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can i take gaba supplement with ativan


Posted by anxious

i take 1mg ativan   twice a day.   i would like to cut down on ativan so can i substitute gaba at least once a day
 
Answers (3)
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Ian Health Maven

Yes, you can. But you'd be wasting your money.  

Firstly, anxiety isn't due to low brain GABA levels. GABA is a byproduct of the Krebs cycle with provides fuel for the brain. So your brain has a great deal of GABA. What it may lack is GABA receptors, aka binding sites (See: http://www.ncbi.nlm.nih.gov/pubmed/10873921 & http://www.ncbi.nlm.nih.gov/pubmed/10873921). However, increasing the amount of GABA is no more likely to reduce anxiety than filling a car's gas tank will fix faulty/missing sparkplugs. Ativan (lorazepam) and the other benzodiazepines don't increase brain GABA levels, they increase the sensitivity and effectiveness of GABA receptors.

Secondly, supplemental GABA cannot cross the blood-brain barrier.  Not only does the barrier block access, it actually contains pumps which remove GABA from the brain as there is so much of it. See: http://www.ncbi.nlm.nih.gov/pubmed/11595763

There are a few anti convulsive drugs which are forms of GABA that can penetrate the BBB but these do not have the same mode of action in the brain as GABA despite increasing brain GABA levels, and appear not be be effective anti anxiety drugs. Psychosis can be a side-effect.

If you want to reduce your benzodiazepine dose, omega-3 fatty acids (fish oil) and exercise will be much more likely to reduce anxiety than GABA supplements. You and your doctor might also consider antidepressants and cognitive/behavioral therapies.

Best wishes

Ian

Here is what I know about Anxiety after studying it for over 17 years. I have heard numerous deficencies have occured could be amino acids, could b B vitamins and I have heard it is Gaba now I wouldn't take Gaba as Ian is correct it will not cross over the brain blood barrier but Suntheanine does. Suntheanine crosses the brain blood barrier to convert into Gaba which we lack along with Serotine. 

I hope this helps do not take the two together though and do not mix antidepressants with natural antidepressants as you can get a serotonine overload and this could become toxic.So please do not mix. 

Ian Health Maven

>"Suntheanine crosses the brain blood barrier to convert into Gaba which we lack along with Serotine."

Sorry, but this is incorrect on both counts.

As per my previous reply, a normally function brain cannot lack GABA. Brains have so much of the stuff that there are GABA pumps in the blood-brain-barrier to remove it. See: http://tiny.cc/dhrsv

Nor are anxiety and depression caused by a serotonin deficiency. It has been known for more than a decade that the 'chemical imbalance/low serotonin' theory was deeply flawed, yet in continues to be promoted in the media and even medical journals.

Serotonergic antidepressants do increase serotonin levels both in synapses and the brain overall within about 30 minutes of the first dose, and levels may remain higher for some weeks. But they drop back to baseline or below at about the time patients begin to feel an improvement in anxiety or depression, usually some 4 to 12 weeks after beginning treatment.[1]

The fact that the boost in serotonin doesn't immediately alleviate anxiety and depression is the first clue that there is more to these disorders than just a lack of serotonin. The second clue is that the first side-effect many experience after beginning to take antidepressants is increased anxiety and agitation. Serotonin is not usually a "feel good" neuotransmitter.

Perhaps, the best indicator that increasing serotonin levels isn't the factor responsible for the therapeutic effect of antidepressants is the French drug trianeptine (Stablon®), a Selective Serotonin Re-Uptake Enhancer/Accelerator. That is, it speeds up the removal of serotonin from the synapses. Yet, it is as effective as Selective Serotonin Re-uptake Inhibitors such as Prozac®, which delay removal of the neurotransmitter. See: http://en.wikipedia.org/wiki/Tianeptine

Further evidence against the hypothesis comes from rat models of depression. Rats bred to have a high genetic predisposition for depression have up to 8 times more serotonin in brain regions associated with anxiety disorders and clinical depression - the nucleus accumbens, prefrontal cortex, hippocampus, and hypothalamus - than controls. Chronic antidepressant treatment reduces serotonin to levels found in 'normal' rats. [2]

How antidepressants work is still a matter of debate. The most likely current theory is that they do so by stimulating Neurogenesis - the formation of new neurons, especially in the hippocampus, and encouraging increased nerve-fiber innervation between limbic structures and the forebrain.

