pathway (resulting from CB1/CB2 agonism).
HV = healthy volunteers; DBP = double-blind placebo; SAD = social anxiety disorder; HC = healthy controls; THC = Δ9-tetrahydrocannabinol; STAI = Spielberger’s state trait anxiety inventory; VAMS = visual analog mood scale; BP = blood pressure; SPST = simulated public speaking test; SCR = skin conductance response; SPECT = single-photon emission computed tomography; SSPS-N = negative self-evaluation subscale; HR = heart rate; VAS = visual analog scale, CBD = cannabidiol
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Clinical and demographic data were analyzed with descriptive statistics and expressed in terms of mean ± standard error of the mean. The Kolmogorov-Smirnov test was used to check for normality. Non-parametric Wilcoxon or Friedman tests analyzed results that failed this test. The remained data was analyzed by two-way repeated-measures ANOVA. A preliminary analysis indicated no gender effect; thus, the factors analyzed were drug, order of drug administration (placebo-CBD versus CBD-placebo), and the interaction between drug and phase. A three-way repeated-measures ANOVA was employed to analyze data throughout the three phases of each exam. In case of significant interactions, paired Student’s t-tests were performed at each phase and/or order to compare the differences between groups. In case of significant time effect, the Bonferroni’s post hoc test was used for multiple comparisons. In cases where sphericity conditions were not reached, the degrees of freedom of the repeated factor were corrected with the Huynh-Feldt epsilon. All the analyses were performed with the Statistical Package for the Social Sciences (SPSS) v.20.0.
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In other words, the greater the amount of CBD oil administered following administration of a 5-HT1A agonist, the more significant the displacement.  Researchers mention that this mechanism differs from THC which is incapable of displacing 5-HT1A agonists from the 5-HT1A receptor.  Partial agonism of the 5-HT1A receptor site is associated with an array of therapeutic effects including: increased serotonin (or serotonergic effects), increased dopamine (in medial PFC, striatum, hippocampus), releasing acetylcholine, and hippocampal neurogenesis.
"It's important to know that the research in this area is in its infancy, partly because we haven't really understood much about CBD until relatively recently," said Marcel Bonn-Miller, an adjunct assistant professor at the University of Pennsylvania Perelman School of Medicine. He pointed out that the classification of marijuana as a Schedule 1 drug by the DEA makes it difficult to get material to use in laboratory studies. Schedule 1 drugs have a high potential for abuse, according to the DEA, and are illegal under federal law.

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