Estrogens are hormones of femininity. What is their role in a woman’s body?

The female hormone estrogen is a substance that determines a woman’s health. There are more than 30 estrogen-like substances, but the most significant are estradiol, estrone and estriol. The mechanism of action of these fractions is to support the reproductive, cardiovascular, nervous systems and musculoskeletal system.

What is the hormone estrogen responsible for?

Estrogen in women is produced from androgen as a result of enzymatic reactions.

The role of estrogens in the functioning of the female body is as follows:

  • building a silhouette according to the female type, a special accumulation of fat in the lower part of the body;
  • growth of the uterus, tubes, ovaries;
  • breast growth in teenagers;
  • female-pattern hair growth, pigmentation of nipples and external genitalia;
  • uterine tone during ovulation, contractile movements of the tubes to promote sperm;
  • regular menstrual cycle, possibility of conception;
  • inhibition of the growth of cholesterol plaques, timely removal of “bad” cholesterol (maintaining normal lipid metabolism);
  • reducing the risk of osteoporosis;
  • maintaining the balance of ferrates and copper in the blood;
  • normalization of cognitive abilities - memorization, concentration;
  • ensuring an adequate course of pregnancy;
  • maintaining healthy nails, hair and skin.

Estrogens, derivatives of progesterone, have a complex effect on a woman’s body. They take part in the work of the heart muscle, support the body’s thermoregulation and the process of calcium absorption. It is under their influence that secondary sexual characteristics are formed in teenage girls - a feminine voice, figure.

Just as estrogen is responsible for femininity, testosterone (a steroid hormone) is responsible for masculinity. If a man has more estrogen than testosterone, he will exhibit feminine characteristics.

Mechanisms of functioning of estrogen receptors

Currently, there are four general mechanisms for receptors to realize their functions (see Fig. 3). This is a direct, “classical” mechanism; associated with other transcription factors (TFs), a non-genomic regulatory mechanism and specifically distinguishes ligand-independent activation of estrogen receptors [5]. It makes sense to examine each in more detail.



Rice. 3. Types of functioning of estrogen receptors in the cell [5].

The classical mechanism is the most common activation of the receptor by a ligand (hormone), which, together with coregulator proteins, somehow changes the expression of individual genes.

The second model is somewhat more complicated. Here the receptor interacts with a complex of other transcription factors that modulate the effect of the receptor on gene expression. It is also a very important regulatory mechanism.

The third type of functioning is called “non-genomic”, since it does not directly affect the genome. It is much less studied and realizes itself through a certain cascade of reactions (currently unknown), the consequence of which is a change in cellular function in the form of opening/closing ion channels, changes in the concentration of NO in the cell. This model mediates “fast responses,” meaning the response to a stimulus occurs in a matter of seconds. It is hypothesized that ERs directly associated with the cell membrane rather than floating freely in the cytoplasm may be involved; There are also hypotheses that these are generally non-estrogen receptors (although they are activated by estradiol).

The previous three mechanisms of receptor functioning are called “ligand-dependent”, since the receptor responds to the hormone. The fourth , ligand-independent method of receptor activation, does not involve the participation of a specific hormone. Any highly active substance (for example, growth factor - GF - grows factor) binds to membrane receptors; this causes a cascade of various reactions, activation of protein kinases, which, interacting with estrogen receptors, phosphorylate it; although there are hypotheses that protein kinases interact not with the ER, but with coregulator proteins [5].

ER-α receptor

This is the first of two types of estrogen receptor discovered; it is predominantly synthesized in the organs and tissues of the reproductive system - mammary glands, uterus, cervix, vagina, etc. [6].

Like most steroid hormone receptors, estrogen receptors carry out their function by activating/deactivating the expression of various genes (genomic function). However, in addition to this, there is also a non-genomic role of the receptor, which manifests itself much faster than the implementation of hereditary information (as already mentioned above). Receptors, being in the cytoplasm, can bind to adenylate cyclase and protein kinases, triggering a certain cascade process. It is the non-genomic functions of estrogen receptors that are of greatest interest to modern researchers [1].

For example, the estrogen receptor initiates transcription at AP-1 sites (encoding AP-1 proteins) [7] using a complex of activator and repressor proteins. AP-1 (activation proteins) are a family of diverse transcription factors that play important roles in the regulation of the cell cycle, dimerization, and overall cell viability [8].

