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Research Cannabis To Treat Anxiety

CarolKing

Always in search of the perfect vaporizer
Natural chemical helps brain adapt to stress
Date:
March 29, 2017
Source:
Vanderbilt University Medical Center
Summary:
A natural signaling molecule that activates cannabinoid receptors in the brain plays a critical role in stress-resilience -- the ability to adapt to repeated and acute exposures to traumatic stress.
Share:
Materials provided by Vanderbilt University Medical Center. Original written by Bill Snyder. Note: Content may be edited for style and length.

A natural signaling molecule that activates cannabinoid receptors in the brain plays a critical role in stress-resilience -- the ability to adapt to repeated and acute exposures to traumatic stress, according to researchers at Vanderbilt University Medical Center.

The findings in a mouse model could have broad implications for the potential treatment and prevention of mood and anxiety disorders, including major depression and post-traumatic stress disorder (PTSD), they reported in the journal Nature Communications.

"The study suggests that deficiencies in natural cannabinoids could result in a predisposition to developing PTSD and depression," said Sachin Patel, M.D., Ph.D., director of the Division of Addiction Psychiatry at Vanderbilt University School of Medicine and the paper's corresponding author.

"Boosting this signaling system could represent a new treatment approach for these stress-linked disorders," he said.

Patel, the James G. Blakemore Professor of Psychiatry, received a Presidential Early Career Award for Scientists and Engineers last year for his pioneering studies of the endocannabinoid family of signaling molecules that activate the CB1 and CB2 cannabinoid receptors in the brain.

Tetrahydrocannabinol (THC), the active compound in marijuana, binds the CB1 receptor, which may explain why relief of tension and anxiety is the most common reason cited by people who use marijuana chronically.

Patel and his colleagues previously have found CB1 receptors in the amygdala, a key emotional hub in the brain involved in regulating anxiety and the fight-or-flight response. They also showed in animal models that anxiety increases when the CB1 receptor is blocked by a drug or its gene is deleted.

More recently they reported anxiety-like and depressive behaviors in genetically modified mice that had an impaired ability to produce 2-arachidonoylglycerol (2-AG), the most abundant endocannabinoid. When the supply of 2-AG was increased by blocking an enzyme that normally breaks it down, the behaviors were reversed.

In the current study, the researchers tested the effects of increasing or depleting the supply of 2-AG in the amygdala in two populations of mice: one previously determined to be susceptible to the adverse consequences of acute stress, and the other which exhibited stress-resilience.

Augmenting the 2-AG supply increased the proportion of stress-resilient mice overall and promoted resilience in mice that were previously susceptible to stress, whereas depleting 2-AG rendered previously stress-resilient mice susceptible to developing anxiety-like behaviors after exposure to acute stress.

Taken together, these results suggest that 2-AG signaling through the CB1 receptor in the amygdala promotes resilience to the adverse effects of acute traumatic stress exposure, and support previous findings in animal models and humans suggesting that 2-AG deficiency could contribute to development of stress-related psychiatric disorders.

Marijuana use is highly cited by patients with PTSD as a way to control symptoms. Similarly, the Vanderbilt researchers found that THC promoted stress-resilience in previously susceptible mice.

However, marijuana use in psychiatric disorders has obvious drawbacks including possible addiction and cognitive side effects, among others. The Vanderbilt study suggests that increasing production of natural cannabinoids may be an alternative strategy to harness the therapeutic potential of this signaling system.

Journal Reference:

  1. Rebecca J. Bluett, Rita Báldi, Andre Haymer, Andrew D. Gaulden, Nolan D. Hartley, Walker P. Parrish, Jordan Baechle, David J. Marcus, Ramzi Mardam-Bey, Brian C. Shonesy, Md. Jashim Uddin, Lawrence J. Marnett, Ken Mackie, Roger J. Colbran, Danny G. Winder, Sachin Patel. Endocannabinoid signalling modulates susceptibility to traumatic stress exposure. Nature Communications, 2017; 8: 14782 DOI: 10.1038/ncomms14782
 

herbivore21

Well-Known Member
Natural chemical helps brain adapt to stress
Date:
March 29, 2017
Source:
Vanderbilt University Medical Center
Summary:
A natural signaling molecule that activates cannabinoid receptors in the brain plays a critical role in stress-resilience -- the ability to adapt to repeated and acute exposures to traumatic stress.
Share:
Materials provided by Vanderbilt University Medical Center. Original written by Bill Snyder. Note: Content may be edited for style and length.

A natural signaling molecule that activates cannabinoid receptors in the brain plays a critical role in stress-resilience -- the ability to adapt to repeated and acute exposures to traumatic stress, according to researchers at Vanderbilt University Medical Center.

