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Does GABA reduce inflammation?

Nielk

Senior Member
Messages
6,970
I have been suffering from acute symptoms of inflammation. This happened soon after I have been
detoxed off of Klonpin three months ago and it has been getting worse as time passes by.

someone told me to look into the fact whether GABA enhancement helps with inflammation and I found this link http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2235846/



Hypothesis

We propose a hypothesis for an inefficient GABA signaling system that results in unchecked proinflammatory cytokine production via the p38 MAPK pathway. This model also supports the need for increasing research in the integration of immunology and neuroscience.

Possible influence of GABA on p38 MAPK pathway in rheumatoid arthritis. This figure illustrates a possible model for how GABA can inhibit the production of proinflammatory cytokines. All molecules are listed by their official gene name.

Does anyone know about this?
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,076
Location
australia (brisbane)
NMDA is said to increase inflammation etc etc and gaba agonists said to have NMDA antagonist properties.
Also of interest is that other NMDA antagonist are said to reduce benzo tolerance, so there is definately a relation between gaba, NMDA and inflammation.
google dextromethorphan(cough medicine) and NMDA antagonist, also said to help with pain and studies done with fibro on this too.

cheers!!!
 

Nielk

Senior Member
Messages
6,970
Thanks heapsreal. I will look this up.
Do you have personal experience with dextromethorphan?
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,076
Location
australia (brisbane)
Thanks heapsreal. I will look this up.
Do you have personal experience with dextromethorphan?
yes been using it for a few weeks, the first week i stopped all benzo meds(only on lowest dose), although it didnt help me sleep i think it helps with symptoms from not using benzo's and does help with nerve/tingling type pain i get under my skin on neck and shoulders. since adding benzo meds back, i take dextro 1/2 hr before benzo sleep meds, but only using benzo's every second or third night for sleep now. when using benzo's for sleep it seems to help them to work without tolerence for now. prior to using the dextro(DXM) my sleep meds werent working at all, so the week off as well as the dxm i think helped. DXM i think helps with that buzzing type feeling in your head from sleep deprivation. When trying to find info on this, alot of the stuff is from people using it to lower their tolerence to benzo's so they can get high,im not doing this though, plus using really high doses of DXM, im only using 40mg which is the lowest dose i read that helps benzo tolerence. When not using benzos for sleep im using a low dose of seroquel with trazadone or mirtazapine or an antihistamine,occassionally use baclofen.
 

Nielk

Senior Member
Messages
6,970
I found this link showing a connection with GABA as an anti-inflammatory:

Could this be the reason why GcMaf works especially well on intestinal issues?

http://www.eurekalert.org/pub_releases/2012-06/asfm-ibp061312.php



Intestinal bacteria produce neurotransmitter, could play role in inflammation



Researchers at Baylor College of Medicine and Texas Children's Hospital have identified commensal bacteria in the human intestine that produce a neurotransmitter that may play a role in preventing or treating inflammatory bowel diseases such as Crohn's disease.
"We identified, to our knowledge, the first bifidobacterial strain, Bifidobacterium dentium, that is capable of secreting large amounts of gamma-aminobutyric acid (GABA). This molecule is a major inhibitory neurotransmitter in the central and enteric nervous systems," says Karina Pokusaeva, a researcher on the study and a member of the laboratory of James Versalovic.
GABA is one of the chief inhibitory neurotransmitters in the human central nervous system. It plays a role in regulating pain and some pain relieving drugs currently on the market act by targeting GABA receptors on neural cells.
Pokusaeva and her colleagues were interested in understanding the role the human microbiome might play in pain and scanned the genomes of potentially beneficial intestinal microorganisms, identified by the Human Microbiome Project, for evidence of a gene that would allow them to create GABA.
"Lab analysis of metagenomic DNA sequencing data allowed us to demonstrate that microbial glutamate decarboxylase encoding gene is very abundant in intestinal microbiota as compared to other body sites," says Pokusaeva. One of the most prolific producers of GABA was B. dentium, which appears to secrete the compound to help it survive the acid environment.
In addition to its pain modulating properties, GABA may also be capable of inhibiting inflammation. Recent studies have shown that immune cells called macrophages also possess GABA receptors. When these receptors were activated on the macrophages there was a decrease in the production of compounds responsible for inflammation.
"Our lab was curious to explore if GABA produced by intestinal human isolate B. dentium could have an effect on GABA receptors present in immune cells," says Pokusaeva. Together with their collaborators Dr. Yamada and Dr. Lacorazza they found that when the cells were exposed to secretions from the bacteria, they exhibited increased expression of the GABAA receptor in the immune cells.
While the findings are preliminary, they suggest the possibility that B. dentium and the compounds it secretes could play a role in reducing inflammation associated with inflammatory bowel diseases.
The next step, says Pokusaeva is to conduct in vitro experiments to determine if the increased GABAA expression correlates with a decrease in production of cytokines associated with inflammation. GABAA receptor signaling may also contribute to pain signaling in the gut and may somehow be involved in abdominal pain disorders.
"Our preliminary findings suggest that Bifidobacterium dentium could potentially have an inhibitory role in inflammation; however more research has to be performed to further prove our hypothesis," says Pokusaeva.