ER-β receptor

In 1996, a new subtype of estrogen receptor was isolated, which was called ER-β [3]. Researchers studied the structure of this protein and found that it is generally quite homologous to the alpha receptor; however, there are also differences (see Fig. 4). In short, the highly conserved DNA-binding domain is almost identical (96% similarity), the ligand-binding domain is only 58% identical in structure; the remaining parts of the molecule are completely different or completely absent, as can be seen from Figure 2. The same study demonstrated that ER-β is also activated by estradiol, although the affinity for it is slightly lower than that of ER-α.

Unlike ERα, this subtype is expressed predominantly in the ovaries, testes, prostate, thymus, spleen, lungs and hypothalamus [6].

Rice. 4. Differences in the amino acid sequence of the ER-α and ER-β receptors [3].

GPER receptor

In the same 1996, another receptor was discovered, which was called the “G-coupled receptor” - GPR30 [9]. In many sources, this protein appears under this name, although officially in 2007 it was given the title of an independent G-coupled estrogen receptor - GPER (G-protein coupled estrogen receptor) [10].

GPER is a 7-segment domain transmembrane receptor that is responsible for special reactions called “rapid effects”, activating various cascade signaling pathways. It is he who is responsible for the “non-genomic” functions of estrogen. GPER is associated with the plasma membrane, as well as with the ER and Golgi complex, and is widely distributed in the cells of the liver, heart, intestine, ovaries, central nervous system, pancreas, immunocompetent cells, adipocytes and cells of the reproductive system [11].

Another new estrogen receptor?

Before scientists had time to recover from previous discoveries, an article was published in 2002 [12], the authors of which notified the discovery of a new estrogen receptor, which they called ER-X. It is associated with the plasma membrane and is detected in high concentrations in the uterus and brain. However, the article seems rather dubious to me: the authors explain why the receptor they discovered is neither an alpha nor a beta subtype, but the study makes no mention of GPER (which, as we recall, was then called GPR30).

Today there is a very meager list of literature on this issue. The ER-X was briefly mentioned in a 2013 review [2]; at the same time (in the same month - March) another article was published, which already talks about several new receptors ER-X and ER-x [13], however, the author politely calls them “candidates” for the role of estrogen receptors.

Be that as it may, there is still no consensus on whether the discovered new receptors can be classified as estrogens, what function they perform, and in general whether these are really “new” receptors and not a methodological error.

Types of female hormone

Three basic factions:

  1. Estradiol is the most important hormone. Before the onset of puberty in boys and girls, its concentration in the blood is the same; the content changes at approximately 12–13 years. Participates in the accumulation of fatty tissue on the chest, hips, development of the mammary glands, and maintains skin tone. In the pubertal phase, it forms sexual characteristics, in adult women it maintains the health of the skin and hair, slows down cellular aging, participates in the construction of bone tissue, utilizes harmful cholesterol, and affects emotional stability. During the gestational period, it helps to increase the size of the uterus along with the growth of the fetus, increases the metabolic rate, forms the bone tissue of the fetus and provides it with nutrients and oxygen.
  2. Estrone. Synthesized by the adrenal cortex, ovaries and fat cells. It is an “intermediate” hormone, used by the body as a raw material for the production of estradiol.
  3. Estriol. It has virtually no effect on hormone levels in women, is inactive in the body, and is found in small quantities. But immediately after conception, its level increases under the influence of gonadotropin to prepare the uterus for growth with an enlarged fetus. It also forms ducts in the breast for lactation, reduces the risk of uterine tone, prevents spasms, and increases blood flow in the uterine cavity. Produced by placental tissue.

PROGESTERONE

When talking about estrogen, one cannot fail to mention progesterone.

The main task of progesterone is the development of the egg and its placement in the uterus, which is why it is often called the pregnancy hormone. In non-pregnant women, progesterone is also present and increases in the second phase of the menstrual cycle, which, unfortunately, negatively affects appearance.

Progesterone promotes fluid retention in the body, increases the permeability of the vascular wall, the skin becomes stretchable, the secretion of sebum increases and acne appears. Facial puffiness may appear due to fluid retention.

