Sponsored by
PuffItUp VapeFully Dynavap Vaposhop
  1. Welcome to VaporAsylum! Please take a moment to read our RULES and introduce yourself here.
    Dismiss Notice
  2. Did you know we have lots of smilies for you to use?
    Dismiss Notice
  3. Did you know that you have two different customized styles/themes to view VaporAsylum in?
    Change your style here.
    Dismiss Notice
  4. Need help navigating the forum? Find out how to use our features here.
    Dismiss Notice

Meds Cannabis Effects on the Brain

Discussion in 'Why Do You Medicate?' started by momofthegoons, May 21, 2017.

  1. momofthegoons

    momofthegoons Vapor Accessory Addict Staff Member

    Likes Received:
    Trophy Points:
    Cannabis could treat traumatic brain injury, Israeli researchers say

    Hebrew University team finds that cannabinoid compounds help recovery in rats, possibly opening door for clinical trials

    Our body’s cannabinoid receptor system may play a part in protecting our nervous system following trauma, Israeli researchers believe.

    A team at the Hebrew University of Jerusalem has found that rats and mice subjected to traumatic brain injury (TBI) showed significantly better recovery when treated with cannabinoid compounds, possibly opening the way for clinical trials in the near future.

    Cannabinoids are chemical compounds, either derived from cannabis or manufactured, that act on specific cannabinoid receptors in our body’s cells. The most well-known is tetrahydrocannabinol, or THC, marijuana’s main psychoactive compound. The endocannabinoid system, our body’s natural cannabinoid receptors, is found in the brain and most organs of the body, and is believed to be a part of the neuroprotective mechanism in mammals, said Prof. Esther Shohami of the Hebrew University of Jerusalem.

    When an external event like stroke or trauma occurs, the body responds by producing these molecules that should protect the brain, Shohami said. In previous studies, the researchers looked at the endocannabinoid 2-AG in mice following a traumatic brain injury. 2-AG is produced by the body naturally, but in relatively low amounts that are not enough to effectively protect the brain.

    The researchers noticed that 2-AG levels were significantly higher following trauma, although they weren’t sure why.

    “A high level doesn’t mean anything, what matters is what it’s there for,” Shohami said.

    They administered additional plant-derived 2-AG to mice following a brain injury, and found that the compound helped the mice recover.

    “It is administered by the brain but it’s not enough to protect the brain, so we had to augment,” Shohami said. “The brain creates protection; we wanted to mimic what the brain does, and we wanted to do it better.”

    The mice only received a single dose, but showed positive effects up to three months after the injury. 2-AG’s main effect is as an anti-inflammatory compound, Shohami said.

    “The outcome of trauma was better, the motor function, the cognitive function,” Shohami said. “All the parameters we looked at as part of the damage were affected by the 2-AG, and were better than the untreated mice.”

    The problem was that both cannabinoid receptors type 1 and 2, or CB1 and CB2, were involved in the response. CB1 is responsible for the psychoactive effects of cannabinoids, and is less stable, so it could not be used as a drug. CB2 is not involved in the psychoactive effects of cannabinoids.

    “If you can distinguish between the two receptors you can make this drug more attractive for pharma, for doctors to prescribe, because the concern about side effects would be significantly reduced,” Shohami said.

    Shohami and her team developed synthetic molecules, modeled on 2-AG, that selectively activate the CB2 receptors and do not bind to the psychoactive, CB1 receptors. The researchers looked at the effect of these molecules, called HU-910 and HU-914, on rats following a closed head injury. They studied the effects of the compounds on both the rats’ brains and on the corticospinal tracts, a neural pathway originating in the brain which extends down the spinal cord and is responsible for the body’s motor control. No one had looked at the effects of cannabis on the corticospinal tract before, Shohami said.

    The researchers found improved recovery after TBI in the brain and in this tract, and improved motor skills, which is one important parameter of recovery.

    There are no drugs approved for treating traumatic brain injury, Shohami said, partly due to failures in developing treatment by the industry in the 1990s and 2000s, which has made drug companies reluctant to endorse new treatments.

    “It’s a very complex condition. Treatment has to be very carefully designed both in terms of mechanism and timing. Timing of treatment is very critical and this was the basis of failure for many of the trials,” Shohami said.

    The drug would need to be administered as a single dose in a specific therapeutic window within a few hours of the injury.

    Not all of the team’s data has been published, but the researchers hope the treatment will advance to clinical trials, and eventually become a prescribed treatment for TBI.

    Prof. Raphael Mechoulam, who collaborated on the research, first discovered the structure of THC. Mechoulam also uncovered the endocannabinoid system in the 1990s.

    Shohami will present her research, titled “The role of CB2 receptors in the recovery of mice after traumatic brain injury,” at the Cann10 International Medical Cannabis Conference, which will be held in Tel Aviv on June 4-6.

    BD9 likes this.
  2. momofthegoons

    momofthegoons Vapor Accessory Addict Staff Member

    Likes Received:
    Trophy Points:
    Posted on September 30, 2015

    Traumatic brain injuries are brain dysfunctions that are caused by an outside blow to the head. Studies have shown marijuana helps limit brain damage and improves recovery when administered shortly after the traumatic blow.

    A traumatic brain injury (TBI) is a disruption of the normal function of the brain caused by a bump or blow to the head. A mild brain injury, or concussion, can cause temporary brain cell dysfunction, while a more serious injury can cause the brain tissue to bruise, tear or bleed and result in long-term complications or death.

    In a TBI, the blow to the head causes damage to the brain cells. The damage can be isolated to the point of impact or can be more widespread if the impact causes the brain to moves back and forth within the skull. In addition, bleeding in the brain, or swelling, can cause greater damage to brain cells.

    According to Mayo Clinic, additional complications can arise from TBI’s, including altered consciousness (coma, vegetative state, locked-in syndrome, brain death, etc…), seizures, fluid buildup, blood vessel damage, nerve damage, and intellectual, communication, sensory and behavioral problems.

    The physical and psychological symptoms of a TBI can vary significantly and can arise immediately after the traumatic blow or even weeks later. Physical symptoms include a loss of consciousness or being dazed, headache, nausea or vomiting, fatigue, sleeping difficulties, sleeping more than usual and dizziness. It’s not uncommon for sensory problems, like blurred vision or ear ringing to occur. Also, memory and concentration problems, mood changes and a feeling of depression are cognitive symptoms of a TBI.

    For mild brain injuries, rest and over-the-counter pain relievers for headaches are often adequate for recovery. More severe brain injuries require emergency care procedures to ensure oxygen, blood levels and blood pressure remain at adequate levels. Medications may be used to help limit secondary damage caused by fluid buildup. In some cases, surgery is required to repair skull fractures or to relief pressure by draining fluid.

    Following the blow that leads to TBI’s, the body releases harmful mediators that lead to excitotoxicity, oxidative stress and inflammation and causes secondary, delayed neuronal death (Biegon, 2004). Cannabis, however, has been shown to offer protection to the neural system, thus reducing the amount of brain damage (Mechoulam, Spatz & Shohami, 2002) (Mechoulam & Shohami, 2007) (Mechoulam, Panikashvili & Shohami, 2002) (Biegon, 2004).

    It’s cannabis’ two major cannabinoids, tetrahydrocannabinol (THC) and cannabidiol (CBD) that are responsible for these beneficial effects following TBI’s. Cannabinoids have been shown to act on the CB1 and CB2 receptors of the endocannibinoid system, which in turn prevents the release of proinflammatory cytokines that are released after brain drama and cause damage (Panikashvili, et al., 2006). Activating of the CB1 and CB2 receptors also has been shown to stimulate the release of minocycline, which reduces brain swelling and neurological impairment, and diffuses further injuries to the brain’s axons (Lopez-Rodriguez, et al., 2015) (Biegon, 2004).

    In one study, cannabinoid administered to mice with brain injuries caused a significant reduction of brain swelling, as well as better clinical recovery, reduced infarct volume, and reduced brain cell death compared to the control group (Panikashvili, et al., 2001). In another, CBD was found to reduce acute and apoptic brain damage (Castillo, et al., 2010). Piglets with brain injuries given CBD experienced less excitotoxicity, oxidative stress and inflammation (Pazos, et al., 2013). Mice that had suffered an impact brain injury showed marked recovery in object recognition and in performing a specific task after CB1 receptors were activated (Arain, Khan, Craig & Nakanishi, 2015). Cannabinoids have even shown to be effective at offering neuroprotection in newborn babies that have experienced a brain injury (Fernandez-Lopez, Lizasoain, Moro & Martinez-Orgado, 2013).

    One study found that patients that had detectable levels of THC in their bodies were less likely to die as a result of a traumatic brain injury than those who didn’t (Nguyen, et al., 2014). Just recently, researchers from the University of Arizona found that trauma patients who tested positive for cannabis upon hospital admission were less likely to die during hospitalization (Singer, et al., 2017).

    Currently, just Illinois, New Hampshire, Washington have approved medical marijuana specifically for the treatment of traumatic brain injuries.

    A number of other states will consider allowing medical marijuana to be used for the treatment of traumatic brain injuries with the recommendation from a physician. These states include: California(any debilitating illness where the medical use of marijuana has been recommended by a physician), Connecticut (other medical conditions may be approved by the Department of Consumer Protection), Massachusetts (other conditions as determined in writing by a qualifying patient’s physician), Nevada (other conditions subject to approval), Oregon (other conditions subject to approval), and Rhode Island (other conditions subject to approval).

