Cannabis Chemical Studied as Schizophrenia Treatment
There has been a lot of press lately about the danger of
Cannabis (Marijuana) causing psychosis and triggering schizophrenia. The main ingredient that is thought to be the trigger for psychosis and schizophrenia is "THC" (tetrahydrocannabinol), which is the active ingredient of marijuana which causes the "high".
Over the years in an effort to get a stronger and more powerful marijuana drug with a stronger "punch" to it, cannabis has been grown to have an increasingly greater amount of THC. This has been at the expense of a lesser known active ingredient of cannabis - a cannabinoid called Cannabidiol (CBD). In fact, the strongest (and most harmful) form of marijuana that has hit the streets in Europe, "skunk", is grown with many more times the amount of THC as the older marijuana had, and very little, if any, CBD. Even small doses of THC can produce temporary psychotic symptoms.
It has been found that Cannabidiol may have a calming, stabilizing effect on the brain - which may help to counteract some of the damage in the brain caused by THC.
Researchers hope to formulate a new medication for schizophrenia based on Cannabidiol.
According to a study which compared this active ingredient, Cannabidiol, with a leading antipsychotic drug (Amisulpride), Cannabidiol might inhibit psychotic symptoms in people with schizophrenia, causing fewer side-effects.
Lead researcher of the study, Dr Marcus Leweke, of the University of Cologne, noted:
"There is a possibility that there are good guys and bad guys in cannabis. THC is the bad guy, but there is a small body of literature that suggested CBD may prevent the induction of psychotic symptoms. Our study supports that view."
Read the original source article:
Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug
Thanks goes to Dugal and Tim for bringing this information to our attention.
Related Reading:
Scientists Show How Cannabis / Marijuana May Trigger SchizophreniaDrug-induced Psychosis up 400% in AustraliaCannabis Abuse May Lead to Earlier Schizophrenia Onset, Worse Outcome
Posted by Jeanie Wolfson at May 8, 2007 07:45 AM
More Information on
Schizophrenia Research Journal Articles
This is good news but unfortunately the pro-cannabis idiots will probably use this as an excuse to continue.
An interesting point is that we know cannabis is a herb and herbs contain a spectrum of chemicals may therefore other psychoactive herbs contain in addition to their mind bending chemicals also antipsychotic type chemicals.
Posted by:
Matt at May 8, 2007 11:37 AM
i agree with Matt. it has already happened. son was able to get cannibas at the legal cannibas club in california. without dr. note or anything. when i e-mailed and alerted them about the detriment this drug causes to schiz, over and over again article after article...they sent back this very article. not surprising. forget all the other articles -dozens- that say otherwise...
Posted by:
ginny at May 11, 2007 07:30 PM
That's why it is important this article has the research from the original with the DISCUSSION linking it back to the other articles (ie the research in context).
It was this very article on schizophrenia.com, that FINALLY got through to a young close family friend about the dangers of smoking pot. It was because the others were just saying its bad its bad its bad and many young people really resent that. This one that said look - there is a good chemical in it that might help counteract the bad chemical, but it is such a small amount, and for some people it only takes a small amount of the bad chemical to do irreprable damage, and in some pot that good chemical is even lacking.... that FINALLY got through to him BECAUSE it presented a wider range of fact... BECAUSE it mentioned the good chemical and talked about both.
Interesting how the same news can be taken in such different ways. Part of the problem is that the original article didn't quite tie it all together with the other research like the one on this website did. The folks at the "medical marijuana" place took research out of context. It helps some to present a more scientific picture.... for others, they will twist anything.
-Naomi
Posted by:
Naomi at May 13, 2007 04:59 AM
Cannabinoids (marijuana…) are known to inhibit calcium channels- glutamate release in schizophrenia
It is generally accepted that the influx of Ca2+ as a result of excessive activation of the NMDA receptor underlies the toxic actions of glutamate in many systems. During periods of ischemia and in many neurodegenerative diseases, excessive stimulation of glutamate receptors is thought to occur. These neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease…, are caused by different mechanisms but may share a final common pathway to neuronal injury due to the overstimulation of glutamate receptors, especially of the NMDA subtype. On the other hand , recently, a hypofunction of glutamatergic neurons has been hypothesized to caused schizophrenia. Functional diversity of NMDA receptors may be expected from the assembly of different subunit combinations, and there is very important „Ca2+-dependent manner” which permits activation of NMDA receptors. So, also dietary calcium deficiency can be important about „NMDA hypofunction“ in schizophrenia…
However, there can be another example about hypoglutamatergic condition; cannabinoids are known to inhibit Ca2+ channels- glutamate release in schizophrenia. Cannabinoids are a group of terpenophenolic compounds present in Cannabis sativa L. Natural cannabinoids are only known to occur naturally in the cannabis plant. The chemical tetrahydrocannabinol (THC) found in marijuana is a cannabinoid, though different from the endogenous cannabinoids naturally produced in the bodies of animals. The broader definition of cannabinoids refer to a group of substances that are structurally related to THC or that bind to cannabinoid receptors. THC is the primary psychoactive component of the plant ,medically, it appears to ease moderate pain and to be neuroprotective. Endocannabinoids serve as intercellular 'lipid messengers', signaling molecules that are released from one cell and activate the cannabinoid receptors present on other nearby cells. So, cannabinoids are naturally occurring compounds in vertebrates, and are known to play an important role in intercellular signaling. In 1992, the first such compound was identified as arachidonoyl ethanolamide and named anandamide. It has a pharmacology similar to THC, although its chemical structure is different.