Progesterone also actively promotes fat storage, preparing us for pregnancy, even if we don't plan for it. Therefore, in the second phase of the cycle, many people gain one or two extra pounds. In addition, progesterone reduces the body's resistance to infections, which has a beneficial effect on the pathogenic microflora of the skin due to weakened immunity and often leads to the formation of acne.

However, its deficiency leads to the occurrence of many female diseases that can lead to cancer.

Estrogen norm

Normal hormone levels are determined by periods of the menstrual cycle:

Type of estrogen1 phase2 phasePregnancyClimax
Estradiol15-60 ng/l27-246 ng/l17-18 thousand ng/l5-30 ng/l
Estrone5-9 ng%3-25 ng%1500-3000 ng%
Estriol0.7-110 nmol/l

Estriol is produced only by the placenta, from the moment of conception to 40 weeks. It is first synthesized from maternal cholesterol by the adrenal glands, then by the fetal liver.

During the gestational period, important values ​​are not only the content of estriol in the mother, but also in the fetus. In the amniotic fluid in the 2nd trimester it should be in the range of 3.5–27.1 nmol/l, in the 3rd trimester – 7.3–69 nmol/l.

IN ADDITION TO DIET CHANGES, YOU NEED TO TAKE CARE OF THE FOLLOWING

  1. Lose excess weight - because adipose tissue cells produce additional estrogen.
  2. Improve the health of the gastrointestinal system. It is necessary to maintain a healthy balance of microbiota (microflora) in the intestines, because “bad” bacteria prevent excess estrogen from being removed from the body, returning it to the blood. While the “good” ones help get rid of it. Here the first and best remedy is massage and restoration of the internal organs of Chi-nei-tsang.
  3. Minimize contact with substances that contain synthetic estrogens: plastics (for example, dishes), many hygiene products, insect repellent aerosols.

Symptoms of Imbalance

Estrogens actively influence the female body from the first menstruation to the development of menopause. Both an increase and a decrease in their volume inhibit reproductive function, spoil a woman’s appearance, the condition of the cardiovascular system, and the structure of bones and cartilage.

Signs of hormone excess in women

Normally, estrogen synthesis increases during puberty and during pregnancy, if it occurs without pathologies. In other periods, an increase in concentration is often caused by improper functioning of the body or the intake of the hormone from food and the environment.

Reasons for estrogen dominance:

  • consumption of foods high in phytoestrogens;
  • incorrectly selected hormone replacement therapy;
  • frequent drinking of alcohol;
  • excess weight;
  • vascular diseases, heart disease, diabetes, hypertension;
  • uncontrolled use of OK (oral contraceptives).

Symptoms of excess estrogen are:

  1. Excessive weight gain
    . With increased levels of female hormones, adipose tissue accumulates mainly in the waist, buttocks, and thighs.
  2. Irregular cycle
    - scanty or, conversely, heavy discharge, breakthrough bleeding, hyperpolymenorrhea, amenorrhea and other disorders.
  3. Breast tenderness and swelling
    . Normally, this condition is observed a few days before the onset of menstruation and during pregnancy. If the mammary glands hurt in the middle of the cycle, this may indicate an increase in estrogen levels.
  4. Increased emotionality
    . PMS, sudden mood swings, depression, anxiety, panic attacks, and insomnia may develop.
  5. Regular headaches
    . Most often they are associated with approaching menstruation.
  6. Hair loss
    , baldness, deterioration of nails and hair.
  7. Memory impairment
    . Some scientists associate Alzheimer's disease with low levels of female estrogen.
  8. Chronic fatigue
    .

Important!
Complications of hyperestrogenism - endometrial hyperplasia, increased risk of bleeding, fibroids, endometriosis, cycle disorders. There are relative and absolute forms:

  • relative hyperestrogenism
    - a decrease in progesterone levels with the same amount of estrogen;
  • absolute hyperestrogenism
    - an increase in estrogen with the same concentration of progesterone.

In adult women, hyperestrogenism can cause a condition similar to the manifestations of menopause - sweating, hot flashes, irritability, frequent headaches.

Symptoms of hormone deficiency

Estrogen deficiency can be caused by the following factors: taking hormonal drugs, thyroid pathologies, therapy for estrogen-dependent tumors in women, taking nootropics or antidepressants, sudden weight loss, pituitary gland diseases, unbalanced nutrition.

