In a series of placebo-controlled studies involving 15 healthy volunteers, Fusar-Poli et al. investigated the effects of CBD and THC on task-related blood-oxygen-level dependent functional magnetic resonance imaging activation, specifically the go/no-go and fearful faces tasks [109, 110]. The go/no-go task measures response inhibition, and is associated with activation of medial prefrontal, dorsolateral prefrontal, and parietal areas [111]. Response activation is diminished in PTSD and other anxiety disorders, and increased activation predicts response to treatment [112]. CBD produced no changes in predicted areas (relative to placebo) but reduced activation in the left insula, superior temporal gyrus, and transverse temporal gyrus. The fearful faces task activates the amygdala, and other medial temporal areas involved in emotion processing, and heightened amygdala response activation has been reported in anxiety disorders, including GAD and PTSD [113, 114]. CBD attenuated blood-oxygen-level dependent activation in the left amygdala, and the anterior and posterior cingulate cortex in response to intensely fearful faces, and also reduced amplitude in skin conductance fluctuation, which was highly correlated with amygdala activation [109]. Dynamic causal modeling analysis in this data set further showed CBD reduced forward functional connectivity between the amygdala and anterior cingulate cortex [110].
The DEA isn’t the only government agency scrutinizing CBD vendors. To fend off the FDA, hemp oil companies contend their wares are not drugs but “dietary supplements.” Despite the suggestive “meds” in the company’s name, HempMedsPx is careful to note on its web site, “Although some of our founders are medical professionals, we cannot make medical claims about the benefits of our products.” Others are not quite so nuanced in their marketing. The internet is flooded with CBD products claiming to treat everything from seizures to arthritis to skin conditions and other maladies.
When formulating a CBD regimen for a specific disease or illness (like sleep disorders), it’s important to understand that CBD should be used regularly for maximum relief. It’s also helpful to understand whether another condition like anxiety, PTSD or pain is actually the root cause of your sleep disorder. The recommended regimen will also vary slightly based on the type of sleeping disorder you have – i.e. those suffering from insomnia will need to consume their CBD at a different time of day than those suffering from excessive daytime fatigue.

Guzmán is a biochemist who’s studied cannabis for about 20 years. I visit him in his office at the Complutense University of Madrid, in a golden, graffiti-splotched building on a tree-lined boulevard. A handsome guy in his early 50s with blue eyes and shaggy brown hair tinged with gray, he speaks rapidly in a soft voice that makes a listener lean forward. “When the headline of a newspaper screams, ‘Brain Cancer Is Beaten With Cannabis!’ it is not true,” he says. “There are many claims on the Internet, but they are very, very weak.”
People claim that cannabis oil can be used to treat a wide range of conditions, though evidence to back up these claims is often lacking. For example, according to Medical News Today, people use cannabis oil for conditions ranging from pain to acne; some even claim the oil can cure diseases like Alzheimer's and cancer. (But again, there is no clinical evidence to support these claims.) 
It’s important to remember that Tetrahydrocannabinol oil has psychoactive properties, so it’s still illegal in states where medical and/or recreational use of marijuana is prohibited. Aside from the illegal nature of THC, many health professionals and medical authorities question it’s efficacy as a treatment option since comes with such profound psychoactive effects. In fact, many doctors and researchers see the oil as more dangerous than it is beneficial.
Funding. AZ, JH, FG, and JC are recipients of fellowship awards from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, Brazil – 1A). The present study was supported by a CNPq grant (CNPq/MS/SCTIE/DECIT N° 26/2014 – Pesquisas sobre Distúrbios Neuropsiquiátricos; 466805/2014-4) and STI-Pharm (Brentwood, United Kingdom) has kindly supplied CBD at no cost. IL and JS are recipients of CNPq Fellowships.
This meant that overall, throughout the entire span of the night, I had ingested 2 doses of 2 BioCBD+ capsules for a cumulative dose of 40 mg (equivalent to 400 mg CBD).  After my second set of capsules, I ended up going over to a friend’s house and an unexpected party was going on (which made me nervous – I don’t like big parties).  I felt somewhat nervous because I didn’t know anyone and they wanted to drink (I didn’t want to) and thought about simply just leaving the party and going home.
Bergamaschi, M. M., Queiroz, R. H. C., Chagas, M. H. N., de Oliveira, D. C. G., De Martinis, B. S., Kapczinski, F., . . . Crippa, J. A. S. (2011, February 9). Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naive social phobia patients. Neuropsychopharmacology, 36(6), 1219-1226. Retrieved from http://www.nature.com/npp/journal/v36/n6/full/npp20116a.html?foxtrotcallback=true
An animal study using mice found repeated administration of CBD may help the hippocampus regenerate neurons, which could be useful for treating anxiety or depression. Research shows both SSRIs and CBD may promote neurogenesis. This is significant, because evidence suggests that severely impaired neuronal plasticity may influence suicidal behavior. Future research comparing CBD and SSRIs effect on neurogenesis could open up promising new avenues in how we understand depression and how to most effectively treat it.

