Snake oil or cure-all? Inside the budding CBD industry | Nightline
CBD became the “it” product of 2019 and believers, including a veteran and soccer star Megan Rapinoe, tout it as a benefit, but there is little regulation and …
Given that CBD use is still a new thing we need more time to see if it’s effect and use is effective and safe. For those that use it regularly, if it helps you then I’m glad it’s helping.
If CBD helped this former military man prevent committing suicide and getting back to living then good for him. Whatever helps people bad long as it’s not an illegal drug or has negative effects on your physical and mental health then why not use it?
I have a sever neurological pain condition CRPS right arm/hand/shoulder/back/eyes/face and CBD oil and vape is a life changer. It works for me personally. I am also in the autistic spectrum and it helps with anxiety for me. I will not take opioids. When i have a flare up I vape cbd 3x and 5 min the pain goes down. learn all about it first be your own self advocate cbdoilusers.com is the up to date educational website. Also do not just buy any cbd oil. This is why you need to go and learn about it first and what top brands do for different conditions. Learn for yourself. Do not let big pharma get you on opioids. Also moderation in all things. never overdo anything.
Very very good video and hoping that more people get well with this type of drug… i believe in the benefits in CBD FOR SOME people and children who can defenitely benefit for a better life!!
Bernie Sanders will legalize it, and people won't have to worry about losing their jobs, and won't have to use big pharma's highly addictive and harmful drugs.
This is why you can't trust corporations. They will cut corners and quality to maximize profits. Use only growers, because you can see how your product is made. Compassion Centers around my part of the US, is ran and owned by slimy politicians and law enforcement, who only care about profit, not the People.
CANNABIS IS THE ONLY DRUG THAT WILL NEVER KILL OR GIVE U OTHER MEDICAL CONDITIONS…LIKE MAN MADE CRACK PILLS…EH?? CBD.OIL SHOULD BE NUMBER ONE MEDICAL MEDICINE. LOL…AMERICAN HAS GUNS BUT THEY DON'T GIVE OUT CANNABIS…"STUPIDS!" UR FDA…NO MEDICAL RESEARCH…😄😅🤣😂🇨🇦🇨🇦🇨🇦🇨🇦🇨🇦🇨🇦….AMAZING FOR PAIN, LIFE SAVING IS CANNABIS. CYMBALT IS YOUR FDA LIFE SAVER…IT WILL SAVE UR KIDNEY'S..🤣😂🥂CHEERS.
The FDA recently came out with a warning re: CBD and liver damage. If you are on a plethora of drugs, it would be unwise to heavily dose CBD due to P450 enzyme reduced activity, other than that? They need to explain just exactly what it is they are getting at.
Sci Rep. 2017 Sep 21;7(1):12064. doi: 10.1038/s41598-017-10924-8. Cannabidiol attenuates alcohol-induced liver steatosis, metabolic dysregulation, inflammation and neutrophil-mediated injury. Wang Y1,2, Mukhopadhyay P1, Cao Z1, Wang H3, Feng D3, Haskó G4, Mechoulam R5, Gao B3, Pacher P6. Author information Abstract
Cannabidiol (CBD) is a non-psychoactive component of marijuana, which has anti-inflammatory effects. It has also been approved by FDA for various orphan diseases for exploratory trials. Herein, we investigated the effects of CBD on liver injury induced by chronic plus binge alcohol feeding in mice. CBD or vehicle was administered daily throughout the alcohol feeding study. At the conclusion of the feeding protocol, serums samples, livers or isolated neutrophils were utilized for molecular biology, biochemistry and pathology analysis. CBD significantly attenuated the alcohol feeding-induced serum transaminase elevations, hepatic inflammation (mRNA expressions of TNFα, MCP1, IL1β, MIP2 and E-Selectin, and neutrophil accumulation), oxidative/nitrative stress (lipid peroxidation, 3-nitrotyrosine formation, and expression of reactive oxygen species generating enzyme NOX2). CBD treatment also attenuated the respiratory burst of neutrophils isolated from chronic plus binge alcohol fed mice or from human blood, and decreased the alcohol-induced increased liver triglyceride and fat droplet accumulation. Furthermore, CBD improved alcohol-induced hepatic metabolic dysregulation and steatosis by restoring changes in hepatic mRNA or protein expression of ACC-1, FASN, PPARα, MCAD, ADIPOR-1, and mCPT-1. Thus, CBD may have therapeutic potential in the treatment of alcoholic liver diseases associated with inflammation, oxidative stress and steatosis, which deserves exploration in human trials.
