~Female Hormone Modulation, Part 4

Safe Hormone Modulation, Without Resorting to Drugs

Some women are able to win the battle against menopausal miseries with natural supplements. While every woman's biochemical makeup varies, the following generalized recommendations can be made concerning nondrug hormone modulation.

Natural Estrogen

A formula called Natural Estrogen contains plant-derived phytoestrogens and nutrients that have been shown to favorably alter estrogen metabolism in the body. The recommended initial dose is one capsule of Natural Estrogen twice a day. While postmenopausal women may start at any time, premenopausal women should begin on the fifth day of their menstrual cycle. It is recommended that women already taking estrogen drugs such as Premarin should wean themselves off the synthetic hormones gradually over several months as follows, using equivalent amounts of Natural Estrogen:
  • First month: Natural Estrogen every other day, previous medication every other day.
  • Second month: Natural Estrogen 2 days in a row, previous medication for 1 day.
  • Third month: Natural Estrogen 3 days in a row, previous medication for 1 day.
  • Fourth month: Natural Estrogen every day.
Natural Progesterone Cream

Natural progesterone cream provides and alternative to artificial progestins so commonly prescribed by conventional physicians. Natural progesterone is far safer than synthetic progestin drugs and it is as easily utilized as the real progesterone manufactured within the human body.

When taken orally, natural progesterone is almost completely degraded by the liver before it can reach the tissues that need it. Even micronized natural progesterone--now available as a prescription drug called Prometrium--must be given in high doses to make it through the first pass through the liver. This puts undue stress on the liver and may create metabolites that have harmful effects.

Natural progesterone can be given in the form of suppositories and injections. Both work to move progesterone into the bloodstream, but the first is messy and the latter is inconvenient. The simplest way to supplement with progesterone is transdermally, in the form of a skin cream that contains bioidentical progesterone made from soy or wild yams. When the cream is smoothed onto the skin, the progesterone molecules are absorbed into the layer of subcutaneous fat. The bioavailability of transdermal progesterone has been proven in several studies.

Once absorbed through the skin, the progesterone molecules gradually diffuse into the circulation. This method provides the closest possible approximation to the natural production of progesterone by the ovaries--as long as the dosages are properly timed.

Massage progesterone cream into the breasts, chest, upper inner arms, face, abdomen, buttocks, inner thighs, or palms of hands. Rotate the site where cream is applied so that subcutaneous fat cells don't become saturated in any one site. Use a cream that contains 500 mg to 700 mg of progesterone per ounce.
  • Premenopausal women: Women who have not gone through menopause and have estrogen dominance symptoms (including fibrocystic breasts and ovarian cysts) should use 1/4 to 1/2 tsp of progesterone cream, an amount which should provide 20-40 mg of progesterone, starting on the 8th day of the cycle. (Day one is the first day of menstruation.) Continue to apply the cream until day 26 of the cycle, and allow 7 days (whether menstruation occurs or not) before beginning to apply it again.
  • PMS: Begin to apply 1/4 tsp of cream on the 12th day after the first day of menstruation and continue until day 26.
  • Endometriosis: Women with endometriosis should use 1/2 tsp twice a day from days 6 through 26 of the menstrual cycle.
  • Menopausal and postmenopausal women: Women who are past menopause or who have had a hysterectomy should use 1/4 to 1/2 tsp of cream twice a day for 25 days, followed by five days off. Repeat this cycle for three months, then decrease the dosage to 1/4 tsp twice a day. If you have a uterus and are using supplemental estrogen of any kind, use progesterone cream every day of the month.
  • Osteoporosis: To help prevent osteoporosis in postmenopausal women, use 1/8 to 1/4 tsp daily from the 12th day to the last day of each monthly cycle. If still menstruating, use the first day of your period to mark the first day of the cycle. Women who have been diagnosed with osteoporosis should apply 1/2 tsp morning and night until the first jar is used up, and then 1/4 tsp morning and night until the second jar is used up. The latter dosage can be used for maintenance, or can be cut in half once again if bone scans show improvement. In addition to progesterone, supplementation with at least 1000 mg a day of calcium along with magnesium, zinc, boron, manganese, vitamin D and vitamin K are essential in the prevention of osteoporosis.
DHEA Replacement

DHEA is a precursor of estrogen and testosterone; therefore, taking DHEA might raise the levels of these other hormones. Most women benefit from 15-25 mg of oral DHEA taken early in the day. Some women need 50 mg and more of DHEA to achieve desired results. A DHEA blood test after 60 days of treatment can enable a woman to adjust the dose of DHEA to restore hormone levels to those of a 21 year old. Refer to the DHEA Replacement Therapy protocol for precautions about who should not take DHEA.

