Quote from: Naomi71 on February 01, 2016, 03:04:00 AM
This year I can finally start with HRT, but I was told that I will probably only get patches, because I had a heart attack last year and other methods might be riskier.
If you read the studies (I have plenty and you can find plenty), you will quickly realize that estrogen is actually CARDIOPROTECTIVE. It increases, for instance, nitric oxide which dilates blood vessels. The problem with older forms of estrogen which weren't
bio-identical (identical to what the body produces) is that they also increased blood pressure and increased clotting to a significant degree. Also, progestins used in combination with these estrogens are now thought to contribute to the increased cardiovascular risks due to their negative impact on blood vessels, counteracting the benefits of estrogen.
The reason why women are less prone to heart problems and heart attacks is due to estrogen. When their estrogen drops after menopause, their cardiovascular risks increase.
Therefore, bio-identical estrogen or ESTRADIOL, delivered through patches, gels, injections, pellets and even pills is beneficial for the heart. It does not increase clotting risks to a significant degree, especially non-orally (where it even protects against it), normalizes blood pressure and is good for the heart. You actually improve your odds in terms of cardiovascular complications and recurrences. Should you take bio-identical progesterone as well, it won't negate the effects of estrogen and might even add to the benefits.
Your options shouldn't be limited when it comes down to bio-identicals.
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Cardiovascular Research 69 (2006) 777 – 780"There is an
abundance of scientific evidence for the protective effect of estrogen against atherosclerosis, such as short-term vasodilating effects as well as long-term vascular protective and anti-atherosclerotic effects [2]. Epidemiological evidence shows that pre-menopausal women have a reduced risk for mortality from cardiovascular diseases [3] and that women are at a lower risk for the development of heart failure [4] and have enhanced cognitive function and reduced neurodegeneration associated with Alzheimer's disease and stroke [5]. Further proof for the protective effect of female gender is the fact that post-menopausal women have a similar or even increased risk for cardiovascular disease compared to men [3] and have an increased risk for adverse outcome after myocardial infarction and acute coronary syndromes, despite similar treatment with thrombolysis and percutaneous interventions [6]. It was therefore postulated that estrogen replacement would be beneficial in preventing cardiovascular diseases in post-menopausal females."
"The cardioprotective effect of estrogen is further supported by the findings that ovariectomy caused a loss of cardioprotection, which was regained by chronic estrogen replacement therapy."
"The vascular protective effects of estrogen and their mechanisms are thus fairly well-established."
The increase in cardiovascular incidences in the Heart and Estrogen/Progestin Replacement Study (HERS) and the WHI (Womens's Health Initiative) study was due to the progestin as no such results were found in women only taking estrogen.
J Am Coll Cardiol. 2000 Dec;36(7):2154-9."This is a randomized controlled primary prevention trial, in which
16,608 postmenopausal women aged 50–79 years with an
intact uterus received conjugated equine estrogens (CEE), plus MPA, or placebo.
The primary outcomes were nonfatal myocardial infarction and coronary
heart disease (CHD) death, with invasive breast cancer as
the primary adverse outcome. While the planned duration of
the treatment was 8.5 years, the CEE+MPA treatment arm
was stopped prematurely after 5.2 years, due to apparent increases
in cardiovascular events and breast cancer incidence
[7].
The evaluation of the CEE-alone treatment arm (women
without a uterus) is still ongoing, due to the absence of such
apparent increases in hazard. This is strongly suggestive
of a potentially harmful effect of the progestin used in the
study (MPA)."
CEE= conjugated equine estrogens
MPA= medroxyprogesterone acetate
Biochem Pharmacol. 2013 Dec 15;86(12):1627-42. "
Cardiovascular disease (CVD), such as coronary heart disease (CHD) and hypertension, is less common in premenopausal women (Pre-MW) than in men of the same age, suggesting vascular benefits of estrogen [1,2]. Also, the risk of CVD increases with age in postmenopausal women (Post-MW) compared with Pre MW, partly due to decreased plasma estrogen levels. Estrogen is the predominant sex hormone in women, affecting the development and function of the female reproductive system. Estrogen is commonly used as a contraceptive, and as a component of menopausal hormone therapy (MHT) for hot flushes, night sweats and vaginal dryness [3]. Earlier observational studies, such as the Nurses' Health Study (NHS) in the mid 1970s, suggested that estrogen therapy in Post-MW reduced the risk of CVD by 35% to 50% [1]. Also, a meta-analysis of observational studies showed 33% reduction in fatal CVD among MHT users compared with nonusers [3]. Experimental studies supported vascular benefits of estrogen. Acute administration of estrogen in female or male patients improves vasodilator responses and ameliorates myocardial ischemia [4]. Also, acute administration of estrogen in dogs and isolated rat and rabbit hearts lowers coronary vascular resistance and enhances coronary blood flow [5]. Estrogen modulates vascular function by targeting estrogen receptor (ER) in endothelial cells (ECs) and vascular smooth muscle (VSM) [1,2]. Estrogen also enhances the release of vasodilator substances such as nitric oxide (NO) and prostacyclin (PGI2), and decreases the production and effects of vasoconstrictors such as endothelin (ET-1) and angiotensin II (AngII) [1,2]."