Two non-psychoactive cannabinoids reduce intracellular lipid levels and inhibit hepatosteatosis. Silvestri C, et al. J Hepatol. 2015. Show full citation Abstract
BACKGROUND & AIMS: Obesity and associated metabolic syndrome have quickly become a pandemic and a major detriment to global human health. The presence of non-alcoholic fatty liver disease (NAFLD; hepatosteatosis) in obesity has been linked to the worsening of the metabolic syndrome, including the development of insulin resistance and cardiovascular disease. Currently, there are few options to treat NAFLD, including life style changes and insulin sensitizers. Recent evidence suggests that the cannabinoids Δ(9)-tetrahydrocannabivarin (THCV) and cannabidiol (CBD) improve insulin sensitivity; we aimed at studying their effects on lipid levels.
METHODS: The effects of THCV and CBD on lipid levels were examined in a variety of in vitro and in vivo systems, with special emphasis on models of hepatosteatosis. Transcriptional, post-translational and metabolomic changes were assayed.
RESULTS: THCV and CBD directly reduce accumulated lipid levels in vitro in a hepatosteatosis model and adipocytes. Nuclear magnetic resonance- (NMR) based metabolomics confirmed these results and further identified specific metabolic changes in THCV and CBD-treated hepatocytes. Treatment also induced post-translational changes in a variety of proteins such as CREB, PRAS40, AMPKa2 and several STATs indicating increased lipid metabolism and, possibly, mitochondrial activity. These results are supported by in vivo data from zebrafish and obese mice indicating that these cannabinoids are able to increase yolk lipid mobilization and inhibit the development of hepatosteatosis respectively.
CONCLUSIONS: Our results suggest that THCV and CBD might be used as new therapeutic agents for the pharmacological treatment of obesity- and metabolic syndrome-related NAFLD/hepatosteatosis.
Fibromyalgia, or myofascial pain syndrome, is an extremely common but controversial condition, whose very basis has been questioned, particularly among neurologists [65]. Even this author must admit to past prejudice in labeling it a “semi mythical pseudo-disease.” Notwithstanding these opinions, the condition is the most frequent diagnosis in American rheumatology practices. Bennett has provided an excellent review [66], emphasizing new insights into fibromyalgia as a condition indicative of “central sensitization” and amplification of somatic nociception. While no clear chemical or anatomical pathology has been clarified in tender muscle points, these present a self-sustaining and amplifying influence on pain perception in the brain over time, and lead to a concomitant disturbances in restful sleep, manifestations of dysautonomia, and prevalent secondary depression. Interestingly, the application of standard antidepressant medication to the latter, and pharmacotherapy in general, provide disappointing results in fibromyalgia treatment. Has a promising therapeutic avenue been missed? Returning to the work of Nicolodi and Sicuteri, the “secondary hyperalgesia” manifested by an increased response to noxious stimuli in areas adjacent to the pain is common to migraine and fibromyalgia (see below).
These authors suggested NMDA blockade as an approach to pain in defects of serotonergic analgesia in fibromyalgia [67]. Several studies of Richardson and her group provide key support for a relation of fibromyalgia and similar conditions to a clinical endocannabinoid deficiency. An initial study [68] demonstrated that intrathecal injection of SR141716A, a powerful cannabinoid antagonist/inverse agonist, resulted in thermal hyperalgesia in mice. This suggests that the endocannabinoid system regulates nociceptive thresholds, and that absence of such regulation, or endocannabinoid hypofunction, underlies hyperalgesia and related chronic pain conditions. In a subsequent study [69], oligonucleotides directed against CB1 mRNA produced significant hyperalgesia. Additionally, the hyperalgesic effect of SR141716A was blocked in a dose-dependent manner by co-administration of two NMDA receptor antagonists, again sup-porting tonic activity of the endocannabinoid system under normal conditions.