DHEA gradually converts into many other hormones, including estrogen and testosterone. To protect against the possible overconversion to dangerous forms of estrogen, women should take a dietary supplement called indole-3-carbinol (I3C) at the dose of 200 mg, two times a day. Women weighing over 180 pounds might need as many as four capsules to adequately saturate cells. Melatonin in doses of 300 mcg-3 mg per night is also recommended to reduce cancer risk and assist with insomnia. For women who cannot tolerate DHEA, pregnenolone can be taken in a dose of 50 mg/day. Pregnenolone is another hormone precursor which occurs earlier in the pathway that leads to cortisol, progesterone, DHEA, estrogen, and testosterone formation. Pregnenolone has anti-aging benefits and is especially helpful with improvement in memory.

These three natural approaches may safely return hormones to the desired levels and eliminate menopausal symptoms. If this does not occur, prescription drug recommendations found in the following sections of the protocol should be considered.

Hormone Replacement Drug Therapy: Today's Conventional Method

Mainstream medicine focuses on the decline and subsequent deficiency of estrogen in the form of estradiol as the only cause of menopausal symptoms. The other hormones are barely recognized as playing a role in this process, although some value has been given to testosterone. Progesterone is only used to prevent uterine cancer in women who have not had a hysterectomy and who take estrogen.

Prior to 1980, conventional physicians used hormone replacement therapy in women for the sole purpose of treating the early symptoms of post-menopause. Estrogen was prescribed for no more than the first 5 years after menopause.

Then, a more preventive strategy was initiated based on observational data demonstrating a protective effect of estrogen on the heart and bone as well as on the observation that coronary artery disease (CHD) was rare in premenopausal women, but increased in a frequency approaching that of men after menopause. Consequently, hormones for prevention were being prescribed for women for the long-term (greater than 5 years). Recent data about side effects of estrogen drugs has caused the pendulum to swing back in the direction of again treating symptoms for the short-term, rather than for long-term prevention.

The Women's Health Initiative study was halted prematurely in mid-2002 due to an overwhelming increase in heart disease and cancer in patients who were taking the traditional combination of conjugated estrogen (Premarin) with progestin (Provera). Since that time, mainstream physicians have been scrambling to find a better approach to this medical problem.

The current recommendations outlined by the American College of Gynecologists (ACOG) and The United States Preventive Services Task Force are to prescribe conjugated estrogen at an oral dose of 0.3-0.625 mg daily for the first 5 years after menopause, adding 2.5 mg of progestin, a synthetic proges-terone, daily only in women who have not had a hysterectomy. Testosterone is not routinely used, but it can be added to the regimen if symptoms persist and/or if testosterone levels are low. The estrogen and progestin are then tapered gradually by omitting one pill each per week to minimize the recurrence of menopausal symptoms.

If symptoms persist after doing this, the recommendation is to start over and taper over 12 weeks instead of 6 weeks (decreasing each hormone by one pill every 2 weeks instead of every week). Some physicians recommend a soy-derived oral estradiol called Estrace (0.5 mg of estradiol) or an estradiol patch such as Vivelle, which comes in various doses. These estrogen drugs are prescribed for the first 5-6 years from the onset of symptoms of menopause.

After this 5- to 6-year period, the recommendation is to slowly decrease this hormone and prescribe raloxifene (Evista), a "select estrogen receptor modulator" to prevent osteoporosis. There is little time spent on analyzing a woman's individual biochemistry. What the drug companies recommend for the "average" woman is typically what every patient is prescribed.

For women in the perimenopausal years (who are still having menstrual cycles), a low-dose oral contraceptive is prescribed to control symptoms until menstrual cycles cease. Then, the birth control pill can be tapered in the same way that estrogen and progestin are tapered, as described above. An estrogen and progestin hormone replacement regimen can commence at that time for 5-6 years if symptoms continue.

Some mainstream physicians are switching from progestin to a more natural micronized progesterone called Prometrium. The starting dose of Prometrium is 100 mg nightly with an added 50-100 mg in the morning if needed.

The conventional approach to hormone replacement can result in multiple hormone deficiencies of estrogen, DHEA, progesterone, and testosterone that leave women vulnerable to many age-related disorders. Conventional medicine does not recognize the value of these hormones in maintaining both a physical and a mental state of youth. For example, DHEA has been shown to alleviate depression and improve emotional well-being in aging females. Progesterone provides many benefits, including protecting the bones. In fact, progesterone may be more important to bone maintenance than estrogen. Some conventional physicians are uneducated regarding all of the effects of these hormones on an aging woman's body. In reality, these hormones have positive critical effects on healthy cellular function.

