I. Introduction
Menstruation, the cyclic shedding of the uterine layer, is a complex control system. Relevant hormones dictate numer-ous negative and positive feedback mechanisms to determine the latency, duration and intensity of each menstrual stage [1]. Consequently, engineers can model the larger control system of menstruation into subsections for each key hor-mone in order to elucidate the cascading effects and causes of each menstrual event. The hypothalamus, pituitary gland and ovaries orchestrate the process by producing and delivering the key hormones via the bloodstream [2]. Gonadotropin-releasing hormone (GnRH) from the hypothalamus stimu-lates the pituitary gland to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH, in turn, cas-cades to stimulate the release of another important hormone, progesterone. Numerous other factors affect menstruation, but the interactions of these four key hormones - GnRH, LH, FSH, and progesterone - play the most major role in menstrual regulation. The menstrual cycle has two main phases: follicular and luteal [3]. The follicular phase lasts about 14 days, during which the levels of GnRH increase, the levels of FSH initially increase and then decrease, and the levels of LH remain low and steady. During the luteal phase, the levels of GnRH decrease in response to ovulation, causing levels of FSH and LH to subsequently decrease as well. The levels of LH are determined by the concentration of estrogen in the blood and the phase of the menstrual cycle. During the follicular phase, low levels of estrogen have a negative feedback relationship with LH and explain the decreasing levels of FSH and low levels of LH. On the other hand, during the luteal phase, high levels of estrogen share a positive feedback relationship with LH and consequently results in an exponential increase in LH.