On this basis, it was suggested that cannabinoid agonists would be applicable to treatment of chronic pain conditions unresponsive to opioid analgesics. Further investigation demonstrated that intrathecal AEA totally blocked carrageenan-induced spinal thermal hyperalgesia, while having no effect on normal thermal sensory and antinociceptive thresholds [70]. Additionally, AEA inhibited K+ and capsaicin-evoked calcitonin gene-related peptide (CGRP) release, and CB1 receptors were identified in rat sensory neurons and trigeminal ganglion. On this basis, the authors recommended cannabinoids for disorders driven by a primary afferent barrage (e.g., allodynia, visceral hyperalgesia, temporomandibular joint pain (TMJ), and reflex sympathetic dystrophy (RSD)), and that such treatment could be effective a sub-psychoactive dosages.
Another study examined peripheral mechanisms [71], wherein AEA acted on CB1 to reduce hyperalgesia and inflammation via inhibition of CGRP neurosecretion in capsaicin activated nerve terminals. This is akin to mechanisms of “sterile inflammation” observed centrally in migraine, where CGRP is felt to be an important mediator [5]. Overall the results supported the notion that endocannabinoids modulate neurogenic inflammation through inhibition of peripheral terminal neurosecretion in capsaicin-sensitive fibers. AEA demonstrated anti-edema effects in addition to anti-hyperalgesia. Similar implications were provided by another study [72], in which WIN 55,212–2, a powerful CB1 agonist, blocked capsaicin-induced hyperalgesia in rat paws. Once more, the benefit occurred at a dosage that did not produce analgesia or motor impairment, suggesting therapeutic benefit of cannabinoids without adverse effects. Similarly, lo-cal THC administration was evaluated in capsaicin-induced pain in rhesus monkeys [73], where, once more, pain was effectively reduced at low dosage, and was blocked by a CB1 antagonist.
OBJECTIVES: Ethan B. Russo’s paper of December 1, 2003 explored the concept of a clinical endocannabinoid deficiency (CECD) underlying the pathophysiology of migraine, fibromyalgia, irritable bowel syndrome and other functional conditions alleviated by clinical cannabis. METHODS: Available literature was reviewed, including searches via the National Library of medicine database and other sources. RESULTS: A review of the literature indicates that significant progress has been made since Dr. Ethan B. Russo’s landmark paper, just ten years ago (February 2, 2004).
Investigation at that time suggested that cannabinoids can block spinal, peripheral and gastrointestional mechanisms that promote pain in headache, fibromyalgia, irritable bowel syndrome and muscle spasm.
CONCLUSION: Subsequent research has confirmed that underlying endocannabinoid deficiencies indeed play a role in migraine, fibromyalgia, irritable bowel syndrome and a growing list of other medical conditions. Clinical experience is bearing this out. Further research and especially, clinical trials will further demonstrate the usefulness of medical cannabis. As legal barriers fall and scientific bias fades this will become more apparent.
THC and CBD phytocannabinoids also act as neuroprotective antioxidants against glutamate neurotoxicity and cell death mediated via NMDA, AMPA and kainate receptors [55], independently of cannabinoid receptors, and exceed the antioxidant potency of vitamins C and E. Migraine is a complex neurochemical disorder with myriad effects beyond pain. Its tendency to produce photophobia and phonophobia, even between discrete attacks [56], may be considered suggestive of a “sensory hyperalgesia,” as these normally tolerated sensations take on painful proportions.The combination of endocannabinoids and their inactive precursors have been dubbed an entourage effect [57], and an analogous synergy of phytocannabinoids, cannabis terpenoids and flavonoids has also been suggested and analyzed at some length [58]. The unique attributes of cannabis to affect serotonergic, dopaminergic, opioid, anti-inflammatory, and NMDA mechanisms of migraine, both acutely and prophylactically, have rendered it a proposed “ideal drug” for its treatment [5].
