This clinical overview article is the third and last in our series Food for Thought. The two-first articles in the series ‘`Marine omega-3 fatty acids and mood disorders – linking the sea and the soul. ‘‘Food for Thought’ I’ by Bronwyn D. Hegarty and Gordon Parker (45) and ‘“D” for depression: any role for Vitamin D? “Food for Thought” II’ by Gordon Parker and Heather L. Brotchie (46) were published earlier this year.
Mood effects of the amino acids tryptophan and tyrosine
‘Food for Thought’ III
Article first published online: 12 APR 2011
© 2011 John Wiley & Sons A/S
Acta Psychiatrica Scandinavica
Volume 124, Issue 6, pages 417–426, December 2011
How to Cite
Parker, G. and Brotchie, H. (2011), Mood effects of the amino acids tryptophan and tyrosine. Acta Psychiatrica Scandinavica, 124: 417–426. doi: 10.1111/j.1600-0447.2011.01706.x
- Issue published online: 14 NOV 2011
- Article first published online: 12 APR 2011
- Accepted for publication March 16, 2011
- amino acids;
Parker G, Brotchie H. Mood effects of the amino acids tryptophan and tyrosine.
Objective: Reflecting increased scientific interest in any nutritional contribution to the onset and treatment of mood disorders, we overview research into two neurotransmitter precursors – the amino acids tryptophan and tyrosine – particularly examining whether any deficiency increases risk to depression and whether those amino acids have any antidepressant properties.
Method: The theoretical relevance of the two amino acids was overviewed by considering published risk and intervention studies, technical papers and reviews.
Results: There is some limited evidence, suggesting that depressed patients, especially those with a melancholic depression, have decreased tryptophan levels. Whether such findings reflect a causal contribution or are a consequence of a depressed state remains an open question. There is a small database supporting tryptophan preparations as benefitting depressed mood states. There is no clear evidence as to whether tyrosine deficiency contributes to depression, while the only randomized double-blind study examining tyrosine supplementation did not show antidepressant benefit.
Conclusion: Acute tryptophan depletion continues to provide a research tool for investigating the relevance of serotonin to depression onset. There is limited evidence that tryptophan loading is effective as a treatment for depression through its action of increasing serotonin production. Most clinical studies are dated, involve small sample sizes and/or were not placebo controlled. The development of the new serotonin reuptake inhibitor drugs seemingly signalled an end to pursuing such means of promoting increased serotonin as a treatment for depression. The evidence for tyrosine loading promoting catecholamine production as a possible treatment for depression appears even less promising, and depletion studies less informative.