    In Washington D.C., any condition can be approved for medical marijuana as long as a DC-licensed physician recommends the treatment.


    Arain, M., Khan, M., Craig, L., and Nakanishi, S.T. (2015, March). Cannabinoid agonist rescues learning and memory after a traumatic brain injury. Annals of Clinical and Translational Neurology, 2(3), 289-94. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369278/.

    Biegon, A. (2004). Cannabinoids as neuroprotective agents in traumatic brain injury. Current Pharmaceutical Design, 10(18), 2177-83. Retrieved from http://www.eurekaselect.com/62903/article.

    Castillo, A., Tolon, M.R., Fernandez-Ruiz, J., Romero, J., Martinez-Orgado, J. (2010, February). The neuroprotective effect of cannabidiol in an in vitro model of newborn hypoxic-ischemic brain damage in mice is mediated by CB(2) and adenosine receptors. Neurobiology of Disease, 37(2), 434-40. Retrieved from http://www.sciencedirect.com/science/article/pii/S096999610900309X.

    Donat, C.K., Fischer, F., Walter, B., Deuther-Conrado, W., Brodhun, M., Bauer, R.., and Brust, P. (2014). Early increase of cannabinoid receptor density after experimental traumatic brain injury in the newborn piglet. Acta Neurobiologiae Experimentalis, 74,197-210. Retrieved from http://www.ane.pl/linkout.php?pii=7419.

    Fernandez-Lopez, D., Lizasoain, I., Moro, M.A., and Martinez-Orgado, J. (2013). Cannabinoids: Well-suited candidates for the treatment of perinatal brain injury. Brain Sciences, 3, 1043-1059. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061885/.

    Injury Prevention and Control: Traumatic Brain Injury. (2015, February 24). Centers for Disease Control and Prevention. Retrieved from http://www.cdc.gov/traumaticbraininjury/get_the_facts.html.

    López Rodríguez, A.B., Mateos Vicente, B., Romero-Zerbo, S.Y., Rodriguez-Rodriguez, N., Bellini, M.J., Rodriguez de Fonseca, F., Bermudez-Silva, F.J., Azcoitia, I., Garcia-Segura, L.M., and Viveros, M.P. (2011, September). Estradiol decreases cortical reactive astrogliosis after brain injury by a mechanism involving cannabinoid receptors. Cerebral Cortex, 21(9), 2046-55. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bhq277.

    Lopez-Rodriguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M., and Viveros, M.P. (2015, January). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex, 25(1), 35-45. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bht202.

    Mechoulam, R., and Shohami, E. (2007, August). Endocannabinoids and traumatic brain injury. Molecular Neurobiology, 36(1), 68-74. Retrieved from http://link.springer.com/article/10.1007/s12035-007-8008-6.

    Mechoulam, R., Spatz, M., and Shohami, E. (2002, April 23). Endocannabinoids and neuroprotection. Science’s STKE, 2002(129). Retrieved from http://stke.sciencemag.org/content/2002/129/re5.full.

    Mechoulam, R., Panikashvili, D., and Shohami, E. (2002, February). Cannabinoids and brain injury: therapeutic implications. Trends in Molecular Medicine, 8(2), 58-61. Retrieved from http://www.cell.com/trends/molecular-medicine/fulltext/S1471-4914(02)02276-1.

    Nguyen, B.M., Kim, D., Bricker, S., Bongard, F., Neville, A., Putnam, B., Smith J., and Plurad, D. (2014, October). Effect of marijuana use on outcomes in traumatic brain injury. The American Surgeon, 80(10), 979-83. Retrieved from http://www.ingentaconnect.com/content/sesc/tas/2014/00000080/00000010/art00015.

    Panikashvili, D., Shein, N.A., Mechoulam, R., Trembovler, V., Kohen, R., Alexandrovich, A., and Shohami, E. (2006, May). The endocannabinoid 2-AG protects the blood-brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines. Neurobiology of Disease,22(2), 257-74. Retrieved from http://www.sciencedirect.com/science/article/pii/S0028390813001238.

    Panikashvili, D., Simeonidou, C., Ben-Shabat, S., Hanus, L., Breuer, A., Mechoulam, R., Shohami, E. (2001, October). An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature, 413(6855), 527-31. Retrieved from https://goo.gl/FNFJPH.

    Pazos, M.R., Mohammed, N., Lafuente, H., Santos, M., Martinez-Pinilla, E., Moreno, E., Valdizan, E., Romero, J., Pazos, A., Franco, R., Hillard, C.J., Alvarez, F.J., Martinez-Orgado, J. (2013, August). Mechanisms of cannabidiol neuroprotection in hyopoxic-ischemic newborn pigs: role of 5HT(1A) and CB2 receptors. Neuropharmacology, 71, 282-91. Retrieved from http://www.sciencedirect.com/science/article/pii/S0028390813001238.

    Presley, C., Abidi, A., Suryawanshi, S., Mustafa, S., Meibohm, B., and Moore, B.M. (2015). Preclinical evaluation of SMM-189, a cannabinoid receptor 2-specific inverse agonist. Pharmacology Research & Perspectives, 3(4), e00159. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506688/.

    Schurman, L. D., and Lichtman, A. H. (2017). Endocannabinoids: A Promising Impact for Traumatic Brain Injury. Frontiers in Pharmacology, 8, 69. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5314139/.

    Shohami, E., Cohen-Yeshurun, A., Magid, L., Algali, M., and Mechoulam, R. (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology, 163(7), 1402–1410. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/.

    Singer, M., Azim, A., O’Keefe, T., Khan, M., Jain, A., Kulvatunyou, N., Gries, L., Jehan, F., Tang, A., and Joseph, B. (2017, August 5). How Does Marijuana Effect Outcomes After Trauma in ICU Patients? A Propensity Matched Analysis. The Journal of Trauma and Acute Care Surgery, doi: 10.1097/TA.0000000000001672. [Epub ahead of print]. Retrieved from http://journals.lww.com/jtrauma/Abs...na_Effect_Outcomes_After_Trauma_in.98956.aspx.

    Traumatic brain injury. (2014, May 15). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/traumatic-brain-injury/basics/definition/con-20029302.

    Xu, Z., Lv, X.Q., Dai, Q. Ge, Y.Q. and Xu, J. Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it’s role in metabolic defects and neuronal apoptosis after TBI. Molecular Brain, 9,75. Retrieved from https://molecularbrain.biomedcentral.com/articles/10.1186/s13041-016-0257-8.
  3. momofthegoons

    momofthegoons Vapor Accessory Addict Staff Member

    Likes Received:
    Trophy Points:
    Healing Brain Injuries with Cannabis
    Cory Hughes | December 13, 2017

    One of the more controversial medical cannabis applications is its use in treating traumatic brain injuries (TBI) and chronic traumatic encephalopathy (CTE).

    However, studies on TBI have shown that the endocannabinoid system plays a crucial role in the brain’s ability to repair damage.

    This system, which spans the entire body and plays an important role in maintaining our day-to-day health, is designed to maintain homeostasis between a stable internal environment and an unstable external environment.

    As a result, cannabinoids are essential to maintaining this homeostasis.

    Traumatic Brain Injuries and Cannabis Use
    Traumatic brain injuries usually result from a single, harsh blow to the head. They can happen in a car crash or other form of critical event.

    Besides the initial injury, TBI can lead to inflammation in the brain, damage to blood vessels, nervous system damage, and interference with processing sensory data.

    For minor TBIs, many patients have no other solution than over-the-counter pain killers. For more serious cases, additional oxygen may be required to overcome imbalances in the blood.

    However, studies are finding that cannabis, with its ability to treat multiple symptoms, is proving to be an extremely effective treatment for patients suffering from TBI.

    Cannabis has already demonstrated its usefulness as an anti-inflammatory. One of hardest aspects of TBI to overcome is brain swelling due to fluid and pressure buildup. Often, brain injuries this severe require surgery to relieve the pressure.

    However, the introduction of cannabinoids, specifically THC and CBD, into the brain has been shown to drastically reduce swelling and allow for normal blood flow.

    When CB1 and CB2 receptors are activated, they stimulate the release of minocycline, which reduces neural swelling and helps to mitigate the damage caused by the injury. These results have been confirmed on studies on both mice and pigs.

    One of the first scientists to study the effects of cannabis on TBI was none other than Dr. Raphael Mechoulam, who is largely credited for being the first person to isolate THC, CBD, and other cannabinoids as far back as the 1960s.

    Mechoulam first published his research on TBI in 2007 in a paper called Endocannabinoids and Traumatic Brain Injury. The study found mice that suffered from a serious brain injury had higher levels of an endocannabinoid known as 2-Arachidonoylglycerol (2-Ag). This endocannabinoid naturally occurs in the body and is mainly found in the central nervous system.

    What Mechoulam and his team discovered was 2-Ag is a natural defense against brain swelling as it is anti-inflammatory by nature. The problem is that the body does not produce enough of it to be effective in accelerating healing.

    The study concluded that the endocannabinoid system and cannabinoids work as a neuroprotectant when the brain is exposed to trauma, and that the full benefit of the endocannabinoid system as it pertains to its regenerative and anti-inflammatory properties can be achieved by supplementing cannabinoids in TBI patients.

    Chronic Traumatic Encephalopathy and Cannabis Use
    Unlike TBI, the neurological effects of CTE are brought about over time instead of from one traumatic event. It was first discovered in football players and other professional athletes exposed to repeated head trauma. Brain tissue exposed to numerous impacts over time eventually dies and leaves behind a protein called tau.

