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cbd and adenosine

Cbd and adenosine

Several enzymes implicated in the regulation of redox have been identified as potential molecular target of CBD [55]. Here, 100 μM CBD applied to mouse hepatic 105,000 g supernatant reduced superoxide dismutase and catalase activity by approximately 76% and 24%, respectively, and nicotinamide adenine dinucleotide (NAD)- and NAD phosphate-dependent NAD(P)H quinone reductase by 80% and 81%, respectively, when compared with controls. Moreover, CBD, at the same concentration, also significantly stimulated glutathione peroxidase and glutathione reductase by 24% and 40%, respectively. However, it is notable that the concentration of CBD used in this study was far in excess of that which can be achieved physiologically [17].

Peroxisome Proliferator-activated Receptors

CBD can directly inhibit enzymes in the ETC in isolated mitochondria [66]. However, brain extracts obtained from rats acutely and repeatedly treated with CBD revealed significantly increased ETC activity [67]. In neurodegenerative disease, the ETC is often impaired [211]. This might therefore suggest that CBD, like many other compounds that can inhibit mitochondrial function, can induce an adaptive upregulation of mitochondrial function and resistance to oxidative stress, a well-described process involving reactive oxygen species [212, 213].

CBD Receptor Targets in Neurodegeneration

100 constituent phytocannabinoids (plant cannabinoids) with therapeutic usefulness, including for neurological disorders such as convulsions and pain [1–9]. However, such traditional use does not constitute valid evidence for the modern medical use of the plant, its extracts or components, and licensed clinical use of cannabis-based medicines remains limited to a small number of disorders such as pain in multiple sclerosis (MS), appetite stimulation in HIV/AIDS, and cancer chemotherapy [10–12]. Moreover, the therapeutic effects of currently licensed cannabis-based treatments rely for the most part upon the pharmacological effects of the principal psychoactive component derived from the C. sativa plant, Δ 9 -tetrahydrocannabinol (Δ 9 -THC) [13].

Cbd and adenosine

The primary purpose of the ECS appears to be maintaining homeostasis, which it does by keeping neurotransmitter levels in check. Consuming CBD could be thought of as supplementing or increasing the activity of your body’s existing endocannabinoid system.

CBD is available as “full spectrum” or “isolate”. Full spectrum CBD products contain CBD and other compounds found in the original plant, which could include small amounts of THC. If the CBD was derived from industrial hemp, the THC content of the original plant is legally supposed to be less than .3% (in Colorado). Products that contain CBD isolate should only contain CBD. CBD isolate and CBD produced from hemp would be a better choice, from an anti-doping standpoint, for anyone with zero-tolerance drug testing at work (i.e. pilots).

Alternative to NSAIDs

Getting more and better sleep is one of the most effective ways an athlete can achieve greater training gains. Anecdotally, athletes who consume CBD report greater ease going to sleep and a more restful night’s sleep. One potential reason for this could be CBD inhibiting the reuptake of adenosine. (7)

Companies that produce and sell CBD products recommend starting with a low dose and gradually increasing it based on the effects you experience.

How to use CBD

Here’s where things get tricky. There is no standard dose that delivers a consistent effect for all people. CBD products are not well regulated, so there can be inconsistencies in how much CBD is in a product. And depending on how you consume CBD (oil, gummy bear, cookie, recovery drink, tincture, vapor), it can be difficult to be precise. The most precise way to consume CBD is probably through capsules, or by calculating how many milligrams of CBD are in a given volume (i.e. 1 milliliter) of a tincture.