Many a time, multiple cannabinoid compounds are used together, either knowingly or unknowingly.  It is, hence, tough to discern the extent to which each compound is involved in causing the desired effect. There are cases where a group of cannabinoids works synergistically in bringing about bodily reactions. Studies selectively employing CBD oil are few in number, but promising.

As of 2018, there are 8 States where the Cannabis plant, including both marijuana and hemp, are completely legal for recreational and medicinal use. These states are Alaska, California, Colorado, Maine, Massachusetts, Nevada, Oregon, and Washington. So if you find yourself in one of these wonderful states, you are free to legally use CBD in any form without a prescription.

We all know of Charlotte’s Web; the miracle strain that is packed with a high concentration of CBD. The Charlotte’s Web Cannabis Strain was named after Charlotte Figi, who suffers from Dravet syndrome and was experiencing several seizures daily until the Stanley Brothers came up with this powerful strain. Since then, Charlotte’s web has been morphed into various products, including their famous Charlotte’s Web CBD oil.

Individuals with sleep disorders are likely to experience more intense pain as the body is unable to complete its natural healing process to alleviate some of the effects caused by arthritis, fibromyalgia, muscle injury, or other type of chronic pain. The danger with chronic pain is that it keeps the nerves engaged in a fight-or-flight state, which makes it extremely difficult to relax and fall asleep. CBD has neuroprotective properties that encourage rest and improve sleep.
This article reviews recent research on cannabinoid analgesia via the endocannabinoid system and non-receptor mechanisms, as well as randomized clinical trials employing cannabinoids in pain treatment. Tetrahydrocannabinol (THC, Marinol®) and nabilone (Cesamet®) are currently approved in the United States and other countries, but not for pain indications. Other synthetic cannabinoids, such as ajulemic acid, are in development. Crude herbal cannabis remains illegal in most jurisdictions but is also under investigation. Sativex®, a cannabis derived oromucosal spray containing equal proportions of THC (partial CB1 receptor agonist ) and cannabidiol (CBD, a non-euphoriant, anti-inflammatory analgesic with CB1 receptor antagonist and endocannabinoid modulating effects) was approved in Canada in 2005 for treatment of central neuropathic pain in multiple sclerosis, and in 2007 for intractable cancer pain. Numerous randomized clinical trials have demonstrated safety and efficacy for Sativex in central and peripheral neuropathic pain, rheumatoid arthritis and cancer pain. An Investigational New Drug application to conduct advanced clinical trials for cancer pain was approved by the US FDA in January 2006. Cannabinoid analgesics have generally been well tolerated in clinical trials with acceptable adverse event profiles. Their adjunctive addition to the pharmacological armamentarium for treatment of pain shows great promise.
Cannabidiol, a non-euphoriant phytocannabinoid common in certain strains, shares neuroprotective effects with THC, inhibits glutamate neurotoxicity, and displays antioxidant activity greater than ascorbic acid (vitamin C) or tocopherol (vitamin E) (Hampson et al 1998). While THC has no activity at vanilloid receptors, CBD, like AEA, is a TRPV1 agonist that inhibits fatty acid amidohydrolase (FAAH), AEA’s hydrolytic enzyme, and also weakly inhibits AEA reuptake (Bisogno et al 2001). These activities reinforce the conception of CBD as an endocannabinoid modulator, the first clinically available (Russo and Guy 2006). CBD additionally affects THC function by inhibiting first pass hepatic metabolism to the possibly more psychoactive 11-hydroxy-THC, prolonging its half-life, and reducing associated intoxication, panic, anxiety and tachycardia (Russo and Guy 2006). Additionally, CBD is able to inhibit tumor necrosis factor-alpha (TNF-α) in its own right in a rodent model of rheumatoid arthritis (Malfait et al 2000). At a time when great concern is accruing in relation to NSAIDs in relation to COX-1 inhibition (gastrointestinal ulcers and bleeding) and COX-2 inhibition (myocardial infarction and cerebrovascular accidents), CBD, like THC, inhibits neither enzyme at pharmacologically relevant doses (Stott et al 2005a). A new explanation of inflammatory and analgesic effects of CBD has recently come to light with the discovery that it is able to promote signaling of the adenosine receptor A2A by inhibiting the adenosine transporter (Carrier et al 2006).
CBD oil has been gaining more attention every day as the compound has been changing countless lives around the globe. The DEA, specifically, has been watching its development closely ever since CBD’s popularity has been increasing at such a rapid pace. So, what is the difference between legal and illegal CBD oil? And how do you know if it really is safe?