Estrogen deficiency can be determined by the following symptoms:

  1. During puberty, there may be a delay in the formation of secondary sexual characteristics - absence of menarche until 15–16 years of age, irregular periods, formation of a male-type figure in girls with a narrow pelvis, broad shoulders and developed muscles. The imbalance is also manifested by a decrease in the size of the uterus, underdevelopment of both external and internal reproductive organs.
  2. During menopause, a decrease in estrogen is normal. If the concentration of hormones falls at the age of 40–45 and earlier, the symptoms of menopause appear more clearly - rapid heartbeat, profuse sweating, hot flashes, dizziness, migraines.
  3. After the age of 35–40, the main symptoms are weight gain, disruption of the gastrointestinal tract, the appearance of wrinkles, cellulite, stretch marks, moles and papillomas in large numbers, decreased libido, high heart rate, and impaired blood circulation in the brain.
  4. In young women, estrogen deficiency leads to frequent colpitis, vaginitis, cycle disruptions, pronounced PMS, decreased performance, joint pain, changes in blood pressure, and lack of lubrication in the vagina.

During pregnancy, such a pathology is fraught with disruptions in the development of the placenta, abruption, miscarriage, abnormalities in the formation of the child’s nervous and cardiac systems, and uterine bleeding. The risk of genetic abnormalities in the fetus, in particular Down syndrome, also increases.

Diabetes

The relationship between the hormone E2 and insulin is quite complex. Studies have shown that postmenopausal women face an extremely high risk of developing metabolic syndrome, diabetes, and obesity. These effects were demonstrated in experiments on ERKO-α mice - due to a deficiency of estrogen receptor type alpha, insulin resistance, hyperinsulinemia, and hyperlipidemia were observed in mice; in the case of knockout of the ERβ gene, there were no such disorders; moreover, there was a slight increase in insulin sensitivity and glucose tolerance. That is, we can say that most of the problems are associated with ERα [4].

In practice, everything turns out to be somewhat more complicated. Numerous studies described in a 2021 paper [23] show that we know too little to draw any conclusions. There is considerable conflicting evidence regarding menopause and the risk of developing type 2 diabetes; Estrogen replacement therapy has shown to be completely ineffective as a prophylactic agent in this case.

Many questions still remain unclear regarding the regulation of insulin and glucose levels by estrogen receptors; and to reduce the risk of developing type 2 diabetes, only an adequate diet and maintaining BMI within the normal range are still suggested.

How to check your estrogen levels?

A basic estrogen test is a blood test.

It contains all 3 fractions of the hormone, the ratio of each type is determined in accordance with the following factors:

  • age;
  • presence or absence of pregnancy;
  • taking medications containing any hormones;
  • weight.

It is important to take the test in accordance with the duration of the cycle:

  • if the cycle is 20–21, blood is taken 2–3 days from the start of the first bleeding;
  • with a cycle of 28 days – 3–5 days;
  • more than 28 days – in the range of 5–7 days from the start of menstruation.

If the cycle is irregular, an ovulation test is first performed.
Within 24 hours of its onset, the concentration of estrogen reaches its peak. Before taking tests, a woman is recommended to limit her intake of hormone-containing drugs, exclude sexual activity, and physical activity. The last meal is possible no later than 10 hours. You can find out the answer in 20–30 minutes.

Cardiovascular diseases

In this matter, women of reproductive age have a huge advantage. Activation of ERα in mice is associated with lower rates of vascular damage by atherosclerosis; estrogen, by acting on ERβ, can prevent cardiac fibrosis. And the GPER receptor is able to reduce ischemic damage and maintain normal cardiac function [2]. Unfortunately, all of these benefits decline with age or oophorectomy, and the effectiveness of estrogen replacement therapy as a preventative or therapeutic option has not been proven to date.

