Understanding Heavy Menstrual Bleeding During Peri -Menopause. The menopause transition, referred to as peri-menopause, gradually begins five to six years preceding true menopause. True menopause tends to occur around age fifty and is noted by the absence of menstrual bleeding for a year. Physiological changes associated with peri-menopause result from alterations in ovarian function due to diminished fertility. During peri menopause these natural alterations in ovarian function often affect changes in the menstrual cycle. The following is a brief over view regarding the hormonal communication that generates a monthly menstrual cycle and the changes in these hormonal messages that gradually shut down the menstrual cycle. In women of childbearing age, the brain sends a monthly message to the ovaries, via follicle stimulating hormone to stimulate the maturation of egg containing follicles in the ovaries. The developing ovarian follicles produce the hormones estrogen and inhibin B. The hormone inhibin B relays a message to the brain to pause the follicle-stimulating hormone message. The hormone estrogen (estradiol) stimulates the cells of the uterine lining to grow and increase in number to generate a nurturing womb in anticipation of pregnancy. However, close to midlife, during peri-menopause, a woman's egg follicles gradually become depleted. There are fewer eggs to become developed and these remaining eggs are less responsive. In an effort to stimulate these less responsive eggs the brain sends more frequent messages of FSH to the ovaries to stimulate egg production. The hormone inhibin B normally switches off (regulates) follicle stimulating hormone. During peri menopause inhibin B levels fall due to the decreased number of ovarian follicles. This reduction of inhibin B contributes to the dys-regulation of follicle stimulating hormone. This normal and gradual lessening of egg production results in erratic fluctuations of follicle-stimulating hormone and estrogen which in turn contribute to the production of very low levels of the hormone progesterone. These fluctuations in hormonal levels often contribute to the physiological symptoms that many women experience during peri-menopause. 
The hormones Inhibin A and B direct follicular development. Inhibin B has a major role in triggering the menopausal transition.
Inhibin B is a glycoprotein synthesized by ovarian granulosa cells. Inhibin B normally switches off (regulates) follicle stimulating hormone. During peri menopause inhibin B levels fall due to the decreased number of ovarian follicles. This reduction of inhibin B contributes to a rise in follicle stimulating hormone. During peri-menopause the gradual lessening of egg production, and thus fertility, often results in anovulatory (non-fertile) menstrual cycles. Essentially, during an anovulatory menstrual cycle an egg follicle is not released from the ovary. As a result, the corpus luteum does not form and only trace amounts of the hormone progesterone are secreted. Anovulatory menstrual cycles are dominated by the estrogen metabolite: estradiol. In addition to the growth and maturation of an egg-bearing follicle, estrogen stimulates the growth and formation of the glands of the uterine lining (the endometrium). During an ovulatory (conceptual) menstrual cycle, luteinizing hormone stimulates a ripened egg follicle to separate from the ovary for fertilization. When the egg follicle separates from the ovary the space that remains is the corpus luteum. The corpus luteum secretes the hormone progesterone. Under the influence of progesterone the glands lining the womb secrete glycogen which will provide energy for the fertilized egg. The secretion of progesterone also helps regulate and suppress the secretion of estrogen. In ovulatory menstrual cycles, the hormone progesterone provides counterbalance to estrogen. However, for many women during peri-menopause an egg does not separate from the ovary which results in no corpus luteum production and levels of progesterone that are to low to counterbalance estrogen. As a result, estrogen dominates the menstrual cycle allowing the cells lining the endometrium to increase in mass and number. The unopposed estrogen allows for the functionalis layer of the endometrium to thicken to more then normal. In addition to un-needed blood vessels, inflammatory *exudates and proteolytic enzymes, menstrual fluid includes the shedding of the functionalis layer of the uterine lining. This extra thicken uterine lining contributes to the increased menstrual flow that many women experience during peri-menopause.
*exudates defined
a fluid with a high concentration of protein and cellular debris which has escaped from blood vessels and has been deposited in tissues, or on tissue surfaces, usually as a result of inflammation.
The functionalis layer of the endometrium grows anew during each cycle.
