Psychiatric Times :: The Role of Cortisol and Depression: Exploring New Opportunities for Treatments
Psychiatric Times
It is now established that in conditions in which there are raised endogenous or exogenous corticosteroids (including Cushing's disease and severe mood disorders), there is also a significant degree of cognitive impairment (Wolkowitz et al., 1990). Studies in experimental animals have shown deficits in learning and memory following chronic administration of glucocorticoids (Lupien and McEwen, 1997), as well as marked atrophy of neurons in the hippocampal formation. It has been postulated that a similar neurodegenerative effect of cortisol may underlie some of the cognitive deficits observed in humans suffering from severe mood disorders (Sapolsky et al., 1986).
While there is substantial evidence to indicate that the hippocampus is particularly sensitive to elevation of glucocorticoids, the effects on other areas of the brain are less clear. Recent clinical data have reported that cortisol treatment induces cognitive deficits in healthy humans, and these deficits appear to be mediated in part via the frontal lobe, suggesting that this brain area may also be sensitive to the neurodegenerative effects of cortisol (Young et al., 1999). The deficits in healthy volunteer study participants are reversible, but this may not be the case with the cognitive deficits induced by hypercortisolemia associated with mood disorders (Ferrier et al., 1999; Young et al., 1999). A more recent study indicated that the frontal lobes are adversely affected by cortisol, which may illustrate a similar pattern of degeneration to that which occurs in the hippocampus (Young et al., in press). Moreover, the traditional assumption that patients with severe mood disorders make a full inter-episode recovery has recently been challenged. Although cognitive deficits do show some improvement on remission of affective symptoms (paralleling the return of normal HPA function), this improvement is not sustained. Studies have identified a specific deficit in executive control in a cohort of patients prospectively verified as euthymic (Thompson et al., 2001), replicating an earlier finding by our group (Ferrier et al., 1999).
This one is a little dense, but basically cortisol creates depression. It also messes with your prefrontal cortex and executive functions of the brain. Like ADD does. Alcohol, caffeine, lack of sleep and external stressors increase cortisol.
It is now established that in conditions in which there are raised endogenous or exogenous corticosteroids (including Cushing's disease and severe mood disorders), there is also a significant degree of cognitive impairment (Wolkowitz et al., 1990). Studies in experimental animals have shown deficits in learning and memory following chronic administration of glucocorticoids (Lupien and McEwen, 1997), as well as marked atrophy of neurons in the hippocampal formation. It has been postulated that a similar neurodegenerative effect of cortisol may underlie some of the cognitive deficits observed in humans suffering from severe mood disorders (Sapolsky et al., 1986).
While there is substantial evidence to indicate that the hippocampus is particularly sensitive to elevation of glucocorticoids, the effects on other areas of the brain are less clear. Recent clinical data have reported that cortisol treatment induces cognitive deficits in healthy humans, and these deficits appear to be mediated in part via the frontal lobe, suggesting that this brain area may also be sensitive to the neurodegenerative effects of cortisol (Young et al., 1999). The deficits in healthy volunteer study participants are reversible, but this may not be the case with the cognitive deficits induced by hypercortisolemia associated with mood disorders (Ferrier et al., 1999; Young et al., 1999). A more recent study indicated that the frontal lobes are adversely affected by cortisol, which may illustrate a similar pattern of degeneration to that which occurs in the hippocampus (Young et al., in press). Moreover, the traditional assumption that patients with severe mood disorders make a full inter-episode recovery has recently been challenged. Although cognitive deficits do show some improvement on remission of affective symptoms (paralleling the return of normal HPA function), this improvement is not sustained. Studies have identified a specific deficit in executive control in a cohort of patients prospectively verified as euthymic (Thompson et al., 2001), replicating an earlier finding by our group (Ferrier et al., 1999).
This one is a little dense, but basically cortisol creates depression. It also messes with your prefrontal cortex and executive functions of the brain. Like ADD does. Alcohol, caffeine, lack of sleep and external stressors increase cortisol.
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