L‐Tryptophan and 5‐hydroxytryptophan in the treatment of depression

d'Elia, G; Hansonan, L.; Raotma, H.

doi:10.1111/j.1600-0447.1978.tb06890.x

Cited by 41 publications

(5 citation statements)

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“…In patients, tryptophan augmentation of 5-HT reuptake therapy is supported by a limited number of clinical trials [47], [48]. These data are, however, not definitive [46], [50] and large follow-up clinical trials have not been reported. In an animal model, behavioral and physiological relevance of the suppression of 5-HT synthesis by SSRIs could be assessed by augmenting 5-HT synthesis in SSRI-treated animals using tryptophan loading [92].…”

Section: Discussionmentioning

confidence: 99%

“…Pharmacological inhibition of 5-HT synthesis can induce a rapid relapse of depression symptoms in SSRI-treated patients with remitted depression, an effect which is not readily observed in subjects with no history of SSRI administration [27], [37]–[44] (also see [45]). Tryptophan itself is considered to be ineffective as an antidepressant [46]; however, tryptophan co-administered with a 5-HT reuptake inhibitor may be more effective as an antidepressant than the reuptake inhibitor administered alone [47]–[50].…”

Section: Introductionmentioning

confidence: 99%

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Chronic Citalopram Administration Causes a Sustained Suppression of Serotonin Synthesis in the Mouse Forebrain

et al. 2009

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BackgroundSerotonin (5-HT) is a neurotransmitter with important roles in the regulation of neurobehavioral processes, particularly those regulating affect in humans. Drugs that potentiate serotonergic neurotransmission by selectively inhibiting the reuptake of serotonin (SSRIs) are widely used for the treatment of psychiatric disorders. Although the regulation of serotonin synthesis may be an factor in SSRI efficacy, the effect of chronic SSRI administration on 5-HT synthesis is not well understood. Here, we describe effects of chronic administration of the SSRI citalopram (CIT) on 5-HT synthesis and content in the mouse forebrain.Methodology/Principal FindingsCitalopram was administered continuously to adult male C57BL/6J mice via osmotic minipump for 2 days, 14 days or 28 days. Plasma citalopram levels were found to be within the clinical range. 5-HT synthesis was assessed using the decarboxylase inhibition method. Citalopram administration caused a suppression of 5-HT synthesis at all time points. CIT treatment also caused a reduction in forebrain 5-HIAA content. Following chronic CIT treatment, forebrain 5-HT stores were more sensitive to the depleting effects of acute decarboxylase inhibition.Conclusions/SignificanceTaken together, these results demonstrate that chronic citalopram administration causes a sustained suppression of serotonin synthesis in the mouse forebrain. Furthermore, our results indicate that chronic 5-HT reuptake inhibition renders 5-HT brain stores more sensitive to alterations in serotonin synthesis. These results suggest that the regulation of 5-HT synthesis warrants consideration in efforts to develop novel antidepressant strategies.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic Citalopram Administration Causes a Sustained Suppression of Serotonin Synthesis in the Mouse Forebrain

et al. 2009

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“…the amino acid precursor of serotonin, with good results. Tryptophan has also been shown by some inves tigators to have antidepressant efficacy [D'Elia et al, 1978]. Additionally, Asberg et al [1976] have posited a biochemical subtype of depression marked by a serotonin deficiency.…”

Section: Pharmacologic Evidencementioning

confidence: 99%

Evidence for a Biological Hypothesis of Obsessive-Compulsive Disorder

Lieberman¹

1984

Neuropsychobiology

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There is scant but provocative evidence to support the concept of a biological etiology in obsessive-compulsive disorder (OCD). This evidence includes the phenomenologic similarities and associations with other major psychiatric disorders for which there is evidence of biologic etiologies; the genetic studies that show an increased familial occurrence of psychiatric illness including OCD and concordance for this disorder in monozygotic twins; biologic evidence and the historical association of OCD and CNS damage; the treatment response of OCD to antidepressant medication and possibly those medications that selectively modify serotonin neuronal activity and to selective anterior limbic leukotomy. This evidence and the evidence linking OCD to depressive illness are specifically reviewed and discussed.

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“…However, clinical trials in which patients have been administered tryptophan or 5-HT have given conflicting results and reached differing conclusions [10,12,[15][16][17]. They also have side-effects (commonly nausea and gastrointestinal distress) [14].…”

mentioning

confidence: 99%

Are Tryptophan and 5-Hydroxytryptophan Effective Treatments for Depression? A Meta-Analysis

Shaw

Turner

Mar

2002

Aust N Z J Psychiatry

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L‐Tryptophan and 5‐hydroxytryptophan in the treatment of depression

Abstract: Trials performed do not provide evidence for an antidepressant effect of 5-HTP. L-TP, without interacting pharmaca, does not appear to be a well-documented antidepressant. The only convincing evidence for L-TP as an antidepressant is that L-TP enhances the effect of MAOI.

Cited by 41 publications

References 54 publications

Chronic Citalopram Administration Causes a Sustained Suppression of Serotonin Synthesis in the Mouse Forebrain

Chronic Citalopram Administration Causes a Sustained Suppression of Serotonin Synthesis in the Mouse Forebrain

Evidence for a Biological Hypothesis of Obsessive-Compulsive Disorder

Are Tryptophan and 5-Hydroxytryptophan Effective Treatments for Depression? A Meta-Analysis

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