After the spongiosa and epithelial layers are shed during menstruation, the endometrium is about 2mm thick. As estrogen levels increase, the endometrium regenerates to a thickness of 11mm late in the follicular phase. Heavy menstrual periods during peri-menopause are often the affect of estrogen dominance, which results from anovulatory (non-fertile) menstrual cycles. Pharmaceutical therapy to help manage heavy or irregular menstrual bleeding during peri-menopause will help to moderate estrogen and progesterone levels and are most effective when individualized to a woman's unique hormonal profile. During perimenopause heavy menstrual bleeding can often be modified with progesterone therapy. Natural micronized progesterone cream or capsules can be obtained from a compounding pharmacy with a physician's prescription. A compounding pharmacy custom blends natural bio-identical hormones. Bio-identical hormones are creams or gels compounded from soy and Mexican Wild Yam. Bio-identical estrogen and progesterone are a match to the ovarian hormones the body naturally produces. Please see the bio-idential hormone replacement gift packages noted on the top right hand corner of this page. Keep in mind, perimenopausal heavy periods will lessen naturally as the menopausal transition progresses, and ovarian estrogen production diminishes.
Click here for overviews regarding menstrual fluid, cramps, clotting and changes in the color of menstrual blood. 
Understanding Why Menstrual Cycles Often Become Closer Together During Peri Menopause Whether a woman has a conceptual or non fertile menstrual cycle, whether a woman is 28 or 48 years old, cyclic menstrual bleeding occurs due to estrogen and/or progesterone withdrawal. When the brain determines that a pregnancy has not occurred hormonal levels (most significantly progesterone) drop, the blood vessels (microvasculature) of the uterine lining regresses and menstrual bleeding occurs. Oral and transdermal contraceptives provide a continuous level of estradiol and/or progesterone usually for three weeks per month. The fourth week of oral contraceptives is a row of placebo pills. Taking the placebo pills allows for hormonal withdrawal, which results in menstrual bleeding. Removing a transdermal contraceptive patch also allows for hormonal withdrawal, which results in menstrual bleeding. Extended cycle oral contraceptives add several more weeks of hormones and then placebo pills which allow for withdrawal menstrual bleeding. Oral contraceptives with fewer placebo pills shorten the days of menstrual bleeding. The key point to understand is that withdrawing the contraceptive drops the hormone levels which results in menstrual bleeding. During peri menopause, estrogen production by the ovary is erratic. Estradiol levels are unpredictable and can fluctuate between low, normal and high. An increase in estrogen contributes to heavier menstrual bleeding. A decrease in estrogen production contributes to less cell growth and maintance of the uterine lining. Essentially estrogen levels are too low to maintain and support the uterine lining. The cells breakdown, the blood vessels regress and menstrual bleeding occurs.
During the reproductive years a woman's menstrual period occurs around the 28th to 32 day. During peri menopause the menstrual period may come around days 22 thru 28. These shorter cycles often result because less estrogen is released due to insufficient follicular development. The decrease in estrogen production contributes to less cell growth and maintance of the uterine lining. The cells breakdown, the blood vessels regress and menstrual bleeding occurs. Many women notice that during day 4 or 5 of the menstrual period, bleeding may stop for several hours and then return briefly. This fluctuation is an example of how estrogen affects the endometrial microvascular. A few days after the onset of menstrual bleeding the functionalis begins to regenerate: grow anew. Estrogen released from primordial follicles, stimulates the regeneration of the surface endometrial epithelium (tissue), while menstruation is occuring. The estrogen secreted by this growing follicle causes prolonged vasoconstriction enabling the formation of a clot over the denuded (shed) endometrial vessels. When bleeding may stop for several hours and then returns during day 4 or 5 of the menstrual period it is because estrogen is beginning to stabilize the arterial blood flow of the functionalis and basilis layers of the endometrium. Irregular cycles and shorter cycles are also the result of nonfertile cycles and diminished progesterone. The hormone progesterone is secreted by the corpus luteum after an egg is released by the ovary. Progesterone allows the cells of the uterine lining to mature, so that the uterine lining (womb) can accept and nourish a fertilized egg. Perimenopause is a transition of diminished egg maturation and release. When an egg is not released from the ovary the corpus luteum does not form and only trace amounts of the hormone progesterone are secreted. Perimenopausal progesterone levels are significantly reduced and will not contribute to maintaining the uterine lining. Keep in mind, it is the withdrawal of progesterone or a blocking of progesterone receptors results in menstrual bleeding. Diminished estrogen production, due to weak egg development combined with diminished progesterone production often results in shorter cycles because these hormone levels are not potent enough to maintain the endometrium. Changes in menstrual bleeding during peri menopause occur naturally due to diminished fertility. Low dose birth control pills, prescription hormone replacement and bio-identical hormone replacement are therapeutic options that can help moderate estrogen and progesterone levels and regulate monthly menstrual cycles during peri-menopause. Keep in mind the menopausal transition is a natural process. Menstrual cycles that occur closer together are part of this natural transition.  Menstrual Bleeding Stops
Insufficient follicular development results in inadequate estrogen production; with little estrogen available to stimulate the endometrium, menstrual bleeding stops (amenorrhea). The peri menopausal gradual lessening of egg production, eventually transitions to menopause: characterized by no menstrual bleeding for a year as a result of no egg production.
