Hormonal breast enhancement or augmentation is a highly experimental potential medical treatment for the breast in which hormones or hormonal agents such as estrogen, progesterone, growth hormone (GH), and insulin- like factors growth 1 (IGF-1) is used or manipulated to produce breast enlargement in women. This is a possible alternative or supplement to surgical breast enlargement with breast implants or fat transfer and other tools of medical breast enlargement.
In addition to drugs, some herbal breast enlargement supplements contain phytoestrogens such as 8-prenylnaringenin (found in hops) and miroestrol (a constituent of Pueraria mirifica ) and thus can be considered as a form of hormonal breast enhancement.. However, evidence of their effectiveness, as well as security data, is lacking.
Video Hormonal breast enhancement
Breast growth
At puberty, estrogen, but not current progesterone, and GH/IGF-1 are essential in mediating breast development, and are synergistic in doing so. Accordingly, hormonal contraceptives and hormone replacement therapy (HRT) with estrogen (and/or progestogen) have been associated with increased breast growth and breast size. In addition, hormonal breast enhancement trials in 45 young women with very high doses (80 mg/injections) intramuscularly, bioidentic estrogen (in the form of estradiol polyphosphate, slow release prodrug estradiol) for six months found that only women increased IGF- 1 occurred after four weeks (46.7% of subjects) had a significant increase in breast size (824.3 mm to 898.5 mm). This is consistent with the established fact that estrogen and IGF-1 appear to be important for breast development, and when present together, is synergistic in mediation.
The administration of estrogen in women with Turner syndrome, which usually does not develop breasts due to hypogonadism, results in normal pubertal breast development. Estrogen and GH are often combined in Turner syndrome. Estrogen in combination with GH or IGF-1 has been used safely and effectively to increase bone density in women with anorexia nervosa. Trans-estrogen-treated women develop normal pubertal breast development similar to the case of girls with Turner syndrome. However, they generally show smaller final breast size compared to their immediate relatives (average size of one cup less). This may be due to the fact that most trans females do not start HRT to adulthood, which is relevant because GH/IGF-1 levels are significantly reduced and decreased after normal teen puberty (from late adolescence/early adulthood and thereafter). Thus, the synergy of estrogen with GH/IGF-1, and with expansion, the potential for maximal breast development, can be reduced.
Systemic administration of GH or IGF-1 causes hyperplasia of mammary (enlarged mammary glands) in animals. For example, in the study of rhesus female apes, treatment with GH alone, IGF-1 alone, and combination of GH and IGF-1, were found to produce milk gland hyperplasia and an increase in the size of the mammary glands and epithelial proliferation by 2-fold, 3 to 4 fold, and 4-5-fold, respectively, changes that directly correlated with serum GH and IGF-1 concentrations. Thus, studies have found that girls with growth hormone deficiency (GHD) treated with GH experience accelerate breast growth and that boys with growth hormone deficiency treated with GH sometimes experience gynecomastia. In addition, levels and activities of IGF-1 have been found to correlate with breast volume in the general female population.
In women with Laron syndrome, in which growth hormone receptor (GHR) is damaged and insensitive to GH and serum IGF-1 levels are very low, puberty, including breast development, is delayed, although full sexual maturity is finally achieved. In addition, breast development and size are normal (though delayed) in spite of GH/IGF-1 axis insufficiency, and in some breasts may actually be large in relation to body size (which has been hypothesized because increased secretion of prolactin is due to the drift phenomenon of somatomammotrophic cells in pituitary gland with high GH secretion). An animal model of Laron's syndrome, GHR KO mice, showed a very disturbed ductal development at 11 weeks of age. However, for 15 weeks, ductal development has been successful with normal mice and the channel has been fully distributed across the breast fat pad, although the ductus remains narrower than the wild rats. However, female GHR knockout mice can lactate normally. Thus, taken together, it is said that the female phenotype with Laron syndrome and GHR knockout mice is identical, with reduced body size and delayed sexual maturity accompanied by normal lactation.
A Vietnamese teenage girl with Laron syndrome treated with high doses of IGF-1 and gonadotropin-releasing hormone analogues for 3-4 years paradoxically develops isolated breast development without other pubertal changes regardless of estrogen levels at low levels. prepubertal range. Noting that gynecomastia is a recognized complication of treatment with GH and IGF-1, the study authors attributed breast development to a high, suprafisiologic, low-grade, suprafisiologic level of oestrogens derived from the aromatization of the adrenal androgen imagery..