Migraine is a strongly genetic disorder, but similar symptoms are acquired under conditions of closed head injury, where the “post-traumatic syndrome” displays similar symptoms. A protective role of endocannabinoids in such settings is evident in the findings that 2-AG is elevated after experimental brain injury, and that it plays an important neuroprotective role [59].Unfortunately, no organized clinical trials of cannabis in migraine have been performed. While documentation of the use of cannabis for migraine suggests a 4000 year history, and it was a major indication for cannabis medicines in Western society between 1842 and 1942 [5], there have been few modern studies beyond the “anecdotal” [5; 60–62]. Surveys in California indicate that of 2480 patients served by the Oakland Cannabis Buyers’ Club, 127, or 5%, sought cannabis for treatment of chronic migraines [63]. Success rates of some 80% with North American strains of cannabis have been estimated based on clinical contact [5]. Experience in prophylactic use of Marinol® (synthetic THC) in some ten patients was disappointing, with some decrement in frequency and severity of attacks, but not total remission or “cures” claimed by 19th century authors with extracts of Indian hemp [5]. The difference may well be due to a nearly total dearth of cannabidiol in North American cannabis strains [64] (see discussion below), and the observed possibility of CBD modulation of serotonergic function [17]. More formal documentation of clinical efficacy would be distinctly welcome.
I know someone who swears CBD fixed his Dupuytren's contracture. His brother got surgery for it, it's a physical build-up of hard tissue in the hand, but he has more mobility just from rubbing CBD on his skin. Thoughts?
Almost all commercially available CBD is hotdog water. CBD is only marginally effective without a THC counterpart, imo. If you are taking CBD only, you're missing out on a lot.
The reason why this haven't fell through and they are only making it Parts in certain areas. Because it's the game they played! Politician the War on Drugs is all a joke. Yes it is a drug problem but it's not these oils. How about big Pharma how about the great work of investigative journalism Gary Webb. Uncover politicians that brought the heroin and cocaine in the US.. Passing laws for Americans can be addicted to 💊 Now you got overdose so high in America it's unreal.
Cbd doses that you find out at stores in gummy form are less than 10 percent the dose needed to actually feel something. Almost always the placebo effect if you eat gas station gummies and think you feel something. You need over 1000 mg to actually start to really feel effects
I live in Canada, a country where it is luckily legal with or without a prescription. Until marijuana became legal in Canada I never risked taking CBD due to my job. I have a chronic illness called Cyclical Vomiting Syndrome (CVS) which causes severe vomiting sometimes for days on end. Often I end up in the hospital with dehydration and often have ulcers. My constant vomiting has caused me to have a large and inoperable hernia in my diaphragm which causes extremely painful acid reflux almost constantly. I have to sleep on a 25% angle (approximately) to keep my stomach acids in my stomach so they don't back up into my esophagus. Anyways. CBD is the only thing that I have found that seems to work getting rid of my acid reflux for a while every day! It allows me to actually get things done and be a normal person. I don't know what I would do without it!
any alternative bs mind altering shit for the mind.
Given that CBD use is still a new thing we need more time to see if it’s effect and use is effective and safe.
For those that use it regularly, if it helps you then I’m glad it’s helping.
If CBD helped this former military man prevent committing suicide and getting back to living then good for him.
Whatever helps people bad long as it’s not an illegal drug or has negative effects on your physical and mental health then why not use it?
