Pros and Cons of Estrogens
Estrogens. Role in the body. Pros and cons
Estrogens are a group of female sex hormones synthesized in the female body by the ovaries and regulating specific sexual functions.
Estrogens are present in both female and male bodies (in men, the male sex hormone testosterone and estrogens work synergistically – without their mutual assistance, muscle mass growth is not observed).
There are two main estrogens (in both women and men). The most active of them is 17-beta estradiol, which is primarily formed in the ovaries from progesterone. Smaller amounts can be produced from testosterone through enzymatic reactions.
In the male body, all 17-beta estradiol is produced by aromatase enzymes in the testes from testosterone secreted by Leydig cells, through enzymatic conversion in Sertoli cells.
The second, weaker estrogen is estrone. In the female body, it is also synthesized by the ovaries from androstendione secreted by the adrenal glands.
Estrogens have multiple effects on the female body.
The normal level of 17-beta estradiol in women during the follicular phase should be 24-195 pg/ml, in the preovulatory phase – 66-411 pg/ml, in the luteal phase – 40-261 pg/ml, during menopause – 10-40 pg/ml. The norm for men is 11-44 pg/ml.
If the estrogen levels are within the normal range, their positive effects manifest as follows.
Estrogens are a group of female sex hormones synthesized in the female body by the ovaries and regulating specific sexual functions.
Estrogens are present in both female and male bodies (in men, the male sex hormone testosterone and estrogens work synergistically – without their mutual assistance, muscle mass growth is not observed).
There are two main estrogens (in both women and men). The most active of them is 17-beta estradiol, which is primarily formed in the ovaries from progesterone. Smaller amounts can be produced from testosterone through enzymatic reactions.
In the male body, all 17-beta estradiol is produced by aromatase enzymes in the testes from testosterone secreted by Leydig cells, through enzymatic conversion in Sertoli cells.
The second, weaker estrogen is estrone. In the female body, it is also synthesized by the ovaries from androstendione secreted by the adrenal glands.
Estrogens have multiple effects on the female body.
The normal level of 17-beta estradiol in women during the follicular phase should be 24-195 pg/ml, in the preovulatory phase – 66-411 pg/ml, in the luteal phase – 40-261 pg/ml, during menopause – 10-40 pg/ml. The norm for men is 11-44 pg/ml.
If the estrogen levels are within the normal range, their positive effects manifest as follows.
Pros of estrogens:
The primary purpose of estrogens (together with progesterone and gonadotropins) is to control the development and functioning of the female reproductive system and to ensure the entire range of activities aimed at preparing the female body for pregnancy, carrying the fetus, and childbirth, namely: the development of secondary sexual characteristics, the emergence of sexual desire, ensuring the release of the egg into the reproductive tract and the possibility of fertilization after ovulation, structural changes in the tissues of the reproductive system (proliferation of the vaginal mucosal epithelium), maintenance of an acidic pH environment, hypertrophy and rhythmic contractions of the uterus, development of mammary glands, distribution of subcutaneous fat characteristic of the female type.
Estrogens are involved in regulating bone tissue metabolism (maintaining strength and preventing bone resorption), the excretory system (regulation of water-salt balance), as well as in the functioning of the cardiovascular system (reducing the levels of circulating low-density lipoproteins = bad cholesterol and thus protecting against atherosclerosis) and the neuroendocrine system.
However, if the estrogen levels in the blood plasma are above normal, negative effects of estrogens may manifest.
Estrogens are involved in regulating bone tissue metabolism (maintaining strength and preventing bone resorption), the excretory system (regulation of water-salt balance), as well as in the functioning of the cardiovascular system (reducing the levels of circulating low-density lipoproteins = bad cholesterol and thus protecting against atherosclerosis) and the neuroendocrine system.
However, if the estrogen levels in the blood plasma are above normal, negative effects of estrogens may manifest.
Cons of estrogens:
The negative influence of estrogens is expressed in the stimulation of carcinogenesis in hormone-dependent organs and tissues. Being key inducers and conduits of intracellular proliferative signals, estrogens (primarily estradiol) under certain conditions can stimulate the growth of benign and malignant tumors in the epithelium of the breast, endometrium, and cervix, as well as in the epithelium and endothelium of mucous membranes (larynx, esophagus, rectum).
The decisive role in the development of breast diseases is currently attributed to progesterone-deficient states, in which an excess of estrogens causes tissue proliferation in the breast and disrupts the receptor apparatus.
Upon entering a cell, estrogen activates the estrogen receptor, which is in an inactive state in the cytoplasm. The interaction of the hormone with the receptor activates the latter and facilitates its penetration into the nucleus. Once in the nucleus, the hormone-receptor complex stimulates the expression of so-called estrogen-dependent genes, most of which directly or indirectly control cellular proliferation and increase the sensitivity of cells to factors that activate hyperplastic processes.
Regularly recurring cycles of estrogen-induced cell division can have a dual effect on the development of tumor processes in hormone-dependent tissues. Firstly, cells that have already undergone malignancy (exposed to external carcinogens or having a set of terminal mutations) can proliferate under the influence of estrogens, and their proliferation leads to the formation of a “tumor clone.” However, more often, a different situation occurs. Periodically recurring cycles of cell division inevitably increase the frequency of new, spontaneous mutations (especially with increasing age of the woman and in the presence of other risk factors). If 3 to 7 such genetic errors accumulate, not eliminated by immune and/or reparative cellular systems, estrogen-dependent proliferation of transformed cells will also lead to tumor formation. In this case, the initiator of the tumor process, in its traditional understanding, is absent in the second scenario.
The decisive role in the development of breast diseases is currently attributed to progesterone-deficient states, in which an excess of estrogens causes tissue proliferation in the breast and disrupts the receptor apparatus.
Upon entering a cell, estrogen activates the estrogen receptor, which is in an inactive state in the cytoplasm. The interaction of the hormone with the receptor activates the latter and facilitates its penetration into the nucleus. Once in the nucleus, the hormone-receptor complex stimulates the expression of so-called estrogen-dependent genes, most of which directly or indirectly control cellular proliferation and increase the sensitivity of cells to factors that activate hyperplastic processes.
Regularly recurring cycles of estrogen-induced cell division can have a dual effect on the development of tumor processes in hormone-dependent tissues. Firstly, cells that have already undergone malignancy (exposed to external carcinogens or having a set of terminal mutations) can proliferate under the influence of estrogens, and their proliferation leads to the formation of a “tumor clone.” However, more often, a different situation occurs. Periodically recurring cycles of cell division inevitably increase the frequency of new, spontaneous mutations (especially with increasing age of the woman and in the presence of other risk factors). If 3 to 7 such genetic errors accumulate, not eliminated by immune and/or reparative cellular systems, estrogen-dependent proliferation of transformed cells will also lead to tumor formation. In this case, the initiator of the tumor process, in its traditional understanding, is absent in the second scenario.