l-Tryptophan in affective disorders: Indoleamine changes and differential clinical effects

Murphy, Dennis L.; Baker, Max; Goodwin, Frederick K.; Miller, Halbert; Kotin, Joel; Bunney, William E.

doi:10.1007/bf00421216

Cited by 110 publications

(18 citation statements)

References 45 publications

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“…Prange et al (1974) found /,-tryptophan to have a similar, if not greater, effect than chlorpromazine, 400 mg daily, in the treatment of mania. A more modest antimanic effect has also been found by Murphy et al (1974). Prange et al (1974) felt this is consistent with the 'permissive hypothesis' which holds a deficiency of serotonin is a necessary precondition for the development of an affective disorder, but it is the level of catecholamines that determines whether it will be depression or mania.…”

Section: -Hydroxy Tryp Tophansupporting

confidence: 66%

Biogenic Amines and Affective Disorders

Luchins¹

1976

Int Pharmacopsychiatry

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The evidence linking biogenic amines and affective disorders is critically reviewed. Surveyed are studies on the level of biogenic amines and their metabolites in the brain, blood, urine and cerebrospinal fluid of patients with affective conditions; the effects of biogenic amine precursors, depletors and blockers on affective states and the action of present methods of treatment of these disorders on the level of biogenic amines. Reference is also made to the existence of various disease states where abnormalities of biogenic amines exist in the absence of affective disorders. The review fails to uncover convincing evidence that affective disorders are related to abnormal levels of biogenic amines. Reasons are outlined why the 'catecholamine hypothesis' and related theories can neither be proven nor disproven with the available techniques.

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Section: -Hydroxy Tryp Tophansupporting

confidence: 66%

Biogenic Amines and Affective Disorders

Luchins¹

1976

Int Pharmacopsychiatry

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“…¿-TP loading has been found to increase 5H1AA and peripheral 5HT in both responders and nonresponders -whether these catego ries were defined in terms of an antidepressant effect (71) or changes in REM latency (74). A similar increased output of 5H1AA has been measured after ¿-5HTP loading, both orally (8,80,81,94) and intravenously (76).…”

Section: Requirement O F Effective Stimulation O F Serotonin Turnoversupporting

confidence: 54%

“…In one study, 7/10 improved with ¿-TP, 3 relapsing again into mania on placebo (71). A second double-blind cross-over study against chlor promazine indicated a more rapid improvement with ¿-TP (82).…”

Section: Indoleamine Precursors In Depression L-tryptophanmentioning

confidence: 99%

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Theoretical and Therapeutic Potential of Indoleamine Precursors in Affective Disorders

Wirz‐Justice¹

1977

Neuropsychobiology

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The strategy of loading with precursor amino acids of the monoamines postulated to be involved in the affective disorders is reviewed. Phenylalanine, tyrosine, L-dopa, L-tryptophan and L-5-hydroxytryptophan (L-5HTP) have been found to induce differential behavioural and biochemical effects in both healthy subjects and endogenous depressives. Indoleamine precursors predominantly cause mood changes. However, the efficacy of these amino acids as antidepressants has been neither clearly established nor refuted, probably due to insufficient consideration of the following criteria; sufficiently high plasma levels to be taken up into the brain, effective stimulation of serotoninergic systems, and selective increase of serotonin turnover with minimal interaction with other neurotransmitters. The use of intravenous L-5HTP as a provocative test in depressive patients, with concomitant neuroendocrinological and psychometric measurements, may be a method adequately fulfilling these requirements. ‘I have no peace of mind’, said Hui-k’o. ‘Please pacify my mind’. ‘Bring out your mind here before me’, replied Bodhidharma, ‘and I will pacify it’. But when I seek my own mind’, said Hui-k’o, ‘I cannot find it’. ‘There!’ snapped Bodhidharma, ‘I have paci-fied your mind!’ Wu-men kuan200

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“…It has been suggested to be as effective as ECT (Coppen, Shaw, Herzberg & Maggs, 1967) and no better than placebo (Carroll, Mowbray & Davies, 1970;Murphy, Baker, Goodwin, Miller, Kotin & Bunney, 1974). Whilst one recent study has indicated that the efficacy of tryptophan is similar to that of imipramine (Jensen, Fruensgaard, Ahlfors, Pihkanan, Tuomikoski, Ose, Dencker, Lindberg & Nagy, 1975) another has suggested that its value alone is small, but that it potentiates other antidepressant drugs such as chlorimipramine or monoamine oxidase inhibitors (d'Elia, Hanson & Raotma, 1978).…”

Section: Introductionmentioning

confidence: 99%

Metabolism of an oral tryptophan load. I: Effects of dose and pretreatment with tryptophan.

Ar¹,

Aronson²,

Curzon³

et al. 1980

Brit J Clinical Pharma

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The Royal Hallamshire Hospital, Sheffield. 1 The metabolism of three oral doses of L-tryptophan (50, 25 and 10 mg/kg) in healthy young males has been investigated. 2 There was a linear relationship between both peak height and area under curve of the total plasma tryptophan concentrations whilst the relationship between these parameters and plasma free tryptophan was hyperbolic. 3 Before the tryptophan load about 85% of plasma tryptophan was bound to albumin. As plasma tryptophan concentrations increased there was a hyperbolic increase in free tryptophan. Scatchard analysis revealed 1.4 binding sites/molecule albumin with a dissociation constant (Kd) of 57.9 ,uM. Following administration of L-tryptophan (50 mg/kg) twice daily for 7 days there was no alteration in the number of binding sites but the dissociation constant (Kd) had decreased to 30.9 ,uM. 4 L-Tryptophan (50 mg/kg twice daily for 7 days) markedly increased both basal plasma total and free tryptophan. However following a further load the total tryptophan curve was comparable to that seen after acute administration. The plasma free tryptophan curve was lowered relative to that seen after an acute dose. 5 Increasing the tryptophan dose shortened the plasma half-life and decreased the volume of distribution and the rate of clearance. Longer term tryptophan administration had no significant effect on plasma half-life or volume of distribution but did decrease the rate of plasma clearance. 6 The plasma kynurenine concentration increased with increasing tryptophan dose and basal concentrations increased markedly after longer term tryptophan administration. 7 Tryptophan administration either acutely or chronically produced little change in urinary tryptophan or 5-hydroxyindole acetic acid excretion. Urinary kynurenine and indole acetic acid excretion increased with increasing doses of tryptophan. 8 Data are discussed in relation to the administration of L-tryptophan for the treatment of depression.

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l-Tryptophan in affective disorders: Indoleamine changes and differential clinical effects

Cited by 110 publications

References 45 publications

Biogenic Amines and Affective Disorders

Biogenic Amines and Affective Disorders

Theoretical and Therapeutic Potential of Indoleamine Precursors in Affective Disorders

Metabolism of an oral tryptophan load. I: Effects of dose and pretreatment with tryptophan.

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