FEMALE HORMONE REPLACEMENT

Cholesterol profile improved by Estradiol
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Estradiol longevity and cardiovascular disease
Taxoxifen is not worth side effects
Estrogens provents hardening of the arteries thus cardiovascular disease
Setting the record straight with journal articles on HRT
HRT for Postmenopausal Women, and PhARMA Profits First
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HRT Studies, much fewer heart attacks, etc.
Breast-Firmer-HRT
Cholesterol profile improved by Estradiol
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healther skin with HRT
Bioidentical Hormone therapy advice
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22% muscle loss prevented with testosterone
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FDA Article on Menopause and HRT
Bioidentical Hormone therapy advice
Prempro settlement $330M
alcohol and higher estradiol and testosterone levels in postmenopausal women

Background: 

Estradiol (E2) is the most bio-active of the 4 human estrogens.  Most progestins, especially MPA and levonorgestrel (LNG) block activity at ER (block healthful effects of E2.  Since the beginning of the millennium Big PhARMA, behaving as a corporation, has assaulted the use of estrogen.  For the best concise analysis of the state of medical science go to http://healthfully.org/rc/id1.html.  The literature shows that the choice of progestins including progesterone have only minor effects on the cholesterol profile, but a great effect upon the oxidative protection offered by estradiol and other estrogens.  It is this lack protection from oxidative damage, and not the level of LDL that is the main causal factor in cardiovascular disease (see bottom article for a study on progestins effects upon cholesterol profile)--jk.  

Estrogen receptors are a group of proteins found inside cells. They are receptors that are activated by the hormone estrogen (17β-estradiol).[1] Two classes of estrogen receptor [ER] exist: ER, which is a member of the nuclear hormone family of intracellular receptors, and the estrogen G protein-coupled receptor GPR30 (GPER), which is a G protein-coupled receptor. This article refers to the former (ER).  [Low estradiol after menopause, the age when most breast cancers occur, would explain why blocking what don’t increase cancer survival.  Moreover it hasn’t been shown that the role of estrogen is to simulate growth/reproduction of breast cells--jk.] The ERα is found in endometrium, breast cancer cells, ovarian stoma cells, and the hypothalamus.[8] In males, ERα protein is found in the epithelium of the efferent ducts.[9]    

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http://circ.ahajournals.org/content/95/6/1378.short 1997; 95: 1378-1385 

American Heart Association

Antioxidant Protection of LDL by Physiological Concentrations of 17β-Estradiol

Background:  Exposure to estrogens reduces the risk for coronary artery disease and associated clinical events; however, the mechanisms responsible for these observations are not clear. Supraphysiological levels of estrogens act as antioxidants in vitro, limiting oxidation of low-density lipoprotein (LDL), an event implicated in atherogenesis. We investigated the conditions under which physiological concentrations of 17β-estradiol (E2) inhibit oxidative modification of LDL.

Conclusions:   Exposure of LDL to physiological levels of E2 in a plasma milieu is associated with enhanced resistance to Cu2+-mediated oxidation and incorporation of E2 derivatives into LDL. This antioxidant capacity may be another means by which E2 limits coronary artery disease in women.

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http://www.atherosclerosis-journal.com/article/S0021-9150(98)00020-3/abstract

Antioxidant protection of LDL by physiologic concentrations of estrogens is specific for 17-beta-estradiol

Atherosclerosis  Volume 138, Issue 2 , Pages 255-262, June 1998

Abstract 

Risk for coronary artery disease is reduced by exposure to estrogens, although the mechanisms of protection are not fully defined. Recent observations have shown that physiologic concentrations of 17-beta-estradiol (E2) exhibit antioxidant activity in vitro, slowing the formation of atherogenic, oxidized low-density lipoprotein (LDL). Using concentrations physiologically relevant for premenopausal women, we compared the antioxidant potency of estrone (E1), E2, and estriol (E3) as measured by their ability to inhibit LDL oxidation. Plasma was incubated with 10 nmol/l estrogens for 4 h at 37C, followed by LDL isolation and Cu2+-mediated oxidation in conjugated diene assays. Only E2 demonstrated antioxidant activity at these physiologic concentrations. Resistance to oxidation was not associated with sparing of endogenous α-tocopherol during plasma incubations. Incubation of plasma with radiolabeled estrogens yielded similar association of E1 and E2 with LDL which was 5–8-fold greater than the association of E3. Chromatographic analysis revealed the association of authenic E1with LDL, while plasma-derived E2 esters were the major form of E2 associated with LDL which was resistant to oxidation. Thus, conjugation in plasma and association of E2 esters with LDL appear to be specific for E2 among these estrogens and render this LDL resistant to oxidation by Cu2+. This antioxidant activity may be another means whereby E2 protects against coronary artery disease in women.