THC mediates the majority of its activities through stimulation of cannabinoid receptors (CB). Two cannabinoid receptors, CB1 and CB2, were discovered only the last ten years. CB1 exists primarily in the central nervous system, while CB2 is found primarily in the peripheral nervous system. Also, endogenous anandamide binds to both the central (CB1) and peripheral (CB2) cannabinoid receptors, and is found in nearly all tissues in a wide range of animals, it is about as potent as THC. Activation of CB1 receptor inhibits neurotransmitter release in many brain regions. CB1 receptors are essentially absent in the medulla oblongata, the part of the brain stem that is responsible for respiratory and cardiovascular functions. Thus, there is not a risk of respiratory or cardiovascular failure as there is with many other drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis.
Some studies suggest that cannabis is neither a sufficient nor necessary factor in developing schizophrenia, but that cannabis may significantly increase the risk of developing schizophrenia and may be, among other things, a significant causal factor. Nevertheless, some previous research in this area has been criticised as it has often not been clear whether cannabis use is a cause or effect of schizophrenia. The goal of this article is to show that cannabis use can be a cause of schizophrenia; characterize two effects on NMDA hypofunction, related to schizophrenia-associated neurodegenerative impairment. See also website www.bse-expert.cz , chapter; Hyperfunction (Alzheimer’s disease and Parkinson disease) and hypofunction (schizophrenia) of glutamatergic neurons;
1. Cannabinoids activity about NMDA glutamate receptor hypofunction; as a ´ schizophreniform effect;
In expression systems and cell bodies, CB1 receptor couples to activation of K+ channels or inhibition of neuronal Ca2+ channels, or both. Either of these mechanisms can reduce Ca2+ influx at nerve terminals and thereby inhibit transmitter release. Activation of K+ channels may change the presynaptic action potential and thus indirectly modulate Ca2+ channel activity. So, communication between the cells requires the release of a glutamate neurotransmitter, triggered by calcium currents passing through a specific Ca2+ channel. Cannabinoids are known to inhibit Ca2+ channels. If we shut down the channel, we shut down the release of glutamate, and profoundly alter the cell's ability to signal.
2. Cannabinoids can regulate NMDA glutamate receptor by reducing intracellular Ca2+ release ; as a neuroprotective effect;
There is evidence that cannabinoids can regulate glutamate release, oxidant free radicals and calcium influxes, which, in excess, can cause neuronal death. Cannabinoids can tonically regulate NMDA glutamate receptor activity in vitro and support the in vivo observation that CB1 regulates NMDA-induced and ischaemic excitotoxicity. Exogenously administered cannabinoids are neuroprotective in several different cellular and animal models. Cannabinoids produce neuroprotection by reducing intracellular Ca2+ release. Emerging evidence indicates that cannabinoids may play a role in slowing the progression of certain neurodegenerative diseases, such as Multiple Sclerosis, Parkinson's disease, Alzheimer's, and Amyotrophic Lateral Sclerosis.
Posted by:
Josef Hlasny at June 19, 2007 01:49 PM
Young people develop schizophenia when they stop taking cannabis. They are very well when taking cannabis. The reason I feel is 1} cabbabis is plagued with fungi causing candida. 2} Candida causes macrophage activation{inflammation} 3} macrophage activation causes glutamate release BUT at the same time cannabis reduces glutamte activation. SO youngsters who have a unhealthy gut {candida}in the first place feel well on cannabis but when they stop taking it their guts have deteriorated badly and hence they they end up with even greater macrophage activation and inflammation and even more glutamate released in their brains causing the schizophrenia. I feel sure this is what is happening and is why some people are OK on cannabis and some are not. Please give me you response P S the youngsters who are suseptible to this are the ones who have food allergies probably milk and gluten leaving them with unhealthy guts.
Posted by:
pamela flavell at February 28, 2008 02:30 PM
An interesting point is that we know cannabis is a herb and herbs contain a spectrum of chemicals may therefore other psychoactive herbs contain in addition to their mind bending chemicals also antipsychotic type chemicals.
It was this very article on schizophrenia.com, that FINALLY got through to a young close family friend about the dangers of smoking pot. It was because the others were just saying its bad its bad its bad and many young people really resent that. This one that said look - there is a good chemical in it that might help counteract the bad chemical, but it is such a small amount, and for some people it only takes a small amount of the bad chemical to do irreprable damage, and in some pot that good chemical is even lacking.... that FINALLY got through to him BECAUSE it presented a wider range of fact... BECAUSE it mentioned the good chemical and talked about both.