    The buildup of this protein affects the brain very much like the plaque buildup found in Alzheimer’s patients. If untreated, it leads to memory issues, cognitive dysfunction, and, in extreme cases, dementia.

    With CTE, it is believed that CBD provides the brain with relief. Cannabidiol is a heavy anti-inflammatory and, as previously mentioned, acts as a strong neuroprotectant.

    It works to slow the release and buildup of these excess tau proteins, thus slowing the advancement of neurological decay.

    This is the same mechanism by which cannabis positively affects patients suffering from the symptoms of Alzheimer’s, which is also caused by excess protein buildup.

    Only recently have doctors come to understand what happens to the brain during a traumatic injury or after years of exposure to lesser traumatic events.

    Simultaneously, cannabis scientists have uncovered an encyclopedia of information about the benefits that cannabinoids like THC and CBD have on the brain.

    The evidence points in only one direction: that there is an inescapable relationship between cannabis, the endocannabinoid system, and the brain’s ability to heal itself.
  4. momofthegoons

    momofthegoons Vapor Accessory Addict Staff Member

    Likes Received:
    Trophy Points:
    Neuroimaging, Cannabis, and Brain Performance & Function

    I think pot should be legal. I don’t smoke it, but I like the smell of it.

    — Andy Warhol

    Cannabis contains various molecules which bind to receptors in the brain, aptly called "cannabinoid receptors". Familiar ligands (which bind to those receptors) include THC (tetrahydrocannabinol) and CBD (cannabidiol), binding to receptors such as the CB1 and CB2 receptors with various downstream functions on the brain. The primary neurotransmitter involved in innate (endogenous) cannabinoid activity is "anandamide", a unique "fatty acid neurotransmitter" whose name means "joy", "bliss" or "delight" in Sanskrit and related ancient tongues. This neurotransmitter system has only relatively recently been investigated in greater detail, and the basic biology is fairly well worked out (e.g. Kovacovic & Somanathan, 2014), improving understanding of therapeutic, recreational and adverse effects of different cannabinoids, and paving the way for novel synthetic drug development.

    Increasing interest in the therapeutic and recreational use of cannabis demands greater understanding of the effects of cannabis on the brain and behavior. Because of the controversial and politicized nature of marijuana in societal discourse, strong beliefs about cannabis obstruct our capacity to have a reasoned conversation about potential pros and cons of cannabis use, and have impeded research initiatives. Nevertheless, many states have permitted medical and recreational use of cannabis preparations, while the federal government is swinging back toward more restrictive policies.

    The jury is out

    Cannabis advocates, on the other hand, may paint too rosy a picture of the benefits of cannabis preparations, downplaying or dismissing relevant information about the hazards of cannabis in specific populations at risk for certain mental disorders, the risks of cannabis use disorders and the negative effects of cannabis on certain cognitive processes accompanied by potentially deleterious, and even dangerous, effects on decision-making and behavior.

    For instance, while cannabis preparations have been shown to be useful for pain management and functional improvement in various conditions, improving quality of life, cannabis may also cause errors in judgment and delays in information processing which can lead not only to individual problems, but may get in the way of relationships and professional activities, even leading to possible harm to others by contributing to accidents. Cannabis has been clearly associated with precipitating the onset of and worsening some illnesses, notably psychiatric conditions. Moreover, there is growing interest in understanding the therapeutic and pathological potential of different compounds contained within cannabis preparations, most notably THC and CBD – though the importance of other components is increasingly recognized. For example, a recent study in the American Journal of Psychiatry strongly suggests that CBD, useful for treating intractable seizures (e.g. Rosenberg et al., 2015), may be of significant benefit as an augmenting agent for some with schizophrenia (McGuire at al., 2017).

    The picture is not either-or, however. A deeper understanding of how cannabis affects different brain regions (under different conditions, e.g. acute vs. chronic use, with and without different mental illnesses and substance use disorder, with individual variations, etc.) is required to ground the debate in knowledge, and provide solid, reliable scientific findings to pave the way for future research. Foundational understanding is lacking, and while there is a growing body of research looking at various aspects of cannabis effect, as is always the case with an evolving body of research early on, methodology has varied across many small studies, without a clear framework to encourage consistent approaches to investigation.

    One question of obvious importance is what are the effects of cannabis on key functional areas of the brain. How do functional and connectivity changes within key anatomic regions (“hubs”, in network theory) spread out to the brain networks in which they are central? How does cannabis use, to the extent we understand its effects, play on within specific tasks used to study cognition? What, in general, is the effect on cannabis on brain networks including the default mode, executive control and salience networks (three key networks in the densely interconnected “rich club” of brain networks)? These and related questions are more important as we come to better understand how the mind/brain gap can be bridged by progress in mapping out the human neural connectome. The expectation is that increases or decreases in activity in different brain areas in users (compared with non-users) will correlate with broad changes across functional brain networks, which are reflected in patterns of differential performance on a large group of commonly used psychological research tools which capture different aspects of mental function and human behavior.

    The current study

    With this key consideration in mind, a multicenter group of researchers (Yanes et al., 2018) set out to collect and examine all the relevant neuroimaging literature looking at the effect of cannabis on the brain and on behavior and psychology. It’s worthwhile to briefly review the meta-analytic approach used and to discuss what kinds of studies were included and excluded, in order to contextualize and interpret the quite significant findings. They looked at literature including studies using fMRI (functional magnetic resonance imaging) and PET scans (positron emission tomography), common tools to measure indicators of brain activity, and conducted two preliminary assessments to organize the data.

    First, they divided the studies into ones where activity in various brain areas was either increased or decreased for users versus non-users, and matched up anatomic areas with the functional brain networks of which they are parts. In the second layer of refinement, they used “functional decoding” to identify and categories different groups of psychological functions measured across the existing literature. For example, studies look at a large but varying set of psychological functions to see how, if at all, cannabis changes cognitive and emotional processing. Relevant functions included decision-making, error detection, conflict management, affect regulation, reward and motivational functions, impulse control, executive functions, and memory, to provide an incomplete list. Because different studies used different assessments under different conditions, developing a pooled analytic approach is necessary to conduct a comprehensive review and analysis.

    Searching multiple standard databases, they selected studies with imaging comparing users with non-users, with data available in the form of standard models suitable for pooled analysis, and which included psychological tests of perception, movement, emotion, thinking, and social information processing, in various combinations. The excluded those with mental health conditions, and studies looking at the immediate effects of cannabis consumption. They analyzed this curated data. Looking at convergence in neuroimaging findings across studies using ALE (Activation Likelihood Estimate, [http://BrainMap.org] which transforms the data onto the standard brain mapping model), they identified which regions were more and less active. Using MACM (Meta-Analytic Connectivity Modeling, which employs the BrainMap database to compute whole-brain activation patterns), they identified clusters of brain regions which activated together. The completed the functional decoding phase by looking at forward and reverse inference patterns to reciprocally link brain activity with mental performance, and mental performance with brain activity to understand how different psychological processes correlate with functions in different brain regions.

    Here is a summary of the overall meta-analytic "pipeline":

    Source: Yanes et al., 2018


    Yanes, Riedel, Ray, Kirkland, Bird, Boeving, Reid, Gonazlez, Robinson, Laird and Sutherland (2018) analyzed a total of 35 studies. All told, there were 88 task-based conditions, with 202 elements related to decreased activation among 472 cannabis users and 466 non-users, and 161 elements regarding increased activation among 482 users and 434 non-users. There were three major areas of findings:

    There were several areas of consistent (“convergent”) changes noticed among users and non-users, in terms of activation and deactivation. Decreases were observed in bilateral (both sides of the brain) ACCs (anterior cingulate cortex) and the right DLPFC (dorsolateral prefrontal cortex). By contrast, there was increased activation consistently observed in the right striatum (and extending to the right insula). Important to note that these findings were distinct from one another, and this lack of overlap means they represent uniquely different effects of cannabis on different systems.

    MACM analysis showed there were three clusters of co-activated brain regions:

    • Cluster 1 – ACC included whole-brain activation patterns, including connections with the insular and caudate cortex, medial frontal cortex (link to last blog), precuneus, fusiform gyrus, culmen, thalamus and cingulate cortex. The ACC is key for decision-making, processing conflict, involved with exploring and committing to a given course of action (e.g. Kolling et al., 2016) and these related areas cover a broad range of functions related to the ACC. The insula is involved with self-perception, a notable example being a visceral experience of self-disgust.
    • Cluster 2 – DLPFC included co-activation with parietal regions, orbitofrontal cortex, occipital cortex and fusiform gyrus. As the DLPFC is involved with important executive functions, including regulating emotions, the experience of mood, and direction of attentional resources (e.g. Mondino at al., 2015) as well aspects of language processing, and the related areas address key functions including social information processing, impulse control, and related.
    • Cluster 3 – Striatum included whole-brain involvement, notably the insular cortex, frontal cortex, superior parietal lobule, fusiform gyrus, and culmen. The striatum is involved with reward – the so-called “dopamine hit” referenced so often – which when properly regulated allows us to pursue optimal success, but in states of under-activity leads to inaction, and in excess contributes to addictive and compulsive behaviors. Evidence reviewed in the original paper suggests that cannabis use may prime reward circuits to predispose toward addiction, and possibly blunt motivationfor ordinary activities.
    While these clusters are functionally distinct in terms of how they are affected by cannabis, they overlap anatomically and spatially, highlighting the crucial importance of viewed brain activity from the connectome, networked point of view in order to grasp the translation of reductive brain findings to how the mind works, and how this plays out for people in day-to-day life.

