Even a quick glance at the list of scientific primary sources behind this topic will make it clear that the powerful qualities of cannabidiol (CBD) as a neuroprotectant and self-resource tool for post-injury rehabilitation are scientifically proven. It is quite difficult to present all the results of scientific research in a publication, so we will write the most simple and understandable. What you will be able to convey to your familiar doctors, relatives of the wounded and just friends over an evening conversation. All the most detailed info on the topic is in the article “Neuroprotection Following Concussion: The Potential Role for Cannabidiol” Singh J. “Neuroprotection Following Concussion: The Potential Role for Cannabidiol” Canadian Journal of Neurological Sciences 7 Feb 2020*., If you are a volunteer medical translator, or if you have the gift of a fundraiser or want to pay for the work of a translator, write to us. In the meantime, read excerpts from research on various aspects of the post-concussion brain protection that CBD can provide.
Cannabidiol (CBD) is of great interest to progressive medicine due to its therapeutic properties and apparent lack of negative side effects. Studies show that high doses of CBD can be taken both once and on an ongoing basis with minimal or no risk (examples of high doses in post dated 07/13/2018 https://cutt.ly/5NQfe8A). This article focuses on the neuroprotective effects of CBD, with an emphasis on its use in recovery from moderate traumatic brain injury (TBI) or concussion.
CBD modulates and nourishes the endocannabinoid system, the body's pervasive rebalancing system that regulates all of its critical functions. At the same time, cannabidiol affects both cannabinoid receptors and other receptors involved in the work of #EKS, for example, vanilloid receptor type 1, adenosine receptors and serotonin receptors as well. Concussions can lead to many physiological consequences, potentially leading to post-concussion syndrome. It often causes the release of pro-inflammatory cytokines, ion imbalance, increased lactate accumulation due to increased glycolysis and oxidative stress, as well as impaired cerebral blood flow. Due to its effects on the vasculature of the brain, as well as its anti-inflammatory and neuroprotective properties, CBD can help reduce the damage caused by concussion. Scientists have even hypothesized that CBD may regulate Ca2+ homeostasis to prevent mitochondrial dysfunction and toxin release.
CBD has been shown to affect:
- the blood-brain barrier (see publication dated 07.10.22 https://cutt.ly/yMuQ5SC),
- brain neurotrophic factor BDNF,
- cognitive ability,
- the vascular system of the brain,
- cardiovascular physiology,
- neurogenesis -
all aspects that undergo changes under the influence of a concussion. Would you like more detailed information on these points (such as CBD and HEB)? Please write in the comments.
Thus, CBD enhances neuroprotection by reducing inflammation, regulating cerebral blood flow, enhancing neurogenesis, and protecting the brain from reactive oxygen species.
Double-blind, randomized controlled trials are still needed to validate the use of CBD as a medicine after moderate brain injuries, such as concussions (perhaps they are timely in Ukraine?).
Due to its neuroprotective properties and lack of intoxicating side effects, CBD shows promising potential in helping patients with brain injuries. Mice with bilateral common carotid artery occlusion were given CBD at 10 mg/kg-1:
- weakened hippocampal neurodegeneration;
- reduced damage to the white matter of the brain;
- increased levels of protein neurotrophic growth factor (BDNF);
- stimulated neurogenesis and dendritic restructuring.
Moreover, administration of CBD to mice both before and after middle cerebral artery occlusion demonstrated that this cannabinoid inhibited cerebral blood flow lesions.
Administration of CBD to piglets with acute hypoxia-ischemia increased brain activity after ischemia to normal levels, as demonstrated by brain electrical activity, brain tissue oxygenation, and neurobehavioral responses, such as locomotor activity.
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It is interesting to know that back in 2015, the pharmaceutical company GW Pharmaceuticals received from the FDA for cannabidiol the status of an orphan drug for newborn children with neonatal hypoxic-ischemic encephalopathy (about the fateful consequences of treatment with cannabidiol immediately after birth injuries - in the publication dated May 4, 2020 at the link https://bit.ly/3WLqmr1). The same indications, tested on babies:
"Scientists are paying particular attention to cannabidiol (CBD), a non-psychoactive cannabinoid from the cannabis plant, as a safe and effective protective and therapeutic tool. It effectively performs a neuroprotective function due to its anti-inflammatory and antioxidant properties in various models neurodegenerative diseases. It modulates excitotoxicity, oxidative stress, inflammation and blood-brain barrier permeability.”
-------
Tag everyone who saves our soldiers. Also tag the soldiers, doctors and medical journalists. We cannot advertise, so sharing this information depends only on you. #contusion
#HempHealing #CannabisScience #cannabidiol #medical_use_of_cannabis
#FSU
List of scientific primary sources:
Singh J. “Neuroprotection Following Concussion: The Potential Role for Cannabidiol” Canadian Journal of Neurological Sciences 7 Feb 2020 https://www.cambridge.org/.../3D24F8E3BB6C2403B9027A183FF...