###

Dr. Pokusaeva will participate in a live webcast media availability to discuss her research on Sunday, June 17, 2012 at 1:00 p.m. EDT. The webcast can be found online atwww.microbeworld.org/asmlive.
This research was presented as part of the 2012 General Meeting of the American Society for Microbiology held June 16-19, 2012 in San Francisco, California. A full press kit for the meeting, including tipsheets and additional press releases, can be found online at http://bit.ly/asm2012pk.
The American Society for Microbiology is the largest single life science society, composed of over 39,000 scientists and health professionals. ASM's mission is to advance the microbiological sciences as a vehicle for understanding life processes and to apply and communicate this knowledge for the improvement of health and environmental and economic well-being worldwide.
 

Nielk

Senior Member
Messages
6,970
I found this link showing a connection with GABA as an anti-inflammatory:

Could this be the reason why GcMaf works especially well on intestinal issues?

http://www.eurekalert.org/pub_releases/2012-06/asfm-ibp061312.php



Intestinal bacteria produce neurotransmitter, could play role in inflammation



Researchers at Baylor College of Medicine and Texas Children's Hospital have identified commensal bacteria in the human intestine that produce a neurotransmitter that may play a role in preventing or treating inflammatory bowel diseases such as Crohn's disease.
"We identified, to our knowledge, the first bifidobacterial strain, Bifidobacterium dentium, that is capable of secreting large amounts of gamma-aminobutyric acid (GABA). This molecule is a major inhibitory neurotransmitter in the central and enteric nervous systems," says Karina Pokusaeva, a researcher on the study and a member of the laboratory of James Versalovic.
GABA is one of the chief inhibitory neurotransmitters in the human central nervous system. It plays a role in regulating pain and some pain relieving drugs currently on the market act by targeting GABA receptors on neural cells.
Pokusaeva and her colleagues were interested in understanding the role the human microbiome might play in pain and scanned the genomes of potentially beneficial intestinal microorganisms, identified by the Human Microbiome Project, for evidence of a gene that would allow them to create GABA.
"Lab analysis of metagenomic DNA sequencing data allowed us to demonstrate that microbial glutamate decarboxylase encoding gene is very abundant in intestinal microbiota as compared to other body sites," says Pokusaeva. One of the most prolific producers of GABA was B. dentium, which appears to secrete the compound to help it survive the acid environment.
In addition to its pain modulating properties, GABA may also be capable of inhibiting inflammation. Recent studies have shown that immune cells called macrophages also possess GABA receptors. When these receptors were activated on the macrophages there was a decrease in the production of compounds responsible for inflammation.
"Our lab was curious to explore if GABA produced by intestinal human isolate B. dentium could have an effect on GABA receptors present in immune cells," says Pokusaeva. Together with their collaborators Dr. Yamada and Dr. Lacorazza they found that when the cells were exposed to secretions from the bacteria, they exhibited increased expression of the GABAA receptor in the immune cells.
While the findings are preliminary, they suggest the possibility that B. dentium and the compounds it secretes could play a role in reducing inflammation associated with inflammatory bowel diseases.
The next step, says Pokusaeva is to conduct in vitro experiments to determine if the increased GABAA expression correlates with a decrease in production of cytokines associated with inflammation. GABAA receptor signaling may also contribute to pain signaling in the gut and may somehow be involved in abdominal pain disorders.
"Our preliminary findings suggest that Bifidobacterium dentium could potentially have an inhibitory role in inflammation; however more research has to be performed to further prove our hypothesis," says Pokusaeva.

###

Dr. Pokusaeva will participate in a live webcast media availability to discuss her research on Sunday, June 17, 2012 at 1:00 p.m. EDT. The webcast can be found online atwww.microbeworld.org/asmlive.
This research was presented as part of the 2012 General Meeting of the American Society for Microbiology held June 16-19, 2012 in San Francisco, California. A full press kit for the meeting, including tipsheets and additional press releases, can be found online at http://bit.ly/asm2012pk.
The American Society for Microbiology is the largest single life science society, composed of over 39,000 scientists and health professionals. ASM's mission is to advance the microbiological sciences as a vehicle for understanding life processes and to apply and communicate this knowledge for the improvement of health and environmental and economic well-being worldwide.
 

xks201

Senior Member
Messages
740
I'm not sure how effective gaba is at reducing inflammation. You would think that if a gaba deficiency was the cause of inflammation that it would reverse CFS symptoms but clearly it does not.