    The functional decoding of the three clusters showed patterns of how each cluster correlates with a group of psychological tests, for example the Stroop test, go/no-go task which involve fast decisions, pain monitoring tasks, and reward-assessing tasks, to name a few. I won’t review them all, but the findings are relevant and some of them stand out (see below). This overview of the cluster-task relationships is useful. Especially notable is the presence of the Go/No-Go task condition in all three functional areas:

    Functional decoding of primary meta-analytic clusters.
    Source: Yanes et al., 2018

    Further considerations

    Taken together, the results of this meta-analysis are profound, and achieve the goals both of focusing in on and distilling findings across the relevant literature investing the effects of cannabis use on brain activation in populations without mental illness, looking at increased and decreased activity in localized brain regions, distributed clusters of distinct relevance, and the impact on key psychological processing tasks and function.

    Cannabis lowers activity in both ACC and DLPFC clusters, and for people with normal brain function this could lead to problems in executive function and decision-making. Cannabis is likely to cause inaccuracy in error monitoring, leading to misperception and performance issues due to mistakes, and may impede function during high-conflict situations, from both errors in judgment as well as from altered decision-making and subsequent execution. Decreased DLPFC activity could lead to emotional regulatory problems as well as decreases in memory and reduced attentional control.

    For people with psychiatric and medical conditions, the same brain effects could be therapeutic, for example reducing pain burden by decreasing ACC activity, alleviating traumatic memories and suppressing post traumatic nightmares, treating anxiety with few side effects, or reducing psychotic symptoms (McGuire, 2017) by inhibiting activity in involved brain areas. But cannabinoids also may trigger pathology, precipitating depression or psychosis, and other conditions, in vulnerable populations. Cannabis use also causes problems for the developing brain, leading to undesirable long-term effects (e.g. Jacobus and Tappert, 2014), such as reduced neurocogntive performance and structural changes in the brain.

    Cannabis was shown, in contrast, to generally increase activity in the striatum and related areas. For people with normal baseline activity, this could lead to priming of reward circuits, and as noted has been observed in numerous studies, increase the risk of addictive and compulsive behaviors, predisposing to some forms of pathology. While this amplification of reward activity (combined with effects on the first two clusters) may contribute to the "high" of marijuana intoxication, enhancing enjoyment and creative activity, making everything more intense and engaging, temporarily.

    The authors note that all three clusters involved the Go/No-Go task, a test situation requiring inhibition or performance of a motor action. They note:

    "Here, the fact that distinct region-specific disruptions were linked
    with the same task classification may be indicative of a cannabis-related compound effect manifest across studies. In other words,
    a diminished capacity to inhibit problematic behaviors may be
    linked to concurrent reduction of prefrontal activity (ACC and
    DL-PFC) and elevation of striatal activity."

    For some patients, cannabis reportedly alleviates symptoms of depression, characterized by core experiences of loss of enjoyment, excessive negative emotional states and lack of motivation, among other symptoms, but heavier users are at increased risk for worsening depression (Manrique-Garcia et al., 2012). However, in addition to potentially priming for addiction to other chemicals and enhancing experiences for those who enjoy being intoxicated with marijuana (others find it produces dysphoria, anxiety, unpleasant confusion, or even paranoia), users may find that in the absence of cannabis use they are less interested in regular activities when they are not high, leading to decreased enjoyment and motivation.

    These effects are different depending on several cannabis use related factors, such as timing and chronicity of use, as well as type of cannabis and relative chemistry, given variations among different species and strains. While this study was not able to distinguish between the effects of THC and CBD, as data were not available on concentrations or ratios of these two key components in cannabis, it is likely that they have different effects on brain function which require further investigation to sort out therapeutic potential from recreational and pathological effects.

    This study is a foundational study, setting the stage for ongoing research on the effects of various cannabinoids on the brain in health and illness, and providing important data to understand therapeutic and damaging effects of different cannabinoids. The elegant and painstaking methodology in this study shines a spotlight on how cannabis affects the brain, providing significant data about overall effects on brain networks as well as on cognitive and emotional function.

    Questions of interest include additional mapping of brain networks and correlating these findings with existing models of the mind, looking at the effect of different types of cannabis and patterns of use, and investigating the effect of cannabinoids (naturally-occurring, endogenous, and synthetic) for therapeutic purposes in different clinical conditions, recreational use, and potentially for performance enhancement. Finally, by providing a coherent framework for understanding the existing literature inclusive of positive and negative effects of cannabis on the brain, this paper centers cannabis research more squarely in the mainstream of scientific study, providing a neutral, de-stigmatized platform to permit the debate on cannabis to evolve in more constructive directions than it historically has.


    Mondino M, Thiffault F & Fecteau S. (2016). Does non-invasive brain stimulation applied over the dorsolateral prefrontal cortex non-specifically influence mood and emotional processing in healthy individuals? Front Cell Neurosci. 2015; 9: 399. Published online 2015 Oct 14.

    Kolling TE, Behrens TEJ, Wittmann MK & Rushworth MFS. (2016). Multiple signals in anterior cingulate cortex. Current Opinion in Neurobiology, Volume 37, April 2016, Pages 36-43.

    McGuire P, Robson P, Cubala WJ, Vasile D, Morrison PD, Barron R, Tylor A, & Wright S. (2015). Cannabidiol (CBD) as an Adjunctive Therapy in Schizophrenia: A Multicenter Randomized Controlled Trial. Neurotherapeutics. 2015 Oct; 12(4): 747–768. Published online 2015 Aug 18.

    Rosenberg EC, Tsien RW, Whalley BJ & Devinsky O. (2015). Cannabinoids and Epilepsy. Curr Pharm Des. 2014; 20(13): 2186–2193.

    Jacobus J & Tapert SF. (2017). Effects of Cannabis on the Adolescent Brain. Cannabis Cannabinoid Res. 2017; 2(1): 259–264. Published online 2017 Oct 1.

    Kovacic P & Somanathan R. (2014). Cannabinoids (CBD, CBDHQ and THC): Metabolism, Physiological Effects, Electron Transfer, Reactive Oxygen Species and Medical Use. The Natural Products Journal, Volume 4, Number 1, March 2014, pp. 47-53(7).

    Manrique-Garcia E, Zammit S, Dalman C, Hemmingsson T & Allebeck P. (2012). Cannabis use and depression: a longitudinal study of a national cohort of Swedish conscripts. BMC Psychiatry201212:112.
    ataxian likes this.
  5. ataxian

    ataxian Well-Known Member

    Likes Received:
    Trophy Points:

    CANNABIS is wonderful 4 R BRAIN'S = CIVILIZED
    momofthegoons likes this.
  6. momofthegoons

    momofthegoons Vapor Accessory Addict Staff Member

    Likes Received:
    Trophy Points:

    The benefits of CBD-rich cannabis concentrates for chronic traumatic encephalopathy (CTE) are well-known among football players and other pro athletes. But the U.S. government still maintains that cannabis is a dangerous drug with no medical value.

    • According to a U.S. government-held patent pertaining to “cannabinoids as antioxidants and neuroprotectants,” CBD and THC can limit “neurological damage following ischemic insults, such as stroke or trauma.”
    • A 2014 study found that traumatic brain injury (TBI) patients who tested positive for THC were more likely to survive with less impairment than TBI patients who abstained from marijuana.
    • Preclinical research and anecdotal accounts indicate that CBD is highly active against brain ischemia, modulating many of the molecular hallmarks of TBI pathology.
    • CBD normalizes post-ischemic heart arrhythmia and limits the size of damaged brain tissue in mice when administered shortly before or after a closed head injury.
    • CBD produces no intoxicating effects, no THC-like high, and its use does not lead to tolerance.
    • As yet there have been no FDA-approved clinical trials to determine the efficacy of CBD-rich cannabis oil extracts for traumatic brain injury.
    Traumatic brain injury (TBI) is one of the leading causes of death worldwide in individuals under the age of 45. Triggered by concussions from car accidents, falls, violent contact sports, explosives or by gunshot and stab wounds, TBI affects 1.7 million Americans annually. It is the most commonly identified cause of epilepsy among adults.

    The social and economic costs of TBI are considerable given that many who survive severe head injuries suffer permanent behavioral and neurological impairment that adversely impacts learning and memory and often requires long term rehabilitation. An estimated 4 million to 6 million Americans are on disability because of TBI. Even so-called mild cases of TBI can result in post-traumatic seizures, refractory cognitive deficits, and lower life expectancy.

    Treatment modalities for TBI are limited with few satisfactory pharmaceutical options available. Surgical intervention, which entails the removal of parts of the skull to reduce intracranial pressure, is an emergency, life-saving measure, and the aftermath can be gruesome.

    But hope is on the horizon, thanks in part to U.S. government-sponsored scientific research – and to extensive anecdotal accounts from medical marijuana patients – which highlight the potential of cannabinoid-based therapies for TBI.

    The patent
    In 1998, the Proceedings of the National Academy of Sciences published a groundbreaking report on the neuroprotective properties of cannabidiol (CBD) and tetrahydrocannabinol (THC), two major components of marijuana. Co-authored by a team of researchers (AJ Hampson, M Grimaldi, D Wink and Nobel laureate J Axelrod) at the National Institutes of Mental Health, this preclinical study on rats would form the basis of a U.S. government-held patent on “Cannabinoids as antioxidants and neuroprotectants.”