Sources:

  1. B. J. Csheskis, J. G. Greger, S. Nagpal, and L. P. Freedman, “Signaling by Estrogens,” J. Cell. Physiol., vol. 213, pp. 610–617, 2007.
  2. R. Li and Y. Shen, “Estrogen and brain: Synthesis, function and diseases,” Trends Mol. Med., vol. 19, pp. 197–209, 2013.
  3. S. Mosselman, J. Polman, and R. Dijkema, “ERβ: Identification and characterization of a novel human estrogen receptor,” FEBS Lett., vol. 392, no. 1, pp. 49–53, 1996.
  4. A. A. Gupte, H. J. Pownall, and D. J. Hamilton, “Estrogen: An Emerging Regulator of Insulin Action and Mitochondrial Function,” vol. 2015, 2015.
  5. N. HELDRING et al., “Estrogen Receptors: How Do They Signal and What Are Their Targets,” Physiol Rev, vol. 87, pp. 905–931, 2007.
  6. J. M. Hall, J. F. Couse, and K. S. Korach, “The Multifaceted Mechanisms of Estradiol and Estrogen Receptor Signaling,” J. Biol. Chem., vol. 276, no. 40, pp. 36869–36872, 2001.
  7. P. J. Kushner et al., “Estrogen receptor pathways to AP-1,” J. Stetoid Biochem. Biol., vol. 74, pp. 311–317, 2000.
  8. M. Karin, Z. g Liu, and E. Zandi, “AP-1 function and regulation,” Curr. Opin. Cell Biol., vol. 9, no. 2, pp. 240–6, 1997.
  9. C. M. Revankar, D. F. Cimino, L. A. Sklar, J. B. Arterburn, and E. R. Prossnitz, “A transmembrane intracellular estrogen receptor mediates rapid cell signaling,” Science (80-.), vol. 307, no. 5715, pp. 1625–1630, 2005.
  10. M. Barton, E. J. Filardo, S. J. Lolait, P. Thomas, M. Maggiolini, and E. R. Prossnitz, “Twenty years of the G protein-coupled estrogen receptor GPER: Historical and personal perspectives,” J. Steroid Biochem. Mol. Biol., vol. 176, pp. 4–15, 2018.
  11. G. Sharma, F. Mauvais-Jarvis, and E. R. Prossnitz, “Roles of G protein-coupled estrogen receptor GPER in metabolic regulation,” J. Steroid Biochem. Mol. Biol., vol. 176, no. 2021, pp. 31–37, 2018.
  12. CD Toran-Allerand et al., “ER-X: A Novel, Plasma Membrane-Associated, Putative Estrogen Receptor That Is Regulated during Development and after Ischemic Brain Injury,” J. Neurosci., vol. 22, no. 19, pp. 8391–8401, 2002.
  13. K. Soltysik and P. Czekaj, “Membrane estrogen receptors—is it an alternative way of estrogen action?,” J. Physiol. Pharmacol., vol. 64, no. 2, pp. 129–142, 2013.
  14. [14] N. J. Kenney, A. Bowman, K. S. Korach, J. C. Barrett, and D. S. Salomon, “Effect of exogenous epidermal-like growth factors on mammary gland development and differentiation in the estrogen receptor-alpha knockout (ERKO) mouse,” Breast Cancer Res. Treat., vol. 79, no. 2, pp. 161–173, 2003.
  15. P. Cowin, T. M. Rowlands, and S. J. Hatsell, “Cadherins and catenins in breast cancer,” Curr. Opin. Cell Biol., vol. 17, no. 5 SPEC. ISS., pp. 499–508, 2005.
  16. G. S. Prins, L. Birch, J. F. Couse, I. Choi, B. Katzenellenbogen, and K. S. Korach, “Estrogen Imprinting of the Developing Prostate Gland Is Mediated through Stromal Estrogen Receptor ␣ : Studies with ␣ ERKO and ␤ ERKO Mice 1,” Environ . Prot., pp. 6089–6097, 2001.
  17. S. Artavanis-Tsakonas, M. D. Rand, and R. J. Lake, “Notch signaling: Cell fate control and signal integration in development,” Science (80-.), vol. 284, no. 5415, pp. 770–776, 1999.
  18. H. A. Harris, “Estrogen Receptor-β: Recent Lessons from in vivo Studies,” Mol. Endocrinol., vol. 21, no. 1, pp. 1–13, 2007.
  19. JF Couse and KS Korach, “Estrogen receptor NULL mice: What have we learned and where will they lead us?,” Endocr. Rev., vol. 20, no. 3, pp. 358–417, 1999.
  20. I. Merchenthaler, M. V. Lane, S. Numan, and T. L. Dellovade, “Distribution of Estrogen Receptor α and β in the Mouse Central Nervous System: In Vivo Autoradiographic and Immunocytochemical Analyses,” J. Comp. Neurol., vol. 473, no. 2, pp. 270–291, 2004.
  21. E. Brailoiu et al., “Distribution and characterization of estrogen receptor G protein-coupled receptor 30 in the rat central nervous system,” J. Endocrinol., vol. 193, no. 2, pp. 311–321, 2007.
  22. F. Lizcano and G. Guzmán, “Estrogen deficiency and the origin of obesity during menopause,” Biomed Res. Int., vol. 2014, 2014.
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  24. H. Samavat and M. S. Kurzer, “Estrogen metabolism and breast cancer,” Cancer Lett., vol. 356, no. 2, pp. 231–243, 2015.
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  28. B. B. Sherwin and J. F. Henry, “Brain aging modulates the neuroprotective effects of estrogen on selective aspects of cognition in women: A critical review,” Front. Neuroendocrinol., vol. 29, no. 1, pp. 88–113, 2008.
  29. M. Bourque, D. E. Dluzen, and T. Di Paolo, “Signaling pathways mediating the neuroprotective effects of sex steroids and SERMs in Parkinson's disease,” Front. Neuroendocrinol., vol. 33, no. 2, pp. 169–178, 2012.

