Estrogen Improves the Quality of Life
OF HORMONE REPLACEMENT
Unlike the highly charged debate about estrogen and breast cancer, the ability of hormone-replacement therapy to relieve bothersome symptoms of menopause and maintain youthfulness is widely acknowledged. In fact, the prevention and relief of menopausal symptoms such as hot flashes is the main reason why many women start taking estrogen -- and then stop taking it a few years later when they perceive it's no longer needed.
Estrogen is actually needed lifelong for the prevention of heart disease, osteoporosis, and Alzheimer's disease. That estrogen also provides for better quality of life and better sex should really be considered "the perks" of using hormone replacement.
The Classic Hot Flash
It's a well-known fact that estrogen relieves hot flashes. Hot flashes affect the large majority of menopausal women. Estimates vary: anywhere from 75 percent to more than 90 percent are affected, with at least 10 to 15 percent of women considering the problem to be severe. Studies calculate that about four million women in the United States are currently severely affected, such that their daily living is disrupted. Though dosage adjustments may be necessary, hormone-replacement therapy cures at least 80 percent (a bit conservative) to nearly 100 percent (more likely) of patients.
In general, hot flashes continue for six months to two years. However, in as many as 25 percent of women, they persist for longer than five years. In some patients, they can continue for ten or twenty years or longer. Obese women ten to have milder symptoms, no doubt due to the ability of fat cells to convert various hormones to estrogen. Conversely, smokers tend to have somewhat more severe symptoms due to the anti-estrogen effects of cigarette smoke.
Variability of symptoms is striking. The onset of hot flashes varies from the premenopausal years to several years after menopause, though the latter is uncommon. The frequency of hot flashes also varies widely and for no observable reason. Hot flashes can occur many times daily or only once in a while and even this pattern often changes. A hot flash itself typically lasts from three to six minutes, with both shorter and longer durations reported.
It is the decline of estrogen from previously normal levels, rather than the low level itself, that causes hot flashes. Abrupt changes in estrogen levels, such as occurs when the ovaries are surgically removed from premenopausal women, generally cause more severe symptoms. In fact, hot flashes have occurred in men when their testicles have been removed surgically, generating an abrupt drop in testosterone -- and estrogen-levels.
The Mechanism of a Hot Flash
In an area of the brain called the hypothalamus are nerve cells that regulate the body's temperature. These nerve cells have estrogen receptors and are directly influenced by estrogen. When estrogen levels decline, the temperature regulatory centers of the hypothalamus are disturbed and cease to function normally. Think of this as a thermostat at home with which people tamper. In the typical American family, one member lowers the thermostat and some time later someone else grouchily puts it back in its original place.
In a woman's body, a hot flash is set in motion when the "thermostat" is placed at a lower setting. The body then tries to cool down to this lower temperature setting by releasing heat. In this attempt, the body sends blood from the inner core to the outer surface (the skin) to cool down. To facilitate the cool-down, blood vessels near the surface of the body widen (causing the flush), the heart rate quickens (palpitations), and skin temperature rises by 10 to 15 degrees (causing the feeling of intense heat). Ultimately the body perspires. At this point the thermostat is raised back to its original setting. The body must now seek to raise its temperature by conserving heat. Often the body shivers in an attempt to create heat and this can be accompanied by a sensation of a chill. At the same time, the peripheral blood vessels constrict in order to return blood to the inner core of the body, diminishing the flush and returning the skin to its normal color.
The opening and closing of the blood vessels, transferring blood from the inner core of the body to the skin and back, gives the hot flash its medical term: "vasomotor instability" (vaso = blood vessel, motor = contracting and dilating).
Many women have a premonition of an impending hot flash -- an aura -- often described as a tingling sensation in the hands and scalp, pressure in the head, along with a sense of anxiety. Though the level of severity is often described as mild, nobody seems to have anything good to say about hot flashes. Consequently, I would simply suggest that you take estrogen in a timely manner, leave the thermostat where it is, and happily avoid the whole problem.
Estrogen receptors have been found in regions of the brain responsible for sleep regulation, such as the hypothalamus, the preoptic area, and the hippocampus. Estrogen may also affect sleep by altering the levels of >neurotransmitters -- including acetylcholine and dopamine, as well as serotonin-- which play a role in regulating sleep patterns.
