>"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.
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. 
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
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