Menopause is a period within which a woman loses her menstrual periods, which is established when a woman goes through 12 months without having menses. A variety of signs are experienced in menopause due to hormonal variations in the body. In addition, there is loss of bone density and increase in the level of cholesterol hence the increased risk of cardiovascular disease. Two kinds of menopause occur in women- premature and perimenopause. In the US, the average age at which women get into menopause is 51, but the standard age of menopause is 48-55 years.
In a few cases, however, menopause begins as early as 40, hence termed as premature. Late menopause occurs beyond 55 years. Premature menopause has a likelihood of occurring in women who smoke and those who have never had pregnancy. The hormones associated with menopause take effect before the final menstrual phase, normally within a 5 year period, hence perimenopause. Surgical menopause occurs when ovaries are amputated through surgical means (The Columbia Encyclopedia, 2007).
The onset of menopause is triggered by the failure of the ovary to respond as a result of the stimulus evoked by gonadotropin hormone. Normally, a female human is born with ovaries holding an estimate of 2 million primordial follicles, each one having a single ovum. Nevertheless not all the ova and follicles grow though the development period; at puberty an estimate of 300, 000 follicles are present. Furthermore, all through the age of 13 to 46 years, a greater majority of the follicles disintegrate- about 299,000, in a process referred to as atresia.
At the end of it, only about 400 follicles develop to form vestibular follicles and finally release an ovum through ovulation (Burger, 2006). Gonadotropin-releasing factor (GnRH) that is secreted by the hypothalamus in the brain stimulates the production of the follicle stimulating hormone (FSH) from the anterior pituitary gland. The role of FSH is to accelerate the development of the vesicular follicle so that it produces estrogen, which together with FSH supports the development of the ovum to maturity and thickening of the uterine walls.
The lutenizing hormone (LH) that is produced by the anterior pituitary gland also activates the development of the ovum and its final release to the fallopian tube. The follicle after releasing the ovum develops further to form the corpus luteum. Corpus luteum is responsible for the secretion of progesterone which is also responsible for the thickening and vascularization of the endometrium walls in preparation for conception. Failure to conceive leads to involution of the corpus luteum and as a result, the production of the progesterone and estrogen stops.
Consequently, the endometrium wall sloughs off and is released out of the uterus as menses. The functioning of the ovary within a woman is considered to be highest before one reaches 30 years, however, as one ages the level of estrogen decreases steadily. During the perimenopausal period, a few occurrence of follicles and ova are noted, hence a reduced level of estrogen and consequently the incapability to act in response to GnRH, FSH and LH.
Nevertheless, the luteal phase is maintained at a constant level as soon as ovulation takes place. Because of these happenings, women are often depressed with the thought that they will never get pregnant. However, research indicates that someone can still be pregnant; unintentional pregnancies have occurred in women aged between 40 and 44 years and their rate has been shown to increase; hence, the necessity of contraceptive use in couples who are heterosexual.
In the early 40s, the menstruation flow reduces in length due to a reduced number of follicles that are functional. When the follicles turn out to be unresponsive to stimulation by the GnRH; the levels of the lutenising hormone and the follicle stimulating hormone within the body rise. Accordingly, the ovary is stimulated leading to an elevated level of estrone and a reduction in the level of estradiol. Similarly, the negative feedback brought about by high levels of FSH leads to low levels of inhibin.
Since estrogen cannot be produced by follicles anymore, the alternative source of estrogen in postmenopausal women is obtained from androstenedione through the ovarian stromal and adrenal secretion. Even though the level of testosterone also declines in menopause, the 17-estradiol level increases much greater than testosterone. When ovulation come to a close, estrogen production through androgen aromatization and in extragonadal places goes unobstructed by progesterone produced by the corpus luteum, thereby leading to an elevated amount of estrogen in the body.
This is dangerous because it can cause endometrial hyperplasia, a potential cause of cancer of the endometrium (Curran, 2008). The onset of menopause and postmenopause, results in low levels of estradiol. However, the level of estrone remains constant; this is responsible for maintenance of estrogen in postmenopausal women. Conversion of androgen to estrogen mostly takes place in the adipose tissue, thus the assumption that women who are overweight have more estrogen than slender women; hence get to menopause late in life.
But this has been disapproved by researches indicating that the menopausal symptoms occur relatively at the same time to heavy-weight women as well as slender women. Menopause is determined clinically by measuring the level of FSH. Higher levels of FSH are noted compared to LH as a result of a decreased rate of FSH renal clearance than LH. On the other hand, this test may not apply since there is a broad variation in the levels of FSH and LH as a reaction to GnRH. The measure of FSH and LH helps to establish whether perimenopausal women are advancing into menopause.
Elevated levels of FSH in women before postmenopause is an indication of a probability of getting pregnant, hence contraception use is encouraged until the high level persists to postmenopause.
References: Curran D. 2008. Menopause. Available from: <http://emedicine. medscape. com/article/264088-overview>. Accessed 2009 March, 30. The Columbia Encyclopedia, Sixth Edition. 2007. Menopause Burger HG. 2006. Physiology and endocrinology of the menopause. Medicine Volume 34(1): 27-30