The Wisdom of Menopause

by Christiane Northrup

  “Estrogen” actually encompasses three distinct estrogenic compounds produced naturally in the body: estradiol, estrone, and estriol. Estriol reaches its highest level during pregnancy; it has weaker biological effects on breast and uterine tissue than do estrone and estradiol. (Women with naturally higher estriol levels appear to have lower breast cancer rates than others, which has led some practitioners to prescribe estriol to decrease the risk of breast cancer.13 Much more research is needed to establish the effectiveness of this approach.)

  There is one area in which supplemental estriol is known to be particularly effective: urogenital symptoms. Applied locally in the vagina, it relieves urinary frequency, vaginal dryness, and other conditions associated with the thinning of these tissues.14

  As I mentioned in chapter 4, there is reason to believe that estrogen’s role during the childbearing years is quite different from its role after menopause. Before menopause, the primary role of estradiol is to stimulate growth in the breasts, ovaries, and uterus and to participate in the growth and maturation of egg-bearing follicles. It also is a major influence in stimulating maternal behavior. In other words, it promotes childbirth and child care. After menopause, estrone becomes the predominant estrogen. No one knows exactly why this happens, but obviously it has nothing to do with procreation. It is likely that estrogen’s ability to protect heart and brain function, as well as bone strength, is part of its purpose in this phase of life.

  FIGURE 9: KINDS OF ESTROGEN

  Recall as well that the ovaries continue to produce small amounts of estradiol, as do the secondary hormone production sites. As a result, it is biologically possible for a woman to produce enough of her own estrogen to support optimal health throughout the second half of her life. This is rarely taken into account, perhaps because stress, unmet spiritual needs, and cultural expectations conspire to impair a woman’s natural ability to produce adequate levels of the estrogens.

  The most obvious and immediate benefit of estrogen therapy is relief from the symptoms of estrogen deficiency. (See box below.) A longer-term benefit is estrogen’s ability to help prevent excessive bone mineral loss leading to osteoporosis. Estrogen also helps maintain the thickness of the collagen layer in skin. Some studies have suggested that it may also help preserve mental function or at least delay the rate of so-called normal, age-related brain changes as well as dementia of the Alzheimer’s type. However, a thorough review of all the major studies that have investigated this does not show a benefit—at least with Prempro or Premarin.15 In general, there is not enough evidence to support prescribing estrogen for cognitive changes alone.

  Estrogen is available in pills, skin patches, and vaginal creams. In low doses, even synthetic estrogen in vaginal creams has negligible systemwide absorption and is generally safe for women who need the local effect of estrogen but don’t want any more exposure than necessary.

  SYMPTOMS OF ESTROGEN DEFICIENCY

  ~ Hot flashes

  ~ Night sweats

  ~ Vaginal dryness

  ~ Mood swings (mostly irritability and depression)

  ~ Mental fuzziness

  ~ Headaches, migraines

  ~ Vaginal and/or bladder infections

  ~ Incontinence; recurrent urinary tract infections

  ~ Vaginal wall thinning

  ~ Vaginal wall thinning

  SYMPTOMS OF ESTROGEN EXCESS

  ~ Bilateral, pounding headache

  ~ Recurrent vaginal yeast infections

  ~ Breast swelling and tenderness

  ~ Depression

  ~ Nausea, vomiting

  ~ Bloating

  ~ Leg cramps

  ~ Yellow-tinged skin

  ~ Excessive vaginal bleeding

  A Note About “Designer Estrogens”: SERMs The selective estrogen receptor modulators (SERMs) are synthetic drugs such as tamoxifen and raloxifene. They get their name from their ability to bind with estrogen receptors and selectively modulate the effects of estrogen in different body tissues. Tamoxifen (trade name Nolvadex) blocks the estrogen receptors on breast cells while maintaining some positive estrogenic effects on bone, uterine tissue, and the cardiovascular system. Raloxifene (trade name Evista) also promotes bone density while decreasing the stimulation of breast tissue by estrogen. This selective activity is possible because there are two different estrogen receptors, ER-alpha and ERbeta, each of which predominates in certain tissue. The same estrogen can produce different effects according to the receptor to which it binds.16