Interesting how the same news can be taken in such different ways. Part of the problem is that the original article didn't quite tie it all together with the other research like the one on this website did. The folks at the "medical marijuana" place took research out of context. It helps some to present a more scientific picture.... for others, they will twist anything.
-Naomi
Cannabinoids (marijuana…) are known to inhibit calcium channels- glutamate release in schizophrenia
It is generally accepted that the influx of Ca2+ as a result of excessive activation of the NMDA receptor underlies the toxic actions of glutamate in many systems. During periods of ischemia and in many neurodegenerative diseases, excessive stimulation of glutamate receptors is thought to occur. These neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease…, are caused by different mechanisms but may share a final common pathway to neuronal injury due to the overstimulation of glutamate receptors, especially of the NMDA subtype. On the other hand , recently, a hypofunction of glutamatergic neurons has been hypothesized to caused schizophrenia. Functional diversity of NMDA receptors may be expected from the assembly of different subunit combinations, and there is very important „Ca2+-dependent manner” which permits activation of NMDA receptors. So, also dietary calcium deficiency can be important about „NMDA hypofunction“ in schizophrenia…
However, there can be another example about hypoglutamatergic condition; cannabinoids are known to inhibit Ca2+ channels- glutamate release in schizophrenia. Cannabinoids are a group of terpenophenolic compounds present in Cannabis sativa L. Natural cannabinoids are only known to occur naturally in the cannabis plant. The chemical tetrahydrocannabinol (THC) found in marijuana is a cannabinoid, though different from the endogenous cannabinoids naturally produced in the bodies of animals. The broader definition of cannabinoids refer to a group of substances that are structurally related to THC or that bind to cannabinoid receptors. THC is the primary psychoactive component of the plant ,medically, it appears to ease moderate pain and to be neuroprotective. Endocannabinoids serve as intercellular 'lipid messengers', signaling molecules that are released from one cell and activate the cannabinoid receptors present on other nearby cells. So, cannabinoids are naturally occurring compounds in vertebrates, and are known to play an important role in intercellular signaling. In 1992, the first such compound was identified as arachidonoyl ethanolamide and named anandamide. It has a pharmacology similar to THC, although its chemical structure is different.
THC mediates the majority of its activities through stimulation of cannabinoid receptors (CB). Two cannabinoid receptors, CB1 and CB2, were discovered only the last ten years. CB1 exists primarily in the central nervous system, while CB2 is found primarily in the peripheral nervous system. Also, endogenous anandamide binds to both the central (CB1) and peripheral (CB2) cannabinoid receptors, and is found in nearly all tissues in a wide range of animals, it is about as potent as THC. Activation of CB1 receptor inhibits neurotransmitter release in many brain regions. CB1 receptors are essentially absent in the medulla oblongata, the part of the brain stem that is responsible for respiratory and cardiovascular functions. Thus, there is not a risk of respiratory or cardiovascular failure as there is with many other drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis.
Some studies suggest that cannabis is neither a sufficient nor necessary factor in developing schizophrenia, but that cannabis may significantly increase the risk of developing schizophrenia and may be, among other things, a significant causal factor. Nevertheless, some previous research in this area has been criticised as it has often not been clear whether cannabis use is a cause or effect of schizophrenia. The goal of this article is to show that cannabis use can be a cause of schizophrenia; characterize two effects on NMDA hypofunction, related to schizophrenia-associated neurodegenerative impairment. See also website www.bse-expert.cz , chapter; Hyperfunction (Alzheimer’s disease and Parkinson disease) and hypofunction (schizophrenia) of glutamatergic neurons;
1. Cannabinoids activity about NMDA glutamate receptor hypofunction; as a ´ schizophreniform effect;
In expression systems and cell bodies, CB1 receptor couples to activation of K+ channels or inhibition of neuronal Ca2+ channels, or both. Either of these mechanisms can reduce Ca2+ influx at nerve terminals and thereby inhibit transmitter release. Activation of K+ channels may change the presynaptic action potential and thus indirectly modulate Ca2+ channel activity. So, communication between the cells requires the release of a glutamate neurotransmitter, triggered by calcium currents passing through a specific Ca2+ channel. Cannabinoids are known to inhibit Ca2+ channels. If we shut down the channel, we shut down the release of glutamate, and profoundly alter the cell's ability to signal.
2. Cannabinoids can regulate NMDA glutamate receptor by reducing intracellular Ca2+ release ; as a neuroprotective effect;
There is evidence that cannabinoids can regulate glutamate release, oxidant free radicals and calcium influxes, which, in excess, can cause neuronal death. Cannabinoids can tonically regulate NMDA glutamate receptor activity in vitro and support the in vivo observation that CB1 regulates NMDA-induced and ischaemic excitotoxicity. Exogenously administered cannabinoids are neuroprotective in several different cellular and animal models. Cannabinoids produce neuroprotection by reducing intracellular Ca2+ release. Emerging evidence indicates that cannabinoids may play a role in slowing the progression of certain neurodegenerative diseases, such as Multiple Sclerosis, Parkinson's disease, Alzheimer's, and Amyotrophic Lateral Sclerosis.