The role of tryptophan in depression has been widely studied but a recent large scale analysis of over 100 previous studies involving more than 10,000 patients indicates that tryptophan is not converted in serotonin efficiently.
Tryptophan is an amino acid found in protein-rich foods, and it is converted into 5-htp and then into serotonin (5-HT). According to the meta-analysis of 101 studies, patients with these psychiatric disorders have lower levels of tryptophan and metabolise tryptophan inefficiently.
Patients with psychiatric disorders have lower levels of tryptophan
researchers at the University of Texas Health Science Centre discovered that the amino acid tryptophan is brain broken differently in patients with major depressive disorder (MDD), bipolar disorder, or schizophrenia . Using the definitions below, they were able to assess 3 psychiatric disorders;
|Psychiatric Disorders assessed in the meta-analysis|
|MDD||low mood that lasts for weeks or months and affects your daily life|
|Bipolar disorder||a mental health condition that causes extreme mood swings|
|Schizophrenia||mental health condition where you may see, hear, or believe things that are not real|
Patients with these psychiatric disorders have lower levels of tryptophan and metabolise tryptophan inefficiently.
Tryptophan doesn’t = serotonin
Tryptophan can be metabolised to either a route where serotonin is produced or to the kynurenine pathway. The kynurenine pathway is advantageous for humans as it plays a critical role in energy production . “People with mood disorders and schizophrenia not only have decreased levels of tryptophan overall, but the tryptophan they do have is being broken down more often in the kynurenine pathway, shifting away from the production of serotonin”.
Overstimulation of this pathway leads to less neuroprotective compounds and the accumulation of neurotoxic compounds. The proliferation of these neurotoxic compounds can induce oxidative stress and further neuronal damage. Oxidative stress is increased in depressed patients  and it might be a cause of some depressive disorders. Is it, therefore, reasonable to hypothesise that increased tryptophan conversion via the kynurenine pathway further exacerbates oxidative stress causing conditions to worsen?
Could 5-HTP be a more effective serotonin enhancer?
There is a challenge with the conversion of tryptophan to serotonin. Tryptophan is unable to enter the brain without a carrier mechanism, resulting in relatively small amounts being converted into serotonin. 5-HTP is an amino acid that can freely cross the blood-brain barrier. It can be synthesised or extracted from the Griffonia seed and can be taken as a food supplement. Given the evidence presented by Marx et al. 5-htp warrants further clinical research into its use in patient groups that fail to efficiently convert tryptophan.
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