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Possible role for glutamic acid decarboxylase in fibromyalgia symptoms: A conceptual model for chronic pain – Source: Medical Hypotheses, Jun 17, 2011

  [ 10 votes ]   [ 3 Comments ]
By Caris T Fitzgerald, Lawrence P Carter • www.ProHealth.com • June 26, 2011


Fibromyalgia (FM) is a condition of chronic generalized musculo-skeletal pain that is thought to be a disorder of central pain sensitization. A number of neurotransmitters [chemicals] in the ascending and descending pain pathways have been implicated in FM including glutamate and GABA.

Glutamic acid decarboxylase (GAD) is the rate-limiting enzyme in the conversion of glutamate to GABA [considered “the cornerstone of the body’s calming system”], and decreased expression or activity of this enzyme could result in an imbalance of excitatory and inhibitory neurotransmission in the ascending and descending pain pathways.

Specifically, the expression and activity of the predominant isoform of GAD (GAD65) is influenced by several factors that are associated with FM such as female sex, poor diet, obesity, sedentary lifestyle, and stress.

We hypothesize that decreased GAD expression and/or activity plays a role in the development and exacerbation of FM leading to impairments in the three common domains of FM symptomatology: increased pain (hyperalgesia and allodynia), disrupted sleep, and disturbances in mood (anxiety and depression).

There are several lines of evidence that appear to support a role of GAD in FM.

First, the defining symptom of FM is pain - and GAD65 knockout mice have been shown to exhibit supraspinal hyperalgesia.

Second, GAD has been implicated in disorders of muscle stiffness and rigidity - and morning stiffness is a common symptom of FM.

Third, stress, depression, and anxiety, which are often comorbid with FM, decrease GAD activity.

Fourth, FM is associated with poor sleep, specifically disrupted non-rapid eye movement (NREM) sleep - and the pharmacological induction of NREM sleep is associated with the activation of GAD-containing neurons in the preoptic hypothalamus.

Fifth, FM is more commonly diagnosed in women than men - and the activity of GAD is reduced by low levels of its cofactor pyroxidine, which is less well-absorbed by women and can be further lowered by diet, tobacco, and alcohol intake.

Sixth, FM patients tend to be overweight or obese - and caloric restriction and exercise have been shown to increase GAD expression and activity.

These six general lines of evidence suggest that GAD expression and/or activity might underlie the pathophysiology of FM.

If this hypothesis is supported by future empirical studies, our understanding of the etiology of FM could be greatly improved.

Moreover, behavioral and pharmacological therapies that modulate or mimic the effects of GAD might hold promise for the treatment of this debilitating and poorly understood disorder.

Source: Medical Hypotheses, Jun 17, 2011. PMID: 21684692, by Fitzgerald CT, Carter LP. Department of Psychiatry, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA. [Email: LCarter2@uams.edu]





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Article Comments Post a Comment

Gad and Gaba
Posted by: IanH
Jun 27, 2011
Do people with FMS have lower GABA or lower functional gaba. Are their GABA(A) or GABA(B) receptors functionally different from "normals" or is it just GABA production that is affected? Is the GAD gene dysfunctional? We know that in Parkinsons disease, direct infusion of the GAD gene into the brain relieves some PD symptoms in about half PD patients. Could this be tried with FM patients? Is the gene in FM an inherited polymorphism? Or has the gene function been affected by a pathogen or by another immunological dysfunction. ( About half of people with ME/CFS fit the criteria of FM) I doubt this is a true co-morbidity but that the FM is a symptom of ME/CFS. FMS researchers and clinicians often forget this strong association with ME/CFS.
Reply Reply

Glutamate Sensitivity
Posted by: Scribelle
Aug 25, 2011
I am wondering. I seem to be sensitive to glutamate intake, which aggravates chem sensitivities as well as fibromyalgia. Do I understand correctly that this could be related to a failure to process the glutamate into its useful form? The relationship between glutamate and glutamic acid decaroxylase is unclear to me.
Reply Reply

glutamic acid decarboxylase
Posted by: inacio
Jul 30, 2012
Hi

There is pregabalin that boosts glutamic acid decarboxylase in dose dependent manner.

The pregabalin is FDA aproved medicine for FM.



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