home - Boilers
The importance of hormones in the body of a pregnant woman. Hormones during pregnancy: what changes await the expectant mother? Estrogens and pregnancy

UDC 577.175.64:618.2(047.31) DOI:

MODERN CONCEPTS ON THE ROLE OF ESTROGEN DURING PREGNANCY

(LITERATURE REVIEW)

I.V.Dovzhikova, M.T.Lutsenko

Federal State Budgetary Scientific Institution "Far Eastern Research Center for Physiology and Pathology of Respiration", 675000, Blagoveshchensk, st. Kalinina, 22

The purpose of the article is to analyze the significance of estrogen during pregnancy. The mechanism of hormone effects is briefly described. The influence of estrogens on uteroplacental blood flow, their necessity for launching the program of tissue morphogenesis in the placenta and uterus, the effect on the production of other steroid and protein hormones, the stimulating effect on the work of 11p-hydroxy-steroid dehydrogenase, and the regulation of low-density lipoprotein expression are considered. Growth factors that serve as estrogen mediators are shown. The conclusion is presented that at the beginning of pregnancy, estrogens contribute to the morphological and functional growth, development and differentiation of the placenta, in the second half of pregnancy, estrogens stimulated functional maturation. In addition, hormones play an important role in the development of the lungs, kidneys, liver, ovarian follicles, fetal bone tissue and contribute to the formation of various changes in the mother's body necessary to maintain pregnancy.

Key words: estrogens, mechanism of action, pregnancy.

MODERN CONCEPTS OF ESTROGENS ROLE AT PREGNANCY (REVIEW)

I.V.Dovzhikova, M.T.Lutsenko

Far Eastern Scientific Center of Physiology and

Pathology of Respiration, 22 Kalinina Str., Blagoveshchensk, 675000, Russian Federation

The article analyzes the importance of estrogen during pregnancy. The mechanism of hormone effects is summarized. The effect of estrogen on utero-placental blood flow, its necessity to run tissue morphogenesis in placenta and uterus, the impact on other steroid and protein hormones production, stimulating effect on 1ip-hydroxysteroid dehydrogenase work, regulation of LDL expression are studied. The growth factors that are mediators of estrogen are shown. There was made a conclusion that in early pregnancy estrogens contribute to morphological and functional growth, development and differentiation of placenta and in the second half of pregnancy estrogens stimulate functional maturation. Furthermore, hormones play an important role in the development of lung, kidney, liver, ovarian follicles, fetal bone and promote the formation of different changes in the mother necessary for the maintenance of pregnancy.

Key words: estrogens, mechanism of action, pregnancy.

Female sex steroid hormones play a huge role during gestation. Recently, however, research efforts have focused mainly on progesterone and its metabolites. When studying estrogens, the emphasis is on the analysis of their influence outside of pregnancy (the mechanism of carcinogenesis, the state of bone tissue, the cardiovascular and nervous systems). Reviews on the importance of estro-

genes during pregnancy, the current literature available to us is insufficiently represented. The aim of our work was to analyze the action of these hormones during the gestational period.

The mechanism of action of estrogens

Estrogens, like other steroid hormones, exercise their action through estrogen receptors (ERs), members of the steroid-receptor superfamily, which are also transcription factors. The most well studied receptors of the most active estrogen - estradiol - a and p. CEA are localized in the organs of the female reproductive system, as well as in the placenta - syncytiotrophoblast and cytotrophoblast. ERs are found in the testes, ovaries, spleen, thymus, adrenals, pituitary, brain, kidneys, and skin. Research has shown that these two RE subtypes respond differently depending on the ligand and may have different roles in gene regulation. The existence of another RE, the so-called receptor, penetrating the membrane 7 times and associated with G-protein (GPER), has been proved. In addition to the receptor mechanism of action, so-called "fast" non-genomic effects are inherent in estrogens. Such effects occurring in a short period of time are also described for other steroid hormones (for example, progesterone). In the placenta, the actions of estrogens are carried out in a classical way - through receptors.

There is an opinion that the value of estrogens during gestation is negligible. This point of view is based on studies of the role of hormones in conditions of their suppressed synthesis (for example, in congenital lipoid hyperplasia of the adrenal glands, insufficiency of placental aromatase or sulfatase). In such studies, it was found that a decrease in estrogen genesis did not lead to termination of pregnancy. The question arises: for what reason does the placenta produce such a large amount of estrogen? To answer it, let's try to understand the role of these hormones during pregnancy.

Effect of estrogen on uteroplacental blood flow

One of the most important functions of estrogens is their ability to influence uteroplacental blood flow. Moreover, the most effective hormone in this case is estriol, the amount of which increases dramatically during gestation.

The mechanisms of such influence are different. Estrogens affect the vascular endothelium by increasing the production of a number of vasodilators, such as nitric oxide, endothelial hyperpolarization factor, and prostacyclin. Estrogen activation of endothelial NO synthase can occur by three different mechanisms: through stimulation of enzyme gene expression by CEA; via activation of a signaling pathway consisting of phosphoinositide 3-kinase - a protein kinase

AKT, which phosphorylates NO-synthase, which leads to an increase in the activity of the latter; and through an increase in the expression of calmodulin, which is required for calcium-dependent stimulation of NO synthase. Estrogens shift the balance of prostanoid synthesis to the vasodilator prostacyclin (PGI2). They increase PGI2 production through stimulation of cyclooxygenase 1 and PGK synthase activity. At the same time, estrogens inhibit the induction of type 2 cyclooxygenase and, accordingly, the synthesis of prostaglandin E2 in the vessels.

In addition, estrogens interfere with the action of traditional vasoconstrictors (for example, endothelin 1) and reduce the expression of angiotensin-converting enzyme in endothelial cells, as well as angiotensin II receptor 1. It has also been found that estrogens affect the blood coagulation system: they lower the level of fibrinogen, antithrombin III and protein S.

With the advent of powerful new molecular methods of research, it is becoming clear that the mechanisms of action of estrogens are much more diverse and complex than originally thought.

Estrogens and morphogenesis of tissues of the uterus and placenta

Estrogens are necessary to launch the tissue morphogenesis program in the placenta and uterus. Previously, it was found that, despite the fact that in vivo uterine cells were highly sensitive to estrogens, in vitro they almost completely ceased to respond to physiological doses of these hormones. This fact was explained by the presence in the body of growth factors that serve as mediators of steroid hormones due to autocrine and paracrine action, which contributes to the regulation of proliferation and differentiation processes. Estrogens potentiate the effects of a number of factors necessary for morphological and functional differentiation.

For maximum exchange between the circulatory systems of the mother and fetus, it is necessary that the capillaries make up more than half the mass of the placental villi. Growth factors and adhesion molecules required for angiogenesis include: fibroblast growth factor, vascular endothelial growth factor, insulin-like growth factor, the epidermal growth factor family, angiopoietins, nitric oxide, and various integrins required for cell attachment.

One of the most powerful and widely recognized factors influencing the development of vessels in the villi is VEGF - vascular epidermal growth factor, also known as vascular permeability factor or vasculotropin. VEGF plays a key role in stimulating the assembly of endothelial cells into capillaries. During pregnancy, the activation of this protein by estrogens underlies vasculogenesis (the formation of the embryonic vascular system) and angiogenesis (the growth of new vessels in already

existing vascular system). It stimulates mitosis, activates the action of serial proteases (uPA and tPA) and collagenases, increases endothelial cell chemotaxis, induces endothelial cell permeability leading to extravasation of plasma proteins to provide a matrix for endothelial cell migration. Most of all, VEFR is produced in the cytotrophoblast (compared to syncytiotrophoblast and Kashchenko-Hofbauer cells).