It wouldn't matter how antidepressants work, just as long as they do, except that the 'chemical imbalance' theory is used to promote sales of the serotonin precursors L-Tryptophan and 5-HTP which not only can't work as advertised, but which, at least in the case of L-Tryptophan, may cause harm through the contaminate, Peak-X. Peak-X is though to trigger the immune system disorder Eosinophilia-myalgia syndrome (EMS). L-Tryptophan linked EMS caused the deaths of 37 people in the late 1980s and permanently damaged the health of another 1,500+.

Despite claims that Peak-X contamination was confined to a few batched produced by one manufacturer, Simat et al (1999) found markers for Peak-X in pharmaceutical grade L-Tryptophan on sale in Germany in 1998. See: http://tiny.cc/zkdsi

Best wishes

Ian


References:

[1] Bosker FJ, Tanke MAC, Jongsma ME, et al. (2010)
Biochemical and behavioral effects of long-term citalopram administration and discontinuation in rats: Role of serotonin synthesis.
Neurochemistry International 2010 Dec;57(8):948-957. [Abstract: http://tiny.cc/51jjg ]

New Rat Study: SSRIs Markedly Deplete Brain Serotonin - http://tiny.cc/0amwf

Honig G, Jongsma ME, van der Hart MC, Tecott LH. (2009)
Chronic citalopram administration causes a sustained suppression of serotonin synthesis in the mouse forebrain.
PLoS One. 2009 Aug 27;4(8):e6797. [Abstract: http://tiny.cc/uylyo ]

Bianchi M, Moser C, Lazzarini C, Vecchiato E, Crespi F. (2002)
Forced swimming test and fluoxetine treatment: in vivo evidence that peripheral 5-HT in rat platelet-rich plasma mirrors cerebral extracellular 5-HT levels, whilst 5-HT in isolated platelets mirrors neuronal 5-HT changes.
Exp Brain Res. 2002 Mar;143(2):191-7. [Abstract: http://tinyurl.com/2gmlym ]

Stenfors C, Yu H, Ross SB. (2001)
Pharmacological characterisation of the decrease in 5-HT synthesis in the mouse brain evoked by the selective serotonin re-uptake inhibitor citalopram.
Naunyn Schmiedebergs Arch Pharmacol, vol 363(2):p 222-32 [Abstract: http://tinyurl.com/ka7xm ]

Alvarez JC, Sanceaume M, Advenier C, et al. (1999)
Differential changes in brain and platelet 5-HT concentrations after steady-state achievement and repeated administration of antidepressant drugs in mice.
Eur Neuropsychopharmacol, vol 10(1):p 31-6 [Abstract: http://tinyurl.com/hdxhc ]

Moret C, Briley M. (1997)
Ex vivo inhibitory effect of the 5-HT uptake blocker citalopram on 5-HT synthesis.
J Neural Transm. 1997;104(2-3):147-60. [Abstract: http://tinyurl.com/l7wzd ]

Trouvin JH, Gardier AM, Chanut E, et al. (1993)
Time course of brain serotonin metabolism after cessation of long-term fluoxetine treatment in the rat.
Life Sci, vol 52(18):p PL187-92 [Abstract: http://tinyurl.com/esqqt ]

Caccia S, Anelli M, Codegoni AM, Fracasso C, Garattini S. (1993)
The effects of single and repeated anorectic doses of 5-hydroxytryptamine uptake inhibitors on indole levels in rat brain.
Br J Pharmacol. 1993 Sep;110(1):355-9. [Abstract: http://tinyurl.com/2483y2]

Caccia S, Fracasso C, Garattini S, Guiso G, Sarati S. (1992)
Effects of short- and long-term administration of fluoxetine on the monoamine content of rat brain.
Neuropharmacology. 1992 Apr;31(4):343-7. [Abstract: http://tinyurl.com/pveto ]

Leonard BE. (1988)
Pharmacological effects of serotonin reuptake inhibitors.
J Clin Psychiatry. 1988 Aug;49 Suppl:12-7. [Abstract: http://tinyurl.com/29w64 ]

[2]

Zangen A, Overstreet DH, Yadid G. (1999)
Increased catecholamine levels in specific brain regions of a rat model of depression: normalization by chronic antidepressant treatment. <br />Brain Res. Apr 10;824(2):243-50. [Abstract: http://tiny.cc/8ac4b ]

Zangen A, Overstreet DH, Yadid G. (1997)
High serotonin and 5-hydroxyindoleacetic acid levels in limbic brain regions in a rat model of depression: normalization by chronic antidepressant treatment.
J Neurochem, vol 69(6):p 2477-83 [Abstract: http://tinyurl.com/egyza ]

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