Erlik and others used EEG (electro-encephalogram, for brain-wave analysis) and skin-temperature measurements to show that postmenopausal women who awoke suddenly during the night did so as a result of hot flashes that occurred during sleep. Shaver and colleagues showed that the quality of sleep is poorer, as measured by the amount of REM (rapid eye movement) sleep in women with hot flashes compared to those who have no hot flashes.
"Night sweats" are hot flashes that occur during sleep, but in fact, falling estrogen levels can cause sleep disruption even if night sweats are not present. Sleep deprivation as a result of nighttime hot flashes can contribute to the daytime fatigue, mood swings, and irritability that have been so closely linked with menopause.
Studies show that women who take estrogen fall asleep more easily and stay asleep longer with fewer periods of wakefulness. Estrogen improves sleep patterns directly by its effect on brain function, and indirectly by relieving debilitating physical symptoms and mood disturbance, which can themselves lead to sleep disturbance. Estrogen's direct effect on the brain is strongly supported by the fact that even women who don't suffer any other menopausal symptoms sleep better if they're taking estrogen.
The tissues that line the entire genitourinary tract are richly endowed with estrogen receptors and are greatly affected by declining estrogen levels. With the loss of estrogen, the vaginal walls get progressively thinner. They lose the elasticity and resilience they had when estrogen was prominent and the vagina itself becomes shorter and narrower. The medical term for this process is, unfortunately, "vaginal atrophy" --and the fact is, eventually it happens to most women.
As they thin out, the vaginal walls can sometimes diminish to only a few cells thick, from their normal thickness of about fifty cells. Not only are the numbers of cells reduced, but a certain type of cells -- namely the "superficial cells," which are rich in glycogen (a natural sugar) becomes nearly absent altogether. These superficial cells, especially when supported by good blood flow, secrete glycogen, which becomes food for healthy vaginal bacteria -- the lactobacilli.
The growth of these helpful bacteria, supported by vaginal glycogen, releases lactic acid, which creates an acidic environment hostile to any invading, opportunistic, or harmful organisms. When estrogen production stops, the acid balance of the vagina slowly shifts away from acidic and toward a more alkaline environment. This makes the vagina more hospitable to hostile bacteria. Dryness and subsequent irritation make vaginal tissues vulnerable to infection as well. Some reports state that the prevalence of this "atrophic vaginitis" affects up to 38 percent of postmenopausal women.
In the absence of estrogen, blood flow to the genitals decreases. So it takes longer to produce lubrication in preparation for intercourse. Vaginal lubrication diminishes as well because low levels of circulating estrogen no longer stimulate the production of cervical and vaginal mucus. Some lubrication may still be derived from small amounts of estrogen still remaining in the body and from the Bartholin's glands, small glands located at the entrance of the vagina.
These physical changes can make sex uncomfortable, painful, or even impossible. As many as 30 percent of postmenopausal women complain of painful intercourse and consequently have sex less often. This is unfortunate, because having sex increases the blood flow to tissues, encourages the production of mucous secretions, helps to maintain muscle tone, and preserves the shape and size of the vagina. Still, even sexually active women may eventually have the same problem other women have unless they use estrogen.
All in all, by several mechanisms, estrogen therapy promotes and maintains the physical and sexual functioning of the vagina. Estrogen increases blood flow to the vagina, builds up vaginal lining to a healthy state, and increases vaginal lubrication for women with a particularly thin and fragile vaginal lining. In the presence of estrogen, the normal acidic environment will return, as will a more normal resistance to infection. Though it may take several months, and even up to a year, for complete restoration of normal anatomy and function, a more pleasurable sex life is often enjoyed in a matter of a few weeks. However, the problem can be avoided entirely by the timely use of estrogen.
In a study of women aged fifty to eighty-two in Madison, Wisconsin, nearly one-half reported an ongoing sexual relationship. Likewise, in the Duke Longitudinal Study on Aging, 50 percent of all older women were still interested in sex. In the same study, however, 70 percent of men were sexually active and 80 percent reported interest in sexual activity. Though these contrasting figures may represent cultural factors, the relative stability of hormone levels in aging men compared to the decreasing levels in menopausal women may also be relevant.