Pazos M.R. et al. "Mechanisms of cannabidiol neuroprotection in hypoxic-ischemic newborn pigs: role of 5HT(1A) and CB2 receptors". Neuropharmacology. 2013; 71 https://pubmed.ncbi.nlm.nih.gov/23587650/
Mishima K. et al. "Cannabidiol prevents cerebral infarction via a serotonergic 5-hydroxytryptamine1A receptor-dependent mechanism". Stroke. 2005;36(5) https://www.ahajournals.org/.../01.STR.0000163083.59201.34
Hind W.H. et al. "Cannabidiol protects an in vitro model of the blood-brain barrier from oxygen-glucose deprivation via PPARγ and 5-HT1A receptors" British Journal of Pharmacology 2016;173(5) https://bpspubs.onlinelibrary.wiley.com/.. ./10.../bph.13368
Esposito G. et al. "Cannabidiol reduces Abeta-induced neuroinflammation and promotes hippocampal neurogenesis through PPARgamma involvement". PLoS One. 2011;6(12) https://pubmed.ncbi.nlm.nih.gov/22163051/
Mecha M. et al. "Cannabidiol provides long-lasting protection against the deleterious effects of inflammation in a viral model of multiple sclerosis: a role for A2A receptors". Neurobiology of Disease. 2013;59:141–50. https://www.sciencedirect.com/.../pii/S0969996113001939
Castillo A. et al. "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 2010;37(2) https://www.sciencedirect.com/.../abs/pii/S096999610900309X
Bisogno T. et al. "Molecular targets for cannabidiol and its synthetic analogues: effect on vanilloid VR1 receptors and on the cellular uptake and enzymatic hydrolysis of anandamide." The British Journal of Pharmacology 2001;134(4) https://pubmed.ncbi.nlm.nih.gov/11606325/
Veldhuis W.B. et al. "Neuroprotection by the endogenous cannabinoid anandamide and arvanil against in vivo excitotoxicity in the rat: role of vanilloid receptors and lipoxygenases". Journal Neuroscience 2003; 23 (10) 103 https://www.jneurosci.org/content/23/10/4127
Correa FG et al. "The endocannabinoid anandamide from immunomodulation to neuroprotection. Implications for multiple sclerosis.” Vitamins and Hormones. 2009;81:207–30. https://pubmed.ncbi.nlm.nih.gov/19647114/
Malek N et. "Anandamide, acting via CB2 receptors, alleviates LPS-induced neuroinflammation in rat primary microglial cultures". Neural Plasticity 2015;2015:130639. https://pubmed.ncbi.nlm.nih.gov/26090232/
Shohami E et al.."Endocannabinoids and traumatic brain injury." British Journal Pharmacology 2011;163(7) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/
Russo, EB et al. "Agonistic properties of cannabidiol at 5-HT1a receptors". Neurochemical Research 2005;30(
https://pubmed.ncbi.nlm.nih.gov/16258853/
Xu, J-Y, Chen, C. “Endocannabinoids in synaptic plasticity and neuroprotection.” Neurosci a Rev J bringing Neurobiol Neurol Psychiatry. 2015;21(2): https://pubmed.ncbi.nlm.nih.gov/24571856/
Mechoulam, R, Spatz, M, Shohami, E. "Endocannabinoids and neuroprotection". Sci STKE. 2002;2002(129):re5. https://pubmed.ncbi.nlm.nih.gov/11972360/
Diana, MA, Marty, A. "Endocannabinoid-mediated short-term synaptic plasticity: depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE)". The British Journal of Pharmacology 2004;142(1) https://bpspubs.onlinelibrary.wiley.com/.../sj.bjp.0705726
Pope, C, Mechoulam, R, Parsons, L. "Endocannabinoid signaling in neurotoxicity and neuroprotection". Neurotoxicology. 2010;31(5) https://pubmed.ncbi.nlm.nih.gov/19969019/
Benyó, Z, et al. "Endocannabinoids in cerebrovascular regulation". Am J Physiol Heart Circ Physiol. 2016;310(7) https://pubmed.ncbi.nlm.nih.gov/26825517/
Linge, R, et al. "Cannabidiol induces rapid-acting antidepressant-like effects and enhances cortical 5-HT/glutamate neurotransmission: role of 5-HT1A receptors". Neuropharmacology.2016;10 https://pubmed.ncbi.nlm.nih.gov/26711860/
Scuderi, C. “Cannabidiol promotes amyloid precursor protein ubiquitination and reduction of beta amyloid expression in SHSY5YAPP+ cells through PPARgamma involvement.” Phytotherapy Research 2014;28(7):1007–13. https://pubmed.ncbi.nlm.nih.gov/24288245/
Ryan, D,".Cannabidiol targets mitochondria to regulate intracellular Ca2+ levels". The Journal of Neuroscience 2009;29(7) https://pubmed.ncbi.nlm.nih.gov/19228959/
Mori MA. et al. "Cannabidiol reduces neuroinflammation and promotes n
Cannabidiol (CBD) is of great interest to progressive medicine due to its therapeutic properties and apparent lack of negative side effects. Studies show that high doses of CBD can be taken both once and on an ongoing basis with minimal or no risk (examples of high doses in post dated 07/13/2018 https://cutt.ly/5NQfe8A). This article focuses on the neuroprotective effects of CBD, with an emphasis on its use in recovery from moderate traumatic brain injury (TBI) or concussion.
