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Cognitive therapy does not prevent a response to tryptophan depletion in patients also treated with antidepressants

Posted on 04/27/2010
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BACKGROUND: Acute tryptophan depletion (ATD) induces depressive symptoms in remitted depressed patients treated with serotonergic medications, but not in patients treated with noradrenergic medications or electroconvulsive therapy. A recent study suggests that cognitive therapy (CT) protects against the effects of ATD, but the evidence is questionable. The present study compared the effect of ATD in patients who were treated with antidepressant medication and CT (n = 17) versus antidepressant medication alone (n = 23) during their latest episode.

METHODS: Forty remitted depressed patients underwent high-dose and low-dose ATD in a randomized double-blind crossover design. RESULTS: There were no differences in response to ATD between treatment groups. This applied to groups defined by lifetime and by recent CT experience.

CONCLUSIONS: Cognitive therapy does not protect against the effects of rapidly lowered plasma tryptophan levels in remitted depressed patients who are also treated with antidepressant medication.

About the Authors

Van der Does AJ, Booij L. (2005) Cognitive therapy does not prevent a response to tryptophan depletion in patients also treated with antidepressants . Biol Psychiatry. 2005 Dec 1;58(11):913-5. Epub 2005 Jul 22.

Comments

NAD_Blood_Tests

Posted on 05/09/2010 08:23 am

It is known that dietary tryptophan can be converted to nicotinamide nucleotides in the body. Both the level of tryptophan and the energy content of the diet have been shown to influence the efficiency of conversion. The rate at which tryptophan is converted to nicotinamide nucleotides in the body may be expected to be influenced by the activities of the enzymes concerned with the tryptophan-NAD pathway.

NAD_Blood_Tests

Posted on 04/29/2010 03:57 am

The ratio of lactate to pyruvate reflects the NAD/NADH ratio and is useful in distinguishing primary defects. Measured enzymatically in blood or CSF as an index of defects of glucose oxidation (fed state) or gluconeogenesis (fasted). (Center Inherited Disorders Energy Metabolism at CWR University School of Medicine, Cleveland, Ohio).