Treatment of hormonal imbalance

The main goal of therapy is to normalize the stages of estrogen production, increase or decrease concentrations to normal.

During the pubertal phase, menopause and or pregnancy, treatment with hormones (gestagens and estrogens) is not carried out.

Medicines

If, in case of hormone deficiency, it is necessary to take drugs that can restore estrogen, then in case of its excess it is strictly forbidden to be treated with such drugs.

To increase estrogen levels

If estrogen is synthesized in a woman in small quantities, the following drugs are prescribed:

NameAction
PremarinConjugated estrogen. Contains natural estrogens. Used for estrogen deficiency, after surgery on the uterus, ovaries, to prevent osteoporosis during the menopause phase.
ProginovaContains estradiol valerate, restores the volume of steroid hormones, improves the condition of cartilage and bone tissue, removes symptoms of menopause, improves skin condition, and slows down aging.
VeroshpironIncludes spironolactone, which has an estrogen-like effect. It has a diuretic effect, reduces testosterone concentrations, and is used in the treatment of polycystic ovary syndrome and menstrual disorders. Reduces the manifestations of female alopecia, skin problems, male pattern hair growth.
HemafeminContains deer pantohematogen, increases the concentration of estrogen in the female body, additionally includes vitamins C, E. Affects the functioning of the ovaries, eliminates hot flashes and pressure surges. Not used during pregnancy, with caution - in case of impaired blood clotting or thrombosis.
StellaStimulates the production of estrogen, reduces the activity of papillomavirus, reduces the risk of developing tumors that produce estrogen. Contains broccoli extract, silicon dioxide, green tea, lactose, soy extract.
OvestinContains estriol. Used to reduce the brightness of menopause, in the treatment of infertility, after surgical extirpation of the uterus, ovaries, and tubes.
OK (Estrogenolite, Janine, Aktivel, Lindinet, Femoden)Monophasic contraceptives contain synthetic estrogens in small doses. They enhance the natural process of hormone production and stop ovulation.

Remedies of this type are often produced in tablets, replenishing the lack of estrogen. Hormone replacement therapy drugs are used for menopause, estrogen deficiency, and infertility. Oral contraceptives are often prescribed to normalize the cycle, for endometriosis, and breakthrough bleeding.

To reduce estrogen levels

In this case, antiestrogenic drugs are used.

Prescribed depending on the cause of low levels of female hormones:

  1. Antitumor drugs: Arimidex, Femara.
  2. For uterine, ovarian and anovulatory infertility: Tamoxifen.
  3. For breast cancer: Letrozole.

Review of tablets containing estrogen →

Estrogen in food

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The effect of drug treatment can be improved with the help of properly selected nutrition.

