Breast growth Hormonal breast enhancement

at puberty, estrogen, not progesterone @ time, , gh/igf-1 critical in mediating development of breasts, , synergistic in doing so. in accordance, hormonal contraception , hormone replacement therapy (hrt) estrogen (and/or progestogens) have been associated increased breast growth , breast size. moreover, trial of hormonal breast enhancement in 45 young women high doses (80 mg/injection) of intramuscular, bioidentical estrogen (in form of estradiol polyphosphate, slow-releasing estradiol prodrug) 6 months found women in whom increase in igf-1 levels occurred after 4 weeks (46.7% of subjects) experienced significant increase in breast size (824.3 mm 898.5 mm). in accordance established fact both estrogen , igf-1 appear essential breast development, , when present together, synergistic in mediating it.

the administration of estrogen women turner syndrome, not develop breasts due hypogonadism, results in normal pubertal breast development. estrogen , gh combined in turner syndrome. estrogen in combination gh or igf-1 has been employed safely , improve bone density in women anorexia nervosa. trans women treated estrogen experience normal pubertal breast development case of girls turner syndrome. however, show smaller final breast size in comparison immediate relatives (one cup size less on average). perhaps due fact trans women not commence hrt until adulthood, of relevance because gh/igf-1 levels , progressively decrease after normal adolescent puberty (from late adolescence/early adulthood , thereafter). such, synergy of estrogen gh/igf-1, , extension, maximal breast development potential, may reduced.

systemic administration of gh or igf-1 causes mammary hyperplasia (enlargement of mammary glands) in animals. example, in study of aged female rhesus macaques, treatment gh alone, igf-1 alone, , combination of gh , igf-1, found produce mammary gland hyperplasia , increased mammary gland size , epithelial proliferation 2-fold, 3- 4-fold, , 4- 5-fold, respectively, changes directly correlated serum concentrations of gh , igf-1. accordingly, research has found girls growth hormone deficiency (ghd) treated gh experience accelerated breast growth , boys ghd treated gh experience gynecomastia. moreover, igf-1 levels , activity have been found correlated breast volume in female general population.

in women laron syndrome, growth hormone receptor (ghr) defective , insensitive gh , serum igf-1 levels low, puberty, including breast development, delayed, although full sexual maturity reached. moreover, breast development , size normal (albeit delayed) in spite of gh/igf-1 axis insufficiency, , in breasts may large in relation body size (which has been hypothesized due increased secretion of prolactin caused drift phenomenon somatomammotrophic cells in pituitary gland high gh secretion). animal model of laron syndrome, ghr knockout mouse, shows severely impaired ductal outgrowth @ 11 weeks of age. however, 15 weeks, ductal development has caught of normal mice , ducts have distributed throughout mammary fat pad, although ducts remain narrower of wild-type mice. in case, female ghr knockout mice can lactate normally. such, taken together, said phenotypes of women laron syndrome , ghr knockout mice identical, diminished body size , delayed sexual maturation accompanied normal lactation.

an adolescent vietnamese girl laron syndrome treated high dosage of igf-1 , gonadotropin-releasing hormone analogue 3–4 years paradoxically experienced isolated progression of breast development without other pubertal changes in spite of estrogen levels in low prepubertal range. noting gynecomastia recognized complication of treatment gh , igf-1, authors of study attributed breast development synergism of high, supraphysiological igf-1 levels low levels of estrogen derived peripheral aromatization of adrenal androgens.

certain long-acting growth hormone secretagogues, such cjc-1295 , ibutamoren (mk-677), capable of reliably , increasing serum gh , igf-1 concentrations in humans. alternatively, exogenous, pharmaceutical gh , igf-1 (as mecasermin or mecasermin rinfabate) themselves, or analogues of igf-1 such des(1-3)igf-1 , igf-1 lr3, may employed increase gh/igf-1 axis function. number of dietary supplements, including l-arginine, l-ornithine, l-lysine, acetyl-l-carnitine, , creatine, may able increase gh levels, although evidence mixed. vitamin d has been found increase igf-1 levels in both healthy subjects , individuals ghd, , vitamin d deficiency associated low igf-1 levels. however, there evidence vitamin d may potently inhibit breast growth via activation of vitamin d receptor.