As stated by Dr. Barbara Sherwin, (Dr. Sherwin cites the work of J. M. Davidson) human sexual behavior comprises two distinct but interrelated processes, libido and potency. Libido refers to sexual desire, sexual fantasies, and satisfaction or pleasure. Potency refers to increased blood flow and resultant swelling of tissues, (pelvic vasocongestion), orgasmic contractions, and other bodily aspects of sexual response.
It is clear that estrogen deprivation affects the physical aspects of a woman's sexual functioning, or potency. As was previously discussed, vaginal changes such as decreased lubrication, increased infection, and anatomic changes including the shortening and narrowing of the vagina can lead to painful intercourse. In addition, the reduced blood flow to the reproductive tissues leads to decreased vasocongestion, which can also lead to decreased lubrication as well as decreased sensation. Fortunately, these physical changes that impact negatively on a woman's sexuality are quite reliably prevented and reversed by estrogen administration.
When physical difficulties impair sexual functioning, concern, anxiety, and diminished pleasure can affect both partners -- leading not only to diminished sexual activity (which, unfortunately, only makes matters worse for vaginal tissues), but also to decreased interest in sex. By ameliorating the physical difficulties and preventing this downward spiral, estrogen indirectly improves libido, no doubt aided by estrogen's additional beneficial effects on mood and psychological well-being.
A direct effect on libido -- the motivational aspects of sexual behavior, including desire and fantasies -- clearly appears to be the province of testosterone. Fortunately, the decrease in testosterone at menopause is not nearly as profound as the decrease in estrogen. In fact, in natural menopause the decrease in circulating testosterone is only about 15 to 25 percent. (After surgical removal of the ovaries, the decrease in testosterone is significantly more pronounced.)
Luckily, the ovary is not a woman's only source of testosterone. In fact, the ovary produces only 25 percent of circulating testosterone. Other sources of testosterone are the adrenal glands and the conversion by the body of other androgenic hormones (andro = male, genic = to generate) into testosterone. In addition, the postmenopausal ovary continues to secrete significant, if not increased, amounts of testosterone. Thus, even though circulating testosterone levels are lower at menopause, this reduction is not necessarily associated with decreased libido in menopausal women.
There is absolutely no question that testosterone supplementation enhances libido. Many studies of postmenopausal women complaining of decreased libido reported a superior response to testosterone-containing regimens when compared to regimens of estrogen alone. The immediate cautionary note to be sounded, however, is that testosterone use may carry a price tag. Namely, it might impair some of estrogen's beneficial, life-saving effects on cholesterol levels and heart disease.
Studies indicate that up to 40 percent of menopausal women have some form of urinary leakage, which is called urinary incontinence. Similar numbers of women complain of frequent urination, a sudden urge to urinate (even though the bladder is not full), and occasional painful urination. Making matters worse, fewer than half of incontinent women seek help -- often because of embarrassment or the misconception that the condition is an inevitable consequence of aging.
Urinary tract tissues in women are embryologically related to the genital tract. Estrogen receptors have been identified in the urethra and bladder, as well as in the muscles of the pelvis. Just as with the lining of the vagina, with menopause, the lining of the urethra may become thin, and the surrounding muscles and elastic tissues may weaken. Estrogen has been shown to enhance the tone of the urethra, allowing it to increase its pressure (think of the urethra as a straw squeezing itself shut) and hold back any undesired flow of urine from the bladder. Estrogen also allows the blood vessels in the urethra to become more swollen (from improved blood flow), which somewhat helps compress the urethra to keep it closed. Given these findings and the known association of the postmenopausal years with increased urinary tract problems, it has been widely assumed that estrogen loss plays a major role in the development of these problems -- and that its replacement will cure them.
Estrogen-replacement therapy does ease some urinary symptoms, but it stops well short of a cure. Though a substantial proportion of patients with urinary problems who take estrogen feel better when you measure their bladder function in a laboratory, estrogen users are not significantly different from nonusers. Why, then, are symptoms relieved by estrogen?