A Progressive Medicine Approach to Hormone Drug Replacement Therapy
  • Urine Test
A small, but growing number of physicians believe that the symptoms of perimenopause and menopause are due to declining estrogen levels as well as declining levels of progesterone, testosterone, and DHEA and a resulting imbalance in these hormones.

Progressive alternative physicians recognize that an imbalance occurs between the types of estrogens as well. As estradiol levels decline, estrone levels decline much more slowly, resulting in more estrone than estradiol. Although both hormones are strong enough to cause concern about the development of breast cancer, the ratio of the hydroxyestrones becomes a more significant factor during this phase of life. Some hydroxyestrones (4- and 16-hydroxy-estrone) may promote cancer, while 2-hydroxyestrone seems to prevent it.

Progesterone declines more rapidly than these estrogens, resulting in a phenomenon called estrogen dominance. During the reproductive years, there is a balance that fluctuates in a cyclical manner between the estrogens and progesterone, according to the menstrual cycle. This shift in dominance of estrogen over progesterone that occurs with age causes a decrease in fertility and the ability to carry a pregnancy to term. Estrogen dominance causes fatigue, depression, thyroid malfunction, fluid retention, and fat storage, resulting in weight gain. The phenomenon of estrogen dominance is exacerbated by environmental exposure to pesticides and obesity.

It is therefore not always lack of estrogen that is the problem. Often there is too much estrogen relative to progesterone and an imbalance not only of estrogen and progesterone, but also an imbalance of the three types of estrogens (estriol, estrone, and estradiol). Testosterone and DHEA may also decline and may need to be replaced to ensure the best outcome.

As the best approach to the menopausal years, a physician well versed on this topic should evaluate the symptoms that the particular woman is experiencing and compare these symptoms with serum, saliva, and/or 24-hour urine levels of the hormones. Then, a personalized compounded formula of the hormones can be prescribed based on the individual's needs. A reevaluation should be done in 60-90 days. The compounded formula can be in either a cream, patch, troche, or oral form.

Some physicians may choose to use an oral form of estriol and natural progesterone cream at onset of menopause because estriol is considered to be the safest form of estrogen. Studies suggest it might help prevent breast and other cancers (Head 1998; Takahashi et al. 2000a,b; Granberg et al. 2002). However, estriol is often not strong enough to prevent osteoporosis on its own and it may or may not relieve hot flashes. Estriol is classified as a "weak" estrogen compared to the more potent estradiol and estrone forms. The dosage for estriol is between 2 and 8 mg/day. Again, trying and evaluating different dosages is the way to achieve the important goal of taking the least amount of estrogen that attains the desired blood or symptom level. Estriol creams in varying potencies may be tried for localized conditions such as vaginal dryness and thinning. Follow the packaging insert regarding the appropriate sites of application. Some estrogen creams are inserted vaginally. For others, the best sites of application of the cream are inner thigh, inner upper arm, and occasionally at the fatty portion of the palms of the hands and the face, alternating sites on a day-to-day basis.

A prescription cream (or gel) would include the estrogen and/or testosterone that have been shown to be deficient. Some estrogen creams contain 100% estriol, while others have varying percentages of the more potent estradiol and estrone forms of estrogen in addition to estriol. Some popular prescription estrogen formulas are called Bi-est or Tri-est. Bi-est consists of estradiol and estriol. Tri-est consists of estradiol, estriol, and estrone in a ratio of 80% estriol to 10% each of estradiol and estrone.

A popular combination is a specially prepared Bi-est formula that usually starts with a combination of 80% estriol and 20% estradiol. This combination is recommended because fat cells, the liver, and to some extent the adrenal glands continue to make more estrone than estradiol during menopause. For women who require more estradiol, the estriol can be titrated downward with the addition of more estradiol if the symptoms are not relieved. Some physicians prefer to start with a 60/40 ratio of estriol to estradiol and go upward or downward from there. In this way, the women gets some estradiol, but with more of the total estrogen dose coming from a weaker, less toxic estriol estrogen.

Progesterone creams and DHEA do not require a prescription. A cream containing estrogen and/or testosterone should not be applied to the face. Overdosing should also be avoided. Adhere to your physician's recommendations.

Estrone is not desirable because it is cancer promoting and tends to be naturally present in higher quantities proportional to the other two estrogens during the menopausal stage of life. However, a saliva and/or blood test can aid a physician in determining your personalized prescription. The goal is to relieve symptoms and prevent bone loss with as little risk as possible.

Why is this progressive approach a better course of action than conventional drug therapy? These natural hormones are biologically identical to the hormones made in a woman's body rather than to those from pregnant mare urine or other synthetic estrogen drugs. These hormones are as natural as currently possible to obtain. Additionally, the doses are titrated to an individual's needs, using the minimum amount required to accomplish the treatment goal by using the symptom profile score and checking blood, saliva, and/or 24-hour urinary excretion levels.