CBD modulates and nourishes the endocannabinoid system, the body's pervasive rebalancing system that regulates all of its critical functions. At the same time, cannabidiol affects both cannabinoid receptors and other receptors involved in the work of #EKS, for example, vanilloid receptor type 1, adenosine receptors and serotonin receptors as well. Concussions can lead to many physiological consequences, potentially leading to post-concussion syndrome. It often causes the release of pro-inflammatory cytokines, ion imbalance, increased lactate accumulation due to increased glycolysis and oxidative stress, as well as impaired cerebral blood flow. Due to its effects on the vasculature of the brain, as well as its anti-inflammatory and neuroprotective properties, CBD can help reduce the damage caused by concussion. Scientists have even hypothesized that CBD may regulate Ca2+ homeostasis to prevent mitochondrial dysfunction and toxin release.
CBD has been shown to affect:
- the blood-brain barrier (see publication dated 07.10.22 https://cutt.ly/yMuQ5SC),
- brain neurotrophic factor BDNF,
- cognitive ability,
- the vascular system of the brain,
- cardiovascular physiology,
- neurogenesis -
all aspects that undergo changes under the influence of a concussion. Would you like more detailed information on these points (such as CBD and HEB)? Please write in the comments.
Thus, CBD enhances neuroprotection by reducing inflammation, regulating cerebral blood flow, enhancing neurogenesis, and protecting the brain from reactive oxygen species.
Double-blind, randomized controlled trials are still needed to validate the use of CBD as a medicine after moderate brain injuries, such as concussions (perhaps they are timely in Ukraine?).
Due to its neuroprotective properties and lack of intoxicating side effects, CBD shows promising potential in helping patients with brain injuries. Mice with bilateral common carotid artery occlusion were given CBD at 10 mg/kg-1:
- weakened hippocampal neurodegeneration;
- reduced damage to the white matter of the brain;
- increased levels of protein neurotrophic growth factor (BDNF);
- stimulated neurogenesis and dendritic restructuring.
Moreover, administration of CBD to mice both before and after middle cerebral artery occlusion demonstrated that this cannabinoid inhibited cerebral blood flow lesions.
Administration of CBD to piglets with acute hypoxia-ischemia increased brain activity after ischemia to normal levels, as demonstrated by brain electrical activity, brain tissue oxygenation, and neurobehavioral responses, such as locomotor activity.
------
It is interesting to know that back in 2015, the pharmaceutical company GW Pharmaceuticals received from the FDA for cannabidiol the status of an orphan drug for newborn children with neonatal hypoxic-ischemic encephalopathy (about the fateful consequences of treatment with cannabidiol immediately after birth injuries - in the publication dated May 4, 2020 at the link https://bit.ly/3WLqmr1). The same indications, tested on babies:
"Scientists are paying particular attention to cannabidiol (CBD), a non-psychoactive cannabinoid from the cannabis plant, as a safe and effective protective and therapeutic tool. It effectively performs a neuroprotective function due to its anti-inflammatory and antioxidant properties in various models neurodegenerative diseases. It modulates excitotoxicity, oxidative stress, inflammation and blood-brain barrier permeability.”
-------
Tag everyone who saves our soldiers. Also tag the soldiers, doctors and medical journalists. We cannot advertise, so sharing this information depends only on you. #contusion
#HempHealing #CannabisScience #cannabidiol #medical_use_of_cannabis
#FSU
List of scientific primary sources:
Singh J. “Neuroprotection Following Concussion: The Potential Role for Cannabidiol” Canadian Journal of Neurological Sciences 7 Feb 2020 https://www.cambridge.org/.../3D24F8E3BB6C2403B9027A183FF...