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http://www.sciencedirect.com/science/article/pii/002604959290295L

The inhibition of low-density lipoprotein oxidation by 17-βestradiol

Metabolism  Volume 41, Issue 10, October 1992, Pages 1110–1114

Abstract

The antioxidant activities of 17-β-estradiol (E2) and other steroid hormones were studied by determining their effect on copper-catalyzed (cell-free) and mononuclear cell-mediated oxidation of low-density lipoproteins (LDL), as measured by the production of thiobarbituric acid-reactive substances (TBARS). The oxidation of LDL increased linearly with copper concentrations ranging from 0 to 10 μmol/L. E2 at a concentration of 1 μmol/L inhibited LDL oxidation by 37% to 62% at the various concentrations of copper. In a time-course study, E2 at 1 μmol/L delayed the onset of LDL oxidation in the presence of 5 μmol/L copper. E2 (1 μmol/L) inhibited TBARS production catalyzed by 5 μmol/L copper by 54%, compared with 60% inhibition by 1 μmol/L butylated hydroxytoluene (BHT), a known inhibitor of lipid peroxidation. Estriol at 5 μmol/L decreased LDL oxidation by 49%. Dehydroepiandrosterone (DHEA), testosterone, and estrone had no significant effects. E2 was also an effective inhibitor of mononuclear cell (MNC)-mediated oxidation of LDL, but had no effect on superoxide production by these cells. The onset of TBARS formation from cell-mediated LDL oxidation was also delayed by incubation with 1 μmol/L E2. The results indicate that estrogen may protect against atherosclerosis by inhibiting lipoprotein oxidation.

 

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This study shows that MPA blocks the anti-oxidation effect of estrogen upon LDL.   

http://www.sciencedirect.com/science/article/pii/S0021915099002191

Estradiol 17β inhibition of LDL oxidation and endothelial cell cytotoxicity is opposed by progestins to different degrees

Atherosclerosis  Volume 148, Issue 1, January 2000, Pages 31–41

Abstract

Progestins oppose the effects of estrogens in many biological systems, but it is not known if progestins oppose the antioxidant effects of estrogen and to differing degrees. To test these questions, the effects of various sex steroids on LDL oxidation and cytotoxicity were studied in the absence or presence of endothelial cells [in large blood vessels]. Freshly isolated LDL was incubated in the presence of Cu++ in the absence or presence of cultured bovine aortic endothelial cells in phenol red-free medium and without or with hormones in 0.5% ethanol. The hormones included 17β-estradiol (E2), progesterone (Pg), norgestimate (NGM), levonorgestrel (LNG), and medroxyprogesterone acetate (MPA). LDL oxidation was measured as formation of conjugated dienes, lipid peroxides, and TBARS, and cyotoxicity by tetrazolium salt reduction (MTT reduction). Progestins diminished conjugated diene lag phase, accelerated lipid peroxide and TBARS production in the absence and presence of cells and accelerated cytotoxicity. When E2 and progestin were incubated with cells at a molar ratio of 1:5, lipid peroxides were reduced from baseline by E2 alone 31%, E2/Pg 29%, E2/NGM 16%, E2/LNG 9% (all P<0.05 or more) and E2/MPA 8% (ns) (E2 or E2/Pg>E2/NGM, E2/LNG and E2/MPA [P<0.001]; E2/NGM>E2/LNG or E2/MPA [P<0.05]). MTT reduction followed a similar gradient, greatest with E2 alone, least with E2/MPA. Conclusions: Progestins promote LDL oxidation and, conjointly, endothelial cell cytotoxicity. Progestins oppose the antioxidant and cytoprotective effects of estrogen when given in combination. MPA and LNG have the strongest prooxidant and cytotoxic effects, which may limit the cardiovascular benefit of estrogen during combined administration in vivo.

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Important article because when considering CVD and morality rates this article confirms that it isn’t the level of cholesterol and bad cholesterol LDL that causes CVD and death, but rather oxidative damage (the articles above).  MPA which doesn’t affect cholesterol levels, but rather blocks estradiol’s anti-oxidative property, and as a consequence very significant increase CVD and death therefrom. 

http://www.fertstert.org/article/S0015-0282%2801%2901699-5/abstract  Fertility and Sterility

Endocrinology and Metabolic Medicine, Division of Medicine, Imperial College School of Medicine, London, United Kingdom. i.godsland@ic.ac.uk Fertility and Sterility

Effects of postmenopausal hormone replacement therapy on lipid, lipoprotein, and apolipoprotein (a) concentrations: analysis of studies published from 1974-2000.

Abstract 

Objective: To establish reference estimates of the effects of different hormone replacement therapy (HRT) regimens on lipid and lipoprotein levels.

Design: Review and pooled analysis of prospective studies published up until the year 2000.

Setting: Clinical trials centers, hospitals, menopause clinics.

Patient(s): Healthy postmenopausal women.

Intervention(s): Estrogen alone, estrogen plus progestogen, tibolone, or raloxifene in the treatment of menopausal symptoms.

Main Outcome Measure(s): Serum high- and low-density lipoprotein (HDL and LDL) cholesterol, total cholesterol, triglycerides, and lipoprotein (a).

Result(s): Two-hundred forty-eight studies provided information on the effects of 42 different HRT regimens. All estrogen alone regimens raised HDL cholesterol and lowered LDL and total cholesterol. Oral estrogens raised triglycerides. Transdermal estradiol 17-beta lowered triglycerides. Progestogens had little effect on estrogen-induced reductions in LDL and total cholesterol. Estrogen-induced increases in HDL and triglycerides were opposed according to type of progestogen, in the order from least to greatest effect: dydrogesterone and medrogestone, progesterone, cyproterone acetate, medroxyprogesterone acetate, transdermal norethindrone acetate, norgestrel, and oral norethindrone acetate. Tibolone decreased HDL cholesterol and triglyceride levels. Raloxifene reduced LDL cholesterol levels. In 41 studies of 20 different formulations, HRT generally lowered lipoprotein (a).

Conclusion(s): Route of estrogen administration and type of progestogen determined differential effects of HRT on lipid and lipoprotein levels. Future work will focus on the interpretation of the clinical significance of these changes.

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