When stimulating vascular morphogenesis, VEFR acts in conjunction with two proteins - angiopoietin-1 and angiopoietin-2. It has been established that type 1 angiopoietin is secreted from both cytotrophoblast and syncytiotrophoblast, while type 2 angiopoietin expression is found predominantly in cytotrophoblast. Angiopoietin-1 promotes the association of endothelial cells, smooth muscle cells, and pericytes for the maturation of nascent blood vessels. Anhypoetin-2, on the contrary, loosens the vascular wall so that endothelial cells become available for VEGF. All together ensures vasculogenesis and thus blood flow in the placenta and, consequently, the growth and development of the fetus.

Estrogens regulate the expression of vascular growth factor and angiopoietins through their receptors, paracrinely ensuring the promotion of the vascular system of the placental villi in the first half of pregnancy. The specific mechanism of regulation is not exactly known, there are suggestions about the involvement of various transcription factors (for example, the protein hypoxia-inducible factor - H1T-1).

The main fibroblast growth factor, bFGF, which is also regulated by estrogens, has been well studied. bFGF, inducing the proliferation of endotheliocytes, leads to an increase in the number of vessels. It also controls the production of enzymes that cause remodeling of the extracellular matrix, in particular collagenase, matrix metalloproteinases and plasminogen activator, which promote vasodilation, and is responsible for chemotaxis. In addition, it was found that changes in the bFGF ligand/receptor system can cause bleeding by disrupting the expression of integrins, which are cell adhesion molecules and are closely involved in the processes of angiogenesis.

Estrogens have a potentiating effect on the family of epidermal growth factors (EGF). It is believed that EGF facilitates implantation, it promotes the growth of the blastocyst and the proliferation of trophoblasts. Estrogens potentiate the action of TGF-R, which belongs to the EGF family. Transforming growth factor regulates cell growth, is involved in the processes of apoptosis and tissue remodeling, and plays a fundamental role in the formation of the extracellular matrix.

The most important effect of EGF is its participation in the regulation of the expression of insulin-like growth factor - IPFR-1. According to many studies

niyam, IPFR-I and, probably, IPFR-II are mediators of estrogen action in tissues. Estrogen stimulates the production and expression of IPFR-I and inhibits the binding protein of insulin-like growth factor (IPGF-3). IPFRSP control the activity of IPFR in the bloodstream and tissues. IPFR ensures cell proliferation, differentiation and survival. IPFR receptors have tyrosine kinase activity and adapters - IRS-I/Shc are used as secondary messengers in signal transmission into the cell, which, through the intracellular signaling pathway IRS/PI3K/AKT, in turn, ensure cell survival through Shc/Ras/Crb2/ MAP kinase - cell proliferation. Many authors insist on the leading role of this factor in myocyte proliferation.

Thus, estrogens play one of the key roles in the process of cell proliferation. In this case, hormones act not only through growth factors. Cell proliferation is regulated by cell cycle control mechanisms, including a set of cyclin-dependent kinases (CDK-cyclin-depended kinases, serine/threonine-protein kinases) along with their activators (cyclins) and inhibitors. Estradiol directly (through a signaling pathway including the sequence of phosphoinositide-3-kinase - AKT - GSK-3P) regulates the cell cycle. In addition, under the action of estradiol, the progression of the cell cycle from G- to S-phase is accelerated by increasing the activity of CDK4 and CDK2, stimulating the expression of cyclin D1, and reducing the level of CDK inhibitors.

Estrogens and mitochondria

Estrogens are able to profoundly affect mitochondrial function by increasing oxidative phosphorylation activity and, at the same time, they reduce superoxide production in mitochondria, which is accompanied by a decrease in lipid peroxidation. The exact mechanism of action of estrogen is unknown. A direct genomic effect is not excluded, since estrogen receptors have been found on mitochondria. In addition, estradiol affects mitochondrial function by modulating the activity of proteins of the PPARg coactivator 1 family (gamma peroxisome proliferator receptors), which are regulators of mitochondrial protein expression.

The role of estrogens in the second half of pregnancy

So, at the beginning of pregnancy, estrogens contribute to the morphological and functional growth, development and differentiation of the human placenta. In the second half of pregnancy, estrogens stimulated functional maturation, which manifested itself in several ways. Firstly, in the form of regulation of the expression of LDL receptors, which specifically stimulates the absorption of lipoproteins. It should be noted that this fact took place only in the placenta and did not affect the maternal organism. In-second-

In other words, estrogens activate the enzyme cytochrome P450scc, thereby promoting the biosynthesis of progesterone in the placenta. In other words, some steroid hormones affect the formation of others and thus regulate their action.

Estrogens, specifically estradiol, stimulate the production of human chorionic gonadotropin. The hormone has a trophic effect on the implanted egg and adjacent tissues, stimulates the development and secretory activity of the corpus luteum, is involved in the regulation of the biosynthesis of progesterone and estrogens in the placenta, promotes the mutual conversion of estrogens and androgens. Data on another protein hormone - chorionic somato-mammotropin are contradictory. Some researchers believe that estrogens stimulate the production of the hormone in the placenta, while others, on the contrary, suppress it. Chorionic somatomammotropin, also known as placental lactogen, is a special peptide hormone produced only by the placenta, it plays an important role in the maturation and development of the mammary glands during pregnancy and in their preparation for lactation.

At the same time, estrogens regulate the localization and development of the 11p-hydroxysteroid dehydrogenase enzyme system in the syncytiotrophoblast, which increases the transplacental oxidation of maternal cortisol to cortisone and leads to maturation of the hypothalamus-pituitary-adrenal axis in the fetus at the end of pregnancy. Before its formation, cortisol from the mother freely penetrated to the fetus and inhibited the fetal synthesis of glucocorticoids. After the formation of the enzyme system, 11p-hydroxysteroid dehydrogenase II inhibits 90% of corticosteroids entering the placenta. As a result of this cascade of events, there is an increase in the pituitary expression of proopiomelanocortin/ACTH and key enzymes, for example, 3p-hydroxysteroid dehydrogenase and P450c17. This leads to adrenocortical self-sufficiency: the adrenal cortex begins to produce glucocorticoids, which are necessary for fetal maturation and neonatal survival.

Estrogen modulates steroidogenesis in the fetal adrenal glands in several ways. Estradiol indirectly increases the production of dehydroepiandrosterone in the fetal adrenal glands by increasing the production of ACTH, which stimulates the synthesis of this estrogen precursor. At the same time, it directly inhibits the production of dehydroepiandrosterone through a decrease in the activity of the P450c17 enzyme. The latter also helps maintain normal estrogen levels during pregnancy.