Follicular atresia is the degeneration and resorption of an ovarian follicle before it reaches maturity and ruptures. After menopause estradiol production drops by 90% due to follicular atresia.
In Summary The are three primary estrogenic compounds, estradiol, estriol and estrone which coincide with the phases of a woman's life. Estradiol is the predominate estrogen produced during a woman's reproductive years. Estriol reaches its highest level during pregnancy and estrone is the predominant estrogen after menopause. The menopausal transition is period during which there is a gradual shift from estradiol to estrone as being the more predominate estrogenic compound. Estrogen receptors are located in the brain, breast, heart, blood vessels, uterus, vagina, bladder, liver, bones, skin and gastrointestinal tract. Therefore, during the menopausal transition, the hormonal shift from estradiol to estrone effects a variety of physiological changes, which may present as symptoms for some women. There have been significant advances in understanding menopausal physiology. This comprehension has lead to a variety of health enhancing therapeutic options to help women ease through this natural transition.
| revised May 2008 For Info About Perimenopausal or Menopausal Consultations click For Info about my Bio-identical Natural Progesterone Gift Package click For Info about my Bio-identical Natural Estrogen Gift Package click 
Follicle Stimulating Hormone Mean follicle stimulating hormone levels
start to increase about 2 years
before the final menstrual period,
increase most rapidly about
10 months before the final menstrual period,
and level off by 2 years
after the final menstrual period.
Source:
The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 11 4025-4030
Prospectively Measured Levels of Serum Follicle-Stimulating Hormone, Estradiol, and the
Dimeric Inhibins during the Menopausal Transition in a Population-Based Cohort of Women.
Henry G. Burger MD, Emma C. Dudley MD
_______________________
Ovarian Cancer Risk in
Peri and Postmenopausal Women
The results from a study of 549 women with
ovarian cancer and 516 women without ovarain cancer (controls) found the consumption of fruits, vegetables and food items high in carotene and lycopene may reduce the risk of ovarian cancer. Food items most strongly related to decreased risk for ovarian cancer were raw carrots and tomato sauce.
Intakes of carotene, especially alpha-carotene, from food and supplements significantly reduced the risk for ovarian cancer, predominantly in postmenopausal women. Intake of lycopene was significantly and inversely associated with risk for ovarian cancer, predominantly in premenopausal women.
Source:
Int J Cancer. 2001 Oct 1;94(1):128-34.
Carotenoids, antioxidants and ovarian cancer risk
in pre- and postmenopausal women.
Obstetrics and Gynecology Epidemiology Center,
Brigham and Women's Hospital, 221 Longwood Avenue,
Boston, MA 02115
A Massachusetts and Wisconsin study of 327 women with ovarian cancer and 3129 women without ovarian cancer found participants with the highest dietary intake of lutein/zeaxanthin (greater than or equal to 24,000 micrograms/week) experienced a 40% lower risk of ovarian cancer compared to those with the lowest intake.
Source:
Cancer Causes Control. 2001 Jan;12(1): 83-90.
A population-based case-control study of
carotenoid and vitamin A intake and ovarian cancer.
Department of Boistatistics and Epidemiology,
University of Massachusetts, Amherst 01003-9304 |