Through an unknown mechanism it decreases the central nervous system activity (brain and spinal cord). That’s why it is an anti-epileptic (epilepsy is an abnormal hyperactivity of the brain and anti-epileptics decrease it). That means that any anti -epileptic has a slowing effect on the brain activity.
This is why all anti-epileptics have a positive effect on any pain. And that is by slowing brain activity. They do not cure the pain, they decrease its feeling.
But, the effect on pain depends on the balance between the pain intensity and the effect on brain slowing activity. If the pain does not change and the effect on brain slowing activity decreases: the pain comes back.
Because the cause of the pain is not treated, at best the pain remains the same, at worst it increases. Like any other medication, anti-epileptics tend to loose their effect over time. The end result is a short-lived betterment.
Then starts the increase of dosage in anti-epileptics. And the side effects increase!
This has always been the same with all anti-epileptics. The more powerful the anti-epileptic effect, the more powerful the anti-pain effect and the worst the side effects.
And we are told that anti-epileptics have more effect on specific pains! That's plain rubbish!
Their effect is the same on any pain, from headaches to central pain. In fact, they are now used by some as pre-operative pre-medications to decrease the post-operative pain! It may be advantageous in some situations, but it is unlikely to become a rule given their side effects!
The end effect on pain tends to be incomplete and short lived. The longest study* of pregabalin (Lyrica) effect on fibromyalgia was over 6 months only! When we know that fibromyalgia is a life long painful disease, that's a bit short!
The end result at 6 months was betterment of 13% whilst the betterment from placebo (sugar) was 10%. Only 3% better than sugar! That's a ridiculous difference.
I know, I know! The numbers are not really presented that way because they're playing with the percentage. Let's take an example: if you have 100 patients and 10 of them get better at 2 months, that's 10% of patients better. Now if you take those 10 patients and at 6 months 5 of them are better, that's 50% of the 10 patients better.
In fact, it is only 5% of the original 100! That's the way they show a result in a better light.
So 3% more than with sugar! But in the meantime, some 40% developed side effects and had to stop the medication. Interestingly, they don't tell us if the side effects corrected! I doubt very much that the gains in weight corrected and that's a cause for concern about the quality of life!
Is it really justified to inflict more problems on some 40% of patients for 3% betterment?
This may very well have played a role in the European decision to refuse pregabalin (Lyrica) its status as a fibromyalgia therapy.
Fibromyalgia status as a recognised disease may suffer from that, but the suffering from the indiscriminate use of a debatable therapy is by far a higher threat.
*Fibromyalgia relapse evaluation and efficacy for durability of meaningful relief (FREEDOM): A 6-month, double-blind, placebo-controlled trial with pregabalin. Crofford LJ, Mease PJ, Simpson SL, et al. Pain. 2008;136:419–31.
GABA and its regulation regularly come back on the fibromyalgia scene. We have said for a long time that fibromyalgia is not in your head but is a muscle disease. Now that an increasing number of specialists are abandoning this fraud of central pain story, we see articles coming back on it such as this one from a psychiatric unit!
It is already suspicious that a psychiatric unit gets involved in fibromyalgia! Fibromyalgia has never been a psychiatric disease and has nothing to do with it even remotely. It has been well known for years that fibromyalgia has no specific psychological profile but for the secondary depression that plagues so many coping chronic pain sufferers.
The main neurotransmitter in the brain is Glutamate. In general it excites. The central nervous system is a fine but highly variable balance between excitation and inhibition. In the inhibition aspect of it, GABA is an important neurotransmitter. Funny enough, it is produced by the transformation of Glutamate under the influence of an enzyme: GAD (glutamic acid decarboxylase). GAD works better in presence of vitamin B6 or pyridoxine (and not pyroxidine as is wrongly written in the summary). So, if there is more glutamate there is more excitation and this is partly compensated by GABA. If GAD is less produced or less active, there is less GABA. That has been known for many years.
What is deadly wrong with the article is a kind of exhaustive list of fibromyalgia symptoms and even of non symptoms! For example, obesity is not part of fibromyalgia as such but as a secondary occurrence (if moving is so painful, you tend to become overweight) or even as a precursor sign of the fact that the muscles are diseased so your physical activities were already limited before you developed the pain!
We have explained in our book on fibromyalgia that the pain of fibromyalgia is called pathological pain and is secondary to the chronic muscle pain! All the other symptoms are only vaguely related or not at all to any supposed GAD deficiency.
We got suspicious with the psychiatric unit origin of this article. The suspicion increases when another fact is highlighted. In a few years, pregabalin, Lyrica, will loose its patent. So Pfizer will bring another similar molecule on the market to keep money pouring in. Already, from gabapentin to pregabalin, we have seen the evolution towards much less good effect and much more bad side effects. We predict that the next one will be even worse. But they are already preparing it as a "new discovery" by throwing around articles about GAD and GABA whose actions will be "supposedly enhanced" by that new incoming toxic molecule! They have already started this "criminal process" by throwing incorrect information on the net like in Wikipedia!
If you want more proof about their reprehensible behavior or a description of side effects of lyrica just click on “Lyrica” in the navigation bar on the left.
Lastly, it would be better that many fibromyalgia blogs stop trumpeting about every new published article without any authoritative ability to criticize them! By doing so they participate in the fraud and we're sure they don't want that! Unless they’re on Pfizer payroll! Pain medications for chronic pain are already difficult to handle, no need to add insult to in jury.
Would Pfizer explain how come statins and muscle pain are related? Oh no! They also sell statins! So they sell you Lyrica that works so poorly but they also sell you Lipitor, atorvastatin, to increase your muscle pain! That's great for them, not for you!
Fitzgerald CT, Carter LP. Possible role for glutamic acid decarboxylase in fibromyalgia symptoms: A conceptual model for chronic pain. Med Hypotheses. 2011 Jun 17
Department of Psychiatry, University of Arkansas for Medical Sciences, 4301 W. Markham St. #843, Little Rock, AR 72205, USA.
Fibromyalgia (FM) is a condition of chronic generalized musculoskeletal pain that is thought to be a disorder of central pain sensitization. A number of neurotransmitters 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 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.
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