Estrogens control the development of fetal ovarian follicles. The regulation of folliculogenesis by estrogens is proved by the presence of EC and a number of experiments in which the number of follicles was significantly reduced when the synthesis of these hormones was suppressed. Oocytes need nutrients that

derived from surrounding cells. Microvilli play an important role in this process. Estrogens regulate the formation of microvilli in the fetal ovaries. In the absence of hormones, oocytes had a significantly smaller number of villi on the plasma membrane, which ensured the absorption of the nutrient substrate from the surrounding cells. As to the mechanism by which estrogens regulate, this remains to be explored. It is assumed that the development of oocyte microvilli requires phosphorylation of the binding protein α-ezrin and expression of α-actinin, which is necessary for the final stage of microvillus formation. The expression of α-actinin, as well as the localization of ezrin phosphate and the SLC9A3R1 gene (encoding the ezrin-binding protein) in the oocyte membrane, are regulated by estrogens.

In addition, estrogens play an important role in the development of the lungs, kidneys, liver, and bone tissue of the fetus.

Effects of estrogen on a woman's body during pregnancy

Estrogens affect not only the development of the fetus and placenta, but also contribute to various changes in the mother's body that are necessary to maintain pregnancy.

Under the influence of estrogens, not only blood circulation in the uteroplacental region changes, but also in the entire cardiovascular system, including the cerebral blood flow of a pregnant woman. For example, during pregnancy there is a 40-50% increase in plasma volume, a 25% increase in erythrocyte mass and, consequently, an increase in maternal blood volume as a whole. These changes are associated with an increase in cardiac output, an increase in uteroplacental blood flow, which accounts for as much as 25% of total cardiac output, and a 20-35% decrease in total peripheral resistance. The exact mechanisms of hormone action are still being studied. For example, plasma volume increases as a result of estrogen stimulation of the renin-angiotensin system, which leads to an increase in aldosterone production and, consequently, the reabsorption of sodium and water ions.

Estrogens increase the availability of protein in the body, maintain a positive nitrogen balance, thereby ensuring the growth of the fetus. In addition, female sex hormones act on the function of the nervous system, mainly through the pituitary-gonadal axis: they affect behavior, response to stress, sleep, heart rate, body temperature.

It is believed that estrogens during gestation have an effect opposite to progesterone. For example, they increase uterine contractility by increasing the excitability of the myometrium through a change in the resting membrane potential and the formation of "gap junctions", and through an increase in the production of prostaglandins.

It is widely believed that estrogens play a fundamental role in regulating the sequence of events leading up to childbirth. They potentiate a series of changes including increased production of prostaglandins G2 and F2, increased expression of prostaglandin receptors, oxytocin receptors, a-adrenergic agonist, modulation of membrane calcium channels, increased connexin synthesis, regulation of the enzyme responsible for muscle contraction (MLCK). All of these changes allow the coordination of uterine contractions.

So, during pregnancy, estrogens improve uteroplacental blood flow, promote neovascularization of the placenta (for optimal gas exchange and the supply of nutrients necessary for the rapid development of the fetus and placenta). Estrogens influence the production of other steroid and protein hormones, stimulate 11P-hydroxysteroid dehydrogenase in the placenta, regulate LDL expression, carry out functional/biochemical differentiation of trophoblast cells, and perform many other functions. Estrogens are believed to play a central, integrating role in modulating placental-fetal dialogue and signaling, leading to the maintenance of pregnancy.

LITERATURE

1. Lutsenko M.T., Samsonov V.P. The main directions and prospects for the development of research work at the Institute of Physiology and Pathology of Respiration, Siberian Branch of the Russian Academy of Medical Sciences // Bulletin of Physiology and Pathology of Respiration. 1998. Issue 2. S.1-9.

2. Lutsenko M.T. Morphofunctional characteristics of the fetoplacental barrier in herpes virus infection // Bulletin of the Far Eastern Branch of the Russian Academy of Sciences. 2004. No. 3. pp. 155-166.

3. Lutsenko M.T., Andrievskaya I.A. The state of the fetoplacental barrier in herpes virus infection in pregnant women. Siberian Scientific Medical Journal. 2008. V.28, No. 5. pp.142-147.

4. Albrecht E.D., Babischkin J.S., Pepe G.J. Regulation of placental villous angiopoietin-1 and -2 expression by estrogen during baboon pregnancy // Mol. reproduction. dev. 2008. Vol.75, No.3. P.504-511.

5. Albrecht E.D., Henson M.C., Pepe G.J. Regulation of placental low density lipoprotein uptake in baboons by estrogen // Endocrinology. 1991. Vol.128, No.1. P.450-458.

6. Albrecht E.D., Pepe G.J. Estrogen regulation of placental angiogenesis and fetal ovarian development during primate pregnancy // Int. J. Dev. Biol. 2010. Vol.54, No.23. P.397-407.

7. Billiar R.B., Pepe G.J., Albrecht E.D. Immunocyto-chemical identification of the estrogen receptor in the nuclei of human placental syncytiotrophoblasts // Placenta. 1997. Vol. 18, No. 4. P.365-370.

8. Brandenberger A.W. Tee M.K., Lee J.Y., Chao V., Jaffe R.B. Tissue distribution of estrogen receptors alpha

(ER-alpha) and beta (ERbeta) mRNA in the midgestational human fetus // J. Clin. Endocrinol. Metab. 1997. Vol.82, No.10. P.3509-3512.

9. Bukovsky A., Caudle M.R., Cekanova M., Fernando R.I., Wimalasena J., Foster J.S., Henley D.C., Elder R.F. Placental expression of estrogen receptor beta and its hormone binding variantcomparison with estrogen receptor alpha and a role for estrogen receptors in asymmetric division and differentiation of estrogen-dependent cells // Re-prod. Biol. Endocrinol. 2003. No. 1. P.36-56.

10. Chen J.Q., Delannoy M., Cooke C., Yager J.D. Mitochondrial localization of ERa and ERp in human MCF7 cells // Am. J Physiol. Endocrinol. Metab. 2004. Vol.286, No.6. P.E1011-E1022.

11. Chobotova K., Spyropoulou I., Carver J., Manek S., Heath J.K., Gullick W.J., Barlow D.H., Sargent I.L., Mardon H.J. Heparin-binding epidermal growth factor and its receptor ErbB4 mediate implantation of the human blastocyst // Mech. dev. 2002. Vol.119, No.2. P.137-144.

12. Cronier L., Guibourdenche J., Niger C., Malassene A. Oestradiol stimulates morphological and functional differentiation of human villous cytotrophoblast // Placenta.

1999. Vol.20, Iss.8. P.669-676.

13. Ferrara N. Vascular endothelial growth factor: basic science and clinical progress // Endocr. Rev. 2004. Vol.25, No.4. P.581-611.

14. Ferrara N, Gerber H.P. The role of vascular endothelial growth factor in angiogenesis // Acta Haematol. 2001. Vol. 106, No. 4. P.148-156.

15. Irwin R.W., Yao J., Hamilton R., Cadenas E., Brinton R.D., Nilsen J. Progesterone and Estrogen Regulate Oxidative Metabolism in Brain Mitochondria // Endocrinology. 2008. Vol.149, No.6. P.3167-3175.

16. Kota S.K., Gayatri K., Jammula S., Kota S.K., Krishna S.V.S., Meher L.K., Modi K.D. Endocrinology of parturition // Indian J. Endocrinol. Metab. 2013. Vol.17, No.1. P.50-59.

17. Lippert C., Seeger H., Mueck A.O., Lippert T.H. The effects of A-ring and D-ring metabolites of estradiol on the proliferation of vascular endothelial cells // Life Sci.

