A clinical endocannabinoid deficiency has been postulated to be operative in certain treatment-resistant conditions (Russo 2004), and has received recent support in findings that anandamide levels are reduced over controls in migraineurs (Sarchielli et al 2006), that a subset of fibromyalgia patients reported significant decreased pain after THC treatment (Schley et al 2006), and the active role of the ECS in intestinal pain and motility in irritable bowel syndrome (Massa and Monory 2006) wherein anecdotal efficacy of cannabinoid treatments have also been claimed.
Some jurisdictions use free voluntary treatment programs and/or mandatory treatment programs for frequent known users. Simple possession can carry long prison terms in some countries, particularly in East Asia, where the sale of cannabis may lead to a sentence of life in prison or even execution. Political parties, non-profit organizations, and causes based on the legalization of medical cannabis and/or legalizing the plant entirely (with some restrictions) have emerged in such countries as China and Thailand.[224][225]

If medical marijuana is illegal in a given state, THC levels determine whether a CBD product is illicit or not. In most places, the limit is extremely low. We’re talking under 1 percent THC, with some states opting for a cap as low as 0.3 percent. In this case, the only source that would work is hemp, and CBD products will, therefore, be hemp-derived.

The FDA relies on applicants and scientific investigators to conduct research. Our role, as outlined in the Federal Food, Drug, and Cosmetic Act, is to review data submitted to the FDA in a marketing application to determine whether a proposed drug product meets the statutory standards for approval. Additional information concerning research on the medical use of marijuana is available from the National Institutes of Health, particularly the National Cancer Institute (NCI) and NIDA.
Going forward, another emerging trend among recreational users are wellness lifestyles built around cannabis. This is certainly part of the influence of California’s new recreational marijuana market, which went online January 1, 2018. California is already an epicenter for health and wellness lifestyles and fads. Expect to see more of the same now that cannabis is completely legal.
CBD, or Cannabidiol, is a compound known as a cannabinoid. Cannabinoids are compounds that act on certain neurotransmitters throughout your body’s Endocannabinoid System (ECS). The ECS is responsible for regulating pain, inflammation, recovery time, sleep, and much more. When CBD is applied, consumed, or vaped, it encourages your ECS to produce more cannabinoids to reduce distress. The CBD in our Pain Rub may be able to alleviate pain and inflammation when it is applied to the desired area.
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The human body also produces cannabinoids, known as endocannabinoids, in a bodily system known as the endocannabinoid system (or ECS). The ECS promotes homeostasis by regulating a wide range of functions, including motor skills, mood, appetite, and sleep. As we age, our ECS produces fewer endocannabinoids; they may also decrease due to physical injury or disease. Replenishing depleted endocannabinoids with phytocannabinoids like CBD can help restore balance to the body.
Cost is another consideration. Most CBD oils are sold in concentrations of 300 to 750 mg, although this may range from less than 100 mg to more than 2,000. A good indicator of price-point is the cost per milligram. Low-cost CBD oils usually fall between five and 10 cents per mg; mid-range prices are 11 to 15 cents per mg; and higher-end oils cost 16 cents per mg or higher. Given these varying per-milligram costs, a bottle of CBD oil may be priced anywhere from $10 or less to $150 or more.

CBD oil alleviates physical pain and anxiety – both of which can have a negative impact on sleep. Additionally, CBD oil can actually prolong sleep for some, leading to more rest from night to night. Most medical experts agree that marijuana is not particularly beneficial for individuals with medical conditions and/or mental health disorders, as the THC can increase their symptoms; this makes CBD oil a good alternative option for people with the following sleep disorders and medical conditions.
Researchers in New Zealand have studied whether cannabis can be used to treat severe motor and vocal tics in those suffering from Tourette syndrome. The study concluded that subjects who took a controlled THC-CBD medicated spray showed marked improvement in the frequency and severity of motor and vocal tics post-treatment. Although the study is only a small clinical trial, it is one of the first to specifically analyze the effects of cannabis on Tourette syndrome.
μ-Opioid receptor agonists (opioids) (e.g., morphine, heroin, hydrocodone, oxycodone, opium, kratom) α2δ subunit-containing voltage-dependent calcium channels blockers (gabapentinoids) (e.g., gabapentin, pregabalin, phenibut) AMPA receptor antagonists (e.g., perampanel) CB1 receptor agonists (cannabinoids) (e.g., THC, cannabis) Dopamine receptor agonists (e.g., levodopa) Dopamine releasing agents (e.g., amphetamine, methamphetamine, MDMA, mephedrone) Dopamine reuptake inhibitors (e.g., cocaine, methylphenidate) GABAA receptor positive allosteric modulators (e.g., barbiturates, benzodiazepines, carbamates, ethanol (alcohol) (alcoholic drink), inhalants, nonbenzodiazepines, quinazolinones) GHB (sodium oxybate) and analogues Glucocorticoids (corticosteroids) (e.g., dexamethasone, prednisone) nACh receptor agonists (e.g., nicotine, tobacco, arecoline, areca nut) Nitric oxide prodrugs (e.g., alkyl nitrites (poppers)) NMDA receptor antagonists (e.g., DXM, ketamine, methoxetamine, nitrous oxide, phencyclidine, inhalants) Orexin receptor antagonists (e.g., suvorexant)
While CBD oil does a fine job of reducing stress, anxiety and the effects of chronic pain, it doesn’t have the same localized effect as CBD cream for pain. For example, if you have severe shoulder pain, CBD cream is a much better option than oil because it will get to work on that area immediately. The CBD in the topical combines with the CB2 receptors in our skin. As it doesn’t reach the bloodstream, it is best used for localized pain since it doesn’t offer full-body pain relief.

^ Fusar-Poli, Paolo; Crippa, José A.; Bhattacharyya, Sagnik; Borgwardt, Stefan J.; Allen, Paul; Martin-Santos, Rocio; Seal, Marc; Surguladze, Simon A.; O'Carrol, Colin; Atakan, Zerrin; Zuardi, Antonio W.; McGuire, Philip K. (2009). "Distinct Effects of Δ9-Tetrahydrocannabinol and Cannabidiol on Neural Activation During Emotional Processing". Archives of General Psychiatry. 66 (1): 95–105. doi:10.1001/archgenpsychiatry.2008.519. PMID 19124693.
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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