This paper contains an expression of gratitude towards the organizers of the congress ‘Psychiatry, Food and Addiction’, and the Board members of the Interdisciplinary Society for Biological Psychiatry, of the Sections ‘Biological Psychiatry’ and ‘Psychiatry and Addiction’ of the Dutch Society of Psychiatry and the former Editorial Board of Acta Neuropsychiatry. The author has been a long-term board member of the society and cofounder of both sections and cofounder and editor-in-chief of this Journal from 1989 to 1999.

In this paper, several experimental models of human depression and cognitive dysfunction, which are designed specifically to mimic the proposed mechanisms of action of many nutritional supplements, are illustrated. These mechanisms of interest are antioxidant effects, glucose utilization, neuronal membrane function and neurotransmitter effects, with particular reference to nutrient-based amino acid manipulations of neurotransmission, such as tryptophan depletion. It is concluded that the application of experimental human models of altered mood and cognitive function may illuminate substantially the quest for nutritional enhancement of human mood and cognitive function.

Depression is a frequent comorbid disorder of many inflammatory diseases and it is suggested that brain inflammatory processes have a pathogenic role in mood dysregulation. Several immunocompromised patients have been treated with cytokines and long-term treatments have resulted in a variety of neuropsychiatric side-effects. The objective of the study was to present evidence for an association between the induction of neuropsychiatric side-effects during treatment with interferon-α (IFN-α) and changes in serotonergic and immunological parameters. Moreover, the use of IFN-α-induced depression as a paradigm for research into the pathophysiology of depressive disorders in general will be discussed. This literature review focused on the relationships between tryptophan, serotonin, cytokines and depression associated with interferon treatment. Immunotherapy with IFN-α influences several immunological and serotonergic parameters, and induces in most patients neurovegetative, somatic and depressive symptoms. Literature findings indicate that the development of depressive symptoms in patients undergoing cytokine therapy are secondary to cytokine induction and could be mediated by a reduced availability of tryptophan to the brain, resulting ultimately in decreased serotonergic activity. Changes in the metabolism of tryptophan and consequently of serotonin may play a role in the pathophysiology of interferon-induced depression. Studies on interferon-induced neuropsychiatric side-effects may be a promising research paradigm and shed light on the role of immunological and serotonergic factors in the pathogenesis of depressive disorders in general. However, first the appropriate symptomatology of the interferon-induced depressive states has to be documented.

In a group of medication-free out-patients suffering from depression and/or panic disorder we investigated the interdependence between psychological parameters such as aggression and biochemical parameters such as serotonin and tryptophan. We compared the findings in the patient group with a reference group. In the group of patients as a whole negative correlations were observed between the concentration of serotonin in platelets and depression and with hostility and aggression against others. Serotonin in plasma and tryptophan correlated negatively with hostility. The findings support the suggested link between aggression and depression with a low functioning serotonergic system.

Prader–Willi syndrome (PWS) is a genetically determined disorder associated with the loss of the paternal contribution to the proximal part of the long arm of chromosome 15. Its pathophysiology is dominated by hypothalamic dysfunctions. The psychopathological phenotype comprises affective and psychotic symptoms as well as an increase of pre-existent obsessive-compulsive behaviors. The present study comprises 19 PWS patients who were referred for neuropsychiatric evaluation because of psychotic deterioration. Patients were assessed by using the elements of semistructured symptom checklists. In the majority a genetic analysis was performed to detect the underlying chromosomal defect. In 16 of the 19 patients a diagnosis of cycloid psychosis could be established. The other three showed a bipolar affective disorder. Of the psychotic patients, 11 were diagnosed as UPD and one as del 15q11–13. The remaining four patients were diagnosed clinically. For various reasons the genetic etiology could not be established. In PWS patients with a psychotic disorder (cycloid psychosis) a disproportional number of UPD is found.