2000. Vol. 67, No. 13. P.1653-1658.

18. Lobov I.B., Brooks PC, Lang RA. Angiopoietin-2 displays VEGF-dependent modulation of capillary structure and endothelial cell survival in vivo // Proc. Natl Acad. sci. USA. 2002. Vol.99, No.17. P.11205-11210.

19. Mesiano S. The endocrinology of human pregnancy and fetoplacental neuroendocrine development // Yen and Jaffe's reproductive endocrinology / J.F. Strauss, R.L. Barbieru (eds). Philadelphia, 2009. 942 p.

20. Mesiano S., Jaffe R.B. Interaction of insulin-like growth factor-II and estradiol directs steroidogenesis in the human fetal adrenal towards dehydroepiandrosterone sulfate production // J. Clin. Endocrinol. Metab. 1993. Vol. 77, No. 3. P.754-758.

21. Miller V.M., Duckles S.P. Vascular Actions of Estrogens: Functional Implications // Pharmacol. Rev. 2008. Vol. 60, No. 2. P.210-241.

22. Miller A.A., Drummond G.R., Mast A.E., Schmidt H.H., Sobey C.G. Effect of gender on NADPH-oxidase ac-

tivity, expression, and function in the cerebral circulation: role of estrogen // Stroke. 2007. Vol.38, No.7. P.2142-2149.

23. Musicki B., Pepe G.J., Albrecht E.D. Functional differentiation of the placental syncytiotrophoblast: effect of estrogen on chorionic somatomammotropin expression during early primate pregnancy // J. Clin. Endocrinol. Metab. 2003. Vol.88, No.9. P.4316-4323.

24. Nakagawa Y., Fujimoto J., Tamaya T. Placental growth by the estrogen-dependent angiogenic factors, vascular endothelial growth factor and basic fibroblast growth factor, throughout gestation // Gynecol. Endocrinol. 2004. Vol.19, No. 5. P.259-266.

25. Nevo O., Soustiel J.F., Thaler I. Maternal cerebral blood flow during normal pregnancy: a cross-sectional study. // Am. J. Obstet. Gynecol. 2010. Vol.203, no.5. P.475e1-e6.

26. Ospina J.A., Duckles S.P., Krause D.N. ^-Estradiol decreases vascular tone in cerebral arteries by shifting COX-dependent vasoconstriction to vasodilation // Am. J Physiol. Heart Circ. physiol. 2003. Vol.285, No.1. P.241-250.

27. Ospina J.A., Krause D.N., Duckles S.P. ^-Estradiol increases rat cerebrovascular prostacyclin synthesis by elevating cyclooxygenase-1 and prostacyclin synthase // Stroke. 2002. Vol.33, No.2. P.600-605.

28. Paech K., Webb P., Kuiper G.G., Nilsson S., Gustafsson J., Kushner P.J., Scanlan T.S. Differential lig-and activation of estrogen receptors ERalpha and ERbeta at AP1 sites // Science. 1997. Vol.277, No. 5331. P.1508-1510.

29. Pepe G.J., Albrecht E.D. Activation of the baboon fetal pituitary-adrenocortical axis at midgestation by estrogen: adrenal A5-3p-hydroxysteroid dehydrogenase and 17a-hydroxylase-17, 20-lyase activity // Endocrinology. 1991. Vol.128, No. 8. P.2395-2401.

30. Pepe G.J., Burch M.G., Albrecht E.D. Estrogen regulates 11 beta-hydroxysteroid dehydrogenase-1 and -2 localization in placental syncytiotrophoblast in the second half of primate pregnancy // Endocrinology. 2001. Vol.142, No. 10. P.496-503.

31. Putney D.J., Pepe G.J., Albrecht E.D. Influence of the fetus and estrogen on serum concentrations and placental formation of insulin-like growth factor I during baboon pregnancy // Endocrinology. 1990. Vol. 127, No. 5. P.2400-2407.

32. Ramayya M.S. Adrenal Organogenesis and steroidogenesis: Role of nuclear nuclear receptor steroidogenic factor-1, dax-1, and estrogen receptor // Adrenal disorders / A.N. Margioris, G.P. Chrousos (eds). Totowa, N.J.: Humana Press, 2001. 437 p.

33. Reynolds L.P., Redmer D.A. Angiogenesis in the Placenta // Biol. reproduction. 2001. Vol. 64, No. 4. P.1033-1040.

34. Rider V., Carlone D.L., Foster R.T. Oestrogen and progesterone control basic fibroblast growth factor mRNA in the rat uterus // J. Endocrinol. 1997. Vol.154, No.1. P.75-84.

35. Rosenthal M.D., Albrecht E.D., Pepe G.J. Estrogen modulates developmentally regulated gene expression in the fetal baboon liver // Endocrine. 2004. Vol.23, No.2-3.

36. Rubanyi G.M., Johns A., Kauser K. Effect of estrogen on endothelial function and angiogenesis // Vascul. Pharmacol. 2002. Vol.38, No.2. P.89-98.

37. St-Pierre J. Drori S., Uldry M., Silvaggi J.M., Rhee J., Jäger S., Handschin C., Zheng K., Lin J., Yang W., Simon D.K., Bachoo R., Spiegelman B.M. Suppression of reactive oxygen species and eurodegeneration by the PGC-1 transcriptional coactivators // Cell. 2006. Vol.127, No.2. P.397-408.

38. Tomooka Y., DiAugustine R., McLachlan J. Proliferation of mouse uterine epithelial cells in vitro // Endocrinology. 1986. Vol.118, No.3. P.1011-1018.

39. Yang S.H., Liu R., Perez E.J., Wen Y., Stevens S.M.Jr., Valencia T., Brun-Zinkernagel A.M., Prokai L., Will Y., Dykens J., Koulen P., Simpkins J.W. Mitochondrial localization of estrogen receptor ß // Proc. Natl Acad. sci. USA. 2004. Vol.101, No.12. P.4130-4135.

40. Yu L., Saile K., Swartz C.D., He H., Zheng X., Kissling G.E., Di X., Lucas S., Robboy S.J., Dixon D. Differential expression of receptor tyrosine kinases (RTKs) and IGF- I pathway activation in human uterine leiomyomas // Mol. Med. 2008. Vol.14, No. 5-6. P.264-275.

1. Lutsenko M.T., Samsonov V.P. Main research directions and development prospects at the Institute of Physiology and Pathology of Respiration. Bulleten "fiziologii i patologii dyhaniâ 1999; 2:1-9 (in Russian).

2. Lutsenko M.T. The morphofunctional description of the fetoplacental barrier under the herpes-viral infection. Vestnik Dal "nevostochnogo otdeleniya Rossiyskoy akademii nauk 2004; 3: 155-166.

3. Lutsenko M.T., Andrievskaya I.A. The State of Fe-toplacental Barrier at Herpes Viral Infection in Pregnant Women. Sibirskiy nauchniy meditsinskiy zhurnal 2008; 28(5):142-147 (in Russian).

4. Albrecht E.D., Babischkin J.S., Pepe G.J. Regulation of placental villous angiopoietin-1 and -2 expression by estrogen during baboon pregnancy. Mol. reproduction. dev. 2008; 75(3):504-511.