To increase performance

The activity of estrogen production can be increased by including foods that are rich in hormone-like substances in the menu:

  • vegetables
    - eggplants, tomatoes, carrots, pumpkin, beets;
  • greens, herbs
    - celery, parsley, asparagus, spinach, basil;
  • fruits and berries
    - pomegranates, dates, cherries, melons, apricots, papaya, grapes, raspberries;
  • dairy products
    - cheese, butter, sour cream, cottage cheese, kefir;
  • sunflower seeds
    , flax seeds, pumpkin seeds, peanuts, sesame seeds;
  • garlic
    , mustard.

To preserve the maximum benefits of products, subject them to minimal heat treatment, include them in the menu every day, choose only fresh vegetables and fruits, and cook them once.

To reduce performance

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The purpose of the diet: weight loss, normalization of the digestive tract:

  • exclude canned food, fatty meats, sausage, coffee, beer and alcohol in general;
  • consume more: mushrooms, citrus fruits, green tea;
  • Replace cow's milk with coconut or rice milk.

Folk remedies that increase estrogen

Estrogen metabolism, as well as hormone concentrations, can be normalized using folk remedies:

  1. Take 20 fresh raspberry leaves and pour 200 ml of boiling water for one hour. Drink instead of regular tea 2 times a day, first strain and cool. Start taking it in the middle of your menstrual cycle.
  2. Pour 100 ml of boiling water over 5 hop cones, simmer for 5 minutes, then add 5 mint leaves, leave for 40 minutes. Drink half a glass three times a day for 1 month.
  3. Pour 100 g of plantain seeds with 50 ml of fresh flaxseed oil. Leave it for a day. Then take one teaspoon before meals three times a day.
  4. Grind 100 g of fresh nettle leaves, squeeze the juice from half a lemon, grate the peel, mix everything. Boil with 300 ml of water over low heat for 10 minutes, leave under a closed lid for half an hour. Then strain, take up to 3 glasses a day instead of tea.
  5. Take equal amounts of dried lemon balm and rose hips, add water so that it covers the dry ingredients. Boil for about half an hour, cool, strain and drink 1 glass in the morning and before bed instead of tea.

You can increase the synthesis of natural hormones in the female body using aromatherapy. Use oil of cypress, rose, lavender, mint, bergamot, orange, birch buds. They can also be used for bathing and massage.

Parkinson's disease

Another common neurodegenerative disease; Unlike Alzheimer's disease, women have a lower risk. In this disease, the striatum and substantia nigra, the structures where all three types of estrogen receptors are expressed, are most affected; The most pronounced effect is ERα, which provides protection to dopaminergic neurons [2].

There is evidence that estradiol, acting on all three types of brain receptors, can have a significant neuroprotective effect in individuals of both sexes; Strategies are being developed that can apply these data to the treatment of Parkinson's disease, but all of them still need to be confirmed [29].

Possible consequences and complications

If estrogens are secreted in insufficient quantities, there is no therapy, and pathological conditions develop:

  • obesity;
  • bone destruction;
  • thrombosis;
  • infertility;
  • mastopathy;
  • breast tumors;
  • metabolic disorders;
  • thyroid pathology;
  • mental and nervous disorders;
  • ovarian cysts;
  • menstrual cycle disorders.

With excess estrogen, weight also increases, skin condition worsens, breast sensitivity increases, and blood pressure rises. Sleep, gastrointestinal function, and psycho-emotional background suffer.

The main task of estrogen is to provide a woman with the opportunity to become pregnant and bear a fetus. It is also thanks to this hormone that girls develop a typically female figure, thinner and more elastic skin than men, and no hair in the chest and abdomen. With an excess or deficiency of all fractions of estrogen, hormonal levels are disrupted, which is fraught with health complications and difficulties in conceiving and bearing a fetus.

Breast cancer

There are various mechanisms for the development of this disease that are not associated with changes in hormonal levels (for example, mutations of the BRCA1 and BRCA2 genes), but in many cases, menopause and a decrease in the amount of circulating estrogens play a significant role in carcinogenesis [24].

In a series of studies, it was found that estradiol in breast tissue can be converted into genotoxic, potentially carcinogenic, forms. ERα knockout mice showed a significant reduction in tumor incidence; oophorectomy also delayed carcinogenesis. The aromatase inhibitor drug letrozole has the same effect [25].

These data may significantly influence the therapy of ER+ breast tumors, however, the mechanisms of carcinogenesis and the exact role of estrogen (and estrogen receptors) remain unclear today.

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