    The patent indicates that CBD and THC were found “to have particular application as neuroprotectants … in limiting neurological damage following ischemic insults, such as stroke or trauma.” These plant cannabinoids were also deemed useful for treating other neurodegenerative conditions, “such as Alzheimer’s disease, Parkinson’s disease and HIV dementia.”

    Whereas TBI results from an external blow to the skull, a stroke is caused internally by an arterial blockage or rupture. But TBI and stroke share many of the same pathological features and aberrant molecular mechanisms.

    Example of a stroke MRI

    TBI and stroke are both acute and potentially lethal injuries, involving a primary ischemic insult that interrupts cerebral blood flow and destroys brain tissue. This is followed by a secondary injury cascade that, if unchecked, can ricochet for several weeks or months, resulting in more brain damage, motor impairment and other adverse “downstream” effects, such as poor concentration, irritability, and sleep problems.

    Whether the cause is an occluded blood vessel or blunt external force, the initial trauma triggers a complex sequence of molecular events characterized by the massive release of glutamate (an excitatory neurotransmitter) and the overproduction of reactive oxygen species (free radicals) and other inflammatory compounds. Excessive glutamate and oxidative stress, in turn, lead to microvascular injury, blood-brain barrier breakdown, swollen brain tissue, mitochondrial dysfunction, calcium ion imbalance, neurotoxicity and cell death. The secondary injury cascade is associated with the development of many of the neurological deficits observed after a TBI or a stroke.

    Cannabinoids to the rescue
    A 2014 article in American Surgeon examined how marijuana use affected people who suffered a traumatic brain injury. “A positive THC screen is associated with decreased mortality in adult patients sustaining TBI,” the study concluded.

    According to this noteworthy report by UCLA Medical Center scientists, TBI-afflicted individuals who consume marijuana are less likely to die and more likely to live longer than TBI patients who abstain.

    How does cannabis, and THC, in particular, confer neuroprotective effects?

    Plant cannabinoids such as THC and CBD mimic and augment the activity of endogenous cannabinoids that all mammals produce internally. Endogenous cannabinoids are part of the endocannabinoid system (ECS). The ECS regulates many physiological processes that are relevant to TBI, such as cerebral blood flow, inflammation, and neuroplasticity.

    A 2011 article in the British Journal of Pharmacology describes the ECS as “a self-protective mechanism” that kicks into high gear in response to a stroke or TBI. Co-authored by Israeli scientist Raphael Mechoulam, the article notes that endocannabinoid levels in the brain increase significantly during and immediately after a TBI. These endogenous compounds activate cannabinoid receptors, known as CB1 and CB2, which protect against TBI-induced neurological and motor deficits.1

    THC activates the same receptors – with similar health-positive effects.

    Of knockout mice and men

    CB1 receptors are concentrated in the mammalian brain and central nervous system. Preclinical research involving animal models of TBI and stroke has shown that heightened CB1 receptor transmission can limit harmful excitoxicity by inhibiting glutamate release. CB1 receptor activation also dilates blood vessels, thereby enhancing cerebral blood flow (and oxygen and nutrient supply to the brain).

    But these beneficial physiological changes were not evident in genetically-engineered “knock out” mice that lack CB1 receptors. Without these crucial receptors, an animal is less able to benefit from the neuroprotective properties of endogenous cannabinoids and plant cannabinoids.

    In 2002, the Journal of Neuroscience reported that the impact of induced cerebral ischemia is much more severe in CB1 knockout mice than in “wild type” mice with cannabinoid receptors. The absence of CB1 was shown to exacerbate TBI-related brain damage and cognitive deficits, indicating that cannabinoid receptors play an important role in neuroprotection.

    The CB1 paradox
    By manipulating cannabinoid receptors and other components of the endocannabinoid system with synthetic and plant-derived compounds, medical scientists have been able to reduce brain injury in animal experiments.

    But CB1 proved to be a tricky target.

    In 2013, the International Journal of Molecular Science reported on how TBI is affected by diurnal variations of the endocannabinoid system. It turns out that the recovery and survival rate of concussed lab rats is significantly higher if a TBI occurs at 1 am, when CB1 receptors are least robust, as compared to 1 pm, when CB1 receptor expression peaks.

    This finding was somewhat perplexing given the protective function of the endocannabinoid system against brain trauma.

    The ECS is a complex, front-line mediator of acute stress, and the pivotal role of the CB1 receptor is contingent on several variables, including time of day, the phase of the ischemic injury, and endocannabinoid concentrations in the brain. Small and large amounts of cannabinoid compounds produce opposite effects.

    When excess glutamate is released, CB1 activity increases to reduce excitotoxic neurotransmission. But CB1also regulates apoptosis (cell death), acting as a switch between cell survival and cell death. Extreme CB1activation could trigger cell death even while it reduces glutamate release. It’s possible that a weak CB1antagonist (that partially blocks CB1 transmission) might limit apoptosis while still reducing glutamate excitotoxicity.2

    CB2 and neurogenesis

    After an initial infatuation with CB1, medical scientists shifted their attention to the CB2 receptor as a drug development target for treating TBI. The CB2 receptor modulates immune function and inflammation. It is expressed primarily in immune cells, metabolic tissue, and the peripheral nervous system.

    CB2 receptor expression, unlike CB1, does not vary according to the hour of the day. But during and after severe head trauma, CB2 receptor expression is dramatically “upregulated” in the brain, which means that these receptors rapidly increase in number and density in response to TBI. According to a 2015 study in Neurotherapeutics, “Upregulation of CB2 with no changes in CB1 have been found in TBI.”

    Preclinical research has shown that CB2 receptor signaling mitigates many of the molecular processes that underlie neuronal deterioration and cell death after TBI. In 2012, the Journal of Neuropsychiatric Researchreported that CB2 receptor activation attenuates blood-brain barrier damage in a rodent model of TBI. Two years later, the Journal of Neuroinflammation noted that the CB2 receptor is instrumental in regulating inflammation and neurovascular responses in the TBI-compromised brain. Genetic deletion of CB2 worsens the outcome of TBI in animal tests, underscoring CB2’s neuroprotective function.

    Other studies have shown that CB2 receptor activation promotes cell repair and survival following an ischemic injury. CB2 receptors are present in progenitor (“stem”) cells and are instrumental in driving neurogenesis (the creation of new brain cells). Neurogenesis enhances motor function and overall recovery after TBI. CB2 knockout mice have impaired neurogenesis.3


    Research involving animal models has shed light on the pathological processes that ensue after a closed head injury. But promising leads focusing on the CB2receptor have not translated into successful clinical results. As Italian scientist Giovanni Appendino remarked: “If drug discovery is a sea, then CB2 is a rock that is surrounded by shipwrecked-projects.”

    But why? For starters, preclinical models only partially reproduce a disease. And synthetic cannabinoids that target a single type of receptor only partially reproduce the multifunctional activities of endogenous cannabinoids and the broad spectrum profile of plant cannabinoids.

    Endocannabinoids and phytocannabinoids are “pleiotropic” agents that interact directly and indirectly with several receptors – not just CB1 and CB2 – which also contribute to remediating the neurodegenerative cascade that ensues after a stroke or TBI.4

    It appears that an exogenous cannabinoid, either synthetic or plant-derived, may need to engage both CB1and CB2 (directly or indirectly) and perhaps other pathways, as well, to confer a clinically-relevant neuroprotective effect. A synthetic single bullet aimed at CB2 or another target is simply not as versatile or as effective as a whole plant synergistic shotgun or a multidimensional endogenous entourage.

    A promiscuous compound
    Cannabidiol is considered to be a promiscuous compound because it produces numerous effects through dozens of molecular pathways. Writing in 2017, Mayo Clinic neurologist Eugene L. Scharf noted that the scientific literature has identified more than 65 molecular targets of CBD. This versatile plant cannabinoid is highly active against brain ischemia, modulating many of the molecular and cellular hallmarks of TBI pathology.

    CBD has been shown to reduce brain damage and improve functional recovery in animal models of stroke and TBI. According to a 2010 report in the British Journal of Pharmacology, CBD normalizes post-ischemic heart arrhythmia and limits the size of damaged tissue when administered after a closed head injury.

    What’s more, CBD produces no intoxicating side effects, no THC-like high. And CBD use does not lead to tolerance.

    A damaged brain can be remarkably plastic, but there is only a circumscribed window of opportunity (the “platinum ten minutes” or “golden hour”) for therapeutic intervention to prevent, attenuate or delay the degenerative domino effect that occurs during a secondary injury cascade. Cannabidiol expands that window of opportunity. Researchers have learned that CBD can convey potent, long-lasting neuroprotection if given shortly before or as much as twelve hours after the onset of ischemia.

    Although it has little direct binding affinity for cannabinoid receptors, CBD confers neuroprotective effects and other benefits via several non-cannabinoid receptors. In 2016, scientists at the University of Nottingham (UK) reported that CBDprotects the blood-brain barrier from ischemia-induced oxygen and glucose deprivation by activating the 5-HT1A serotonin receptor and the PPAR-gamma nuclear receptor. CBD also acts through numerous receptor-independent channels – for example, by delaying endocannabinoid “reuptake,” which increases the concentration of neuroprotective endocannabinoids in the brain.

    Spanish scientists, presenting at the 2016 conference of the International Cannabinoid Research Society, compared the impact of CBD and hypothermia (cooling) on newborn piglets deprived of oxygen because of an ischemic injury. Hypothermia is typically the go-to therapy for treating newborn infants after a stroke. But in this animal model, the administration of CBD was more effective than hypothermia in protecting neonatal brain function. Preliminary data suggests that a synergistic combination of CBD and hypothermia may produce the best results.

