How to Use CBD for Anxiety: Products, Research, and Safety

A quality product should be free of contaminants and the levels of cannabinoids should closely match the product label (small variations are expected), and it should comply with the legal requirement of less than 0.3% THC. A real benefit of marijuana or THC is that they don’t cause overdose, which makes them especially attractive as an alternative to opioids for chronic pain. Side effects specific to smoking marijuana include coughing, increased phlegm, and a higher risk of lung illness and infection. However, smoking marijuana doesn’t appear to increase the risk of lung cancer. An important difference between your endocannabinoids and cannabinoids from an outside source, however, is that yours work in precise coordination with only the system that needs correcting at that moment.

• The influence of CBD on cardiovascular system in humans might depend not only on a dose [98] and duration of administration [97], but also on the delivery method of CBD.
• In another study, oral CBD (200, 400 and 800 mg) does not alter the subjective, reinforcing and cardiovascular effects of smoked cannabis (1/2 of cigarette containing ~800 mg of cannabis; 5.3–5.8% THC) [93].
• CBD is metabolized in the liver and the intestine by cytochrome P450 (CYP) CYP2C19 and CYP3A4, and 5′-diphosphoglucuronosyltransferase (UGT) UGT1A7, UGT1A9, and UGT2B7 isoforms, mainly producing hydroxylated and carboxylated metabolites [19].
• How fast your body absorbs the oil varies based on how it’s administered.
• CBD has been studied for its use in seizures, chronic pain, anxiety, inflammation, and more.

AEs occurred more frequently in the CBD than the placebo group, with somnolence (36% vs 10%) being the most common AE. The greatest success for CBD treatment is the reduction in seizures in children with refractive epilepsy. In a randomized, double-blind, placebo-controlled trial, CBD reduced atonic seizures in Lennox-Gastaut patients, who also received clobazam, valproate, lamotrigine, levetiracetam, or rufinamide [65].

Medications changed by the liver (Cytochrome P450 1A2 (CYP1A substrates) interacts with CANNABIDIOL (CBD)

Therefore, some authors suggest that the proposed endothelial cannabinoid receptor may be GPR18. However, not all experimental observations confirm it explicitly [73]. In addition, GPR18-independent activation of high-conductance Ca2+-activated K+ (BKCa) channels might contribute to vasodilatory action of Abn-CBD [157]. Abn-CBD can also lower blood pressure after intra-RVLM administration via GPR18 activation which leads to sympathoinhibition [158]. Moreover, this compound is an agonist of GPR55, however this receptor does not mediate vasorelaxant response to Abn-CBD [150].

Tremors were observed at all doses and CNS inhibition (depression, sedation, and prostration) was evident within 30 min. CBD’s neuroprotective effect was investigated in human neuroblastoma SH-SY5Y cells during and after neuronal differentiation [60]. Terminally-differentiated cells incubated with 2.5 µM CBD were not protected against ROS produced by exposure to glycolaldehyde, methylglyoxal, 6-hydroxydopamine, and hydrogen peroxide. During SH-SY5Y cell differentiation, CBD did not induce changes in antioxidant potential, nor neurite density.

Possible Side Effects

Pathological states might also modify action of administered cannabinoids, e.g., depressor response to THC is stronger in hypertensive than in normotensive patients [20]. Moreover, the influence of cannabinoids on the cardiovascular system may be achieved through their modulating effect on immune processes or redox balance occurring via cannabinoid and non-cannabinoid receptors. Cannabinoids can cause oxidative stress and proinflammatory effects (mainly through CB1 receptors) as well as antioxidative and anti-inflammatory effects (mainly through CB2 receptors) [27.31].

Gastrointestinal disturbances could be due to other co-administered anti-epileptic drugs making it difficult to assign responsibility to CBD. In a randomized, double-blind, placebo-controlled trial, CBD was efficacious in reducing atonic seizures in patients with Lennox-Gastaut syndrome, also taking clobazam, valproate, lamotrigine, levetiracetam, or rufinamide [65]. Treatment-related AEs, including somnolence, were mostly mild and occurred in 62% of 86 patients treated with 20 mg/kg/day CBD for 14 weeks. Severe AEs included sedation occurring in 23% of 86 patients receiving CBD; 14% patients treated with CBD and one (1%) treated with placebo withdrew from the study. CBD’s anti-inflammatory and antioxidant properties may offer a new pharmacological approach for neuroprotection and a reduction in hippocampal volume loss [23, 40, 41]. CBD protects against hippocampal pathology following chronic frequent THC use [42].

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That, combined with the absence of a high that impairs cognition, makes this drug especially attractive to many people with chronic pain. Cannabinoids affect your body through the endocannabinoid system (ECS). That system is named for substances your body naturally produces—and depends on—that are very like plant-based cannabinoids. The ECS has far-reaching effects is cannabidiol addictive on your body, and that’s why cannabinoids are believed to have so many different medicinal uses. Ultimately, the primary reasons why people use CBD is because it tends to have calming, relaxing, pain-reducing effects. It has been used to alleviate joint pain and nerve pain, reduce anxiety and stress, treat insomnia, improve migraines, and address nausea.

This is also considered a benefit for some people, but Jas Matharu-Daley, MD, a physician and chief medical officer for a CBD brand, notes that the effects might be too strong if you’re also taking CBD with other sedating medications. The most comment side effects of CBD include drowsiness, gastrointestinal issues, dry mouth, reduced appetite, nausea, and interaction with other medications. According to federal law, all hemp-derived CBD products must contain less than 0.3% THC.

Topical CBD

Potential uses for the products listed here are not health claims made by the manufacturers. The information in this article is intended to be general in nature. It’s not intended to be a substitute for medical advice from a healthcare professional. Healthline encourages you to make any treatment https://ecosoberhouse.com/ decisions with your healthcare professional. Amongst all of these positive developments, unapproved CBD products are being sold across the US and in other countries without rigorous standardization of CBD potency, the content of other constituents, and with unproven claims of health effects.

• Cannabinoids can cause oxidative stress and proinflammatory effects (mainly through CB1 receptors) as well as antioxidative and anti-inflammatory effects (mainly through CB2 receptors) [27.31].
• This variation highlights the need for more high quality, large-scale clinical trials to help establish standardized dosing and clinical usage guidelines for CBD therapy.
• For the oral route, on the other hand, maximum concentrations are reached after 1–2 or up to six hours after intake, and bioavailability is less than 20%, due to the first-pass metabolism [4,58].
• The anti-inflammatory and vascular-stabilizing effects of CBD have been also revealed in the murine encephalitis induced by lipopolysaccharide (LPS) administration (Table 4).
• Studies defining CBD’s beneficial effects were included to provide balance in estimating risk/benefit.

Severe AEs in Lennox-Gastaut patients receiving CBD treatment included increased ALT, AST, and GGT concentrations [65]. In 2017, Garberg et al. administered 50 mg/kg IV CBD to four piglets to evaluate drug safety and potential neuroprotective effects. CBD significantly reduced brain-derived neurotrophic factor (BDNF) expression and other signaling proteins in the hippocampus and frontal cortex with no effect in the striatum. It was concluded that CBD did not provide neuroprotection during early global hypoxia-ischemia [63].