Progestins are NOT progesterone


I want to make this very very clear:  natural progesterone  is beneficial and lessens cancer risk whereas synthetic “progestin” which is a near-miss, a knock off of progesterone is dangerous and worsens cancer risk.  This is a classic example of a near miss, a half-truth if you will, being worse than a lie.   So, why do scientists like Dr. Pasqualini (below) spend millions of dollars researching progestins and why do Big Pharma spend millions marketing progestins despite their product having been considered so dangerous that a huge multi-center study was halted (PremPro)?  Because,d ear reader, natural progesterone, despite being safe and effective when prescribed appropriately, is unpatentable and therefore not profitable. The patented progestin (again a synthetic knock-off) however promises profits, if only it can somehow be seen to not be lethal…

1: Gynecol Endocrinol. 2007 Oct;23 Suppl 1:32-41.

Progestins and breast cancer.

Pasqualini JR.

Hormones and Cancer Research Unit, Institut de Puériculture et de Périnatalogie, Paris, France.

Progestins exert their progestational activity by binding to the progesterone receptor (form A, the most active and form B, the less active) and may also interact with other steroid receptors (androgen, glucocorticoid, mineralocorticoid, estrogen). They can have important effects in other tissues besides the endometrium, including the breast, liver, bone and brain. The biological responses of progestins cover a very large domain: lipids, carbohydrates, proteins, water and electrolyte regulation, hemostasis, fibrinolysis, and cardiovascular and immunological systems. At present, more than 200 progestin compounds have been synthesized, but the biological response could be different from one to another depending on their structure, metabolism, receptor affinity, experimental conditions, target tissue or cell line, as well as the biological response considered. There is substantial evidence that mammary cancer tissue contains all the enzymes responsible for the local biosynthesis of estradiol (E(2)) from circulating precursors. Two principal pathways are implicated in the final steps of E(2) formation in breast cancer tissue: the ‘aromatase pathway’, which transforms androgens into estrogens, and the ‘sulfatase pathway’, which converts estrone sulfate (E(1)S) into estrone (E(1)) via estrone sulfatase. The final step is the conversion of weak E(1) to the potent biologically active E(2) via reductive 17beta-hydroxysteroid dehydrogenase type 1 activity. It is also well established that steroid sulfotransferases, which convert estrogens into their sulfates, are present in breast cancer tissues. It has been demonstrated that various progestins (e.g. nomegestrol acetate, medrogestone, promegestone) as well as tibolone and their metabolites can block the enzymes involved in E(2) bioformation (sulfatase, 17beta-hydroxysteroid dehydrogenase) in breast cancer cells. These substances can also stimulate the sulfotransferase activity which converts estrogens into the biologically inactive sulfates. The action of progestins in breast cancer is very controversial; some studies indicate an increase in breast cancer incidence, others show no difference and still others a significant decrease. Progestin action can also be a function of combination with other molecules (e.g. estrogens).

In order to clarify and better understand the response of progestins in breast cancer (incidence, mortality), as well as in hormone replacement therapy or endocrine dysfunction, new clinical trials are needed studying other progestins as a function of the dose and period of treatment.   (DR. WEEKS COMMENT:  FORGET THE PROGESTINS, USE PROGESTERONE!)

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