I’m 48 and have been diagnosed with anxiety disorder, depression, ptsd and have had panic attacks that have lead me to the ER 3 or 4 times. My psychiatrist put me on wellbutrin and klonopin for the anxiety and depression… I’m taking very low dosages of each but from what I’ve read when you come off of the klonopin it has physical side effects. I’m wanting to come off of both and my psychiatrist doesn’t think good things about cannabis and says that it interferes with the GABA receptors in the brain. I’m trying to find a doctor than can explain to me face to face how CBD and THC work on the brain and what he/she would recommend I do to get off the big pharma train. I’m in Puerto Rico.
In the United States, approximately 70 million people suffer from insomnia, insufficient sleep or another sleep disorder. CBD has been mistakenly described as sedating. In modest doses, CBD is mildly alerting. Cannabidiol activates the same adenosine receptors as caffeine, a stimulant. But several patients with sleep issues report that ingesting a CBD-rich tincture or extract a few hours before bedtime has a balancing effect that facilitates a good night’s sleep.
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 ). 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 . 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 . 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].
Blake Pearson, founder of GreenlyMed and a practicing doctor in Ontario, Canada, specializes in cannabinoid medicine and said he has personally seen patients who have lowered their intake of prescription medications or reduced the negative side effects of taking other medications. However, Pearson would like to see more robust research, including random controlled trials.
“THC”—the more-famous, high-inducing compound in cannabis—“works directly on the cannabinoid system, meaning it attaches to receptors and mimics some of our own internal endocannabinoids,” says Igor Grant, a professor and chair of psychiatry at the University of California, San Diego School of Medicine. But CBD’s interaction with the endocannabinoid system is subtler. “Normally, these endocannabinoid-signaling molecules are broken down by enzymes, and one thing CBD does is interfere with the actions of those enzymes.”
CBD is shorthand for cannabidiol, one of the more than 100 cannabinoids found in cannabis. CBD products are said to deliver their many claimed benefits by boosting the body’s endocannabinoid system, which is a system that “is a unique signaling pathway that controls the function of a variety of systems throughout the body, including the cardiovascular system,” says Nicholas DiPatrizio, Ph.D., a professor of biomedical sciences at the University of California, Riverside School of Medicine. (More on the endocannabinoid system later.)
It’s important to note that each state has its own individual laws on possession limits. Many states now have their own laws on the books for CBD oil specifically. Tennessee, for example, has made cannabis oil legal if it’s derived from hemp rather than marijuana. As Professor Elliot Altman of the Botanical Medical Research Center at Middle Tennessee State University, explains, “The legal definition is hemp is less than point three percent THC which is the psychotropic agent. Marijuana is point three percent or greater.” (14)
Hi, I have had spondylolisthesis since age 11 which left me with extreme nerve pain...restless leg syndrome. Had 3 spinal ops and also had hip surgery 2 years ago. have asthma and hypothyroidism. I can deal with everything else but this nerve pain is insane. Used Gabapentin for 9 years and now its not in the market in Nairobi, Kenya where I live. Am on Lyrica, which is not working. I started Cbd oil in August but now found my body has become immune to the effects of pain releif I was getting. Can anyone suggest what strength oil/cbd supplement I should aim for? Currently am making flapjacks with weed, have one every night but this makes me high which I dont want. I still wake up in pain at night, please help.
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.
The lab also has studied how the chemicals in cannabis, as well as cannabinoids like the anandamide produced by our bodies, protect our brains against various types of insults, such as physical and emotional trauma. “Our brain needs to remember things, of course,” says Guzmán, “but it also needs to forget things—horrific things, unnecessary things. It’s much like the memory in your computer—you have to forget what is not necessary, just like you need to periodically delete old files. And you have to forget what is not good for your mental health—a war, a trauma, an aversive memory of some kind. The cannabinoid system is crucial in helping us push bad memories away.”
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.
Sample sizes: As was already mentioned, the sample sizes used to test the effects of CBD for anxiety were relatively small-scale. Although the results from these small-scale studies may be accurate, larger-scale trials (with larger sample sizes) are warranted to confirm preliminary outcomes. A therapeutic effect found in just 10-20 patients may not hold up in a group of several hundred.
Administration of CBD reduced the anxiogenic effects of THC, suggesting that it is capable of decreasing anxiety in animal models. It was also documented that standalone CBD treatment reduced expression of c-Fos in the central nucleus of the amygdala. Reduction in c-Fos is understood to yield anxiolytic effects – possibly another mechanism by which cannabidiol attenuates symptoms of anxiety.
CBD does not appear to have any psychotropic ("high") effects such as those caused by ∆9-THC in marijuana, but may have anti-anxiety and anti-psychotic effects. As the legal landscape and understanding about the differences in medical cannabinoids unfolds, it will be increasingly important to distinguish "medical marijuana" (with varying degrees of psychotropic effects and deficits in executive function) – from "medical CBD therapies” which would commonly present as having a reduced or non-psychoactive side effect profile.
My favorite thing about it is how incredibly mild it is – like I said, the effects just kind of slowly ooze their way in without you even really noticing. Also, I love how seemingly long-lasting the effects are. I’ve read that some people prefer vaping over taking the oil drops because they say vaping is more potent, but I also understand that the effects of vaping are much shorter lived.
Currently available pharmacological treatments include serotonin reuptake inhibitors, serotonin–norepinephrine reuptake inhibitors, benzodiazepines, monoamine oxidase inhibitors, tricyclic antidepressant drugs, and partial 5-hydroxytryptamine (5-HT)1A receptor agonists. Anticonvulsants and atypical antipsychotics are also used to treat PTSD. These medications are associated with limited response rates and residual symptoms, particularly in PTSD, and adverse effects may also limit tolerability and adherence [7–10]. The substantial burden of anxiety-related disorders and the limitations of current treatments place a high priority on developing novel pharmaceutical treatments.
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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