The secretariat of certain long-term growth hormone, such as CJC-1295 and ibutamoren (MK-677), is able to reliably and effectively increase serum GH and IGF-1 concentrations in humans. Alternatively, exogenous, pharmaceutical GH and IGF-1 (as mecasermin or mecasermin rinfabate) alone, or IGF-1 analogues such as des (1-3) IGF-1 and IGF-1 LR3, may be used to increase GH/IGF -1 axis function. A number of dietary supplements, including L -arginine, L -ornithine, L -syssine, acetyl- L -carnitine , and creatine, may significantly increase GH levels, although evidence varies. Vitamin D has been found to increase IGF-1 levels in healthy subjects and individuals with GHD, and vitamin D deficiency is associated with low levels of IGF-1. However, there is evidence that vitamin D also has the potential to inhibit breast growth through activation of vitamin D receptors.
Oral estrogen therapy suppresses the production of IGF-1 in the liver, where about 80% of serum IGF-1 is derived from, and decreases serum IGF-1 levels (about 15-40%, depending on the dosage and type of estrogen given), as well as binding growth factor proteins such as insulin 1 (IGFBP1) (a carrier protein that inhibits the bonding/activity of IGF-1). This results in a functioning state of GH resistance (since GH induces the production and secretion of IGF-1 in the liver to mediate most of its effects), with a combination of oral estrogens and GH being less effective in generating GH clinical effects relative to GH alone. in individual clinical studies with hypopituitarism/GHD. In contrast, treatment with a combination of GH and transdermal estrogens has been found not to lower IGF-1 levels or to increase IGFBP1 levels. Thus, estrogen is administered via other routes of liver-cutting administration, such as transdermal (in patch estrogen), sublingual, intranasal, intramuscular injection, and subcutaneous injection, possibly significantly more effective than oral estrogens.
Non-androgenic progesterone and progestin, such as dydrogesterone, do not affect serum IGF-1 levels regardless of route of administration. However, androgenic progestin, such as 19-nortestosterone derivatives such as norethisterone and levonorgestrel and others like, to a lesser extent, medroxyprogesterone acetate (MPA), when taken orally, induces the production of IGF-1 through activation of androgen receptors (AR) in the liver. However, at the same time, androgens potentially inhibit estrogen actions in the breast, such as by suppressing ER expression in breast tissue, and this action is expected to undo any benefit. Accordingly, a small clinical study found that the addition of oral MPA to estrogen in trans females undergoing genital replacement therapy did not result in an increase in breast size.
Diet and nutrients have been found to affect serum levels of IGF-1. In particular, low protein intake, fasting, and malnutrition were associated with low levels of IGF-1, whereas obesity was associated with high or normal levels of IGF-1 and reduced levels of IGFBP1 and IGFBP3 (resulting in higher free IGF-1 concentrations). In addition, milk consumption and circulating levels of IGF-1 have been found to be positively correlated. In addition to diet and nutrition, exercise has also been found to increase GH levels significantly.
Androgens, such as testosterone and dihydrotestosterone (DHT), strongly suppress the action of estrogen in the breast. At least one way they do this is by reducing expression of estrogen receptor in breast tissue. In women with complete androgen insensitivity syndrome (CAIS), which is completely insensitive to androgens and has only low estrogen levels (50 pg/ml), relatively low estrogen levels mediate significant breast development, and breast size CAIS Women, on average, is actually larger than non-CAIS women. In men treated with antiandrogens, gynecomastia (breast enlargement in men) and mastodynia (pain/breast tenderness) usually occur. Antiandrogens, such as spironolactone, are also known to cause breast augmentation and mastodynia in women. Some examples of widely used and very powerful antiandrogens include cyproterone acetate and bicalutamide.
The expression of Cyclooxygenase-2 (COX-2) in the mammary gland tissue results in milk gland hyperplasia as well as the early development of mammalian glands in female rats, suggesting a strong stimulatory effect of this enzyme on the growth of the mammary gland. This effect appears to be a downward step of increasing prostaglandin prescription activation of EP 2 , EP 3 , and EP 4 , but not on EP 1 receptor, in the mammary gland tissue, which in turn produces a strong induction of amphiregulin expression, an important growth factor involved in the development of normal milk glands. In addition, epidermal growth factor receptor agonists (EGFRs), molecular targets of amphiregulin, induce COX-2 expression in the mammary gland tissue, potentially generating self-amplification amplification cycles by COX-2. This mechanism is closely related to the formation, growth, and spread of cancer with a poor prognosis, and in accordance with the fact that long-term aspirin, COX inhibitors, and other nonsteroidal anti-inflammatory inhibitors of COX (NSAID) have been found to slightly reduce cancer risk breasts in women (the important thing here is that breast growth/size and risk of breast cancer are positively associated). Taken together, these findings suggest that COX-2 inhibitors, such as aspirin, ibuprofen, naproxen, paracetamol (acetaminophen), and celecoxib, can suppress breast tissue growth.