I have a sever neurological pain condition CRPS right arm/hand/shoulder/back/eyes/face and CBD oil and vape is a life changer. It works for me personally. I am also in the autistic spectrum and it helps with anxiety for me. I will not take opioids. When i have a flare up I vape cbd 3x and 5 min the pain goes down. learn all about it first be your own self advocate cbdoilusers.com is the up to date educational website. Also do not just buy any cbd oil. This is why you need to go and learn about it first and what top brands do for different conditions. Learn for yourself. Do not let big pharma get you on opioids. Also moderation in all things. never overdo anything.
Snake oil, poisons is what comes out of the normal medical system. No healing
That is one loud drone they use to film the farm.
Very very good video and hoping that more people get well with this type of drug… i believe in the benefits in CBD FOR SOME people and children who can defenitely benefit for a better life!!
Bernie Sanders will legalize it, and people won't have to worry about losing their jobs, and won't have to use big pharma's highly addictive and harmful drugs.
This is why you can't trust corporations. They will cut corners and quality to maximize profits. Use only growers, because you can see how your product is made. Compassion Centers around my part of the US, is ran and owned by slimy politicians and law enforcement, who only care about profit, not the People.
30 years from now pot will have a warming on it that it causes cancer or someother thing
Beware of cbds if you are on depakote.The combo can blow out your liver.Why is this not common knowledge?
CANNABIS IS THE ONLY DRUG THAT WILL NEVER KILL OR GIVE U OTHER MEDICAL CONDITIONS…LIKE MAN MADE CRACK PILLS…EH?? CBD.OIL SHOULD BE NUMBER ONE MEDICAL MEDICINE. LOL…AMERICAN HAS GUNS BUT THEY DON'T GIVE OUT CANNABIS…"STUPIDS!" UR FDA…NO MEDICAL RESEARCH…😄😅🤣😂🇨🇦🇨🇦🇨🇦🇨🇦🇨🇦🇨🇦….AMAZING FOR PAIN, LIFE SAVING IS CANNABIS. CYMBALT IS YOUR FDA LIFE SAVER…IT WILL SAVE UR KIDNEY'S..🤣😂🥂CHEERS.
It's not produced from the cannabis plant though…lying twat!…its produced from the hemp plant, cannabis's cousin…which is legal to grow
Maybe if I smoke enough I'll get the healing effects of CDB oil
CBD doesn’t make you high, but it does work. I use CBD gummy bears. It doesn’t kill the pain, but it makes it tolerable
Kratom changed my life
*edit: saved my life
The FDA recently came out with a warning re: CBD and liver damage. If you are on a plethora of drugs, it would be unwise to heavily dose CBD due to P450 enzyme reduced activity, other than that? They need to explain just exactly what it is they are getting at.
Sci Rep. 2017 Sep 21;7(1):12064. doi: 10.1038/s41598-017-10924-8.
Cannabidiol attenuates alcohol-induced liver steatosis, metabolic dysregulation, inflammation and neutrophil-mediated injury.
Wang Y1,2, Mukhopadhyay P1, Cao Z1, Wang H3, Feng D3, Haskó G4, Mechoulam R5, Gao B3, Pacher P6.
Author information
Abstract
Cannabidiol (CBD) is a non-psychoactive component of marijuana, which has anti-inflammatory effects. It has also been approved by FDA for various orphan diseases for exploratory trials. Herein, we investigated the effects of CBD on liver injury induced by chronic plus binge alcohol feeding in mice. CBD or vehicle was administered daily throughout the alcohol feeding study. At the conclusion of the feeding protocol, serums samples, livers or isolated neutrophils were utilized for molecular biology, biochemistry and pathology analysis. CBD significantly attenuated the alcohol feeding-induced serum transaminase elevations, hepatic inflammation (mRNA expressions of TNFα, MCP1, IL1β, MIP2 and E-Selectin, and neutrophil accumulation), oxidative/nitrative stress (lipid peroxidation, 3-nitrotyrosine formation, and expression of reactive oxygen species generating enzyme NOX2). CBD treatment also attenuated the respiratory burst of neutrophils isolated from chronic plus binge alcohol fed mice or from human blood, and decreased the alcohol-induced increased liver triglyceride and fat droplet accumulation. Furthermore, CBD improved alcohol-induced hepatic metabolic dysregulation and steatosis by restoring changes in hepatic mRNA or protein expression of ACC-1, FASN, PPARα, MCAD, ADIPOR-1, and mCPT-1. Thus, CBD may have therapeutic potential in the treatment of alcoholic liver diseases associated with inflammation, oxidative stress and steatosis, which deserves exploration in human trials.
