Effects of acute tryptophan depletion on affective processing in first-degree relatives of depressive patients and controls after exposure to uncontrollable stress.
BACKGROUND
Individuals with a family history of depression may be more likely to develop depression due to an innate vulnerability of their serotonergic system. However, even though serotonergic vulnerability may constitute a risk factor in the development of depression, it does not seem to be sufficient to cause a depressive episode. Based on previous data, it is suggested that stress may be a mediating factor.


OBJECTIVE
This study examined the role of serotonin (5-HT) in stress coping in individuals with or without a family history of depression.


METHODS
Nineteen healthy first-degree relatives of depressive patients (FH+) and 19 healthy controls without a family history of depression (FH-) were tested in a double-blind placebo-controlled design for affective processing under acute stress exposure, following acute tryptophan depletion (ATD) or placebo.


RESULTS
Significant negative effects were found of stress on affective processing in FH- and FH+. In addition, FH- responded slower to positive words after stress only following ATD, whereas FH+ responded marginally slower under stress already after placebo and before stress following ATD.


CONCLUSIONS
Acute stress exposure reduces positive affective bias; supporting the role of stress as an important predecessor in the development of depression. Furthermore, FH+ may be more susceptible than FH- to the negative effects of stress as well as to the negative effects of ATD. The results support the assumption that the 5-HT system is involved in stress resilience and may be more vulnerable in first-degree relatives of depression.
Department of Clinical Psychological Science, Faculty of Psychology, Maastricht University, Maastricht, The Netherlands. christine.firk@psychology.unimaas.nl
Christine
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D000293:Adolescent; D000339:Affect / Q000502:physiology*; D000596:Amino Acids / Q000097:blood / Q000378:metabolism / Q000494:pharmacology; D001923:Brain Chemistry / Q000235:genetics / Q000502:physiology; D018592:Cross-Over Studies; D003866:Depressive Disorder / Q000235:genetics* / Q000378:metabolism / Q000523:psychology*; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D008297:Male; D011930:Reaction Time / Q000502:physiology; D013315:Stress, Psychological / Q000235:genetics* / Q000378:metabolism / Q000523:psychology*; D014364:Tryptophan / Q000172:deficiency / Q000502:physiology*; D055815:Young Adult
D000596:Amino Acids; D014364:Tryptophan