The findings in a mouse model could have broad implications for the potential treatment and prevention of mood and anxiety disorders, including major depression and post-traumatic stress disorder (PTSD), they reported in the journal Nature Communications.

"The study suggests that deficiencies in natural cannabinoids could result in a predisposition to developing PTSD and depression," said Sachin Patel, M.D., Ph.D., director of the Division of Addiction Psychiatry at Vanderbilt University School of Medicine and the paper's corresponding author.

"Boosting this signaling system could represent a new treatment approach for these stress-linked disorders," he said.

Patel, the James G. Blakemore Professor of Psychiatry, received a Presidential Early Career Award for Scientists and Engineers last year for his pioneering studies of the endocannabinoid family of signaling molecules that activate the CB1 and CB2 cannabinoid receptors in the brain.

Tetrahydrocannabinol (THC), the active compound in marijuana, binds the CB1 receptor, which may explain why relief of tension and anxiety is the most common reason cited by people who use marijuana chronically.

Patel and his colleagues previously have found CB1 receptors in the amygdala, a key emotional hub in the brain involved in regulating anxiety and the fight-or-flight response. They also showed in animal models that anxiety increases when the CB1 receptor is blocked by a drug or its gene is deleted.

More recently they reported anxiety-like and depressive behaviors in genetically modified mice that had an impaired ability to produce 2-arachidonoylglycerol (2-AG), the most abundant endocannabinoid. When the supply of 2-AG was increased by blocking an enzyme that normally breaks it down, the behaviors were reversed.

In the current study, the researchers tested the effects of increasing or depleting the supply of 2-AG in the amygdala in two populations of mice: one previously determined to be susceptible to the adverse consequences of acute stress, and the other which exhibited stress-resilience.

Augmenting the 2-AG supply increased the proportion of stress-resilient mice overall and promoted resilience in mice that were previously susceptible to stress, whereas depleting 2-AG rendered previously stress-resilient mice susceptible to developing anxiety-like behaviors after exposure to acute stress.

Taken together, these results suggest that 2-AG signaling through the CB1 receptor in the amygdala promotes resilience to the adverse effects of acute traumatic stress exposure, and support previous findings in animal models and humans suggesting that 2-AG deficiency could contribute to development of stress-related psychiatric disorders.

Marijuana use is highly cited by patients with PTSD as a way to control symptoms. Similarly, the Vanderbilt researchers found that THC promoted stress-resilience in previously susceptible mice.

However, marijuana use in psychiatric disorders has obvious drawbacks including possible addiction and cognitive side effects, among others. The Vanderbilt study suggests that increasing production of natural cannabinoids may be an alternative strategy to harness the therapeutic potential of this signaling system.

Journal Reference:

  1. Rebecca J. Bluett, Rita Báldi, Andre Haymer, Andrew D. Gaulden, Nolan D. Hartley, Walker P. Parrish, Jordan Baechle, David J. Marcus, Ramzi Mardam-Bey, Brian C. Shonesy, Md. Jashim Uddin, Lawrence J. Marnett, Ken Mackie, Roger J. Colbran, Danny G. Winder, Sachin Patel. Endocannabinoid signalling modulates susceptibility to traumatic stress exposure. Nature Communications, 2017; 8: 14782 DOI: 10.1038/ncomms14782
Great stuff! Thanks for sharing @CarolKing


However, marijuana use in psychiatric disorders has obvious drawbacks including possible addiction and cognitive side effects, among others. The Vanderbilt study suggests that increasing production of natural cannabinoids may be an alternative strategy to harness the therapeutic potential of this signaling system.
I should add here that these are not really 'limitations'.

Cognitive side effects of even high THC containing cannabis derivatives are mild, and very well tolerated when compared to other psychiatric medications prescribed for these conditions (I am sure all of you who've got these conditions and been prescribed pharma will have plenty of stories to tell about this!). Cannabis 'addiction' is also a very controversial topic in the psychiatric literature, and not all researchers agree that it even exists.

Most crucially, the phytocannabinoid which acts most similarly on the endocannabinoid receptors (CB2 primarily) to 2-AG is actually CBD. CBD is obviously not correlated with the abovementioned side effects.
 
Last edited:

Baron23

Well-Known Member
Natural chemical helps brain adapt to stress
Date:
March 29, 2017
Source:
Vanderbilt University Medical Center
Summary:
A natural signaling molecule that activates cannabinoid receptors in the brain plays a critical role in stress-resilience -- the ability to adapt to repeated and acute exposures to traumatic stress.
Share:
Materials provided by Vanderbilt University Medical Center. Original written by Bill Snyder. Note: Content may be edited for style and length.

A natural signaling molecule that activates cannabinoid receptors in the brain plays a critical role in stress-resilience -- the ability to adapt to repeated and acute exposures to traumatic stress, according to researchers at Vanderbilt University Medical Center.