https://www.ncbi.nlm.nih.gov/m/pubmed/25595882/?i=2&from=Fatty%20liver%20cannabidiol
Two non-psychoactive cannabinoids reduce intracellular lipid levels and inhibit hepatosteatosis.
Silvestri C, et al. J Hepatol. 2015.
Show full citation
Abstract
BACKGROUND & AIMS: Obesity and associated metabolic syndrome have quickly become a pandemic and a major detriment to global human health. The presence of non-alcoholic fatty liver disease (NAFLD; hepatosteatosis) in obesity has been linked to the worsening of the metabolic syndrome, including the development of insulin resistance and cardiovascular disease. Currently, there are few options to treat NAFLD, including life style changes and insulin sensitizers. Recent evidence suggests that the cannabinoids Δ(9)-tetrahydrocannabivarin (THCV) and cannabidiol (CBD) improve insulin sensitivity; we aimed at studying their effects on lipid levels.
METHODS: The effects of THCV and CBD on lipid levels were examined in a variety of in vitro and in vivo systems, with special emphasis on models of hepatosteatosis. Transcriptional, post-translational and metabolomic changes were assayed.
RESULTS: THCV and CBD directly reduce accumulated lipid levels in vitro in a hepatosteatosis model and adipocytes. Nuclear magnetic resonance- (NMR) based metabolomics confirmed these results and further identified specific metabolic changes in THCV and CBD-treated hepatocytes. Treatment also induced post-translational changes in a variety of proteins such as CREB, PRAS40, AMPKa2 and several STATs indicating increased lipid metabolism and, possibly, mitochondrial activity. These results are supported by in vivo data from zebrafish and obese mice indicating that these cannabinoids are able to increase yolk lipid mobilization and inhibit the development of hepatosteatosis respectively.
CONCLUSIONS: Our results suggest that THCV and CBD might be used as new therapeutic agents for the pharmacological treatment of obesity- and metabolic syndrome-related NAFLD/hepatosteatosis.
It doesn’t work for me.
Fibromyalgia, or myofascial pain syndrome, is an extremely common but controversial condition, whose very basis has been questioned, particularly among neurologists [65]. Even this author must admit to past prejudice in labeling it a “semi mythical pseudo-disease.” Notwithstanding these opinions, the condition is the most frequent diagnosis in American rheumatology practices. Bennett has provided an excellent review [66], emphasizing new insights into fibromyalgia as a condition indicative of “central sensitization” and amplification of somatic nociception. While no clear chemical or anatomical pathology has been clarified in tender muscle points, these present a self-sustaining and amplifying influence on pain perception in the brain over time, and lead to a concomitant disturbances in restful sleep, manifestations of dysautonomia, and prevalent secondary depression. Interestingly, the application of standard antidepressant medication to the latter, and pharmacotherapy in general, provide disappointing results in fibromyalgia treatment. Has a promising therapeutic avenue been missed? Returning to the work of Nicolodi and Sicuteri, the “secondary hyperalgesia” manifested by an increased response to noxious stimuli in areas adjacent to the pain is common to migraine and fibromyalgia (see below).