Menopause. 2014 Jan 6."According to the National Heart, Lung, and Blood Institute,
24 which amassed data from seven major epidemiologic
studies, CVD incidence is 4 cases per 1,000 person-years for
women aged 45 to 54 years and 8 to 9 cases per 1,000 person-years
for women aged 55 to 64 years. The incidence of CHD
alone is 1 to 2 cases per 1,000 person-years in women aged 45
to 54 years and 3 to 6 cases per 1,000 person-years in women
aged 55 to 64 years. »
« Menopause is accompanied by a dramatic rise in the prevalence
of hypertension (HTN) in women, suggesting a protective
role for endogenous estradiol in BP regulation"
"Hassager et al40: This 2-year placebo-controlled study was
conducted on 110 early postmenopausal women to examine
the effects of percutaneous and oral estradiol, alone or with
progestogen, on BP. The investigators found that systolic BP
(SBP) and diastolic BP (DBP) remained unchanged in both
HT groups, whereas DBP tended to rise in the placebo groups.
Both estradiol regimens may have protected against the agerelated
increase in DBP noted in early postmenopausal
women. »
Eur J Endocrinol. 2014 Mar 10."The incidence of heart disease increases with age, but is lower in women than in men up to 75 years. A protective effect of female sex hormones or, alternatively, acceleration in male heart disease by testosterone at younger ages, could explain this sex difference."
Horm Mol Biol Clin Investig. 2014 May;18(2):89-103."The cardiovascular protection observed in females has been attributed to the beneficial effects of estrogen on endothelial function."
"estrogen alone or combined with progesterone has been associated with decreased blood pressure"
"Estrogens physiologically stimulate the release of endothelium-derived vasodilator factors and inhibit the renin-angiotensin system."
Rev Prat. 1993 Dec 15;43(20):2631-7."This favourable effect of estrogens is completed by other mechanisms which modify platelet aggregation, prostacyclin/thromboxane equilibrium, endothelin, etc., and which improve arterial wall morphology and vasoactive reactions. Some synthetic progestogens, given with oestrogens for endometrium control, may compromise these spectacular vascular benefits, but this is not the case with natural progesterone."
"there is no known theoretical risk when oestradiol is given parenterally, which in France is the favoured method. This type of replacement therapy with oestradiol should be more often prescribed to subjects with atherogenic hyperlipidaemia,
arterial hypertension or ischaemic coronary disease: not only it is not contraindicated, but it should soon become an indication."
Ann Clin Res. 1983;15 Suppl 38:1-121. (on oral estradiol)"Estradiol-17 beta substitution decreased the systolic and diastolic blood pressure in normotensive, hypertensive and borderline hypertensive postmenopausal women. The blood pressure of the hypertensive subjects decreased on average more than the blood pressure of the normotensive subjects."
"Estradiol-17 beta substitution decreased the systolic and diastolic blood pressure in normotensive, hypertensive and borderline hypertensive postmenopausal women."
"Irrespective of the pretreatment blood pressure levels, heart rate decreased during estradiol-17 beta substitution"
"Estradiol-17 beta substitution caused an increase in the blood volume in all groups of postmenopausal women"
"Cardiac output increased in the normotensive test subjects but decreased in the hypertensive and borderline hypertensive subjects"
Climacteric. 2012 Apr;15 Suppl 1:11-7. "There is a wealth of evidence to suggest that, unlike oral estrogens, transdermal estradiol does not increase the risk of venous thromboembolism, probably due to its lack of effect on the coagulation cascade, including thrombin generation and resistance to activated protein C, and does not increase the risk of stroke. It is cardioprotective, significantly reducing the incidence of myocardial infarction compared with non-users; it significantly reduces the incidence of new-onset diabetes, a risk factor for myocardial infarction. Micronized progesterone has also been shown not to increase the risk of venous thromboembolism and further reduced the incidence of new-onset diabetes when combined with transdermal estrogen. Micronized progesterone has a neutral effect on the vasculature, including a neutral or beneficial effect on blood pressure. Therefore, experimental and clinical data indicate that transdermal estradiol and micronized progesterone could represent the optimal HRT, particularly in women at risk of adverse events."
Oral estrogens referred to in this study are non bio-identical estrogens.
Lancet. 1993 Jul 17;342(8864):133-6."Acute administration of oestradiol-17 beta therefore has a beneficial effect on myocardial ischaemia in women with coronary artery disease. This effect may be due to a direct coronary-relaxing effect, to peripheral vasodilation, or to a combination of these mechanisms. Oestradiol-17 beta may prove to be a useful adjunct to the treatment of angina in postmenopausal women with coronary heart disease."
J Lipid Res. 2006 Feb;47(2):349-55."This prospective pilot study of 18 men with androgen-independent prostate cancer receiving ADT measured effects of TDE on lipid and inflammatory CVD risk factors before and after 8 weeks of TDE (...). During treatment, estradiol levels rose 17-fold; total cholesterol, LDL cholesterol, and apolipoprotein B levels decreased. HDL2 cholesterol increased, with no changes in triglyceride or VLDL cholesterol levels. Dense LDL cholesterol decreased and LDL buoyancy increased in association with a decrease in HL activity. Highly sensitive C-reactive protein levels and other inflammatory markers did not worsen. Compared with ADT, short-term TDE therapy of prostate cancer improves lipid levels without deterioration of CVD-associated inflammatory markers and may, on longer-term follow-up, improve CVD and mortality rates."