  Tamoxifen, the most widely used SERM, was first approved by the FDA for the treatment of patients with estrogen-receptor-positive (ER-positive) breast cancer in 1978. It is now prescribed for about half of all women diagnosed with breast cancer in the United States. It has been shown to reduce the risk of developing breast cancer in the remaining breast, as well as breast cancer recurrences and deaths. Tamoxifen is also approved for breast cancer prevention in women who are at high risk or perceived high risk for the disease. It helps prevent bone loss and also has a beneficial effect on LDL cholesterol but does not decrease the risk of heart disease.

  Since the 2002 WHI study results underscored the risks of estrogen, especially in older women, raloxifene is being prescribed more than ever to protect women against osteoporosis. However, it doesn’t protect bones as well as estrogen does. With or without estrogen, most women can get all the bone protection they need by doing weight-bearing exercise, getting enough vitamin D and minerals, and following the guidelines I’ve outlined for maintaining healthy bones in chapter 12. Why put yourself at risk with a relatively untested drug?

  I’m very concerned about SERMs. They are not found anywhere in nature and have not been around long enough for us to truly assess their benefits and risks. Touted for their ability to stimulate the “good” effects of estrogen without the “bad” ones, these drugs are riding the current wave of panic about breast cancer and are being requested by women who really don’t need them, or for whom there are far safer alternatives. If a young woman who fears breast cancer begins taking a SERM drug, she likely will be taking it for many years. This long-term blockage of some estrogen sites with stimulation of others is a double-edged sword. What if we find that these drugs actually increase the risk of Alzheimer’s disease by blocking the estrogen receptors in the brain?

  Troubling side effects of tamoxifen have already been documented, including an increased risk of certain visual disturbances, fatal pulmonary embolism, and endometrial cancer. Though studies indicate that raloxifene, unlike tamoxifen, can protect against endometrial cancer, both tamoxifen and raloxifene have been implicated in increasing the risk for colon cancer.17 They also increase hot flashes in many women, the very symptom for which most perimenopausal women seek treatment in the first place.18

  Even more disturbing is the finding that after five years of use, the antiestrogenic effects of tamoxifen on breast cells appear to reverse. A 2009 study showed that women who take tamoxifen for at least five years following a lumpectomy or mastectomy more than quadruple their risk of developing ER-negative breast cancer, a rare but more aggressive and difficult-to-treat cancer, in their healthy breast.19 Although using tamoxifen for less than five years wasn’t linked to the more aggressive cancer, it doesn’t really matter all that much because women don’t get the full benefit of the drug until they’ve taken it for five years. So while the majority of breast cancer patients will lower the risk of their cancer recurring by taking tamoxifen, 24 percent of them will actually increase their risk of getting an even more deadly form of breast cancer. I’m simply not comfortable with those odds, especially considering that tamoxifen also raises the risk of blood clots, stroke, and uterine cancer. Though this study was in women with cancer, not ductal carcinoma in situ (DCIS), women with DCIS are routinely put on tamoxifen. Given that most DCIS isn’t likely to progress to invasive cancer in the first place, is tamoxifen really worth the risk?

  The bottom line is this: unless you have no other alternative, I r
ecommend that you avoid SERMs or limit their use to five years or less. Better yet, stick with bioidentical hormones or the alternatives I outline in chapter 6.

  Progesterone

  A decline in progesterone is the first hormonal change to cause symptoms in a woman approaching menopause—sometimes years before she suspects she may be nearing the change. Because the body is designed for progesterone and estrogen to be present in a dynamic counterbalance with each other, the result is estrogen dominance, with symptoms of both progesterone deficiency and relative estrogen excess.

