Lecture 7: Barbara Sperner-Unterweger - Affective disorders: Depression and somatic co-morbidity

HBP Curriculum: Interdisciplinary Brain Science | Brain medicine for non-specialists | 4th Teaching Cycle
Lecture 7: Affective disorders: Depression and somatic co-morbidity
Speaker: Barbara Sperner-Unterweger, Medical University Innsbruck, Austria
Major Depressive Disorder (MDD) is a heterogeneous disease with a lifetime prevalence of approximately 15%. On Friday 31 March 2017, the World Health Organization (WHO) ranks MDD as leading cause of disability worldwide. By their estimates, more than 300 million people live with the condition-an 18 percent increase since 2005. But nearly half of these people don't get the treatment they need. Depressed patients experience reduced general functioning and quality of life, as well as increased physical morbidity and mortality. Several studies have shown that MDD predicts the onset and the progression of both physical and social disability. The 12-month prevalence rates of mental disorders, especially MDD, are 1.5 to 2 times higher in patients with chronic somatic diseases compared to the general population. In general hospitals, depressive disorders are present in 10 to 60 percent of somatically ill patients, depending on the somatic diagnosis.
During the past twenty years the relationship between depressive symptoms and somatic conditions such as cardiovascular disease, diabetes, cancer, and neurodegenerative disorders has received increasing attention in research. Depressive symptoms may be a secondary reaction to the development of the somatic disease, or to complications and aversive symptoms; in addition, they may also be related to side effects of medications administered to treat the illness. Aside from these indirect effects, as well as disease- specific direct pathophysiological effects on the brain (i.e. stroke, or multiple sclerosis), inflammation is the common underlying condition of these chronic somatic diseases). Thus, patients who suffer from chronic inflammatory processes due to autoimmune syndromes, infections, or
cancer, etc., have an increased risk of developing fatigue and depression. Similar clinical abnormalities can develop as side effects in patients under treatment with pro-inflammatory cytokines such as interleukins, interferons or tumor necrosis factor. Immune activation and the serotonergic system are linked by the activity of the enzyme indoleamine 2,3-dioxygenase (IDO), which is involved in the breakdown of tryptophan, the essential precursor of 5-HT. The activity of IDO is enhanced by proinflammatory cytokines.
Immunbiochemical interactions between the metabolism of serotonin but also of catecholamines might indeed account for the increased prevalence of clinical depression in chronically ill people).
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