5. Albrecht E.D., Henson M.C., Pepe G.J. Regulation of placental low density lipoprotein uptake in baboons by estrogen. Endocrinology 1991; 128(1):450-458.

6. Albrecht E.D., Pepe G.J. Estrogen regulation of placental angiogenesis and fetal ovarian development during primate pregnancy. Int. J. Dev. Biol. 2010; 54(2-3):397-407.

7. Billiar R.B., Pepe G.J., Albrecht E.D. Immunocyto-chemical identification of the estrogen receptor in the nuclei of human placental syncytiotrophoblasts. Placenta 1997; 18(4):365-370.

8. Brandenberger A.W. Tee M.K., Lee J.Y., Chao V., Jaffe R.B. Tissue distribution of estrogen receptors alpha (ER-alpha) and beta (ERbeta) mRNA in the midgestational human fetus. J.Clin. Endocrinol. Metab. 1997; 82(10):3509-3512.

9. Bukovsky A., Caudle M.R., Cekanova M., Fernando R.I., Wimalasena J., Foster J.S., Henley D.C., Elder R.F.

Placental expression of estrogen receptor beta and its hormone binding variant-comparison with estrogen receptor alpha and a role for estrogen receptors in asymmetric division and differentiation of estrogen-dependent cells. Reprod. Biol. Endocrinol. 2003. 1:36-56.

10. Chen J.Q., Delannoy M., Cooke C., Yager J.D. Mi-tochondrial localization of ERa and ERp in human MCF7 cells. Am. J Physiol. Endocrinol. Metab. 2004; 286(6):E1011-E1022.

11. Chobotova K., Spyropoulou I., Carver J., Manek S., Heath J.K., Gullick W.J., Barlow D.H., Sargent I.L., Mardon H.J. Heparin-binding epidermal growth factor and its receptor ErbB4 mediate implantation of the human blastocyst. Mech. dev. 2002; 119(2):137-144.

12. Cronier L., Guibourdenche J., Niger C., Malassene A. Oestradiol stimulates morphological and functional differentiation of human villous cytotrophoblast. Placenta 1999; 20(8):669-676.

13. Ferrara N. Vascular endothelial growth factor: basic science and clinical progress. Endocr. Rev. 2004; 25(4):581-611.

14. Ferrara N., Gerber H.P. The role of vascular endothelial growth factor in angiogenesis. Acta Haematol. 2001; 106(4):148-156.

15. Irwin R.W., Yao J., Hamilton R., Cadenas E., Brinton R.D., Nilsen J. Progesterone and Estrogen Regulate Oxidative Metabolism in Brain Mitochondria. Endocrinology 2008; 149(6):3167-3175.

16. Kota S.K., Gayatri K., Jammula S., Kota S.K., Krishna S.V.S., Meher L.K., Modi K.D. Endocrinology of parturition. Indian J. Endocrinol. Metab. 2013; 17(1): 5059.

17. Lippert C., Seeger H., Mueck A.O., Lippert T.H. The effects of A-ring and D-ring metabolites of estradiol on the proliferation of vascular endothelial cells. life sci. 2000; 67(13):1653-1658.

18. Lobov I.B., Brooks P.C., Lang R.A. Angiopoietin-2 displays VEGF-dependent modulation of capillary structure and endothelial cell survival in vivo. Proc. Natl Acad. sci. USA 2002; 99(17):11205-11210.

19. Mesiano S. The endocrinology of human pregnancy and fetoplacental neuroendocrine development. In: Strauss J.F., Barbieru R.L. (eds). Yen and Jaffe's reproductive endocrinology. Philadelphia; 2009.

20. Mesiano S., Jaffe R.B. Interaction of insulin-like growth factor-II and estradiol directs steroidogenesis in the human fetal adrenal towards dehydroepiandrosterone sulfate production. J.Clin. Endocrinol. Metab. 1993; 77(3):754-758.

21. Miller V.M., Duckles S.P. Vascular Actions of Estrogens: Functional Implications. Pharmacol. Rev. 2008; 60(2):210-241.

22. Miller A.A., Drummond G.R., Mast A.E., Schmidt H.H., Sobey C.G. Effect of gender on NADPH-oxidase activity, expression, and function in the cerebral circulation: role of estrogen. Stroke 2007; 38(7):2142-2149.

23. Musicki B., Pepe G.J., Albrecht E.D. Functional differentiation of the placental syncytiotrophoblast: effect of estrogen on chorionic somatomammotropin expression

during early primate pregnancy. J.Clin. Endocrinol. Metab. 2003; 88(9):4316-23.

24. Nakagawa Y., Fujimoto J., Tamaya T. Placental growth by the estrogen-dependent angiogenic factors, vascular endothelial growth factor and basic fibroblast growth factor, throughout gestation. Gynecol. Endocrinol. 2004; 19(5):259-266.

25. Nevo O., Soustiel J.F., Thaler I. Maternal cerebral blood flow during normal pregnancy: a cross-sectional study. Am. J. Obstet. Gynecol. 2010; 203(5):475. e1-6.

26. Ospina J.A., Duckles S.P., Krause D.N. 17ß-Estra-diol decreases vascular tone in the cerebral arteries by shifting COX-dependent vasoconstriction to vasodilation. Am. J Physiol. Heart Circ. physiol. 2003; 285(1):H241-250.

27. Ospina J.A., Krause D.N., Duckles S.P. 17ß-Estra-diol increases rat cerebrovascular prostacyclin synthesis by elevating cyclooxygenase-1 and prostacyclin synthase. Stroke 2002; 33(2):600-605.

28. Paech K., Webb P., Kuiper G.G., Nilsson S., Gustafsson J., Kushner P.J., Scanlan T.S. Differential lig-and activation of estrogen receptors ERalpha and ERbeta at API sites. Science 1997; 277(5331):1508-1510.

29. Pepe G.J., Albrecht E.D. Activation of the baboon fetal pituitary-adrenocortical axis at midgestation by estrogen: adrenal A5-3ß-hydroxysteroid dehydrogenase and 17a-hydroxylase-17, 20-lyase activity. Endocrinology 1991; 128(8):2395-2401.

30. Pepe G.J., Burch M.G., Albrecht E.D. Estrogen regulates 11 beta-hydroxysteroid dehydrogenase-1 and -2 localization in placental syncytiotrophoblast in the second half of primate pregnancy. Endocrinology 2001; 142(10):496-503.

31. Putney D.J., Pepe G.J., Albrecht E.D. Influence of the fetus and estrogen on serum concentrations and placental formation of insulin-like growth factor I during baboon pregnancy. Endocrinology 1990; 127(5):2400-2407.

32. Ramayya M.S. Adrenal Organogenesis and Steroidogenesis: Role of Nuclear Nuclear Receptor Steroidogenic Factor-1, DAX-1, and Estrogen Receptor. In: Margioris A.N., Chrousos G.P., editors. adrenal disorders. Totowa, N.J.: Humana Press; 2001:11-45.

33. Reynolds L.P., Redmer D.A. Angiogenesis in the Placenta. Biol. reproduction. 2001; 64(4):1033-1040.

34. Rider V., Carlone D.L., Foster R.T. Oestrogen and progesterone control basic fibroblast growth factor mRNA in the rat uterus. J. Endocrinol. 1997; 154(1):75-84.

35. Rosenthal M.D., Albrecht E.D., Pepe G.J. Estrogen modulates developmentally regulated gene expression in the fetal baboon liver. Endocrine 2004; 23(2-3):219-228.