  Progesterone comes primarily from the ovaries both before and after menopause, but it is also produced in both the brain and the peripheral nerves.20 Its main job during the childbearing years is to prepare and maintain the uterus for its most important function: pregnancy. It also is a uterine muscle relaxant, preventing premature contractions. Progesterone levels rise in anticipation of pregnancy and stimulate the uterine lining to thicken with rich, well vascularized tissue to support an embryo, then fall precipitously if pregnancy does not occur. This abrupt drop-off in progesterone is what signals the shedding of the “nest” (that thickened uterine lining) in the form of menstrual bleeding.

  Progesterone also affects brain function. It produces a sense of calmness, and its sedating, antianxiety effect helps promote rejuvenating sleep.

  Progesterone comes from a temporary yellowish gland in the ovary called the corpus luteum, formed quickly in the small cystlike structure left behind when a follicle ovulates. The corpus luteum produces increasing amounts of progesterone until the body sends the signal “We’re not pregnant,” at which point the corpus luteum is reabsorbed. As a woman reaches her mid-thirties to early forties, the follicle is more likely (at least in this culture) to fail to ovulate, which means the corpus luteum does not form.21 Over time, this contributes to an increasing deficiency of progesterone.

  Note: Our bodies are designed to accommodate very high levels of progesterone during pregnancy. For that reason, symptoms from excessive progesterone are rare. However, depression is a common side effect of synthetic progestins such as Provera. And a few women are so sensitive to progesterone that they become depressed even on very small doses of natural, bioidentical progesterone. Women who have this side effect should try using chasteberry (Vitex agnus-castus) to increase their body’s progesterone naturally.

  SYMPTOMS OF PROGESTERONE DEFICIENCY

  ~ Premenstrual migraine

  ~ PMS-like symptoms

  ~ Irregular or excessively heavy periods

  ~ Irregular or excessively heavy periods

  SYMPTOMS OF EXCESS PROGESTERONE

  ~ Sleepiness

  ~ Drowsiness

  ~ Depression

  Bioidentical Progesterone

  Bioidentical progesterone supplementation can help alleviate the symptoms of both progesterone deficiency and estrogen excess, restoring the body’s balance. This provides long-term as well as short-term benefits. As I’ve noted, a growing body of evidence points to estrogen dominance as a major factor in promoting breast or uterine cancer in susceptible women. Studies show that when estrogen therapy is taken in concert with an appropriate dose of progesterone, the incidence of uterine cancer does not increase. This is true whether the progesterone is synthetic or bioidentical. It is also clear that Prempro (Premarin and Provera) at the dosages used in the WHI study increases the risk of breast cancer. The latest analysis of the WHI data, published in 2011, shows the risk of breast cancer is greater for women using a combination estrogen-progestin than for those taking only estrogen.22 The same study also showed that with both estrogen-progestin HT and estrogen-only HT, the risk of breast cancer increases when women begin HT either before menopause or less than five years after menopause—yet there’s little or no increased risk if women begin use of HT five years or more after menopause. The effect may not be the same with bioidentical hormones, however.

  One of the largest studies to compare bioidentical hormones with synthetic hormones showed that the bioidentical hormones (including progesterone) have significantly less associated risk of breast cancer. This 2008 study conducted in France followed more than 80,000 postmenopausal women for more than eight years.23 A 2009 follow-up study by the same French researchers looked at when HT therapy was begun. The results showed no significant increase in risk for breast cancer among women using estrogen plus natural progesterone for short durations, whether HT use began three years or less after menopause, or whether HT use began three years following menopause.24 (See chapter 13, “Creating Breast Health.”)

  The latest research also shows that natural progesterone is very helpful in relieving midlife chest pain from coronary artery spasm at very low doses (¼ tsp or 20 mg of 2 percent progesterone cream) applied to the skin.25 A company called Dimera, partially funded by grants from the National Institutes of Health (NIH), has recently developed the first heart drug for women—a transdermal form of natural progesterone (www.dimera.net). The drug is currently in clinical trials and is not yet on the market but shows enormous promise.