These authors suggested NMDA blockade as an approach to pain in defects of serotonergic analgesia in fibromyalgia [67]. Several studies of Richardson and her group provide key support for a relation of fibromyalgia and similar conditions to a clinical endocannabinoid deficiency. An initial study [68] demonstrated that intrathecal injection of SR141716A, a powerful cannabinoid antagonist/inverse agonist, resulted in thermal hyperalgesia in mice. This suggests that the endocannabinoid system regulates nociceptive thresholds, and that absence of such regulation, or endocannabinoid hypofunction, underlies hyperalgesia and related chronic pain conditions. In a subsequent study [69], oligonucleotides directed against CB1 mRNA produced significant hyperalgesia. Additionally, the hyperalgesic effect of SR141716A was blocked in a dose-dependent manner by co-administration of two NMDA receptor antagonists, again sup-porting tonic activity of the endocannabinoid system under normal conditions.
On this basis, it was suggested that cannabinoid agonists would be applicable to treatment of chronic pain conditions unresponsive to opioid analgesics. Further investigation demonstrated that intrathecal AEA totally blocked carrageenan-induced spinal thermal hyperalgesia, while having no effect on normal thermal sensory and antinociceptive thresholds [70]. Additionally, AEA inhibited K+ and capsaicin-evoked calcitonin gene-related peptide (CGRP) release, and CB1 receptors were identified in rat sensory neurons and trigeminal ganglion. On this basis, the authors recommended cannabinoids for disorders driven by a primary afferent barrage (e.g., allodynia, visceral hyperalgesia, temporomandibular joint pain (TMJ), and reflex sympathetic dystrophy (RSD)), and that such treatment could be effective a sub-psychoactive dosages.
Another study examined peripheral mechanisms [71], wherein AEA acted on CB1 to reduce hyperalgesia and inflammation via inhibition of CGRP neurosecretion in capsaicin activated nerve terminals. This is akin to mechanisms of “sterile inflammation” observed centrally in migraine, where CGRP is felt to be an important mediator [5]. Overall the results supported the notion that endocannabinoids modulate neurogenic inflammation through inhibition of peripheral terminal neurosecretion in capsaicin-sensitive fibers. AEA demonstrated anti-edema effects in addition to anti-hyperalgesia. Similar implications were provided by another study [72], in which WIN 55,212–2, a powerful CB1 agonist, blocked capsaicin-induced hyperalgesia in rat paws. Once more, the benefit occurred at a dosage that did not produce analgesia or motor impairment, suggesting therapeutic benefit of cannabinoids without adverse effects. Similarly, lo-cal THC administration was evaluated in capsaicin-induced pain in rhesus monkeys [73], where, once more, pain was effectively reduced at low dosage, and was blocked by a CB1 antagonist.
http://nel.edu/journal/search/?q=cannabinoids
OBJECTIVES: Ethan B. Russo’s paper of December 1, 2003 explored the concept of a clinical endocannabinoid deficiency (CECD) underlying the pathophysiology of migraine, fibromyalgia, irritable bowel syndrome and other functional conditions alleviated by clinical cannabis. METHODS: Available literature was reviewed, including searches via the National Library of medicine database and other sources. RESULTS: A review of the literature indicates that significant progress has been made since Dr. Ethan B. Russo’s landmark paper, just ten years ago (February 2, 2004).
Investigation at that time suggested that cannabinoids can block spinal, peripheral and gastrointestional mechanisms that promote pain in headache, fibromyalgia, irritable bowel syndrome and muscle spasm.
CONCLUSION: Subsequent research has confirmed that underlying endocannabinoid deficiencies indeed play a role in migraine, fibromyalgia, irritable bowel syndrome and a growing list of other medical conditions. Clinical experience is bearing this out. Further research and especially, clinical trials will further demonstrate the usefulness of medical cannabis. As legal barriers fall and scientific bias fades this will become more apparent.
THC and CBD phytocannabinoids also act as neuroprotective antioxidants against glutamate neurotoxicity and cell death mediated via NMDA, AMPA and kainate receptors [55], independently of cannabinoid receptors, and exceed the antioxidant potency of vitamins C and E. Migraine is a complex neurochemical disorder with myriad effects beyond pain. Its tendency to produce photophobia and phonophobia, even between discrete attacks [56], may be considered suggestive of a “sensory hyperalgesia,” as these normally tolerated sensations take on painful proportions.The combination of endocannabinoids and their inactive precursors have been dubbed an entourage effect [57], and an analogous synergy of phytocannabinoids, cannabis terpenoids and flavonoids has also been suggested and analyzed at some length [58]. The unique attributes of cannabis to affect serotonergic, dopaminergic, opioid, anti-inflammatory, and NMDA mechanisms of migraine, both acutely and prophylactically, have rendered it a proposed “ideal drug” for its treatment [5].
