Holy shit, I think you just broke the Internet, 
well........maybe just the noogleberry. 
Fantastic growth.
Lovely, do you mean Glucocorticoids and Mineralocorticoids?, or something else?.
The glucocorticoid receptor: Pivot of depression and of antidepressant treatment?
There is strong evidence for the notion that antidepressants exert these effects by modulating the GR. Such modulations, however, can be manifold and range from regulation of receptor expression to post-translational modifications, which may result in differences in GR nuclear translocation and GR-dependent gene transcription. The idea that the therapeutic action of antidepressants is mediated, at least in part, by restoring GR function, is consistent with studies showing that decreased GR function contributes to HPA axis hyperactivity and to the development of depressive symptoms. Conversely, excessive glucocorticoid signalling, which requires an active GR, is associated with functional impairments in the depressed brain, especially in the hippocampus, where it results in reduced neurogenesis and impaired neuroplasticity.
http://www.ncbi.nlm.nih.gov/pmc/articles...-32323.pdf
well........maybe just the noogleberry. Fantastic growth.
(01-07-2015, 12:50 AM)lovely11 Wrote: Mood problems are also from different types of progestogens forming into mineralcoiterroids, and gluccoriods inefficiently.
Lovely, do you mean Glucocorticoids and Mineralocorticoids?, or something else?.
The glucocorticoid receptor: Pivot of depression and of antidepressant treatment?
There is strong evidence for the notion that antidepressants exert these effects by modulating the GR. Such modulations, however, can be manifold and range from regulation of receptor expression to post-translational modifications, which may result in differences in GR nuclear translocation and GR-dependent gene transcription. The idea that the therapeutic action of antidepressants is mediated, at least in part, by restoring GR function, is consistent with studies showing that decreased GR function contributes to HPA axis hyperactivity and to the development of depressive symptoms. Conversely, excessive glucocorticoid signalling, which requires an active GR, is associated with functional impairments in the depressed brain, especially in the hippocampus, where it results in reduced neurogenesis and impaired neuroplasticity.
http://www.ncbi.nlm.nih.gov/pmc/articles...-32323.pdf