The cyclic nature of depressive illness, the diurnal variations in its symptomatology and the existence of disturbed sleep-wake and core body temperature rhythms, all suggest that dysfunction of the circadian time keeping system may underlie the pathophysiology of depression. As a rhythm-regulating factor, the study of melatonin in various depressive illnesses has gained attention. Melatonin can be both a 'state marker' and a 'trait marker' of mood disorders. Measurement of melatonin either in saliva or plasma, or of its main metabolite 6-sulfatoxymelatonin in urine, have documented significant alterations in melatonin secretion in depressive patients during the acute phase of illness. Not only the levels but also the timing of melatonin secretion is altered in bipolar affective disorder and in patients with seasonal affective disorder (SAD). A phase delay of melatonin secretion takes place in SAD, as well as changes in the onset, duration and offset of melatonin secretion. Bright light treatment, that suppresses melatonin production, is effective in treating bipolar affective disorder and SAD, winter type. This review discusses the role of melatonin in the pathophysiology of bipolar disorder and SAD.
There is evidence in the literature that there are associations between advancing paternal age and psychosis or more specifically schizophrenia, but not enough to support a strong link between advancing paternal age and common mental disorders.
There are several reports of reduced levels of polyunsaturated fatty acids (PUFA), particularly arachidonic acid (AA) and docosahexaenoic acid (DHA), in membrane phospholipid from various tissues including red blood cells (RBC) taken from schizophrenic patients. However, reports have not been entirely consistent and most studies have been confounded by the potential effects of environmental factors including antipsychotic medication and diet. We measured PUFA levels in RBC from two separate groups of unmedicated patients and control subjects from India and Malaysia, populations which have substantial differences in diet. We found no significant difference in levels of AA between patients and control subjects in either population. Levels of adrenic acid were significantly reduced, and levels of DHA significantly increased in both clinical populations. However, diet-related differences in DHA between the populations from India and Malaysia were much greater than differences between schizophrenic patients and controls. It is concluded that reduced RBC membrane levels of AA and DHA are not pathognomic of schizophrenia but that variations in cell membrane fatty acid levels are an epiphenomenon which may reflect underlying abnormalities of phospholipid and fatty acid metabolism and their interaction with environmental factors including medication and diet.