    CBD for CTE
    Chronic traumatic encephalopathy (CTE), a particularly severe form of TBI, is caused by the accumulation of numerous concussions, which increases the risk of neurological problems later in life and hastens the progression of dementia. Football players are particularly vulnerable given the violent nature of the sport.

    After years of official National Football League neglect and cover-up, a cascade of suicide and mental health disorders among former star athletes has generated public attention. So has CBD. The anecdotal benefits of CBD-rich cannabis oil for CTE are well known among football players, boxers, and other professional athletes who are prone to head injuries.

    CBD, in and of itself, has a unique, broad-spectrum profile that can augment multiple aspects of our innate, endocannabinoid biology. As a single-molecule compound, CBD has delivered impressive neuroprotective results in preclinical experiments. But let’s not forget about THC, given that TBI patients who tested positive for THC did better than TBI patients who abstained from cannabis.

    The entourage effect is real. CBD works even better when combined with THC and other constituents of the cannabis plant. Beyond CBD and THC, dozens of cannabis components with specific medical attributes interact synergistically so that the therapeutic impact of the whole plant is greater than the sum if its parts.

    For many TBI patients, it’s late in the game and the clock is ticking. A phytocannabinoid remedy that combines CBD and THC and acts at multiple targets simultaneously would seem to be an ideal therapeutic candidate to treat TBI. Thus far, however, there have been no FDA-sanctioned clinical trials to ascertain the efficacy of whole plant, CBD-rich cannabis oil for traumatic brain injury. And in many places, cannabis is still not available as a legal therapeutic option.

    Complementary Therapies for TBI
    A pathology as complex as a stroke or a traumatic brain injury can benefit from a multifaceted treatment regimen that encompasses a combination of healing modalities, including:
    Whole plant cannabis oil. CBD-rich extracts with as much THC as a person is comfortable with.
    Terpenes. Cannabis products and strains with beta-caryophyllene and terpinolene.
    Diet. A high fat/low carbohydrate/low sugar diet with plenty of leafy greens, omega 3 oils (DHA, EPA), and fermented foods (probiotics).
    Nutritional supplements and antioxidants. Magnesium, vitamin D, curcumin, glutathione – and melatonin to restore circadian rhythms and sleep.
    Ancient therapies. Acupuncture, exercise, and caloric restriction (fasting), which increase endocannabinoid levels.
    Modern therapies. Neurofeedback, low-level laser therapy (photobiomodulation), hyperbaric oxygen, traßnscranial direct current stimulation, flotation tank therapy, and hypothermia (cooling).

    Martin A Lee is the director of Project CBD and the author of Smoke Signals: A Social History of Marijuana – Medical, Recreational and Scientific.


    1. The greater the neurological impairment, the higher the levels of endogenous cannabinoids in response to acute brain trauma, according to a May 2010 report in Lipids Health & Disease.
    2. Initial studies of CB1 knockout mice demonstrated increased injury following a stroke, indicating that CB1 receptor activation was neuroprotective. But later studies with selective CB1 antagonists (compounds that block CB1) given at the time of ischemia also demonstrated a protective effect. It appears that CB1 can either buffer or facilitate a concussive head wound, depending in part on the phase of the injury. According to a 2008 report in Neuroscience, “The greatest degree of neuroprotection was obtained by combining an inhibitor of CB1 activation with an exogenous CB2 agonist.”
    3. Adult neurogenesis occurs in specific brain areas – the subventricular zone of the lateral ventricles and in the subgranular zone of the dentate gyrus. Italian scientists reported that adult neural stem cells and progenitor cells originating within these brain structures protect neurons from glutamate-mediated toxicity. According to a November 2012 study by Italian scientists in Brain, CB2 receptor signaling regulates the migration of progenitor cells and stem cells to injured brain tissue. And a 2016 article in Stroke reported that animals with genetic deletions of CB2 receptors displayed a “significant decrease in the number of new neurons generated in the injured cortex of CB2-deficient mice compared to wild-type controls.”
    4. For example, anandamide, a major endocannabinoid, activates the CB1 cannabinoid receptor. Anandamide also confers neuroprotective effects by binding to TRPV1, an ion channel that regulates vasodilation and blood-brain-barrier permeability. CBD binds to the same ionotropic receptor, TRPV1, thereby relaxing blood vessels and enhancing blood-brain-barrier integrity. THC protects against cerebral ischemia in an animal model through a mechanism involving both cannabinoid and opioid receptors, according to a December 2007 report in the British Journal of Pharmacology.

    Amenta PS, Jallo JI, Tuma RF, Elliott MB. A cannabinoid type 2 receptor agonist attenuates blood-brain barrier damage and neurodegeneration in a murine model of traumatic brain injury. J Neurosci Res. 2012 Dec;90(12):2293-305. doi: 10.1002/jnr.23114. Epub 2012 Aug 18. PubMed PMID: 22903455.

    Amenta PS, Jallo JI, Tuma RF, Hooper DC, Elliott MB. Cannabinoid receptor type-2 stimulation, blockade, and deletion alter the vascular inflammatory responses to traumatic brain injury. J Neuroinflammation. 2014 Nov 22;11:191. doi: 10.1186/s12974-014-0191-6. PubMed PMID: 25416141; PubMed Central PMCID: PMC4248435.

    Arain M, Khan M, Craig L, Nakanishi ST. Cannabinoid agonist rescues learning and memory after a traumatic brain injury. Ann Clin Transl Neurol. 2015 Mar;2(3):289-94. doi: 10.1002/acn3.163. Epub 2015 Feb 16. PubMed PMID: 25815355; PubMed Central PMCID: PMC4369278.

    Ashton JC, Rahman RM, Nair SM, Sutherland BA, Glass M, Appleton I. Cerebral hypoxia-ischemia and middle cerebral artery occlusion induce expression of the cannabinoid CB2 receptor in the brain. Neurosci Lett. 2007 Jan 29;412(2):114-7. Epub 2006 Nov 22. PubMed PMID: 17123706.

    Barata L, et al. “Cerebral and extracerebral effects of combining cannabidiol and hypothermia after hypoxia-ischemia in newborn piglets,” presentation at the International Cannabinoid Research Society conference, June 26-July 1, 2016.

    Biegon A. Cannabinoids as neuroprotective agents in traumatic brain injury. Curr Pharm Des. 2004;10(18):2177-83. Review. PubMed PMID: 15281893.

    Bittigau P, Sifringer M, Felderhoff-Mueser U, Hansen HH, Ikonomidou C. Neuropathological and biochemical features of traumatic injury in the developing brain. Neurotox Res. 2003;5(7):475-90. Review. PubMed PMID: 14715432.

    Bravo-Ferrer I, Cuartero MI, Zarruk JG, Pradillo JM, Hurtado O, Romera VG, Díaz-Alonso J, García-Segura JM, Guzmán M, Lizasoain I, Galve-Roperh I, Moro MA. Cannabinoid Type-2 Receptor Drives Neurogenesis and Improves Functional Outcome After Stroke. Stroke. 2017 Jan;48(1):204-212. doi: 10.1161/STROKEAHA.116.014793. Epub 2016 Nov 29. PubMed PMID: 27899748.

    Butti E, Bacigaluppi M, Rossi S, Cambiaghi M, Bari M, Cebrian Silla A, Brambilla E, Musella A, De Ceglia R, Teneud L, De Chiara V, D’Adamo P, Garcia-Verdugo JM, Comi G, Muzio L, Quattrini A, Leocani L, Maccarrone M, Centonze D, Martino G. Subventricular zone neural progenitors protect striatal neurons from glutamatergic excitotoxicity. Brain. 2012 Nov;135(Pt 11):3320-35. doi: 10.1093/brain/aws194. Epub 2012 Sep 24. PubMed PMID: 23008234.

    Ceprián M, Jiménez-Sánchez L, Vargas C, Barata L, Hind W, Martínez-Orgado J. Cannabidiol reduces brain damage and improves functional recovery in a neonatal rat model of arterial ischemic stroke. Neuropharmacology. 2017 Apr;116:151-159. doi: 10.1016/j.neuropharm.2016.12.017. Epub 2016 Dec 21. PubMed PMID: 28012949.

    Elliott MB, Tuma RF, Amenta PS, Barbe MF, Jallo JI. Acute effects of a selective cannabinoid-2 receptor agonist on neuroinflammation in a model of traumatic brain injury. J Neurotrauma. 2011 Jun;28(6):973-81. doi: 10.1089/neu.2010.1672. Epub 2011 Jun 1. PubMed PMID: 21332427.

    Fernández-López D, Lizasoain I, Moro MA, Martínez-Orgado J. Cannabinoids: well-suited candidates for the treatment of perinatal brain injury. Brain Sci. 2013 Jul 10;3(3):1043-59. doi: 10.3390/brainsci3031043. PubMed PMID: 24961520; PubMed Central PMCID: PMC4061885.

    Fernández-Ruiz J, Moro MA, Martínez-Orgado J. Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications. Neurotherapeutics. 2015 Oct;12(4):793-806. doi: 10.1007/s13311-015-0381-7. Review. PubMed PMID: 26260390; PubMed Central PMCID: PMC4604192.

    Fowler CJ. Plant-derived, synthetic and endogenous cannabinoids as neuroprotective agents. Non-psychoactive cannabinoids, ‘entourage’ compounds and inhibitors of N-acyl ethanolamine breakdown as therapeutic strategies to avoid pyschotropic effects. Brain Res Brain Res Rev. 2003 Jan;41(1):26-43. Review. PubMed PMID: 12505646.