36. Rubanyi G.M., Johns A., Kauser K. Effect of estrogen on endothelial function and angiogenesis. Vascul. Pharmacol. 2002; 38(2):89-98.

37. St-Pierre J. Drori S., Uldry M., Silvaggi J.M., Rhee J., Jäger S., Handschin C., Zheng K., Lin J., Yang W., Simon D.K., Bachoo R., Spiegelman B.M. Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. Cell 2006; 127(2):397-408.

38. Tomooka Y., DiAugustine R., McLachlan J. Prolif-

eration of mouse uterine epithelial cells in vitro. Endocrinology 1986; 118(3):1011-1018.

39. Yang S.H., Liu R., Perez E.J., Wen Y., Stevens S.M.Jr., Valencia T., Brun-Zinkernagel A.M., Prokai L., Will Y., Dykens J., Koulen P., Simpkins J.W. Mitochondrial localization of estrogen receptor ß. Proc. Natl Acad. sci.

USA 2004; 101(12):4130-4135.

40. Yu L., Saile K., Swartz C.D., He H., Zheng X., Kissling G.E., Di X., Lucas S., Robboy S.J., Dixon D. Differential expression of receptor tyrosine kinases (RTKs) and IGF- I pathway activation in human uterine leiomyomas. Mol. Med. 2008; 14(5-6):264-275.

Received 03/11/2016

Contact information Inna Viktorovna Dovzhikova, Doctor of Biological Sciences, Leading Researcher, Laboratory of Mechanisms of Etiopathogenesis and Recovery Processes of the Respiratory System

for nonspecific lung diseases, Far Eastern Research Center for Physiology and Pathology of Respiration,

675000, Blagoveshchensk, st. Kalinina, 22.

Email: [email protected] Correspondence should be addressed to Inna V. Dovzhikova,

PhD, DSc, Leading staff scientist of Laboratory of Mechanisms of Etiopathogenesis and Recovery

Processes of the Respiratory System at Non-Specific Lung Diseases, Far Eastern Scientific Center of Physiology and Pathology of Respiration, 22 Kalinina Str., Blagoveshchensk, 675000, Russian Federation.

Hello girls! Today, our topic of conversation will be the hormone estrogen, to which we owe our rounded hips and small, compared to men, growth. Of particular importance is estrogen during pregnancy, since it is he who is responsible to a greater extent for its preservation.

How does the amount of the hormone change?

To better understand the topic, let's start with the basic concepts. The ovaries, adrenal cortex, and placenta are the sites where estrogen is created and released. Its dominance over other hormones is observed in the first couple of weeks of the cycle, when the follicular phase is noted. Starting with insignificant indicators, its amount gradually increases, and the maximum level occurs at the time of ovulation. Then the volume goes down, increases a little in the third week, and then continues to fall further. It is at a very high level towards the end of your first trimester. Then its amount stabilizes and remains unchanged for the entire period of bearing the baby.

It is interesting!

At different periods of life in the female body, one of its three types predominates:

  • estrone (E1) during pregnancy;
  • estradiol (E2) is responsible for femininity;
  • estriol (E3) after menopause.

In the early stages, estradiol is responsible for your baby's development and plays an important role in preventing miscarriage. It is believed that this hormone allows women to become pregnant. To accurately measure your estrogen levels during pregnancy, your doctor will do blood tests that look at your levels, as well as a protein called alpha-fetoprotein (AFP) and human

Body transformation during pregnancy

The effect of estrogen, invisible to our eyes, is manifested in improving the functioning of the uterus and ensuring the body's ability to further respond to oxytocin. If you've thought about it, why do you need estrogen, then know that it is he who increases blood circulation, activates and regulates the production of other key hormones.

When there is an increase in its level, such symptoms:

  • increase in appetite;
  • nausea;
  • the appearance of spider veins;
  • change in skin color;
  • the occurrence of pigmentation spots.

It is the female hormone that causes an increase in breast volume and skin sensitivity, and promotes milk production. You may notice nipple engorgement and colostrum discharge. Due to increased blood flow to the mucous membranes, they swell and soften. Therefore, when carrying a baby, you may have a constantly stuffy nose. Red spots on the face - the so-called glow, which many mothers wear with pride - are also the result of the activity of the female hormone. Increased blood flow to your skin can show up as reddened palms.

The hormone estrogen, along with melanocyte cells, often causes darkening of the skin (hyperpigmentation), which manifests itself, for example, in a change in the color of the areola on the chest, the appearance of a vertical strip across the entire abdomen and a “pregnancy mask” on the face. Since the skin becomes extremely sensitive to sunlight, take extra care.

With an increase in the content of the female hormone in the body, such unpleasant manifestations, how:

  • headache;
  • irritability;
  • aggression;
  • sudden mood swings;
  • rapid weight gain.

Effects of low estrogen levels on pregnancy

This hormone is considered a trigger for the development of the baby's organs and regulates bone density, therefore, if its level is lowered, serious negative consequences are possible, especially if a woman is expecting the birth of a girl.

Low estrogen during pregnancy can cause:

  • metabolic disorders;
  • failures in the development of the genital organs of the fetus;
  • fertility problems in a newborn girl.

If your hormone level is less than normal (the indicator itself is quite specific), then it is imperative to talk with your doctor to assess individual risks and problems. It seems to me that you will be interested in the norm by weeks. The table with numbers is shown below:

Gestational age, in weeks Estriol concentration, ng/ml
6–7 0,06–0,2
8–9 0,23–1
10–12 0,66–2,45
13–14 1,64–4,32
15–16 1,55–6,04
17–18 1,9–7,2
19–20 2,16–8,06
21–22 3,46–11,81
23–24 2,36–14,69
25–26 5,76–17,28
27–28 6,05–18,29
29–30 5,76–19,58
31–32 5,62–20,16
33–34 6,62–23,33
35–36 7,2–29,09
37–38 8,64–32,26
39–40 10,08–31,97

So that a pregnant woman does not panic for no reason, doctors usually recommend checking estrogen levels not too often. Like any other hormone, it tends to decrease during the bearing of a baby, so only a doctor can accurately determine the range that is acceptable specifically for you, which will be considered normal within the generally accepted fluctuations.

Here are the acceptable limits for each trimester of pregnancy:

  • first trimester - 187–2498 pg / ml;
  • second trimester - 1276–7193 pg / ml;
  • third trimester - 3461–6138 mcg / ml.

Conclusion

From week to week, the level of this hormone changes dramatically, so do not despair if it is slightly increased or decreased relative to the specified range. Hormonal imbalance is considered normal during pregnancy, and only in severe cases, therapy with appropriate medications is required. Usually in late pregnancy, the amount of estrogen increases. This is necessary in order to ensure the sensitivity of the uterus to substances that cause it to contract.

So, now you know that estrogen during pregnancy is responsible for breast enlargement, skin pigmentation, redistribution of fat in the lower body, mood swings and changes in well-being. Hair loss is another phenomenon that is caused by estrogen, although many women during gestation have to deal with an increase in body hair. In fact, you can deal with this problem quite simply if you purchase portable trimmer for trimming and hair removal. The presence of interchangeable nozzles will allow you to carefully care for sensitive areas of the body and quickly remove unwanted hairs. My dear readers, watch your beauty and be healthy! See you soon on this blog.