Pazos M.R. et al. "Mechanisms of cannabidiol neuroprotection in hypoxic-ischemic newborn pigs: role of 5HT(1A) and CB2 receptors". Neuropharmacology. 2013; 71 https://pubmed.ncbi.nlm.nih.gov/23587650/
Mishima K. et al. "Cannabidiol prevents cerebral infarction via a serotonergic 5-hydroxytryptamine1A receptor-dependent mechanism". Stroke. 2005;36(5) https://www.ahajournals.org/.../01.STR.0000163083.59201.34
Hind W.H. et al. "Cannabidiol protects an in vitro model of the blood-brain barrier from oxygen-glucose deprivation via PPARγ and 5-HT1A receptors" British Journal of Pharmacology 2016;173(5) https://bpspubs.onlinelibrary.wiley.com/.. ./10.../bph.13368
Esposito G. et al. "Cannabidiol reduces Abeta-induced neuroinflammation and promotes hippocampal neurogenesis through PPARgamma involvement". PLoS One. 2011;6(12) https://pubmed.ncbi.nlm.nih.gov/22163051/
Mecha M. et al. "Cannabidiol provides long-lasting protection against the deleterious effects of inflammation in a viral model of multiple sclerosis: a role for A2A receptors". Neurobiology of Disease. 2013;59:141–50. https://www.sciencedirect.com/.../pii/S0969996113001939
Castillo A. et al. "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 2010;37(2) https://www.sciencedirect.com/.../abs/pii/S096999610900309X
Bisogno T. et al. "Molecular targets for cannabidiol and its synthetic analogues: effect on vanilloid VR1 receptors and on the cellular uptake and enzymatic hydrolysis of anandamide." The British Journal of Pharmacology 2001;134(4) https://pubmed.ncbi.nlm.nih.gov/11606325/
Veldhuis W.B. et al. "Neuroprotection by the endogenous cannabinoid anandamide and arvanil against in vivo excitotoxicity in the rat: role of vanilloid receptors and lipoxygenases". Journal Neuroscience 2003; 23 (10) 103 https://www.jneurosci.org/content/23/10/4127
Correa FG et al. "The endocannabinoid anandamide from immunomodulation to neuroprotection. Implications for multiple sclerosis.” Vitamins and Hormones. 2009;81:207–30. https://pubmed.ncbi.nlm.nih.gov/19647114/
Malek N et. "Anandamide, acting via CB2 receptors, alleviates LPS-induced neuroinflammation in rat primary microglial cultures". Neural Plasticity 2015;2015:130639. https://pubmed.ncbi.nlm.nih.gov/26090232/
Shohami E et al.."Endocannabinoids and traumatic brain injury." British Journal Pharmacology 2011;163(7) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/
Russo, EB et al. "Agonistic properties of cannabidiol at 5-HT1a receptors". Neurochemical Research 2005;30(
https://pubmed.ncbi.nlm.nih.gov/16258853/
Xu, J-Y, Chen, C. “Endocannabinoids in synaptic plasticity and neuroprotection.” Neurosci a Rev J bringing Neurobiol Neurol Psychiatry. 2015;21(2): https://pubmed.ncbi.nlm.nih.gov/24571856/
Mechoulam, R, Spatz, M, Shohami, E. "Endocannabinoids and neuroprotection". Sci STKE. 2002;2002(129):re5. https://pubmed.ncbi.nlm.nih.gov/11972360/
Diana, MA, Marty, A. "Endocannabinoid-mediated short-term synaptic plasticity: depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE)". The British Journal of Pharmacology 2004;142(1) https://bpspubs.onlinelibrary.wiley.com/.../sj.bjp.0705726
Pope, C, Mechoulam, R, Parsons, L. "Endocannabinoid signaling in neurotoxicity and neuroprotection". Neurotoxicology. 2010;31(5) https://pubmed.ncbi.nlm.nih.gov/19969019/
Benyó, Z, et al. "Endocannabinoids in cerebrovascular regulation". Am J Physiol Heart Circ Physiol. 2016;310(7) https://pubmed.ncbi.nlm.nih.gov/26825517/
Linge, R, et al. "Cannabidiol induces rapid-acting antidepressant-like effects and enhances cortical 5-HT/glutamate neurotransmission: role of 5-HT1A receptors". Neuropharmacology.2016;10 https://pubmed.ncbi.nlm.nih.gov/26711860/
Scuderi, C. “Cannabidiol promotes amyloid precursor protein ubiquitination and reduction of beta amyloid expression in SHSY5YAPP+ cells through PPARgamma involvement.” Phytotherapy Research 2014;28(7):1007–13. https://pubmed.ncbi.nlm.nih.gov/24288245/
Ryan, D,".Cannabidiol targets mitochondria to regulate intracellular Ca2+ levels". The Journal of Neuroscience 2009;29(7) https://pubmed.ncbi.nlm.nih.gov/19228959/
Mori MA. et al. "Cannabidiol reduces neuroinflammation and promotes n