    Galve-Roperh I, Aguado T, Palazuelos J, Guzmán M. The endocannabinoid system and neurogenesis in health and disease. Neuroscientist. 2007 Apr;13(2):109-14. Review. PubMed PMID: 17404371.

    Grundy RI. The therapeutic potential of the cannabinoids in neuroprotection. Expert Opin Investig Drugs. 2002 Oct;11(10):1365-74. Review. PubMed PMID: 12387700.

    Guzmán M, Sánchez C, Galve-Roperh I. Control of the cell survival/death decision by cannabinoids. J Mol Med (Berl). 2001;78(11):613-25. Review. PubMed PMID: 11269508.

    Hampson AJ, Grimaldi M, Axelrod J, Wink D. Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8268-73. PubMed PMID: 9653176; PubMed Central PMCID: PMC20965.

    Hampson AJ, Grimaldi M, Lolic M, Wink D, Rosenthal R, Axelrod J. Neuroprotective antioxidants from marijuana. Ann N Y Acad Sci. 2000;899:274-82. Review. PubMed PMID: 10863546.

    Hayakawa K, Mishima K, Abe K, Hasebe N, Takamatsu F, Yasuda H, Ikeda T, Inui K, Egashira N, Iwasaki K, Fujiwara M. Cannabidiol prevents infarction via the non-CB1 cannabinoid receptor mechanism. Neuroreport. 2004 Oct 25;15(15):2381-5. PubMed PMID: 15640760.

    Hayakawa K, Mishima K, Nozako M, Hazekawa M, Aoyama Y, Ogata A, Harada K, Fujioka M, Abe K, Egashira N, Iwasaki K, Fujiwara M. High-cholesterol feeding aggravates cerebral infarction via decreasing the CB1 receptor. Neurosci Lett. 2007 Mar 6;414(2):183-7. Epub 2006 Dec 23. PubMed PMID: 17208374.

    Hayakawa K, Mishima K, Fujiwara M. Therapeutic Potential of Non-Psychotropic Cannabidiol in Ischemic Stroke. Pharmaceuticals (Basel). 2010 Jul 8;3(7):2197-2212. Review. PubMed PMID: 27713349; PubMed Central PMCID: PMC4036658.

    Hillard CJ. Role of cannabinoids and endocannabinoids in cerebral ischemia. Curr Pharm Des. 2008;14(23):2347-61. Review. PubMed PMID: 18781985; PubMed Central PMCID: PMC2581413.

    Hind WH, England TJ, O’Sullivan SE. Cannabidiol protects an in vitro model of the blood-brain barrier from oxygen-glucose deprivation via PPARγ and 5-HT1A receptors. Br J Pharmacol. 2016 Mar;173(5):815-25. doi: 10.1111/bph.13368. Epub 2016 Feb 3. PubMed PMID: 26497782; PubMed Central PMCID: PMC4761095.

    Jennings JS, Gerber AM, Vallano ML. Pharmacological strategies for neuroprotection in traumatic brain injury. Mini Rev Med Chem. 2008 Jun;8(7):689-701. Review. PubMed PMID: 18537724.

    Martinez-Vargas M, Morales-Gomez J, Gonzalez-Rivera R, Hernandez-Enriquez C, Perez-Arredondo A, Estrada-Rojo F, Navarro L. Does the neuroprotective role of anandamide display diurnal variations? Int J Mol Sci. 2013 Nov 27;14(12):23341-55. doi: 10.3390/ijms141223341. PubMed PMID: 24287910; PubMed Central PMCID: PMC3876049.

    Mechoulam R, Spatz M, Shohami E. Endocannabinoids and neuroprotection. Sci STKE. 2002 Apr 23;2002(129):re5. Review. PubMed PMID: 11972360.

    Nguyen BM, Kim D, Bricker S, Bongard F, Neville A, Putnam B, Smith J, Plurad D. Effect of marijuana use on outcomes in traumatic brain injury. Am Surg. 2014 Oct;80(10):979-83. PubMed PMID: 25264643.

    Panikashvili D, Simeonidou C, Ben-Shabat S, Hanus L, Breuer A, Mechoulam R, Shohami E. An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature. 2001 Oct 4;413(6855):527-31. PubMed PMID: 11586361.

    Parmentier-Batteur S, Jin K, Mao XO, Xie L, Greenberg DA. Increased severity of stroke in CB1 cannabinoid receptor knock-out mice. J Neurosci. 2002 Nov 15;22(22):9771-5. PubMed PMID: 12427832.

    Royo NC, Shimizu S, Schouten JW, Stover JF, McIntosh TK. Pharmacology of traumatic brain injury. Curr Opin Pharmacol. 2003 Feb;3(1):27-32. Review. PubMed PMID: 12550738.

    Schmidt W, Schäfer F, Striggow V, Fröhlich K, Striggow F. Cannabinoid receptor subtypes 1 and 2 mediate long-lasting neuroprotection and improve motor behavior deficits after transient focal cerebral ischemia. Neuroscience. 2012 Dec 27;227:313-26. doi: 10.1016/j.neuroscience.2012.09.080. Epub 2012 Oct 13. PubMed PMID: 23069763.

    Schomacher M, Müller HD, Sommer C, Schwab S, Schäbitz WR. Endocannabinoids mediate neuroprotection after transient focal cerebral ischemia. Brain Res. 2008 Nov 13;1240:213-20. doi: 10.1016/j.brainres.2008.09.019. Epub 2008 Sep 18. PubMed PMID: 18823959.

    Schurman LD, Lichtman AH. Endocannabinoids: A Promising Impact for Traumatic Brain Injury. Front Pharmacol. 2017 Feb 17;8:69. doi: 10.3389/fphar.2017.00069. eCollection 2017. Review. PubMed PMID: 28261100; PubMed Central PMCID: PMC5314139.

    Shohami E, Cohen-Yeshurun A, Magid L, Algali M, Mechoulam R. Endocannabinoids and traumatic brain injury. Br J Pharmacol. 2011 Aug;163(7):1402-10. doi: 10.1111/j.1476-5381.2011.01343.x. Review. PubMed PMID: 21418185; PubMed Central PMCID: PMC3165950.

    Tuma RF, Steffens S. Targeting the endocannabinod system to limit myocardial and cerebral ischemic and reperfusion injury. Curr Pharm Biotechnol. 2012 Jan;13(1):46-58. Review. PubMed PMID: 21470162.

    Vink R, Van Den Heuvel C. Recent advances in the development of multifactorial therapies for the treatment of traumatic brain injury. Expert Opin Investig Drugs. 2004 Oct;13(10):1263-74. Review. PubMed PMID: 15461556.

    Vink R, Nimmo AJ. Multifunctional drugs for head injury. Neurotherapeutics. 2009 Jan;6(1):28-42. doi: 10.1016/j.nurt.2008.10.036. Review. PubMed PMID: 19110197; PubMed Central PMCID: PMC5084254.

    Walsh SK, Hepburn CY, Kane KA, Wainwright CL. Acute administration of cannabidiol in vivo suppresses ischaemia-induced cardiac arrhythmias and reduces infarct size when given at reperfusion. Br J Pharmacol. 2010 Jul;160(5):1234-42. doi: 10.1111/j.1476-5381.2010.00755.x. PubMed PMID: 20590615; PubMed Central PMCID: PMC2936031.

    Ward SJ, Castelli F, Reichenbach ZW, Tuma RF. Surprising outcomes in cannabinoid CB1/CB2 receptor double knockout mice in two models of ischemia. Life Sci. 2018 Feb 15;195:1-5. doi: 10.1016/j.lfs.2017.12.030. Epub 2017 Dec 27. PubMed PMID: 29288767; PubMed Central PMCID: PMC5810406.

    Zani A, Braida D, Capurro V, Sala M. Delta9-tetrahydrocannabinol (THC) and AM 404 protect against cerebral ischaemia in gerbils through a mechanism involving cannabinoid and opioid receptors. Br J Pharmacol. 2007 Dec;152(8):1301-11. Epub 2007 Oct 29. PubMed PMID: 17965746; PubMed Central PMCID: PMC2189998.

    Zhang M, Martin BR, Adler MW, Razdan RK, Jallo JI, Tuma RF. Cannabinoid CB(2) receptor activation decreases cerebral infarction in a mouse focal ischemia/reperfusion model. J Cereb Blood Flow Metab. 2007 Jul;27(7):1387-96. Epub 2007 Jan 24. PubMed PMID: 17245417; PubMed Central PMCID: PMC2637559.

    Zhang M, Martin BR, Adler MW, Razdan RK, Ganea D, Tuma RF. Modulation of the balance between cannabinoid CB(1) and CB(2) receptor activation during cerebral ischemic/reperfusion injury. Neuroscience. 2008 Mar 27;152(3):753-60. doi: 10.1016/j.neuroscience.2008.01.022. Epub 2008 Jan 25. PubMed PMID: 18304750; PubMed Central PMCID: PMC2577828.

