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This study cannot make the conclusion AT ALL.  They claim to say hormones should not be used to prevent chronic disease. Yet, the study they use to support this statement, the WHI, did not look at hormones.  The WHI looked at premarin and medroxyprogesterone acetate, a progestin.  They are not the hormones the body makes. Second, the WHI looked at women that were 6 years postmenopausal, on average, and then they added in bad drugs, disguised as hormone like, and then were dosed high.   If one desires to truly make a statement of prevention, one needs to pre-empt testing and therapy before disease.  Additionally, the study needs to match the hormones needed at the right physiologic level in the right balance.   One must also ensure proper hormone metabolism and know hormone receptor status.  This study does non of the above and the conclusion of this study is irrelevant.  In fact, I think the authors of this study have undergone scientific malpractice in their conclusions.

Fantastic read on the effects of progesterone metabolism on tumor and cancer growth.  Tumorigenesis is not just about the hormone, hormone balance, but about the metabolism of hormones.  This is why premarin is so carcinogenic: it is primarily metabolized by the 4-OH estrone pathway.

very nice article that looks at the balance of ER-alpha/ER-beta and their role in metabolic syndrome.  This article discusses the balance of  these receptors are tissue dependent in their effect.  I like their conclusion: "...but these mechanisms will never be completely understood if they are not considered in the context of a whole system.

Fantastic article written by John Lee, MD.  This article is a great review on saliva testing and hormone therapy as it relates to both men and women; even though this article is in reference to men.  Worth your time to read

Awesome article discusses the different balance of ER alpha and ER beta and the effects on tissue as it relates to proliferation versus differentiation.  This has clear implications in disease.  Physicians prescribing hormones without a knowledge and understanding of this are only causing potential harm to their clients.

thyroid hormone plays important role in heart failure and heart repair; thyroid balance critical

Balance of progesterone receptor A and B shown to influence survival rates in ER+/PR+ breast cancer on hormonal therapy.

Might the enzymes be more important than the hormones themselves?  The number is important i.e. progesterone, but how the number came to be is more important as it points to the underlying etiology.  Here, the balance of enzymes are found to direct cell line tumor potential.  The enzyme 5alpha-reductase increased production of the 5alpha-pregnanes which increased tumor potential.  In contrast, the enzymes 20alpha-hydrosteroid oxidoreductase and 3alpha-hydroxysteroid oxidoreductase increase production of the 4alpha-pregnanes, which decreased tumor potential.

The progesterone metabolites effect ER expression.

better cortisol pattern seen in women with good social support.  This is indicative of a better balanced HPA axis and thus immune system balance.  Significant implications in women with metastatic breast cancer.  Cortisol evaluated by saliva

saliva testing will benefit breast cancer patients in more ways than just checking hormone balance

good review of the physiology behind adolescent PCOS.  Though I hate this term because it treats PCOS as a diagnostic disease when it is simply a metabolically induced hormone balance.

oxytocin shown to inhibit appetite as an anorexigen.  As a hormone, prolactin, regulates energy balance

Meta-analysis finds that men with low total Testosterone, free Testosterone, and SHBG are more at risk for MetS than those with elevated levels.

The risks of estrogen metabolism are not clear cut.  Likely never will be due to the complexity of individual metabolism.  This study found no correlation between 2OH-Estrone and 2OH:16alpha-Estrone and breast cancer risk in ER+/PR+ breast cancer.  Translated: no benefit in breast cancer risk in 2OH-Estrone metabolism or increased 2OH:16alpha estrone metabolism.  There was a positive association between 2OH-Estrone and 2:16alpha-Estrone in women with ER-/PR- tumors and low BMI.

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Awesome article on progesterone metabolism in breast cancer.  The author, weibe, describes 2 categories of progesterone metabolites in breast tissue: 5alpha-pregnanes and 4-pregnenes.  The author describes 3 primary enzymes that control the balance between these 2 metabolites--5alpha reductase, 3alpha-HSO, and 20alpha-HSO.  The resultant balance of 5alpha-dihydroprogesterone and 3alpha-dihydroprogesterone helps to determine the cancer potential of breast tissue.

long endurance competitive events associated with catabolic hormone balances found in a low T:C ratio.  This occurs primarily through an elevation in cortisol and small drop in Testosterone.  The recovery phase is anabolic through a rise in T:C, primarily through a return to baseline by cortisol and an increase in Testosterone.

Progesterone metabolites are present on the membrane of ER/PR + as well as ER/PR - breast cancer cell lines.  The balance of 5 alpha pregnane:3 alpha pregnane regulates tumor genesis.  Estradiol increased 5 alpha pregnane receptors as well as 5 alpha pregnane unregulated itself via autocrine activity.  The 3 alpha pregnenes, 3 alpha hydroxyprogesterone and 20 alpha-dihydroprogesterone, decrease the 5 alpha pregnane receptors via paracrine activity.

Good discussion of the different effects of progesterone metabolites in breast cancer cell lines (in vitro).  This article focused on the biochemical balance of 5alpha pregnane: 3alpha HP.  The increase in this ration promoted proliferation and metastasis, where a decreased ratio did the opposite

Study finds that Testosterone regulates glucose metabolism, in part, through adiponectin production.  Early state of low T will slow the use of fats as a source of fuel and this results in an increased energy balance and results in the increased adiponectin production to increase metabolism.  Testosterone and adiponectin exist in an inverse relationship. This study does not mimic normal physiology.  Men with low T are unhealthy with significant metabolic dysfunction.  These young, "healthy" men were induced to a low T state--that is not a clear picture as the physiology of a "young healthy" man is quite different than that of one with low T.   Testosterone conversion to DHT increases GLUT4 and thus glucose uptake--another mechanism of Testosterone's effect on glucose metabolism.