The use of cannabis for pain relief dates back to ancient China, according to a report published in the journal Cannabis and Cannabinoid Research. It’s thought that CBD oil might help ease chronic pain in part by reducing inflammation. In addition, CBD oil is said to promote sounder sleep and, in turn, treat sleep disruption commonly experienced by people with chronic pain.
The Marinol patient monograph cautions that patients should not drive, operate machinery or engage in hazardous activities until accustomed to the drug’s effects ( The Sativex product monograph in Canada ( suggests that patients taking it should not drive automobiles. Given that THC is the most active component affecting such abilities, and the low serum levels produced in Sativex therapy (vide supra), it would be logical that that patients may be able to safely engage in such activities after early dose titration and according to individual circumstances, much as suggested for oral dronabinol. This is particularly the case in view of a report by an expert panel (Grotenhermen et al 2005) that comprehensively analyzed cannabinoids and driving. It suggested scientific standards such as roadside sobriety tests, and THC serum levels of 7–10 ng/mL or less, as reasonable approaches to determine relative impairment. No studies have demonstrated significant problems in relation to cannabis affecting driving skills at plasma levels below 5 ng/mL of THC. Prior studies document that 4 rapid oromucosal sprays of Sativex (greater than the average single dose employed in therapy) produced serum levels well below this threshold (Russo 2006b). Sativex is now well established as a cannabinoid agent with minimal psychotropic effect.
In the United States, we're in the middle of a cannabis revolution. Our nation is slowly waking up to the truth that cannabis, what was once dubiously considered a dangerous psychoactive substance, is not only safe but extremely versatile in its medical benefits. This has been reflected in the sales of legal cannabis products, which is expected to grow from $6.6 billion in 2016 to $24.1 billion in 2025.
Strains such as Charlotte's Web, that started out being classified as "marijuana" strains, have now been able to be reclassified as Hemp strains, due to the meeting of the .3% THC threshold. This is an important designation, as breeders are now breeding Cannabis strains down to acceptable THC levels, while still offering a plant that carries all of the other combinations of naturally occurring Cannabinoids, which provide a synergistic effect when taken together along with the plants given Terpenoid and Flavanoid profiles.
Cannabis is a generic term used to denote the several psychoactive preparations of the plant Cannabis sativa. The major psychoactive consituent in cannabis is ∆-9 tetrahydrocannabinol (THC). Compounds which are structurally similar to THC are referred to as cannabinoids. In addition, a number of recently identified compounds that differ structurally from cannabinoids nevertheless share many of their pharmacological properties. The Mexican term 'marijuana' is frequently used in referring to cannabis leaves or other crude plant material in many countries. The unpollinated female plants are called hashish. Cannabis oil (hashish oil) is a concentrate of cannabinoids obtained by solvent extraction of the crude plant material or of the resin.
Cannabis has been around for thousands of years and is believed to have originated in South or Central Asia. The two main species of cannabis are Cannabis sativa and Cannabis indica. Both Cannabis sativa and indica contain varying amounts of psychoactive and nonpsychoactive components. Cannabis sativa is more commonly known for its stimulatory, mental effects while Cannabis indica is more known for its relaxing, body-calming effects.
The vast majority of subjects in Sativex clinical trials do not experience psychotropic effects outside of initial dose titration intervals (Figure 2) and most often report subjective intoxication levels on visual analogue scales that are indistinguishable from placebo, in the single digits out of 100 (Wade et al 2006). Thus, it is now longer tenable to claim that psychoactive effects are a necessary prerequisite to symptom relief in the therapeutic setting with a standardized intermediate onset cannabis-based preparation. Intoxication has remained a persistent issue in Marinol usage (Calhoun et al 1998), in contrast.
In 2000, 65% of Nevada voters approved Question 9, amending the state constitution to allow the use, possession and cultivation of marijuana by qualifying patients who participate in a confidential state-run registry that issues identification cards. Currently, registered patients may possess up to 2 ½ ounces of cannabis in a single 14-day period, as well as cultivate up to 12 plants or designate a primary caregiver to assist them. Patients who possess more than the law allows or do not have a registration card can still be prosecuted, but are entitled to a medical necessity defense in court.

The results of the three large European cohort studies have been confirmed in two smaller New Zealand birth cohorts. Arsenault and colleagues (2002) reported a prospective study of the relationship between adolescent cannabis use and psychosis in a New Zealand birth cohort (n = 759). They found a relationship between cannabis use by age 15 and an increased risk of psychotic symptoms by age 26. The relationship did not change when they controlled for other drug use, but it was no longer statistically significant after adjusting for psychotic symptoms at age 11. The latter probably reflected the small number of psychotic disorders observed in the sample. Fergusson et al. (2003) found a relationship between cannabis dependence at age 18 and later symptoms that included those in the psychotic spectrum reported at age 21 in the Christchurch birth cohort. Fergusson and colleagues adjusted for a large number of potential confounding variables, including self-reported psychotic symptoms at the previous assessment, other drug use and other psychiatric disorders, but whether the association represents a link between cannabis use and psychotic symptoms specifically, or more general psychiatric morbidity, remains unclear.

At an epidemiological level, a dose response relationship exists between cannabis use and increased risk of psychosis[126][127][128] and earlier onset of psychosis.[129] Although the epidemiological association is robust, evidence to prove a causal relationship is lacking.[130] But a biological causal pathway is plausible, especially if there is a genetic predisposition to mental illness, in which case cannabis may be a trigger.[131][better source needed]
The endocannabinoid system is tonically active in control of pain, as demonstrated by the ability of SR141716A (rimonabant), a CB1 antagonist, to produce hyperalgesia upon administration to mice (Richardson et al 1997). As mentioned above, the ECS is active throughout the neuraxis, including integrative functions in the periacqueductal gray (Walker et al 1999a; Walker et al 1999b), and in the ventroposterolateral nucleus of the thalamus, in which cannabinoids proved to be 10-fold more potent than morphine in wide dynamic range neurons mediating pain (Martin et al 1996). The ECS also mediates central stress-induced analgesia (Hohmann et al 2005), and is active in nociceptive spinal areas (Hohmann et al 1995; Richardson et al 1998a) including mechanisms of wind-up (Strangman and Walker 1999) and N-methyl-D-aspartate (NMDA) receptors (Richardson et al 1998b). It was recently demonstrated that cannabinoid agonists suppress the maintenance of vincristine-induced allodynia through activation of CB1 and CB2 receptors in the spinal cord (Rahn et al 2007). The ECS is also active peripherally (Richardson et al 1998c) where CB1 stimulation reduces pain, inflammation and hyperalgesia. These mechanisms were also proven to include mediation of contact dermatitis via CB1 and CB2 with benefits of THC noted systemically and locally on inflammation and itch (Karsak et al 2007). Recent experiments in mice have even suggested the paramount importance of peripheral over central CB1 receptors in nociception of pain (Agarwal et al 2007)

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