    Zhang M, Adler MW, Abood ME, Ganea D, Jallo J, Tuma RF. CB2 receptor activation attenuates microcirculatory dysfunction during cerebral ischemic/reperfusion injury. Microvasc Res. 2009 Jun;78(1):86-94. doi: 10.1016/j.mvr.2009.03.005. Epub 2009 Mar 28. PubMed PMID: 19332079; PubMed Central PMCID: PMC3319431.
  7. momofthegoons

    momofthegoons Vapor Accessory Addict Staff Member

    Likes Received:
    Trophy Points:
    Some new evidence that THC and CBD are beneficial for brain injuries like concussion syndrome, etc.
    Cannabis is Healing the Injured Brain – Here’s the Latest
    Dragana Komnenov PhD May 26, 2018, 10:52 PM

    The devastating consequences of Traumatic Brain Injury (TBI) are reduced through the use of cannabis medicine.
    Traumatic brain injury (TBI) accounts for approximately 1.5 million visits to the emergency room and hospitalizations every year. Young men are vastly over-represented within this population. Still, the majority of head injuries are considered mild and do not receive the medical treatment.

    Image Credit: Puwadol Jaturawutthichai

    The most alarming statistic, perhaps, is that individuals suffering from TBI have a lower life expectancy, deteriorating at about 3-fold faster rate than the average population. This is because the pathophysiological events of TBI lead to cell death, excitotoxicity, neuroinflammation and cerebrovascular breakdown. These cell-level damaging mechanisms are associated with long term physical, cognitive, and psychological disorders that impact immensely on the quality of life.

    Image Credit: Blurry Me

    Even if TBI is considered “mild”, the devastating consequences of this injury can result in the same consequences. Despite the sizeable healthcare burden imposed by TBI, successful therapies are lacking and the existing pharmacotherapies are ineffective.

    A growing body of evidence points to the potential of the endocannabinoid system to alter the cellular events that occur in the hours, months and days post-TBI, which may be critical in reducing the neuronal damage and downstream functional outcomes.

    Image Credit: Dougie Jones

    Pre-clinical work has shown that in the hours-to-days following the injury, there is a gradual increase in the endogenous cannabinoid, anandamide, in the brain, suggesting that perhaps this reflects a self-neuroprotective response. After the initial insult, the area of the contusion is referred to as the primary lesion, or the infarct, and the area surrounding the infarct is the paracontusional area. So not only is the of area of impact damaged, but also the physiology of the surrounding area becomes affected, effectively expanding the area of the brain that will be damaged.

    Image Credit: Teeadej

    At the cellular and the molecular level, neuroinflammation ensues, which further promotes cell death. Cerebrovascular breakdown follows, compromising the integrity of the blood-brain barrier, which serves as a protective gate-keeper between the systemic circulation and the brain. The accumulated research of cannabinoids on traumatic brain cell death have so far proven efficacious in two areas: downgrading neurodegeneration and reducing lesion size.

    Image Credit: Canna Obscura

    The death of neurons immediately following a TBI is greatly reduced with the administration of CB2 receptor agonists, or inhibitors of enzymes that normally degrade endocannabinoids. Also, when CB1 receptor was blocked alone, or in combination with CB2 receptor, making them unavailable for binding by cannabinoids, the protective effects on lesion volume and neuroinflammation were not observed, indicating that CB1 and CB2 receptor signaling are instrumental in therapeutics of TBI.

    Image Credit: Shutterstock

    TBI-related neuroinflammation has been shown to be initiated by activated microglia, the scavenger cells of the brain, and inhibiting the activation of microglia may be an important therapeutic strategy. Indeed, it has been shown that elevation of endogenous cannabinoids resulted in prevention of TBI-associated microglia activation.

    Image Credit: Hug You

    Although the studies conducted so far focused on administering cannabinoid agonists after TBI had occurred, one study did look at the patients who sustained TBI after cannabis use. The hope was to gain insight into whether administration of THC prior to injury had a protective effect. The researchers found, in this 3-year retrospective study, that the individuals who suffered from TBI (and in whom the urine toxicology screens were found positive for THC prior to TBI), had lower mortality rates compared to those in which the THC screens were negative. Based on previous work conducted in mice, it is possible that low dose THC provides impairment protection and serves as pre-conditioning.

    Image Credit: Shutterstock

    Furthermore, another cannabinoid, CBD, given its anti-inflammatory properties, may be of particular therapeutic potential in TBI. Although there are no studies at present that investigated the use of CBD in TBI therapeutics, it is a promising future avenue of investigation for two reasons. Firstly, CBD is a potent anti-inflammatory molecule that in the context of TBI would downregulate neuroinflammation of the brain tissue at both the contusion site and in the paracontusional area. Secondarily, reduced inflammatory cells and their damaging action on the surrounding tissue would be expected to result in reduction of lesion volume, and thus reduce the extent of the injury.

    Image Credit: Puwadol Jaturawutthichai

    Overall, the abundant and growing pre-clinical research suggests that cannabinoids, both endogenous and phytocannabinoids (found in the plant) exert many beneficial effects that may ameliorate multifactorial TBI pathology. Distribution of CB1 and CB2 receptors in the neural tissue may be one of the key aspects of these effects. Another relevant factor is the dosing of THC and CBD, and in case of THC it has been suggested that ameliorative effects in TBI are observed with low dose administration.
    ataxian likes this.
  8. momofthegoons

    momofthegoons Vapor Accessory Addict Staff Member

    Likes Received:
    Trophy Points:
    Your Brain On Weed: Concussions And Cannabis

    During the 2019 Cultivation Classic, Dr. Ethan Russo of the International Cannabis and Cannabinoids Institute presented his latest research findings on cannabis and traumatic brain injury.

    Conventional wisdom is that if the symptoms persist for a year, the symptoms will be present. But as Dr. Russo illustrated during his talk, this conventional wisdom is not always the case and certain things can be done. This includes some promising research into the role cannabis can play in recovery from traumatic brain injuries.

    THC and CBD As Recovery Agents
    Both THC and CBD are neuroprotective antioxidants, which Dr. Russo observes is a fancy way of saying they help reduce the effects brain damage whether due to trauma or things like strokes or other disease. An antioxidant is something that prevents rust. And according to Dr. Russo, “rust in the brain means deterioration in the brain structures.”

    Glutamine is a neurotransmitter that produces an over abundance of glutamine following a head injury that produces glutamate excitotoxicity whereby the cells stimulate themselves to death. This can lead to a neuronal demise after a traumatic brain injury. In Dr. Russo’s research, he’s observed that CBD and THC may help prevent glutamate excitotoxicity. Also, THC and CBD, have been extremely helpful in treatment of chronic traumatic encephalopathy (CTI) symptoms experienced by football players and anyone else engaged in contact sports.

    Using Cannabis to Treat Concussions
    While one should consult with their personal medical provider before beginning any regime, Dr. Russo offered these overall guidelines for those looking to treat a conclusion with cannabis.

    If one choose to inhale cannabis via smoking or vaping, tiny doses should be utilized sequentially with 10 to15 minute pauses. This should help lift “brain fog or allay symptoms such as headache or dizziness. For chronic problems, oral administration of low doses via capsules or tinctures are preferable.

    While THC-predominant chemovars can be very effective, in Dr. Russo’s practice, what would be more appropriate would be Type II or III chemovars with low THC and high CBD. In those tepenes that are proven to be particularly effective α-pinene-inene is helpful to reduce SIN- and cognitive impairment; limonene will elevate mood; and carvophyllene will reduce pain and inflammation.

    In addition to cannabis, other natural treatments recommended by Dr. Russo include ginkgo biloba, ginger, and chelated agnesium. Other existing treatments for concussions include rest, avoidance of excessive light, avoidance of alcohol, the low resumption of aerobic activity as tolerated, and antidepressants (SSRIs et al). As Dr. Russo notes, the success of these approaches is variable at best.
    Helios, Madri-Gal and ataxian like this.
  9. Madri-Gal

    Madri-Gal Well-Known Member

    Likes Received:
    Trophy Points:
    Excellent news! I've had more than my share of concussions, and if THC and CBD help, sign me up.
    BD9, ataxian, Helios and 1 other person like this.
  10. ataxian

    ataxian Well-Known Member

    Likes Received:
    Trophy Points:
    I have more strains however 2 R out in da lead!

    Lemon Haze is one! (High CBD)
    Maui WOWIE 4 reading?
    momofthegoons and Madri-Gal like this.
  11. Killick

    Killick Well-Known Member

    Likes Received:
    Trophy Points:
    Cascadia Norte
    Cannabinoids create effects by activating or blocking what are known as G-protein-coupled receptors, often abbreviated to GPCR. One such site in the body is called GPR55, known as an 'orphan receptor', and its importance has been studied at a highly scientific level, yet the average user may not yet be aware of its existence. This is partially because, despite pharmaceutical giants GlaxoSmithKline and AstraZenica applying for a GPR55-related patent back in 2001, no peer-reviewed research supported the claim that GPR55 was indeed a cannabinoid receptor until an article was published in the British Journal of Pharmacology in 2007 [Ryberg et al]. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2095107/]

    The study also states that, “GPR55 was activated by a range of plant, synthetic and endogenous cannabinoids and blocked by the non-psychoactive phytocannabinoid, cannabidiol.” It continues by outlining the pharmacological differences between GPR55, CB1 and CB2 receptors, pointing out that while some receptors are triggered by certain cannabinoids, others are blocked; this action reverses and/or varies, depending upon which receptor and which cannabinoid is being discussed. All of this information highlights the natural inclination of our bodies to accept cannabinoids as medicine, whether they are produced within our bodies or sourced from plants or synthetic means. Thus, cannabinoids are an effective, natural way to fix inadequacies in our systems – one that is purposeful and intended to actually help at a cellular level, rather than a simple ploy to get high, as opponents have been claiming.

  1. This site uses cookies to help personalise content, tailor your experience and to keep you logged in if you register.
    By continuing to use this site, you are consenting to our use of cookies.
    Dismiss Notice