The Expanded Female Hormone Panel

An expanded female hormone panel is tabulated based upon 11 saliva samples provided from the patient over a 28 day range.  In a cycling female, levels of estrogen and progesterone, and their pituitary precursors: FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone) vary highly over a 28-35 day range.  As such basing decisions or even putting much credence at all in to levels tested via one blood test, on one day of the cycle is substantially incomplete.  In order to get the entire picture, 11 saliva samples, submitted every few days throughout the cycle can chart the optimal peaks and dips (or lack thereof) of  the 4 above mentioned hormones, along with associated levels of other critical players in DHEA (precursor to testosterone and estrogen) and insulin.

Panel is often performed to help provide further insight into an erratic or atypical menstrual cycle, heavy, light or no bleeding, history of oral contraceptives (birth control pills) or HRT (Hormone Replacement Therapy), severity of PMS symptoms, planning for or after child birth, and no take a deeper look into conditions like PCOS (Polycystic Ovarian Syndrome).

BACKGROUND:

In order to fully comprehend the results and their potential implications, an understanding of optimal levels and timing measured by this panel is necessary.  Reviewing the physiological sequence involved further demonstrates why recording samples submitted throughout the entire cycle is imperative and highly useful in thoroughly understanding and thus addressing the underlying issue at hand.

In ideal terms, we can break the monthly cycle into two phases consisting of the follicular phase (day 1-14) and the luteal phase (day 15-28).

(It is acknowledged that levels and timing/duration will vary, however the general characteristics described are to serve as a general blueprint for which relevant comparisons and hypotheses can be formulated.)

Generally, around day 1, we should see Follicle Stimulating Hormone (FSH) rising by way of the anterior pituitary gland.  This signals down to the ovaries and as the name implies, stimulates the follicles within as they basically compete to become the winner or “maybe baby,” (aka the graafian follicle).  The follicles mainly compete by releasing estrogen, which will play a large part in determining the health, strength and robustness of not just the individual follicle and it’s likelihood of survival, but the entire cycle.

(This is a key point to note.  If the follicles do not respond to the pituitary gland’s release of FSH, or if the pituitary does not release sufficient FSH, there will be no estrogen surge, the cycle is a potential loss and ovulation may not even occur.)

The estrogen being released due to the FSH from the pituitary then signals back to the pituitary in a positive feedback loop that triggers the release of more FSH, leading to more estrogen, which causes proliferation (growth & thickening) of the endometrium (uterine lining).  Around day 7-9 we should see climbing FSH and the cycle dependent E2 (estradiol) surge, which subsequent progesterone production and the entire second half of the cycle (luteal phase), including ovulation is contingent upon.

In order to provide the most robust surge of E2 as possible, any progesterone and testosterone is converted to E2 via an important enzyme called AROMATASE.  This is another demonstration of the importance of the E2 surge.  Factors to focus on here that play a major role in this E2 surge include FSH from the pituitary and the health of the ovaries and the follicle itself.  If any piece of this puzzle is lacking, there can be an inhibition of uterine lining proliferation, upon which progesterone is reliant on.

In the presence of an adequate E2 surge, between day 12-14, the pituitary gland recognizes this increase in estradiol and thickening of the endometrium as representation of a quality follicle, and releases LH (lutenizing hormone).  At this point in the presence of an LH surge, the dominant follicle will have migrated to the ovary wall, and ovum to the follicle wall, setting the stage for the follicle to exit the ovary and erupt, releasing the egg to the fallopian tube and thus ovulation has occurred.

The now empty follicle turns in on itself, becoming the corpus luteum (with the follicle no longer present, FSH should drop). The corpus luteum now feeds the ovum and uterine wall by producing massive amounts of progesterone (which should be represented by a bell curve on the second half of the graph) which also causes FSH & LH to drop by way of negative feedback to the pituitary gland.  Whereas estrogen caused growth/thickening of the uterine lining, progesterone causes maturation and vascularization of the wall necessary to support implantation and fertilization.

At this point, if fertilization does not occur, progesterone drops and the uterine lining sloughs off or sheds leading to menstruation and setting the stage for another cycle to occur.

(This is an oversimplified summary of this miraculous, potentially life creating, monthly process, of which many other variables can and do play pivotal parts in this delicate dance.  However, it does provide a basic overview, allowing us to go into more detail where necessary, and subsequently identify and address areas of concern.)