Immediately after the conception of a child in the body of a woman, the so-called pregnancy hormones are revived, which help the fetus in full development, set the woman up for motherhood.

Why do you need to control the level of hormones during pregnancy?

In the body of a pregnant woman, cardinal changes occur, especially hormonal ones. The endocrine system is no exception. All conditions must be created for the successful bearing of a child.

Of great importance are the hormonal indicators of the body - they can be used to judge the intrauterine development of the fetus. The attending physician controls the level of hormones with the help of prenatal screenings - they are done at least twice during the entire pregnancy: during the first trimester (11-12 weeks) and during the second (16-19 weeks). What indicators are included in this survey?

Hormones that "create" the body of the unborn baby

  1. human chorionic gonadotropin - HCG. It begins to be actively produced by chorion cells as soon as the fetus attaches to the wall of the uterus. The production of hCG is vital to maintain and maintain a pregnancy. It is this hormone that controls the production of the main pregnancy hormones - progesterone and estrogen. With a significant deficiency of hCG, the embryo detaches from the uterus - this ends in a spontaneous miscarriage. The concentration of hCG in the blood of a pregnant woman should continuously increase, reaches a maximum at 10-11 weeks, after which the concentration of this hormone gradually decreases, after which it remains constant until the end of the term.
    The hCG hormone is similar in structure to the thyroid stimulating hormone produced by the pituitary gland and stimulating the action of the thyroid gland. The accumulation of thyroid hormones under the influence of hCG increases. This leads to an acceleration of metabolism, and this renews all the cells of the body.
    An hCG test during pregnancy is of great importance because:
    1) when passing an analysis for the level of hCG, it is possible to accurately determine the “interesting position” of a woman in less than a week after conception;
    2) the test helps to determine the timing of pregnancy with great accuracy;
    3) the level of hCG can quite fully tell how the baby develops.
  2. Chorionic somatomammotropin causes the growth of the mammary glands.
  3. Placental lactogen and free estriol . It is very important to control the level of these hormones in order to assess the risk of hereditary chromosomal abnormalities in a child.
  4. Free estriol which is produced by the placenta. It improves the flow of blood through the vessels of the uterus, helps the functioning of the ducts of the mammary glands, which helps prepare the mother for feeding the baby.
  5. Placental lactogen (PL) is also produced by the placenta. It rises to a maximum of 937-38 weeks), after which it decreases. But its level must be monitored throughout pregnancy - in order to constantly monitor the condition of the placenta and diagnose placental insufficiency in time.

Hormones responsible for pregnancy

Estradiol and progesterone. Tests for the level of these hormones during pregnancy are included in hormonal studies and are considered mandatory. They support the normal conditions in which pregnancy proceeds.

Estradiol produce the ovaries, and during pregnancy and the placenta. At this time, the level of estradiol rises sharply. A decrease in its level indicates a real danger, which is fraught with interruption of gestation. At the end of pregnancy, its density reaches a maximum for a natural reason - it acts as a strong natural pain reliever.

Progesterone. Its main task is to create the necessary conditions for the development of the child. Its normal level provides the very conception. Together with estrogen, it helps the embryo to attach to the wall of the uterus and prevents a miscarriage from happening. During pregnancy, this hormone stimulates the growth of the mammary glands and their maturation. Its side effect is nausea, drowsiness, chest pain, frequent urination.

With a deficiency of progesterone, pregnancy can take place with great problems and the risk of a frozen pregnancy and spontaneous abortion.

thyroid hormones

TSH, T3, T4 - this is the name of the hormones responsible for the normal functioning of the thyroid gland, they can tell about its hypo- or hyperfunction.

The hormones of motherhood

Pituitary hormones play a huge role during pregnancy. It is an endocrine gland located in the hypothalamic region of the brain. During childbirth, the hormone oxytocin enters the bloodstream of a woman, thanks to the pituitary gland. It stimulates uterine contractions. After childbirth, the hormone prolactin is actively synthesized - with its deficiency, a woman cannot fully breastfeed her baby.

Adrenal hormones

This is the common name for mineralocorticoids and glucocorticoids. Stimulates their secretion of the specific pituitary hormone ACTH - adrenocorticotropic hormone. An increase in its level means the body's response to stress - in this case, pregnancy. ACTH affects skin pigmentation. Mineralocorticoids correct fluid and salt in the body. They suppress the immune system, which prevents the rejection of the fetus.

An imbalance of hormones leads not only to problems in the functioning of internal organs, but also to changes in appearance and mood. The most important of them is called the creator of female behavior and appearance.

Often, the female body of the level of estrogen is not only due to age-related changes, but also from substances that enter from outside.

The main reasons include:

  • the use of meat containing substances similar to estrogen, the appearance of which is possible due to the feeding of the animal with harmful additives and “growth” hormones;
  • a vegetarian diet that promotes the appearance of a large number of legumes in the diet, especially soy, rich in natural phytoestrogens;
  • the use of non-natural means for washing and cleaning, cosmetics, inhaling the vapors of which endocrine disorders are possible;
  • frequent consumption of alcoholic beverages, especially beer;
  • some diseases of the heart system;
  • high blood pressure;
  • prolonged stressful state;
  • diabetes;
  • taking drugs based on hormones.

Interesting! Often, women over 30 years of age are not even aware of the presence of a problem associated with a hormone surge, however, in 50% of them, doctors detect this disease during examination.

Increase symptoms

In order to suspect this problem in yourself in time, you need to carefully monitor the body, paying attention to such important signs as:

  • uncontrolled weight gain;
  • multiple rashes on the skin;
  • increased hair loss;
  • excessive sensitivity of the nipples;
  • nausea, vomiting;
  • dizziness;
  • frequent hypertension;
  • disruptions in the menstrual cycle;
  • pain in the lower abdomen;
  • prolonged headaches;
  • compaction and engorgement of the mammary glands;
  • irritability leading to sleep disturbances;
  • general exhaustion of the body, expressed in increased fatigue and a constant feeling of weakness.

With a long stay of the level of estrogen above the permissible, the appearance of:

  • calf cramps;
  • osteoporosis;
  • thrombosis;
  • obesity;
  • pathological changes in the thyroid gland;
  • the development of a malignant tumor of the mammary gland and the appearance of mastopathy;
  • obvious changes in the mental state;
  • no pregnancy;
  • decrease in the ability to remember the information received.

Important! Doctors consider the main signs of estrogen dominance to be breast and uterine cancer, endometriosis, hypertension, and persistent depression.

Diagnostics

If any of the above signs are noticed, you should immediately contact a gynecologist, and then an endocrinologist.

Diagnostics will include:

  • direct examination and collection of complaints;
  • search during the examination of the vagina for loose mucous membranes, an increased amount of discharge, a symptom of the "pupil" of the cervix, polyps, tumors, clearly indicating an excess of estrogen;
  • ultrasound examination;
  • taking a blood test from a vein for the amount of hormones of the reproductive system and thyroid gland.

Important! Hormones such as FSH, estradiol, testosterone, prolactin and thyroid hormones should be taken on the 5th-7th day of the cycle and only on an empty stomach.

How to influence the increased content?

Before taking medication, it makes sense to try to adjust the level by changing your lifestyle.