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.”


So Mechoulam called the Israeli national police and scored five kilos of confiscated Lebanese hashish. He and his research group isolated—and in some cases also synthesized—an array of substances, which he injected separately into rhesus monkeys. Only one had any observable effect. “Normally the rhesus monkey is quite an aggressive individual,” he says. But when injected with this compound, the monkeys became emphatically calm. “Sedated, I would say,” he recalls with a chuckle.
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 [46]. 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 [48]. 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].
It is unclear as to what the optimal dosage of CBD is for anxiety disorders.  Most literature suggests that a single 600 mg dose of CBD is sufficient to alleviate anxiety.  However, the source from which you attain your CBD may make a major difference.  Various companies are selling CBD formatted with nanotechnology and/or co-factors (to maximize bioavailability) and a significantly lesser dose may be required than agents without specialized formatting.
I put two drops in my coffee (yes, I realize mixing hemp oil with caffeine is a bananas thing to do, but I need coffee and it is recommended on the website). The oil is much less unpleasant to take this way, although it does hugely change the taste of your coffee, so perhaps save it for your instant coffee, rather than your $5 slow-roasted French drip latte.
Given what you know about CBD already, you likely won’t be surprised to learn that it does not work like typical sleep medications do. In fact, some studies have shown it to actually be mildly alerting, and even to activate some of the same receptors that caffeine does. With this in mind, how can it possibly work to promote a healthy night’s sleep?
Until 2017, products containing cannabidiol that are marketed for medical purposes were classed as medicines by the UK regulatory body, the Medicines and Healthcare products Regulatory Agency (MHRA) and could not be marketed without regulatory approval for the medical claims.[82] CBD oil with THC content not exceeding 0.2% was legalized throughout the UK in 2017.[citation needed] Cannabis oil, however, remained illegal to possess, buy and sell.[83]
THC, an intoxicating and illegal substance, is responsible for causing marijuana users to get “high.” Unlike THC, CBD is non-psychoactive because it does not act on the same pathways as THC. Thus, it is impossible to get “high” by smoking or ingesting CBD or CBD oil extracted from industrial hemp plants, as they only have minuscule traces of THC (<0.3%).

I found I was too groggy during work hours if, on a typical day, I took CBD in the morning and at night. A dose of 25 milligrams an hour before going to bed, plus occasional topical use, has become my norm. The main exception is after an especially long or hard weekend run, when I have an additional 25 milligrams if I’m planning to mostly lounge about the house.


Epidemiological studies of various neuropsychiatric disorders indicate that a higher CBD content in chronically consumed cannabis may protect against adverse effects of THC, including psychotic symptoms, drug cravings, memory loss, and hippocampal gray matter loss [115–118] (reviewed in [119]). As THC acutely induces anxiety, this pattern may also be evident for chronic anxiety symptoms. Two studies were identified, including an uncontrolled retrospective study in civilian patients with PTSD patients [120], and a case study in a patient with severe sexual abuse-related PTSD [121], which showed that chronic cannabis use significantly reduces PTSD symptoms; however, these studies did not include data on the THC:CBD ratio. Thus, overall, no outcome data are currently available regarding the chronic effects of CBD in the treatment of anxiety symptoms, nor do any data exist regarding the potential protective effects of CBD on anxiety potentially induced by chronic THC use.
“It can affect everything from emotion to pain to appetite to energy metabolism to brain function to even the immune system and inflammation,” says Hector Lopez, M.D., a consultant to PlusCBD Oil, one of the top-selling brands. “When you have a system that cross talks with all those pathways, then there are very few things the endocannabinoid system does not influence.”
No statistically significant differences were found between groups in the VAMS, STAI, Digit Symbol Substitution and Symbol Copying Tests, and PVT. In the analysis of the WAIS, the results in the Symbol Copying Tests showed no effects of drug (F1,24 = 2.46; p > 0.05) or order of administration (F1,24 = 0.44; p > 0.05), but the interaction between drug and order was significant (F1,24 = 4.9, p < 0.05). To check if this interaction could have potentially interfered with the results, we split the subjects, comparing the placebo and CBD groups separately in the two orders (first placebo or CBD). Again, there was no difference between groups in the two situations.
Kane fingers one of his innocuous-looking plants, expressing mild bemusement at the U.S. ban on commercial hemp cultivation. “Hemp produces fibers of unparalleled quality,” he notes. “It’s a tremendously high biomass crop that replenishes the soil and doesn’t require much in terms of inputs. We import tons and tons of hemp each year from China and even Canada, yet as a matter of federal policy, we can’t legally grow it. There are places where farmers in the U.S. can literally look across the Canadian border and see fields that are yielding huge profits.”
Subjectively, I’d say it took around 15 to 20 minutes before I noticed some sort of an effect; could’ve been shorter or longer (I didn’t have a timer out).  I wasn’t stressed or anxious prior to taking the capsule, so there may not have been as much neurophysiological contrast.  That said, I noticed that I felt psychologically more relaxed and as if I stopped thinking critically about every little thing.

