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I recognize that the scientific community is aware that the chemical stress pathway is mediated by glucocorticoids. The pathway response initializes as a result of some sort of stress (potentially chemical, such as low glucose) and the hypothalamus secretes corticotropin-releasing hormone which binds to targets on the pituitary gland. This causes the release of adrenocorticotropin-releasing hormone, which binds to targets on the adrenal cortex and promotes the production of cortisol.

In the event of hypoglycemic stress, cortisol concentrations rise everywhere in the body as a result of this stress signaling. For Type 1 diabetics specifically, hypoglycemia is a common side-effect of treatment.

I also recognize that the anxiety response is largely mediated by amygdalae activity, and the amygdalae are known to have receptors for cortisol (they are the ‘fear’ center, after all). From my research, the morphology of dendrites in this brain structure as well as other centers for mood/emotion are shifted into less functional patterns as a consequence of chronic exposure to glucocorticoids such as cortisol (Krugers 2010). Additionally, glucocorticoids cause serotoninergic receptors to become less sensitive to activation (van Riel 2003).

So my questions are:

if hypofunctioning of serotonergic receptors in the Raphe Nucleus leads to excess firing of hippocampal and amygdalae neurons, which is believed to be one of the primary mechanism through which anxiety manifests itself, why hasn't chronically high levels of cortisol, as a result of hypoglycemia, been implicated more in anxiety disorders in Type 1 diabetics? Is there a link to clinical depression from here?

SSRIs are consistently used to treat anxiety in the short term, but for diabetics, the crux of the issue seems to be the chronic exposure to high levels of cortisol. Has anyone studied or seen this in their practices/research?

Sources:

Krugers 2010 http://www.ncbi.nlm.nih.gov/pubmed/20820185

van Riel 2003 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059694/

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