  Another advantage of progesterone supplementation relates to this hormone’s relatively unique ability to be converted into other hormones as needed. If progesterone levels are adequate, for example, but testosterone levels are on the low side, supplemental progesterone can actually transform itself into testosterone. It also increases the levels of DHEA. (See How to Restore Your Adrenal Function, page 135.) Under the right circumstances, supplemental progesterone can even be metabolized into estrogen. This is one reason using natural progesterone cream in early perimenopause, when there’s a great deal of variation in the levels of all three hormones, allows so many women to enjoy symptomatic relief.

  FIGURE 10: KINDS OF PROGESTERONE

  Progesterone cream is available over the counter in a 2 percent strength, and I’ve been recommending it for years. You can rub the cream anywhere on your body. One of the best places is right into your hands, because they are very well vascularized. But many women love the way progesterone cream works as a face or body cream. (I recommend Pro-Gest Cream by Emerita—which now comes in single-dose, 20 mg foil packets as well as a tube—and PhytoGest Cream by Kevala, available through Emerson Ecologics at www.emersonecologics.com.) Recent research shows that even small amounts of topical progesterone are indeed absorbed by the body and increase salivary levels of the hormone.26

  Natural progesterone is also available as a 4 to 8 percent gel (e.g., Crinone or Prochieve) or in an oral, micronized form (Prometrium). (Both require a prescription.) Though the manufacturer doesn’t endorse this use, Prometrium capsules can be opened and the contents applied to the skin. I’ve found that this works very well for individuals who do not tolerate oral progesterone well but who require a higher dosage than is available with an over-the-counter cream.

  THE YAM CREAM CAVEAT

  Because bioidentical progesterone is often produced from wild Mexican yams, some women try to save money by buying one of a number of wild Mexican yam creams. The problem is, yam contains only a progesterone precursor, which remains inactive when it is absorbed through the skin. The conversion of wild yam into bioidentical progesterone can only occur in a laboratory setting. Yam creams may offer some beneficial phytoestrogens, but they certainly don’t provide the documented benefits of laboratory-grade USP progesterone.

  The Problem with Synthetics

  Synthetic progestin is an altogether different story. The most commonly prescribed progestin is medroxyprogesterone acetate (MPA; trade names Provera, Amen). Others include norethindrone, norgestrel, and norgestimate. Progestin actually causes or exaggerates many symptoms. (See list on page 174.) That’s yet another reason why I don’t recommend any of the hormone therapy programs that employ synthetic progestins. Given the 2002 Women’s Health Initiative findings, synthetic progestins are also implicated as a risk factor in strokes, heart disease, and breast cancer.

  MPA has been shown to attenuate some of estrogen’s well-documented posi
tive effect on blood vessels. It increases vascular resistance, inhibits blood flow, and increases cerebral artery resistance. A large study of women receiving continuous therapy consisting of estrogen plus MPA (Prempro is an example of this type of therapy) showed a marked increase in myocardial infarction, death from coronary artery disease, and venous thrombosis (blood clots in the veins) during the first two years of therapy.27

  New analysis of the WHI data released in 2010 confirmed that this risk is present even for women who began synthetic HT within ten years of menopause—although risk drops after six years of use (which is longer than most women take HT anyway).28 An earlier reanalysis of the WHI and Nurses’ Health studies data from 2006 is also interesting because it supports an adverse effect from synthetic progestin. Younger women taking Prempro had a 30 percent decreased risk of heart disease when they started HT within ten years of menopause. But those who were on estrogen only had a 44 percent decreased risk. I suspect that the difference in the two groups was due to the adverse effect of MPA.

  Natural bioidentical progesterone contains no such risk and in fact has many benefits. In the famous PEPI (Postmenopausal Estrogen/ Progestin Intervention) trial, oral natural progesterone in micronized form prevented the adverse effects on cholesterol that were seen in women on Provera.