I have spent the last year + researching over 200 CBD companies and their products. I learned how the CBD is extracted, the difference between IH (Industrial Hemp) and THC producing cannabis that is harvested early, so that is is given the legal term Hemp, but technically it is the marijuana plant, etc. First, I chose not to take CBD orally, because of how the body breaks down CBD, when you digest it, it goes through the liver first, meaning less than 20% of what you take ends up in your body. Very expensive!! With vaping CBD oil about 70% makes it right into your bloodstream. With the CBD wax/shatter/dab, it is the same. So I stopped the oral route altogether. If you would oral or vape (inhaling vapor, no combustion), you want to look to see or email the company to ask how they extract the CND, and ask if they use CBD frown in the US. I highly suggest CBD frown in the US! The old law had people growing it overseas, and shipping it here to be extracted. Make sure no solvents were used to extract the CBD, like Butane. Whatever they tell you about how they extract it, look it up! This is a MUST! The most common ways to extract are via CO2 extraction using cold temperatures sometimes called subcritical or supercritical temperatures, same with ethanol extraction, there is no solvent in that either. Please research online both methods. There are a couple of other methods, one comes to mind, but it does not stay fresh long, and I cannot recall the name, I have not found any products which use that method, which is why I cannot name it. After making sure it is not done with anything dangerous, you want to make sure they have batch lab reports that check for heavy metals, mold, and how much CBD,CBG,CBC, etc is in the product. CBD, Cannabidiol is the most common Cannabinoid found in the marijuana or hemp plant. Did you know that IH contains a very small amount of THC? it is at or under.3%, so it is low, but it does help the CBD work.
Oral dronabinol (THC) is marketed in synthetic form as Marinol® (Solvay Pharmaceuticals) in various countries, and was approved in the USA for nausea associated with chemotherapy in 1985, and in 1992 for appetite stimulation in HIV/AIDS. Oral dronabinol’s expense, variability of action, and attendant intoxication and dysphoria have limited its adoption by clinicians (Calhoun et al 1998). Two open label studies in France of oral dronabinol for chronic neuropathic pain in 7 subjects (Clermont-Gnamien et al 2002) and 8 subjects (Attal et al 2004), respectively, failed to show significant benefit on pain or other parameters, and showed adverse event frequently requiring discontinuation with doses averaging 15–16.6 mg THC. Dronabinol did demonstrate positive results in a clinical trial of multiple sclerosis pain in two measures (Svendsen et al 2004), but negative results in post-operative pain (Buggy et al 2003) (Table 1). Another uncontrolled case report in three subjects noted relief of intractable pruritus associated with cholestatic jaundice employing oral dronabinol (Neff et al 2002). Some authors have noted patient preference for whole cannabis preparations over oral THC (Joy et al 1999), and the contribution of other components beyond THC to therapeutic benefits (McPartland and Russo 2001). Inhaled THC leads to peak plasma concentration within 3–10 minutes, followed by a rapid fall while levels of intoxication are still rising, and with systemic bioavailability of 10%–35% (Grotenhermen 2004). THC absorption orally is slow and erratic with peak serum levels in 45–120 minutes or longer. Systemic bioavailability is also quite low due to rapid hepatic metabolism on first pass to 11-hydroxy-THC. A rectal suppository of THC-hemisuccinate is under investigation (Broom et al 2001), as are transdermal delivery techniques (Challapalli and Stinchcomb 2002). The terminal half-life of THC is quite prolonged due to storage in body lipids (Grotenhermen 2004).
I have suffered from Neuropathy to both feet for about six years. The symptoms are numbness and pins and needs to the metatarsal region as well as the toes. There is also an intermittent very intense internal itching to the soles of both feet, which changes in location. I have been offered painkilling prescription drugs, but have refused these. I am very interested to learn of the benefits of Hemp/CBD Oil, and would appreciate some advice on which product you feel would most benefit my condition. Many thanks for your anticipated assistance. You may wish to reply to me by e-mail.
In 2019, the European Food Safety Authority (EFSA) announced that CBD and other cannabinoids would be classified as "novel foods",[83] meaning that CBD products would require authorization under the EU Novel Food Regulation stating: because "this product was not used as a food or food ingredient before 15 May 1997, before it may be placed on the market in the EU as a food or food ingredient, a safety assessment under the Novel Food Regulation is required."[84] The recommendation – applying to CBD extracts, synthesized CBD, and all CBD products, including CBD oil – was scheduled for a final ruling by the European Commission in March 2019.[83] If approved, manufacturers of CBD products would be required to conduct safety tests and prove safe consumption, indicating that CBD products would not be eligible for legal commerce until at least 2021.[83]

In addition to the daily pain management program outlined above, many people find they still need a safe way to manage acute flare ups. Whether it’s caused by a recent injury, cold weather, or general aggravation  – we recommend vaporizing CBD isolate to combat these acute pain flare ups. The benefit of vaporizing or dabbing CBD isolate is that the relief can be felt almost instantaneously. CBD isolate is 99% pure CBD and provides a wave of relief that can be felt throughout the whole body.
Figure 2. Receptor Systems Involved in CBD’s Potential Therapeutic Applications. CBD interacts, either directly or indirectly, with many different receptor systems in the brain. It indirectly influences the major cannabinoid receptor in the brain by decreasing THC’s ability to stimulate this receptor. It also interacts with a variety of other receptors. A subset of these are shown here. Each red shape represents a different brain receptor that might be found on a neuron. Some of the potential therapeutic applications associated with CBD’s interaction with each receptor system are listed below each receptor.

Understanding CBD’s analgesic, or pain-relieving, interactions with the ECS can shed light on CBD’s other interactions and effects. Importantly, the ECS participates in our bodies’ pain processing, but when CBD is introduced to our ECS, it stops the body from absorbing a pain-regulating compound known as anandamide — one of our body’s’ own natural cannabinoid molecules. Inhibiting the absorption of this compound shunts excess quantities into the bloodstream that in turn reduces pain. One study has revealed that CBD targets alpha-3 (α3) glycine receptors to suppress chronic pain and inflammation associated with dysfunctional glycine receptors, which are an important target for pain processing in the spine. In both humans and animal models, CBD has been shown to have a variety of anti-inflammatory properties.
The glutamatergic system is integral to development and maintenance of neuropathic pain, and is responsible for generating secondary and tertiary hyperalgesia in migraine and fibromyalgia via NMDA mechanisms (Nicolodi et al 1998). Thus, it is important to note that cannabinoids presynaptically inhibit glutamate release (Shen et al 1996), THC produces 30%–40% reduction in NMDA responses, and THC is a neuroprotective antioxidant (Hampson et al 1998). Additionally, cannabinoids reduce hyperalgesia via inhibition of calcitonin gene-related peptide (Richardson et al 1998a). As for Substance P mechanisms, cannabinoids block capsaicin-induced hyperalgesia (Li et al 1999), and THC will do so at sub-psychoactive doses in experimental animals (Ko and Woods 1999). Among the noteworthy interactions with opiates and the endorphin/enkephalin system, THC has been shown to stimulate beta-endorphin production (Manzanares et al 1998), may allow opiate sparing in clinical application (Cichewicz et al 1999), prevents development of tolerance to and withdrawal from opiates (Cichewicz and Welch 2003), and rekindles opiate analgesia after a prior dosage has worn off (Cichewicz and McCarthy 2003). These are all promising attributes for an adjunctive agent in treatment of clinical chronic pain states.

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