Más argumentos a mi favor:
1: Ther Umsch 1994 Nov;51(11):748-54
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[Cardiovascular effects and estrogen/gestagen substitution therapy]
[Article in German]
Kuhl H.
Abteilung fur gynakologische Endokrinologie, Universitats-Frauenklinik Frankfurt am Main.
After the menopause there is a profound increase in cardiovascular diseases which is mainly based on an enhanced development of atherosclerosis caused by an estrogen deficiency. The most important pathomechanisms are the rise in LDL-cholesterol and triglycerides as a result of an impaired elimination of LDL and remnants in the liver, and an enhancement of LDL oxidation in the arterial intima. Moreover, at the site of endothelial lesions the occurrence of vasospasms and platelet aggregation is facilitated in estrogen-deficient women which may lead to ischemia.
Epidemiological studies revealed that replacement therapy with natural estrogens reduces the risk of cardio-vascular diseases by 30 to 50%, whereby the protective effect is not impaired by the addition of progestogens. The mechanism of action is only partly based on the favorable effect of estrogens on lipid metabolism. Besides an increase in HDL, estrogens may reduce LDL-cholesterol by means of an enhancement of receptor-mediated elimination of LDL and remnants in the liver. A rise in triglycerides is of no clinical relevance, if based on an estrogen-induced increase in triglyceride synthesis and VLDL-LDL turnover. Even in the case of an unfavorable lipid pattern
estrogens may protect from atherosclerosis, as they inhibit LDL oxidation by scavenging free oxygen radicals. Finally, estrogens may cause vasodilation which is partly endothelium - dependent, but presumably is also based on the blockade of calcium influx into smooth muscle cells. This may be of particular importance in women with endothelial lesions, e.g. coronary sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 7839333 [PubMed - indexed for MEDLINE]
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1: Ann Endocrinol (Paris) 1979 Jan-Feb;40(1):47-8
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[Ischemic cardiovascular accidents during treatment with progestins alone. Apropos of 3 cases]
[Article in French]
de Gennes JL, Turpin G, Baulac L.
Three cases of ischaemic cardio-vascular accidents are reported under progestative treatment; the drug used was chlormadinone acetate (0,5 mg daily) in one patients, and norethisterone (5 mg daily) in two others. The accident was observed in two cases at the end of the second menstrual cycle and in one case after three years.
Lipid abnormalities have been detected in the three cases: minor type IV (two patients) and mixed hyperlipidaemia (one patient).
PMID: 87143 [PubMed - indexed for MEDLINE]
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1: Prog Clin Biol Res 1985;192:233-9
Related Articles, Links
Progesterone derivatives that bind to the digitalis receptor.
LaBella FS.
Examination of mammalian steroid hormones, their metabolites and semi-synthetic analogs in a radioreceptor binding assay for cardiac glycosides led to the identification of active derivatives of hydroxyprogesterone. The active compounds are potent inhibitors of purified sodium, potassium-ATPase and of the sodium pump in isolated tissues.
Metabolism of progesterone offers a mechanism for the generation of endogenous substances that resemble, both structurally and biologically, the digitalis cardioactive steroids.
PMID: 3001755 [PubMed - indexed for MEDLINE]
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A ver muchachones, quiero argumentos sólidos
Saludos.
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), son los prostágenos los que incrementan el riesgo cardiovascular, los cuales son componentes de muchas formulaciones anticonceptivas, no el estrógeno, el cual tiene un efecto positivo en los lípidos en la sangre.