The findings in a mouse model could have broad implications for the potential treatment and prevention of mood and anxiety disorders, including major depression and post-traumatic stress disorder (PTSD), they reported in the journal Nature Communications.

"The study suggests that deficiencies in natural cannabinoids could result in a predisposition to developing PTSD and depression," said Sachin Patel, M.D., Ph.D., director of the Division of Addiction Psychiatry at Vanderbilt University School of Medicine and the paper's corresponding author.

"Boosting this signaling system could represent a new treatment approach for these stress-linked disorders," he said.

Patel, the James G. Blakemore Professor of Psychiatry, received a Presidential Early Career Award for Scientists and Engineers last year for his pioneering studies of the endocannabinoid family of signaling molecules that activate the CB1 and CB2 cannabinoid receptors in the brain.

Tetrahydrocannabinol (THC), the active compound in marijuana, binds the CB1 receptor, which may explain why relief of tension and anxiety is the most common reason cited by people who use marijuana chronically.

Patel and his colleagues previously have found CB1 receptors in the amygdala, a key emotional hub in the brain involved in regulating anxiety and the fight-or-flight response. They also showed in animal models that anxiety increases when the CB1 receptor is blocked by a drug or its gene is deleted.

More recently they reported anxiety-like and depressive behaviors in genetically modified mice that had an impaired ability to produce 2-arachidonoylglycerol (2-AG), the most abundant endocannabinoid. When the supply of 2-AG was increased by blocking an enzyme that normally breaks it down, the behaviors were reversed.

In the current study, the researchers tested the effects of increasing or depleting the supply of 2-AG in the amygdala in two populations of mice: one previously determined to be susceptible to the adverse consequences of acute stress, and the other which exhibited stress-resilience.

Augmenting the 2-AG supply increased the proportion of stress-resilient mice overall and promoted resilience in mice that were previously susceptible to stress, whereas depleting 2-AG rendered previously stress-resilient mice susceptible to developing anxiety-like behaviors after exposure to acute stress.

Taken together, these results suggest that 2-AG signaling through the CB1 receptor in the amygdala promotes resilience to the adverse effects of acute traumatic stress exposure, and support previous findings in animal models and humans suggesting that 2-AG deficiency could contribute to development of stress-related psychiatric disorders.

Marijuana use is highly cited by patients with PTSD as a way to control symptoms. Similarly, the Vanderbilt researchers found that THC promoted stress-resilience in previously susceptible mice.

However, marijuana use in psychiatric disorders has obvious drawbacks including possible addiction and cognitive side effects, among others. The Vanderbilt study suggests that increasing production of natural cannabinoids may be an alternative strategy to harness the therapeutic potential of this signaling system.

Journal Reference:

  1. Rebecca J. Bluett, Rita Báldi, Andre Haymer, Andrew D. Gaulden, Nolan D. Hartley, Walker P. Parrish, Jordan Baechle, David J. Marcus, Ramzi Mardam-Bey, Brian C. Shonesy, Md. Jashim Uddin, Lawrence J. Marnett, Ken Mackie, Roger J. Colbran, Danny G. Winder, Sachin Patel. Endocannabinoid signalling modulates susceptibility to traumatic stress exposure. Nature Communications, 2017; 8: 14782 DOI: 10.1038/ncomms14782
Thanks for posting this, @CarolKing !

I know from reading that many find MJ to help with their anxiety. As for me, I have been diagnosed quite some time ago with chronic anxiety (hey, who knew....I've been like this my whole life) and I have to be careful as some cannabis products sends my anxiety through the roof....particularly in social situations.

It seems to be that individual brain chemistry is so varied that its tenuous to extrapolate from a mouse experiment to all humans. But I hope this is a good avenue of research that will eventually really help people with PSTD.
 

herbivore21

Well-Known Member
I know from reading that many find MJ to help with their anxiety. As for me, I have been diagnosed quite some time ago with chronic anxiety (hey, who knew....I've been like this my whole life) and I have to be careful as some cannabis products sends my anxiety through the roof....particularly in social situations.
Man we are so very alike in all aspects of this!

It seems to be that individual brain chemistry is so varied that its tenuous to extrapolate from a mouse experiment to all humans. But I hope this is a good avenue of research that will eventually really help people with PSTD.
This is an important comment. Whilst what I said above in relation is demonstrable in humans, the original study is what we call 'pre-clinical', as in it does not work with human subjects. Whilst most good medical science is first supported by these pre-clinical studies, we would ideally like to see this study replicated with human beings to confirm the usefulness of the application :peace: This is a very recent study and given the results, I am sure testing with human subjects could be justified on the merits of the research topic, we may do well to watch this space!
 

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