Migraine is a strongly genetic disorder, but similar symptoms are acquired under conditions of closed head injury, where the “post-traumatic syndrome” displays similar symptoms. A protective role of endocannabinoids in such settings is evident in the findings that 2-AG is elevated after experimental brain injury, and that it plays an important neuroprotective role [59].Unfortunately, no organized clinical trials of cannabis in migraine have been performed. While documentation of the use of cannabis for migraine suggests a 4000 year history, and it was a major indication for cannabis medicines in Western society between 1842 and 1942 [5], there have been few modern studies beyond the “anecdotal” [5; 60–62]. Surveys in California indicate that of 2480 patients served by the Oakland Cannabis Buyers’ Club, 127, or 5%, sought cannabis for treatment of chronic migraines [63]. Success rates of some 80% with North American strains of cannabis have been estimated based on clinical contact [5]. Experience in prophylactic use of Marinol® (synthetic THC) in some ten patients was disappointing, with some decrement in frequency and severity of attacks, but not total remission or “cures” claimed by 19th century authors with extracts of Indian hemp [5]. The difference may well be due to a nearly total dearth of cannabidiol in North American cannabis strains [64] (see discussion below), and the observed possibility of CBD modulation of serotonergic function [17]. More formal documentation of clinical efficacy would be distinctly welcome.
Literally every pot head thinks their form is superior to other pot heads.
I know someone who swears CBD fixed his Dupuytren's contracture. His brother got surgery for it, it's a physical build-up of hard tissue in the hand, but he has more mobility just from rubbing CBD on his skin. Thoughts?
Snake oil… fucking seriously.
Potheads are the only believers. Rational people know not to buy into the hype.
Almost all commercially available CBD is hotdog water. CBD is only marginally effective without a THC counterpart, imo. If you are taking CBD only, you're missing out on a lot.
The reason why this haven't fell through and they are only making it Parts in certain areas.
Because it's the game they played!
Politician the War on Drugs is all a joke.
Yes it is a drug problem but it's not these oils.
How about big Pharma how about the great work of investigative journalism Gary Webb. Uncover politicians that brought the heroin and cocaine in the US..
Passing laws for Americans can be addicted to 💊
Now you got overdose so high in America it's unreal.
There is plenty of research since it’s been used for centuries for medical reasons.
7:33 super bad grammar!
Should be: “The public HAS….”
I take it. It works. Some brands better than others
No, not snake oil.. it's weed oil moron
Cbd doses that you find out at stores in gummy form are less than 10 percent the dose needed to actually feel something. Almost always the placebo effect if you eat gas station gummies and think you feel something. You need over 1000 mg to actually start to really feel effects
Cbd= gay
Thc= cool
It’s sad how marijuana enthusiast still won’t admit this is a sham
I live in Canada, a country where it is luckily legal with or without a prescription. Until marijuana became legal in Canada I never risked taking CBD due to my job. I have a chronic illness called Cyclical Vomiting Syndrome (CVS) which causes severe vomiting sometimes for days on end. Often I end up in the hospital with dehydration and often have ulcers. My constant vomiting has caused me to have a large and inoperable hernia in my diaphragm which causes extremely painful acid reflux almost constantly. I have to sleep on a 25% angle (approximately) to keep my stomach acids in my stomach so they don't back up into my esophagus. Anyways. CBD is the only thing that I have found that seems to work getting rid of my acid reflux for a while every day! It allows me to actually get things done and be a normal person. I don't know what I would do without it!
It's science
Obvious Propaganda ! – Always Broadcasting Crap !