We’re standing in a laboratory greenhouse on the campus of the University of Colorado Boulder looking at ten hemp plants that Kane recently procured for research purposes. They’re spindly, stalky little things, like gangling teenagers, a far cry from the lascivious crop that Hague had shown me. These plants, like nearly all hemp varieties, carry extremely low levels of THC.
In 1937, the U.S. Treasury Department introduced the Marihuana Tax Act, which imposed a levy of $1 per ounce for medicinal use of cannabis and $100 per ounce for recreational use. This was opposed by physicians who were not required to pay a special tax for prescribing cannabis, use special order forms to obtain it and keep records detailing its professional use. The American Medical Association believed that evidence of cannabis’ harmful effects was limited and the act would prevent further research into its medicinal worth.
In recent years, CBD has generated a tremendous amount of interest among consumers, clinicians, and scientists. Why? Not only does evidence suggest CBD counteracts many of THC’s adverse effects, but numerous animal studies and accumulating evidence from human experimental, clinical, and epidemiological studies suggest CBD has powerful anti-anxiety properties. Administered acutely (“as needed”), it appears safe, well-tolerated, and may be beneficial to treat a number of anxiety-related disorders, including:
CBD has also been shown to enhance extinction of contextually conditioned fear responses. Extinction training involves repeated CS exposure in the absence of the US, leading to the formation of a new memory that inhibits fear responses and a decline in freezing over subsequent training sessions. Systemic CBD administration immediately before training markedly enhanced extinction, and this effect depended on CB1R activation, without involvement of TRPV1 receptors . Further studies showed CB1Rs in the infralimbic cortex may be involved in this effect .
During the study, 50 participants with PTSD coexisting with alcohol use disorder will be given either 400 milligrams of CBD daily, or a placebo. The goal is to see if the participants who take CBD end up drinking less and whether this leads to an improvement in PTSD symptoms. The participants will be given a pharmaceutical-grade CBD, which is more reliable in strength and purity than the supplements that are currently available for sale to the public.
You should always start low with just tiny drops. Each tiny drop is about the size of a grain of rice. Try 2 tiny drops under tongue for 4 days. If no results, do 4 tiny drops for 4 days. If no results, do 6 tiny drops for 4 days and so on. It’s true that everybody is different. You have to play around until you get the dose that’s right for you. We have found that if we take too much, it does nothing and we just waste money. I use the Elixinol 3600 for sleep and I take 6 drops. My son uses Charlotte’s Web for PTSD and he takes a 1/4 dropper in morning and 1/4 dropper at night. I use Elixinol 3600 for my 95 year old with vascular dementia and I give him 6 drops about 3 or 4 times a day to help with confusion and prevent sundowners. He sleeps ALL night long!!!!
When appropriate doses of CBD are taken during the day (which should be determined in consultation with your doctor, but often include one dose in the morning and one in the evening), daytime performance is drastically improved, and in turn, both the “strength and consistency” of the sleep-wake cycle is also improved. Naturally, this enhances the ability of the body to enter the all-important non-REM sleep cycle at night.
Several complexities of the eCB system may impact upon the potential of CBD and other CB1R-activating agents to serve as anxiolytic drugs. First, CB1R agonists, including THC and AEA, have a biphasic effect: low doses are anxiolytic, but higher doses are ineffective or anxiogenic, in both preclinical models in and humans (reviewed in [33, 45]). This biphasic profile may stem from the capacity of CB1R agonists to also activate TRPV1 receptors when administered at a high, but not low dose, as demonstrated for AEA . Activation of TRPV1 receptors is predominantly anxiogenic, and thus a critical balance of eCB levels, determining CB1 versus TRPV1 activation, is proposed to govern emotional behavior [27, 47]. CBD acts as a TRPV1 agonist at high concentrations, potentially by interfering with AEA inactivation . In addition to dose-dependent activation of TRPV1 channels, the anxiogenic versus anxiolytic balance of CB1R agonists also depends on dynamic factors, including environmental stressors [33, 49].
Yet the DEA has stated unequivocally that it considers CBD to be illegal under the Controlled Substances Act. “CBD derived from the cannabis plant is controlled under Schedule I of the CSA because it is a naturally occurring constituent of marijuana,” Joseph Rannazzisi, the deputy assistant administrator of the DEA, told a congressional panel in June. “While there is ongoing research into a potential medical use of CBD, at this time, CBD has no currently accepted medical use in the USA.” Moreover, DEA spokesman Eduardo Chavez told the New Republic that Medical Marijuana, Inc.’s in-house opinion with regards to CBD has no merit. “The bottom line,” Chavez said, “is the oil is part of the marijuana plant, and the marijuana plant is currently a Schedule I controlled substance under federal law.”
However, Bonn-Miller told Live Science that he thinks cannabis research is on the upswing. "If we flash forward five years I think you'll see more studies," he said. Those studies could reveal more conditions that CBD may be helpful for and may also reveal that some of the reasons why people say they use CBD oil are not supported by the science but are instead a placebo effect. "And that's why we need to do the studies," he said.
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