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Whether the drug and non-drug, cultivated and wild types of Cannabis constitute a single, highly variable species, or the genus is polytypic with more than one species, has been a subject of debate for well over two centuries. This is a contentious issue because there is no universally accepted definition of a species.[54] One widely applied criterion for species recognition is that species are "groups of actually or potentially interbreeding natural populations which are reproductively isolated from other such groups."[55] Populations that are physiologically capable of interbreeding, but morphologically or genetically divergent and isolated by geography or ecology, are sometimes considered to be separate species.[55] Physiological barriers to reproduction are not known to occur within Cannabis, and plants from widely divergent sources are interfertile.[43] However, physical barriers to gene exchange (such as the Himalayan mountain range) might have enabled Cannabis gene pools to diverge before the onset of human intervention, resulting in speciation.[56] It remains controversial whether sufficient morphological and genetic divergence occurs within the genus as a result of geographical or ecological isolation to justify recognition of more than one species.[57][58][59]

In response to the FDA’s historic decision, the Drug Enforcement Administration (DEA) announced in September 2018 that it had removed Epidiolex from Schedule I classification, a category reserved for dangerous drugs with no medical value. Henceforth, Epidiolex would be considered a Schedule V drug, the least dangerous designation under the Controlled Substances Act.
One of CBD’s chief properties is its anticonvulsant nature. Clinical trials have shown that CBD is effective at reducing seizures in children, and the FDA is likely to approve Epidiolex, a pharmaceutical-grade version of CBD for this use, in summer 2018. Although CBD has been documented as an antiepileptic since 1881, CBD’s anticonvulsant mechanisms still remain unclear. Not enough studies have been conducted to understand this relationship fully. One possible explanation for CBD’s neuroprotective effects is its interaction with NMDA receptors, which play a key role in the overly active neuron activity that is a hallmark of epilepsy.
Consumers report using CBD for a huge variety of health and wellness reasons, but a lot more research is needed to determine which symptoms and ailments it works best for. Currently, there are more than 40 clinical trials enrolling patients to examine the effectiveness of CBD for a variety of diseases, including substance use disorder, chronic pain, post-traumatic stress disorder (PTSD), depression, schizophrenia, and many others. Most importantly, CBD is incredibly safe, and not addictive. Even young children can tolerate daily doses of up to twenty milligrams (20 mg) per kilogram (1 kg) of body weight (for a 175 pound adult, that’s more than 1,500 mg). The most common side effect of high-dose CBD is sleepiness.
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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