One idea is that estrogen makes the bladder less sensitive to stimuli. Without estrogen, the bladder may overreact with increased contractions -- creating an urge to urinate, or leading to an increased frequency of urination, especially at night. "Nocturia" (noct = nocturnal), can be particularly bothersome. By decreasing the sensitivity and "hyper" functioning of the bladder, there is less disruption of daily living.
Another mechanism by which estrogen provides improvement is the prevention of urinary tract infections (which also cause a frequent urge to urinate). Unlike other urinary problems, the ability of estrogen to prevent these infections in menopausal women has unequivocal scientific support. Estrogen users have significantly fewer urinary tract infections, presumably because estrogen returns the vaginal environment to its original state, encouraging the return of lactobacilli, and removing the offending bacteria. Indeed, compared to nonusers, many estrogen users remain free of urinary tract infection.
In sum, regarding the urinary tract, estrogen may best be considered a role player, providing supportive therapy and improving comfort level. Still, all urinary complaints should receive prompt and expert attention. Proper diagnosis and individualized treatment-which may be a combination of medical, surgical, and behavioral therapy -- is essential.
In general, as people age, their skin-cell replacement slows down, as does the elastic fiber content. As a result, the skin becomes drier, thinner, less elastic, and more inclined to wrinkle. In women, it has been shown that skin collagen and skin thickness steadily decrease with time after menopause. Women can lose up to 30 percent of skin collagen in the first five years following menopause. Happily, this decrease is prevented by hormone-replacement therapy. The fact that collagen loss accelerates during the first several years after menopause suggests that if supplemental estrogens do indeed benefit skin, it might be best to begin therapy early.
Also of considerable importance is the natural diminishing of the layer of fat cells of the skin. This subcutaneous fat provides inner support, firmness, and resilience to the skin. Estrogen helps maintain this layer by stimulating the production of hyaluronic acid, which holds water and maintains the moisture of the tissues.
In the first randomized, double-blind, placebo-controlled study addressing the effects of estrogen-replacement therapy on skin thickness, a 1994 Canadian study evaluated sixty postmenopausal nuns (aged fifty-one to seventy-one) whose limited exposure to sun and smoking provided a clearer reading of what changing hormone levels themselves could do to skin. After twelve months of taking estrogen, those in the treated group showed a 30 percent increase in the thickness of the dermis (the inner layer of the skin), and an 11.5 percentincrease in overall skin thickness. No significant skin changes were observed in the placebo group.
Similar studies found that estrogen can inhibit the loss of skin collagen and thickness within six months, and can even restore a substantial amount of what was lost. There is also some indication that as skin thickness increases, wrinkling might be reduced. However, once a certain threshold is reached, long-term hormone use does not appear to have any further effect on skin.
Since everybody thinks that estrogen causes weight gain, let me state an accepted fact: Estrogen therapy doesn't cause an ounce of weight gain.
A study of five hundred postmenopausal women by Judith Wurtman at the Massachusetts Institute of Technology revealed that 64 percent of nonobese women gained an average of ten to fifteen pounds after menopause. Obese menopausal women fared even more poorly -- 94 percent gained an average of twenty-one to twenty-three pounds after menopause. When estrogen replacement was factored into the equation-that is, when women taking estrogen were measured against women not taking estrogen, there was no difference in weight gain. In fact, in most studies (seven of eleven by one count) the hormone users actually weighed slightly less.
Still another "perk" estrogen users enjoy involves fat distribution. It appears estrogen is responsible for keeping a woman's fat in the right places. Scientists call this "gynecoid fat distribution," measured by the waist-to-hip ratio. Estrogen users maintain a more favorable waist-to-hip ratio (less waist, more hip), whereas nonusers begin after menopause to redistribute their fat to the waist and abdomen, attaining a more "android" fat distribution somewhat reminiscent of their spouses, or yours truly.
From ESTROGEN: How and Why It Can Save Your Life, by Adam Romoff, M.D. and Ina Yalof. Copyright © 1999 by Adam Romoff, M.D. and Ina Yalof. Excerpted by arrangement with St. Martin's Press. $16. Available in local bookstores or call 800-288-2131 or click here.