One nutrient may be all it takes to keep the prostate healthy
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How to lower estrogen and prevent prostate cancer
Prostate cancer is one of the most common cancers on the planet.
But it remains thoroughly misunderstood by common medical thinking and practitioners.
Androgens like testosterone and even DHT have been identified as the culprits behind prostate cancer, when this is far from reality.
Aging men have much less testosterone and DHT and yet they are the population most susceptible to prostate cancer.
Why is that? The answer is probably estrogen.
Estrogen is a major player in prostate cancer, but it is barely even mentioned on the wikipedia page for prostate cancer.
Quite the opposite, estrogen has even been used as a treatment (!) for prostate cancer in the past.
The rationale was that estrogen could suppress androgen levels, but it was obviously a terrible idea.
“Prolonged treatment of adult rodents with estrogens (…) leads to epithelial metaplasia (…) even adenocarcinoma of prostate speaking for the role of estrogen in prostate cancer development.” – Härkönen & Mäkelä
In particular, too little attention is given to the enzyme aromatase, which makes estrogen by turning testosterone into estrogen.
“This study demonstrates local estrogen biosynthesis in prostate-induced aromatase gene expression in malignancy and potential alteration of aromatase promoter use with disease progression. These data provide a basis for continued investigation of local estrogen production and its potential role in prostate disease.” – Ellem et al. (2004)
Estrogen is an hormone of proliferation and unconstrained growth, which characterizes the states of cancer involving tumors:
“Locally produced or metabolically transformed estrogens may differently affect proliferative activity of prostate cancer cells. Aberrant aromatase expression and activity has been reported in prostate tumor tissues and cells, implying that androgen aromatization to estrogens may play a role in prostate carcinogenesis or tumor progression.” – Carruba (2007)
This might be difficult to understand in a context where the androgen theory for prostate cancer has permeated the culture for so long:
“In summary, although multiple consistent evidence suggests that estrogens are critical players in human prostate cancer, their role has been only recently reconsidered, being eclipsed for years by an androgen-dominated interest.” – Carruba (2007)
Knowing this, the most important target for intervention is probably suppressing aromatase activity, which turns protective androgens like testosterone into estrogen.
What modulates aromatase? As it turns out, the answer is quite straightforward:
‘’The enzyme that makes estrogen, aromatase, is activated by anything that stresses cells.” – Ray Peat (2013)
Any type of stress, be it nutritional, psychological or environmental (lack of light, EMF exposure, toxins etc.) contributes to this state of aromatase activity and excess estrogen.
Several things, like sunshine exposure, vitamin D supplementation, good nutrition and something like white button mushrooms, have potent anti-aromatase effects.
These can all be protective against the effects of estrogen on prostate cancer.
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Härkönen PL, Mäkelä SI. Role of estrogens in development of prostate cancer. J Steroid Biochem Mol Biol. 2004 Nov;92(4):297-305. doi: 10.1016/j.jsbmb.2004.10.016. Epub 2004 Dec 19. PMID: 15663993.
Carruba G. Estrogen and prostate cancer: an eclipsed truth in an androgen-dominated scenario. J Cell Biochem. 2007 Nov 1;102(4):899-911. doi: 10.1002/jcb.21529. PMID: 17786930.
Ellem SJ, Schmitt JF, Pedersen JS, Frydenberg M, Risbridger GP. Local aromatase expression in human prostate is altered in malignancy. J Clin Endocrinol Metab. 2004 May;89(5):2434-41. doi: 10.1210/jc.2003-030933. PMID: 15126575.
[25:25] Learned Helplessness, Nervous System, Stress, Thyroid. KMUD Ask Your Herb Doctor, September 2013
Chen S, Oh SR, Phung S, Hur G, Ye JJ, Kwok SL, Shrode GE, Belury M, Adams LS, Williams D. Anti-aromatase activity of phytochemicals in white button mushrooms (Agaricus bisporus). Cancer Res. 2006 Dec 15;66(24):12026-34. doi: 10.1158/0008-5472.CAN-06-2206. PMID: 17178902.