Increased levels of HGF and, to a lesser extent, IGF-1 (5.4 fold and 1.8-fold respectively), in breast stromal tissue, have been found in macromastia, a very rare condition of very large breast size and excessive. Exposure of macromastatic breast stromal tissue to non-macromastric breast tissue was found to cause elevated alveolar morphogenesis and epithelial proliferation in the latter. Neutralizing antibodies to HGF, but not for IGF-1 or EGF, were found to weaken the proliferation of breast epithelial tissue caused by exposure of macromastatic breast stromal cells, potentially directly involved in breastfeeding and enlargement seen in macromastia. Thus, treatment with HGF or its receptor agonist, c-Met, or potentiator from the HGF-c-Met axis (such as dihexa) may have the potential to induce breast growth similar to macromastia by relying on exposure. However, genomic association studies are strongly associated with HGF and c-Met in aggressive breast cancer, and a study of women with macromastia indicates that there may be a significant association between macromastia and an increased risk of breast cancer.
Maps Hormonal breast enhancement
Possible increases in cancer risk
The risk of breast cancer in women is about 100 times that of men. Thus, typical female-breast development is associated with a dramatic increase in breast cancer risk. In addition, breast size and breast cancer are positively correlated, and macromastia, a condition of too large a breast size, is considered a risk factor for breast cancer. Accordingly, it has been hypothesized that there may be a further increase in risk of breast cancer with hormonal breast enhancement.
Long-term treatment with estrogen and/or progestogen in women, especially in the form of oral contraceptives, appears to be associated with a slightly increased risk of breast cancer. The risk seems to be highest in younger women, especially in those who start using oral contraceptives before the age of 20 years. This could be attributed to increased estrogen synergies with higher GH/IGF-1 levels present at a younger age.
Studies have shown that elevated growth factor pathways, including from GH/IGF-1, may potentially increase the risk of various cancers, including breast cancer. Increased proliferation due to increased activity of IGF-1 has been suggested for the possibility of playing a key role in high-risk breast cancer seen in women with BRCA1 mutations. Several large studies have found correlations in premenopausal women between serum IGF-1 levels in the upper quartile of the normal range and the level of IGFBP-3 in the lower quartile (ie, high circulating IGF-1 levels and low circulating IFGBP-3 levels) and the risk of developing various cancer, including breast cancer. However, an increased risk of breast cancer has been found to be simple (for example, just more than twice the usual risk). Subsequent studies have found the increased risk to be less clear, and it should be noted that high-normal IGF-1 levels have been found to correlate only with premenopause and not with the incidence of postmenopausal breast cancer. In any case, mice that are engineered to have lower levels of circulating IGF-1 show a lower risk of developing various cancers, including breast cancer. In contrast to the case of IGF-1, upper quintiles (20%) of postmenopausal women with the highest estrogen and androgen levels in circulation have been found to have a significantly increased risk of breast cancer (relative to the lowest quintile, the risk is 2- to 3-fold higher). A significant positive association with breast cancer risk has also been found with prolactin levels in postmenopausal women.
In acromegaly, a condition caused and maintained by extremely high GH/IGF-1 levels, overall, there appears to be little or no increased risk of breast cancer or certain other cancers (eg, prostate cancer, lung cancer) relative to the general population. That said, the risk of cancer appears to be consistently increased in individuals specifically with uncontrolled illness. In addition, there appears to be an increased risk of colorectal cancer and pre-malignant tubular adenomas in acromegaly. However, individuals with acromegaly do not appear to show an increased risk of cancer mortality or general mortality after treatment (ie, after their GH/IGF-1 levels have been normalized with medical care), and this includes breast cancer. (Research with a larger scale may be necessary.) Unlike acromegaly, people with Laron syndrome, a condition characterized by insensitivity to GH and very low levels of IGF-1, have large reductions, in fact virtually none, the risk of developing cancer , including breast cancer. There are concerns expressed about doping in athletes with GH/IGF-1 and the possible increased risk of cancer, including breast cancer.
See also
- Hormone therapy
- Mammoplasia
- Galactagogue
- Micromastia
- Breast atrophy
- Pre-menstrual water retention
- Clitoral enlargement method
- Penis enlargement
References
Source of the article : Wikipedia
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