Mar 18, 2013
USA / Europe
As many forum users probably know, glucocorticoid treatment is one of the main lines of therapies in cancer. It is considered highly beneficial due to reducing inflammation and swelling/pain in inflamed/cancerous tissue. However, recent studies have shown that immune dysfunction is perhaps the main reason behind the initiation and progression of cancer, and that restoring immune activity may be as simple as blocking estrogen.
Immune Decline (Not Genetics) Causes Cancer And It Can Be Easily Fixed
Reducing Estrogen Synthesis Regenerates Thymus Destroyed By Aging

Considering that glucocorticoid are the most potent agents known for destroying the thymus gland (i.e. thymolytic), and that glucocorticoids are among the most potent inducers of estrogen synthesis, it seems that administering glucocorticoid to cancer patients would be a rather bad idea.
The study below corroborates this idea and suggests that glucocorticoid therapy in cancer could be rather dangerous except in a very small proportion of patients.

Corticosteroid co-treatment induces resistance to chemotherapy in surgical resections, xenografts and established cell lines of pancreatic cancer. - PubMed - NCBI
"...In conclusion, we show by in vitro,ex vivo and in vivo studies that application of DEX renders pancreatic cancer cells resistant to apoptosis and promotes proliferation following cytotoxic therapy. This is in contrast to the effect of GCs in lymphoid cells and may involve cell type specific regulation of survival molecules such as SGK-1 and MKP-1 together with anti-apoptotic molecules such as X-IAP and Bcl-2. Thus, while some properties of GCs may be of benefit, induction of resistance in tumour cells towards cancer therapy may be dangerous for patients. Prospective clinical studies which do not exist until now, are urgently needed."


Thread starter
Mar 18, 2013
USA / Europe

I disagree.
Comparison of the effect of cortisol on aromatase activity and androgen metabolism in two human fibroblast cell lines derived from the same individ... - PubMed - NCBI
Cortisol induces aromatase expression in human placental syncytiotrophoblasts through the cAMP/Sp1 pathway. - PubMed - NCBI

Btw, the studies you posted do not show corticoids decreasing aromatase. They talk about the GR receptors and show cortisol sometimes antagonizes the ER. That is not the same as inhibiting aromatase. As far as estrogen - if estrogen blocks the GR then it does not induce GR resistance but actually treats it. Agonists induce resistance by downregulating a receptor, so if estrogen inhibits GR then it is an antagonist. RU486 is a GR antagonist and it is used to reverse GR resistance.
Finally, in Cushing syndrome (excess cortisol) about 80% of the male patients have gyno. Gyno is caused by estrogen/prolactin, so the high cortisol in those patients must be increasing estrogen/prolactin somehow, which matches what I mentioned before and the studies I posted.
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