Botanical Breast Enhancement: Guide



Breast development

The hormones of estrogens, progestogens, prolactin and androgens influence breast tissue through Estrogen Receptor Alpha (ERα), Progesterone Receptor B (PRB) and Prolactin Receptor (PrlR). ERα, Estrogen Receptor Beta (ERβ) and progesterone receptors (PR) in the reproductive tract are important for estrogen balance and fertility. As each receptor is positively stimulated by its respective hormone, it also becomes desensitized. There are more receptor types in the breast and body that cannot be ignored due to health reasons.

Positive estrogenic stimulation, or agonism, of ERα causes lengthening of milk ducts. Branching of milk ducts, which increases the amount of end buds, is caused by progestogenic agonism on PRB. The formation of milk lobules converted from the end of milk ducts and their continued growth is caused by prolactin’s effects on PrlR. Progesterone also has a role in differentiation, or conversion of end points into milk lobules, by influencing prolactin, during secretory phase.


Of ERα, ERβ and PRB, mild potentencies of their non-respective steroid hormone enhances each hormone receptor’s response to its respective hormone, known as receptor upregulation. Without compatible synergistic action, the response to a receptor’s own specific hormone dulls with quantity or potency, known as receptor downregulation. Upregulation and downregulation also applies to non-steroid hormone receptors like PrlR. Too much of a potent hormone can damage its own and other interacting receptors. An imbalance of too much of one type of hormone is a cancer and fertility risk. The breast and reproductive tract contain more types of cell receptors, but the mentioned above are the focus so far.

Estrogens are formed from androgens through a process called aromatase, and aromatase enzymes are located within tissue where ERα and ERβ are also present. ERβ is located in ovarian, egg, bone, brain and adipose tissue. Within the ovarian follicle or corpus luteum, androgen production by theca cells, and estrogen production by granulosa cells are together important for reproductive health.

Estrogens, progestogens, androgens, glucocorticoids and mineralocorticoids are steroid hormones which are fat soluble. Steroid hormones react with their respective receptors within cells.

Follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (Prl), anti-müllerian hormone (AMH) and inhibin are amino acid based hormones that regulate the menstrual cycle. These hormones do not last as long in the body as steroid hormones, and these hormones interact with receptors at cells walls. Balance of these non-steroid hormones, and the health of their corresponding receptors is also important.

Menstrual cycle


The menstrual cycle will be divided into the following 4 phases to simplify timing: menses (menstruation), proliferative, secretory and premenstrual. Follicular phase has been divided up into menses and proliferative phases. Menstruation is when the uterus lining is shed. The proliferative phase is when the uterus rebuilds to prepare for potential pregnancy, and this lasts from the end of menstruation until ovulation. Ovulation is an intermediate time between proliferative and secretory phases. The luteal phase has been divided into secretory and premenstrual phases. The corpus luteum, which produces progesterone, is present during the secretory phase. Premenstrual phase begins after the corpus luteum disintegrates, and it lasts until menstruation starts.

During menstruation, FSH increases menstruation intensity, and prolactin decreases menstruation intensity. Estrogen is not a dominant hormone during menstruation. FSH develops the follicle, but it also causes follicles to be released.

During proliferative phase, one or few follicles continue to develop which raises inhibin and estrogen. Inhibin signals the pituitary to not release FSH, and for new follicles not to be released. Rising estrogen levels prepare the reproductive tract for egg implantation. Estrogen suppresses LH at first, but a buildup of estrogen eventually causes the body to release LH.

LH allows ovulation to occur, releasing the egg from the follicle, leaving behind the corpus luteum in the ovary. The sequential rise of LH, then FSH initially matures the corpus luteum within the ovary during ovulation. FSH then pushes the egg towards the uterus.

Progesterone is produced by the corpus luteum, which is a temporary organ whose function is to signal to the pituitary gland to momentarily prevent menstruation, for purposes of maintaining fertilization or pregnancy. Lower amounts of estrogens than progestogens are produced during the luteal phase and pregnancy. The pituitary gland releases prolactin, which signals the corpus luteum (and if during pregnancy, the placenta) to release more progesterone, creating a feedback loop. Progesterone increases prolactin, and prolactin lowers FSH and LH.

If the egg is not fertilized, the corpus luteum dies within the ovaries. Once progesterone levels drop during premenstrual phase, the pituitary gland begins to release FSH, allowing menstruation to begin. Outside of the secretory phase, early premenstrual phase or pregnancy, progesterone amounts in the body are existent (due to the adrenal glands), but negligible.


This is from chapter 1 from breast-endocrinology.pdf. The next chapter is Hormone Imbalances. super-bazongas.pdf continues on herb use.

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