In case you are unfamiliar, ipsapirone is classified as a 5-HT1A partial agonist that is understood to exert antidepressant and anxiolytic effects.  Although it isn’t approved by the FDA to treat any conditions, it is commonly used as a research chemical.  Additionally, the drug Valium is understood to be a potent benzodiazepine that acts as a positive allosteric modulator at GABAA receptors; it is FDA approved for acute anxiety.

CBD likewise communicates with a neurotransmitter called GABA (gamma-aminobutyric corrosive). GABA transfers messages from one brain cell, or neuron, to another; that message usually is “Back off” or “stop pushing.” GABA advises the body when it’s a great opportunity to shut down, and since a huge number of neurons in the cerebrum react to GABA, the impacts include lessening anxiety, quieting the sensory system, assisting with rest, unwinding the muscles.
Food and beverage products containing CBD were introduced in the United States in 2017.[51] Similar to energy drinks and protein bars which may contain vitamin or herbal additives, food and beverage items can be infused with CBD as an alternative means of ingesting the substance.[52] In the United States, numerous products are marketed as containing CBD, but in reality contain little or none.[53] Some companies marketing CBD-infused food products with claims that are similar to the effects of prescription drugs have received warning letters from the Food and Drug Administration for making unsubstantiated health claims.[54]

Following cloning of the endogenous receptor for THC, namely the CB1R, endogenous CB1R ligands, or “endocannabinoids” (eCBs) were discovered, namely anandamide (AEA) and 2-arachidonoylglycerol (reviewed in [22]). The CB1R is an inhibitory Gi/o protein-coupled receptor that is mainly localized to nerve terminals, and is expressed on both γ-aminobutryic acid-ergic and glutamatergic neurons. eCBs are fatty acid derivatives that are synthesized on demand in response to neuronal depolarization and Ca2+ influx, via cleavage of membrane phospholipids. The primary mechanism by which eCBs regulate synaptic function is retrograde signaling, wherein eCBs produced by depolarization of the postsynaptic neuron activate presynaptic CB1Rs, leading to inhibition of neurotransmitter release [23]. The “eCB system” includes AEA and 2-arachidonoylglycerol; their respective degradative enzymes fatty acid amide hydroxylase (FAAH) and monoacylglycerol lipase; the CB1R and related CB2 receptor (the latter expressed mainly in the periphery); as well as several other receptors activated by eCBs, including the TRPV1 receptor, peroxisome proliferator-activated receptor-γ, and G protein-coupled 55 receptor, which functionally interact with CB1R signaling (reviewed in [21, 24]). Interactions with the TRPV1 receptor, in particular, appear to be critical in regulating the extent to which eCB release leads to inhibition or facilitation of presynaptic neurotransmitter release [25]. The TRPV1 receptor is a postsynaptic cation channel that underlies sensation of noxious heat in the periphery, with capsacin (hot chili) as an exogenous ligand. TRPV1 receptors are also expressed in the brain, including the amygdala, periaqueductal grey, hippocampus, and other areas [26, 27].
(FYI, if you're concerned about whether or not Charlotte's Web is legal, their PR kindly sent me this statement: "Regarding legality, CW Hemp is compliant with U.S. law regarding the manufacture and sale of dietary or food supplements. Our products meet the EU standard of less than 0.2% THC to be regarded as hemp and we market our products as a food supplement and adhere to those labeling laws." Phew.)
Both Bonn-Miller and Ward stress that it's up to the consumer to be well-educated about the material they're purchasing and the research that's out there. "The companies that are creating [cannabis oils] are offering lots of claims about its use that are not necessarily substantiated by any research," Bonn-Miller said. So "I think there needs to be, from a consumer standpoint, a lot of vigilance," he added.

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