...with due respect, your experience Locsta is almost precisely what happened with my....chihuahua. Degenerative disc disease, excruciating pain, prednisone worked, but couldn't keep her on it..pain killers and muscle relaxants didn't help, really thought I would have to put her down. Chi bloggers suggested CBD; gave PetReleaf a shot--like you, literally within minutes I could see the difference, in days she was pain free and now is back in charge of our world. The real key here is that with my dog, there is zero, nada, chance that there was any placebo effect...
Devinsky puts more weight behind the scientific advancements: In June, the FDA approved an epilepsy drug called Epidiolex, which contains a purified form of CBD oil. In controlled clinical trials, the drug was proven to reduce seizures in people with Dravet syndrome and Lennox-Gastaut syndrome — and it didn't produce as many of the unpleasant side-effects that come with other epilepsy medications.
5-HT1A agonist: 5-HT1A is a subtype of the serotonin receptor, which is important because anxiety and depression can sometimes be treated with medications that target the serotonin system. This is why drug companies developed selective serotonin reuptake inhibitors (SSRIs) like Prozac and Zoloft. SSRIs work by blocking reabsorption of serotonin in the brain, which increases availability of serotonin in the synaptic space. This helps brain cells transmit more serotonin signals, which can reduce anxiety and boost mood in certain cases (although the full biological basis for this is more complicated and not fully understood).
This evidence supports the idea that CBD decreases autonomic stress responses (e.g. increased blood pressure, faster heart rate, etc.) associated with stress in animal models. Additionally, the reduction in stress associated with CBD is induced predominantly via its binding to the 5-HT1A receptor sites. Based on the results, we could speculate that CBD may be equally therapeutic in attenuating exaggerated autonomic stress responses in humans.
THC (Tetrahydrocannabinol) Cannabis oil and Cannabidiol (also called CBD) have similarities but some important differences for users. Both cannabinoids, chemical compounds that can be found in all cannabis plants, including hemp and marijuana. Cannabinoids are the substances secreted by the flowers of the cannabis plant and contain natural medicinal properties, offering relief from conditions including anxiety, pain, nausea, and inflammation. There are plant-based cannabinoids and also phytocannabinoids, both with a variety of health benefits.
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 . Response activation is diminished in PTSD and other anxiety disorders, and increased activation predicts response to treatment . 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 . Dynamic causal modeling analysis in this data set further showed CBD reduced forward functional connectivity between the amygdala and anterior cingulate cortex .
Bonn-Miller also explained that it's imperative to exhaust the traditional and established front-line treatments that are available before seeking out these products. "CBD is not really a first-line treatment for anything," he said. "You don’t want situations where somebody says, 'I have cancer I'm going to forgo chemotherapy because I read something about CBD or THC helping with cancer.'" That's not a good idea, Bonn-Miller said. "Not only is the science not there, but you may end up worse off."
Preclinical evidence conclusively demonstrates CBD’s efficacy in reducing anxiety behaviors relevant to multiple disorders, including PTSD, GAD, PD, OCD, and SAD, with a notable lack of anxiogenic effects. CBD’s anxiolytic actions appear to depend upon CB1Rs and 5-HT1ARs in several brain regions; however, investigation of additional receptor actions may reveal further mechanisms. Human experimental findings support preclinical findings, and also suggest a lack of anxiogenic effects, minimal sedative effects, and an excellent safety profile. Current preclinical and human findings mostly involve acute CBD dosing in healthy subjects, so further studies are required to establish whether chronic dosing of CBD has similar effects in relevant clinical populations. Overall, this review emphasizes the potential value and need for further study of CBD in the treatment of anxiety disorders.
There are two types of cannabinoid receptors. CB1 receptors are located in the central and peripheral nervous system and are credited with creating homeostasis with health and disease. CB2 receptors are located in the immune system, gastrointestinal system, and the brain. In a 2001 study, researchers from Vanderbilt conducted a study on mice to search for CB1 receptors in the central amygdala — an area of the brain associated with anxiety and stress responses. They found the presence of receptors in the mouse brain and furthermore, discovered that when endocannabinoids interacted with them that the excitability of these brain cells decreased. Further studies are needed to prove this finding.
Cannabidiol has been found to act as an antagonist of GPR55, a G protein-coupled receptor and putative cannabinoid receptor that is expressed in the caudate nucleus and putamen in the brain. It has also been found to act as an inverse agonist of GPR3, GPR6, and GPR12. Although currently classified as orphan receptors, these receptors are most closely related phylogeneticaly to the cannabinoid receptors. In addition to orphan receptors, CBD has been shown to act as a serotonin 5-HT1A receptor partial agonist, and this action may be involved in its antidepressant, anxiolytic, and neuroprotective effects. It is an allosteric modulator of the μ- and δ-opioid receptors as well. The pharmacological effects of CBD have additionally been attributed to PPARγ agonism and intracellular calcium release.
Human activities—including pollution, deforestation, overpopulation, poaching, warming oceans and extreme weather events tied to climate change—are predicted to drive so many mammals to extinction in the next five decades that nature will need somewhere between 3 to 7 million years to restore biodiversity levels to where it was before modern humans evolved, according to an alarming new analysis published Monday in the Proceedings of the National Academy of Sciences.
Fear and anxiety are adaptive responses essential to coping with threats to survival. Yet excessive or persistent fear may be maladaptive, leading to disability. Symptoms arising from excessive fear and anxiety occur in a number of neuropsychiatric disorders, including generalized anxiety disorder (GAD), panic disorder (PD), post-traumatic stress disorder (PTSD), social anxiety disorder (SAD), and obsessive–compulsive disorder (OCD). Notably, PTSD and OCD are no longer classified as anxiety disorders in the recent revision of the Diagnostic and Statistical Manual of Mental Disorders-5; however, excessive anxiety is central to the symptomatology of both disorders. These anxiety-related disorders are associated with a diminished sense of well-being, elevated rates of unemployment and relationship breakdown, and elevated suicide risk [1–3]. Together, they have a lifetime prevalence in the USA of 29 % , the highest of any mental disorder, and constitute an immense social and economic burden [5, 6].
Research has shown that administration of cannabidiol actually inhibits agonist effects at the CB1/CB2 receptor sites. Although the effects of CB1 inverse agonism aren’t fully elucidated, many speculate that CB2 inverse agonism may contribute to cannabidiol’s anti-inflammatory effects. Due to the fact that neuroinflammation is associated with anxiety disorders, we could hypothesize that a decrease in inflammation may yield anxiolytic responses in a subset of CBD users.
"It's important to know that the research in this area is in its infancy, partly because we haven't really understood much about CBD until relatively recently," said Marcel Bonn-Miller, an adjunct assistant professor at the University of Pennsylvania Perelman School of Medicine. He pointed out that the classification of marijuana as a Schedule 1 drug by the DEA makes it difficult to get material to use in laboratory studies. Schedule 1 drugs have a high potential for abuse, according to the DEA, and are illegal under federal law.
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