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The entry of tryptophan to the brain is crucial in the proper synthesis of the neurotransmitter serotonin in the brain.
One way to acutely cause depression or bulimia or anxiety in humans, in order to assess an individual's vulnerability to those disorders, is to supplement with a formula with all or most amino acids except tryptophan.
The protein synthesis elicited by the amino acids leads circulating amino acids, including tryptophan, to be incorporated into proteins.
Tryptophan thus lowers in the brain as a result of the protein synthesis enhancement ( causing circulating tryptophan to lower more than other amino acids ), and perhaps also competition of large neutral amino acids for transport across the blood – brain barrier through the large neutral amino acid transporter 1 ( LNAA1 ).
The consequence is acute tryptophan depletion ( ATD ) in the brain and a consecutive lowering of serotonin synthesis.
ATD, which is basically a diagnostic procedure, is not a treatment for GA1.

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