Mood disorders cortisol

Yehuda R, Boisoneau D, Mason JW, Giller EL (1993a) Glucocorticoid receptor number and cortisol excretion in mood, anxiety, and psychotic disorders. Biol Psychiatry 34 18-25... 

Adverse early environmental stress has also been investigated in human populations. Observations of the effects of early childhood experience of environmental adversity have led investigators to propose a stress vulnerability mediated by changes in stress-responsive CRF systems implicated in both mood and anxiety disorders (Heim and Nemeroff, 1999). Granger et al. (1996) measured children s adrenocortical reactions to a conflict-oriented mother-child interaction task and found that children s pretask cortisol scores were negatively associated with anxiety symptoms. 

Most attempts of using hormones as psychotropic medications were conducted with gonadal or with thyroid hormones, mainly because of the apparent mood changes associated with physiological or disorder-associated changes in levels or activity of these hormones. However, as shown in Table 17-1, current applications are broader and involve several hormones and systems. It is anticipated that, with acquired knowledge on mood effects of several other hormones, that list will continue to expand. Here, I focus on psychotropic effects of gonadal and thyroid hormones. Cortisol and melatonin are only briefly discussed. 

Mental disorders, also called affective disorders, are multi-level, multi-scale and multiple-system diseases (Fig. 7.1). Mental disturbances generally go along with disturbances of autonomous functions. These essentially are (1) sleep disturbances, both sleep duration and sleep pattern, and (2) disturbances of the hypothalamic-pituitary-adrenal (HPA) axis, the so-called stress axis with elevated cortisol levels. It can be expected that disturbances of autonomous control systems as well as mood are caused by neuronal malfunctioning which may concern practically all neuronal levels systemic interactions, neuronal network connections, single neuron dynamics, synaptic transmitters and/or receptors, ion channels, second messengers, and gene expression (Fig. 7.1a). Nevertheless, despite a manifold of data, there are only vague ideas so far about the differences in neuronal dynamics in the brain of a chronically depressed person compared with a person with a sensitive but balanced mood. 

For further progress towards mechanisms based models, such phenomenological descriptions shall also be examined in context with disease-related disturbances of autonomous functions. This mainly concerns disturbances of sleep-wake cycles and cortisol release which are the most reliable biological markers of mental diseases, especially major depression, and can provide objective and quantifiable parameters (e.g. EEG frequency components, cortisol blood level) for the estimation of an otherwise mainly subjective and only behaviorally manifested illness. Moreover, there is a manifold of data which interlink the alterations of the autonomous system parameters (sleep states, cortisol release) with alterations of neural dynamics. Therefore, the most promising approach also to understand the interrelations between neural dynamics and affective disorders probably goes via the analysis of mood related disturbances of autonomous functions. 

The significant meshing of the neuronal control areas for sleep and hormone release and their connections to mood relevant brain areas suggest that functional interdependencies also exist and that these also become evident in the system disturbances. The block diagram in Fig. 7.5 mainly emphasizes on the parts which are of particular relevance for those autonomous parameters which are the most clearly accessible markers of mental disorders the increased blood cortisol level and changes of the sleep EEG pattern. 

In mental disorders, in contrast to other neural diseases like epilepsy or Parkinson s disease, not much is known about the relevant alteration of neural dynamics. It can be just assumed from the pa lien I s inappropriate environmental responsiveness that neuronal adaptability and flexibility are disturbed, accompanied by a changed neuronal sensitivity on external stimuli. Fortunately, there is more information with regard to the neural control of sleep-wake cycles and cortisol release, which are very reliable biological markers of mental disorders and therefore may provide a link for a better understanding also of the neuronal dynamics which control mood. 

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