oral estrogen treatment suppresses igf-1 production in liver, approximately 80% of serum igf-1 originates from, , reduces total serum igf-1 levels (by 15–40%, dependent on dose , type of estrogen administered), increases levels of insulin-like growth factor-binding protein 1 (igfbp1) (a carrier protein inhibits igf-1 binding/activity). results in state of functional gh resistance (as gh induces igf-1 production , secretion in liver mediate of effects), combined oral estrogen , gh being less effective in evoking clinical effects of gh relative gh alone in clinical studies of individuals hypopituitarism/ghd. in contrast, treatment combined gh , transdermal estrogen has been found not decrease igf-1 levels or increase igfbp1 levels. such, estrogen administered via other routes of administration bypass liver, such transdermal (in form of estrogen patches), sublingual, intranasal, intramuscular injection, , subcutaneous injection, may more effective oral estrogen.

progesterone , non-androgenic progestins, such dydrogesterone, not affect serum igf-1 levels regardless of route of administration. however, androgenic progestins, such 19-nortestosterone derivatives norethisterone , levonorgestrel , others like, lesser extent, medroxyprogesterone acetate (mpa), when taken orally, induce igf-1 production via activation of androgen receptor (ar) in liver. however, @ same time, androgens potently inhibit estrogen action on breast, such suppressing er expression in breast tissue, , action expected cancel out benefit. in accordance, single small clinical study found addition of oral mpa estrogen in trans women undergoing sex reassignment therapy did not result in increased breast size.

diet , nutrition have been found affect serum igf-1 levels. specifically, low protein intake, fasting, , malnourishment associated low igf-1 levels, whereas obesity associated high or normal igf-1 levels , lowered igfbp1 , igfbp3 levels (resulting in higher free igf-1 concentrations). in addition, milk consumption , circulating igf-1 levels have been found positively correlated. aside diet , nutrition, exercise has been found increase gh levels.

androgens, such testosterone , dihydrotestosterone (dht), powerfully suppress action of estrogen in breasts. @ least 1 way reducing expression of estrogen receptor in breast tissue. in women complete androgen insensitivity syndrome (cais), insensitive androgens , have modest levels of estrogen (50 pg/ml), relatively low levels of estrogen capable of mediating significant breast development, , breast sizes of cais women, on average, in fact larger of non-cais women. in males treated antiandrogens, gynecomastia (enlargement of breasts in males) , mastodynia (breast tenderness/pain) commonly occur. antiandrogens, instance spironolactone, known cause breast enlargement , mastodynia in women. examples of used , highly-potent antiandrogens include cyproterone acetate , bicalutamide.

cyclooxygenase-2 (cox-2) overexpression in mammary gland tissue produces mammary gland hyperplasia precocious mammary gland development in female mice, indicating strong stimulatory effect of enzyme on growth of mammary glands. these effects appear downstream actions of increased activation of prostaglandin ep2, ep3, , ep4 receptors, not ep1 receptor, in mammary gland tissue, in turn results in potent induction of amphiregulin expression, critical growth factor involved in normal mammary gland development. in addition, agonists of epidermal growth factor receptor (egfr), molecular target of amphiregulin, induce cox-2 expression in mammary gland tissue, potentially resulting in self-perpetuating cycle of growth amplification cox-2. mechanism closely related formation, growth, , spreading of cancers poor prognosis, , in accordance fact long-term administration of aspirin, cox inhibitor, of other cox-inhibiting nonsteroidal anti-inflammatory drugs (nsaids), have been found reduce risk of breast cancer in women (it notable here breast growth/size , breast cancer risk positively associated). taken together, these findings indicate cox-2 inhibitors, such aspirin, ibuprofen, naproxen, paracetamol (acetaminophen), , celecoxib, may suppress growth of breast tissue.

elevated levels of hgf and, lesser extent, igf-1 (by 5.4-fold , 1.8-fold, respectively), in breast stromal tissue, have been found in macromastia, rare condition of extremely , excessively large breast size. exposure of macromastic breast stromal tissue non-macromastic breast epithelial tissue found cause increased alveolar morphogenesis , epithelial proliferation in latter. neutralizing antibody hgf, not igf-1 or egf, found attenuate proliferation of breast epithelial tissue caused exposure macromastic breast stromal cells, potentially directly implicating hgf in breast growth , enlargement seen in macromastia. such, treatment hgf or agonists of receptor, c-met, or potentiators of hgf-c-met axis (such dihexa) might have potential induce macromastia-like breast growth in exposure-dependent manner. however, genome-wide association study highly implicated hgf , c-met in breast cancer aggressiveness, , study of women macromastia indicated there may significant association between macromastia , increased risk of breast cancer.