For this you should:

  • buy and eat organic products grown on their own or bought on the market and which are as clean as possible from chemical components and hormones;
  • adhere to a balanced and fortified diet, taking vitamins and trying to eat mainly sea fish, beef liver, nuts, buckwheat, peas, oatmeal, beans, lamb, almonds, sea kale, barley groats;
  • give up alcohol, because the function of the liver is the production of estrogens, which means that the balance of these hormones depends on its proper functioning;
  • increase fiber intake in the form of fruits and vegetables, which actively remove toxins and excess estrogen from the body;
  • regularly drink rosemary essential oil, which helps reduce the amount of estradiol, which is the worst type of estrogen, as well as strengthens the immune system, stimulates hair growth, improves memory;
  • try to eat more foods with a low content of phytoestrogens, such as barley, oats, pears, apples, berries, flaxseed or oil;
  • use in everyday life household chemicals and cosmetics, consisting of natural ingredients that do not contain harmful xenoestrogens;
  • avoid stressful situations, or simply not react to problems too violently;
  • increase the consumption of fermented milk products, rich in bifidobacteria and displacing harmful bacteria and excess hormones.

Attention! Women who drink a large glass of alcohol or more per day have a higher risk of developing breast cancer.

red brush

Plants contain phytohormones, similar to those found in medicines, but with fewer side effects. The red brush is often used in the form of an alcohol tincture or decoction in the treatment of various problems of the genital area in women.

When using a red brush, you can achieve:

  • hormonal balance;
  • an even menstrual cycle;
  • elimination of painful sensations during critical days.

Cannot be used for:

  • hypertension;
  • infections;
  • breastfeeding;
  • gestation.

Attention! It is necessary to carry out treatment with traditional medicine after consulting a doctor.

Treatment methods to reduce the amount

The choice of drug depends on the anamnesis of a particular woman and the results of the tests.

Basically, drugs are used to lower:

  • plant-based mastodinone;
  • phaslodex;
  • tamoxifen;
  • Arimidex;
  • aromasin;
  • femara.

To suppress the work of the ovaries, which cause an increase in estrogen, in premenopause and postmenopause, the following are used:

  • lupron;
  • zoladex.

Any method of dealing with excess, prescribed by the attending physician, will positively affect the level and reduce the risk of malignant neoplasms.

Is it possible to get pregnant?

Pregnancy with a temporary increase is possible, but this will affect its course, and there is a high probability of having 2 or more children. If estrogen is still above normal during pregnancy, this will indicate:

  • high probability of miscarriage;
  • intrauterine infection;
  • fetal pathology.

If it was in excess for a long period, then serious problems can arise with the onset of pregnancy, because with such a hormonal background, changes begin in the endometrium and cervix, polyps and cancerous tumors can occur.

Every woman is obliged to monitor her health, detect and eliminate malfunctions in the body in time, timely seeking help from a doctor.

  • What is estrogen?

One of the most common problems during pregnancy is an extreme imbalance of hormones, and this imbalance can lead to numerous problems. One of the most important hormones during pregnancy is estrogen. It plays a huge role in the health and well-being of the mother, as well as in the development of the child.

What is estrogen?

The human body has many hormones that help in the development and maintenance of the human body. Two of these hormones are dominant - testosterone and estrogen. All humans have both hormones, but women have estrogen as their dominant hormone (while men have testosterone as their dominant hormone).

Estrogen is normally produced in the placenta and ovaries in women. One of the most important forms of estrogen produced by the female human body is estradiol. In fact, it is the most important hormone for your child's developmental well-being. This hormone allows women to become pregnant and after that plays an important role in preventing miscarriages.

What role does estrogen play during pregnancy?

Here are some of the roles estrogen plays during pregnancy:

1. Helps carry baby to term

Estrogen is the main hormone, which includes many minor hormones such as estradiol, which was mentioned above. The estrogen hormones in women are crucial as they are produced by the placenta and ovaries and play a key role in determining the duration of pregnancy. They do this by supporting the lining of the uterus, which provides a safe space for the baby to grow. They also help regulate other hormones, such as progesterone, which are essential for fetal growth.

2. Impact on fertility prospects

Research by the University of Maryland Medical Center shows that women who are pregnant and have low estrogen levels may, in turn, reduce the chances of their children being fertile enough to have a child of their own, the same study shows that too high amounts of estrogen can lead to other fertility problems and increase the chance of your baby miscarrying. Balanced and healthy estrogen levels will greatly improve not only your child's health, but also his chances of having children of his own.

3. Reduces Fetal Malnutrition

Estrogen is an extremely important hormone due to the fact that it plays an important role in feeding the developing fetus to a healthy baby that is ready to enter the world, and healthy estrogen levels ensure that the fetus is well nourished. Low or high estrogen levels during pregnancy can increase the risk of fetal malnutrition.

How is estrogen testing done?

Estrogen tests are done as part of your four-stage pregnancy tests and can also be tested whether you are pregnant or not. To check estrogen levels, doctors will draw some blood and test the blood for components of estrogen called estriol and a protein called alpha-fetoprotein, or AFP. They will also test for human chorionic gonadotropin, or hCG. By measuring these three aspects through the blood, doctors can accurately measure estrogen levels.

Impact of low estrogen during pregnancy

Low estrogen levels during pregnancy can adversely affect the overall pregnancy and the children born, especially women. Low estrogen levels during pregnancy can lead to:

  • Miscarriage
  • Fewer eggs in female babies born from pregnancy
  • Fertility problems in women born from pregnancy

The result is very specific to each person, so if you have low estrogen, it's a good idea to talk to your doctor to understand what your specific risks and concerns are.

Changes in estrogen levels and normal range during pregnancy

During pregnancy, your hormones will rise and fall, estrogen is no different. Doctors often advise women not to check their estrogen too often for fear that they might panic for no reason. Usually during pregnancy, doctors regularly access estrogen levels and provide a range that is considered healthy due to fluctuations in hormone levels. Here are the normal ranges for each trimester during pregnancy.

  • First trimester- 187-2498 pg / ml
  • Second trimester- 1276-7193 pg / ml
  • third trimester- 6138-3461 pg / ml

It is important to remember that estrogen levels fluctuate. The above ranges are considered safe, and you can expect estrogen levels during pregnancy to fluctuate drastically from week to week. Don't panic if it is within the range above or slightly above or below.

If you are worried about your level or estrogen and pregnancy risks associated with it, we recommend that you consult your doctor and ease your fears. Remember that hormonal imbalances are normal during pregnancy and hormonal imbalances can be treated with medication.



 


Read:



Presentation on the topic "Modal verbs and their meaning"

Presentation on the topic

Modal Verbs Do not have the -s ending in the 3rd person singular present tense. He can do it. He may take it. He must go there. He...

I need to write an essay on the topic "How to treat your own talent"

I need to write an essay on the topic

Talent in a person's life 02/10/2016 Snezhana Ivanova To develop talent, you need to have confidence, take concrete steps, and this is connected with...

I need to write an essay on the topic "How to treat your own talent"

I need to write an essay on the topic

I believe that every person is talented. But the talent of each manifests itself in different areas. Someone draws excellently, someone achieves ...

Jack London: biography as a search for an ideal

Jack London: biography as a search for an ideal

Jack London is a famous American writer, prose writer, socialist, journalist and public figure. He painted his works in the style of realism and...

feed image RSS