Using this progressive approach, all hormones are considered. Urine levels of the hydroxyestrones are measured to decrease the risk of cancer. If the ratio is unfavorable, indole-3-carbinol (I3C) can be consumed to increase the levels of beneficial 2-hydroxy-estrone and reduce levels of the more dangerous 4- and 16-hydroxyestrone. I3C is found in cruciferous vegetables. It is abundant in broccoli sprouts and Brussels sprouts and can be found in standardized dietary supplements.

Another method of delivery of these hormones is by vaginal absorption. According to Dr. Uzzi Reiss, an obstetrics/gynecology physician who specializes in natural hormone replacement, vaginal delivery of progesterone is an excellent method of delivery to the uterus; however, it is not an ideal method of delivery to the rest of the body (Reiss et al. 2001).

The progressive medicine approach to hormone replacement consists of an analysis of the woman's symptoms, an evaluation of her hormone levels, and then a compounded formula of natural hormones that suit her individual needs. Adjustments are continually made to maintain a youthful hormonal state.

Urine Test for Women Concerned about Estrogen-Induced Cancer

An emerging area of scientific and clinical data indicates that many risk factors for breast cancer are mediated through alterations in estrogen metabolism. The metabolism of estrogens depends upon a woman's unique genetic makeup, her lifestyle, and her diet. Consideration of the ways various estrogens are metabolized and whether they are comprised of potentially harmful or beneficial derivatives may help assess the risk of breast cancer (and possibly other estrogen-sensitive cancers) in women. Measurement of these estrogen derivatives in urine presents a new opportunity for the prevention, management, and treatment of estrogen-dependent conditions, including breast cancer.

The three most widely known estrogens are: estrone (E1), estradiol (E2), and estriol (E3). Estradiol and estrone interconvert freely, and both may be metabolized to 2-hydroxylated, 16-hydroxylated, or other forms. These hydroxylation steps take place in various tissues, including breast, kidney, and liver. 2-Hydroxyestrone has even been found to exert a modest antiestrogenic effect (Schneider et al. 1984; Vandewalle et al. 1989) and has been called "the good estrogen" (Bradlow et al. 1996). A high level of the 16-hydroxyestrone metabolite is considered to be a potential risk factor for estrogen-induced cancers (Fishman et al. 1980).

There has been extensive basic and clinical research regarding the role of the 2-hydroxy- and 16-hydroxyestrone metabolites in breast cancer and which of these estrogens might be useful as markers to assess breast cancer risk. In this discussion pertaining to these estrogen metabolites, only estrone metabolites will be addressed because of the easy interconversion of estrone and estradiol in the body.

Various studies support an active role for 2-hydroxyestrone in the inhibition of estrogen-induced cancers. 2-Hydroxyestrone can also be considered to be a naturally occurring antiestrogen or selective estrogen receptor modulator (Schneider et al. 1984; Imoto et al. 1992). At the least, it is a neutral or nonestrogenic metabolite (Westerlind et al. 1998). 2-Hydroxyestrone may also inhibit cancer via conversion to an inhibitor of cellular division (Zhu et al. 1998). In addition, it has been argued that an increase in the formation of 2-hydroxyestrone is anticarcinogenic in that it diverts estrone away from formation of the genotoxic and extremely potent estrogen metabolite, 16-hydroxyestrone (Bradlow et al. 1995b).

Some dietary and lifestyle factors that increase circulating levels of 2-hydroxyestrone include ingestion of cruciferous vegetables (Auborn et al. 1998); the supplement indole-3-carbinol (I3C) (Bradlow et al. 1995a; Rosen et al. 1998); lignins found in flaxseed (Haggans et al. 1999); isoflavones in enriched soy (Lu et al. 2000); omega-3 and omega-6 fatty acids in fish oils (Osborne et al. 1988); a high-protein diet (Anderson et al. 1984); and an athletic lifestyle (Snow et al. 1989; Frisch et al. 1993). Two factors that are known to decrease 2-hydroxyestrone levels are obesity (Michnovicz 1998) and a diet high in fat (Longcope et al. 1987). In most cases, note that the factors that increase 2-hydroxylation of estrogens are those already known to prevent breast cancer.

There is abundant clinical evidence that 16-hydroxyestrone is elevated in women with breast cancer. Early radiometric studies found the formation of 16-hydroxylated estrogens to be dramatically elevated in women with breast cancer (Schneider et al. 1982; Osborne et al. 1993); women at high risk for breast cancer (Osborne et al. 1993); and in strains of mice with a high incidence of spontaneous mammary tumors (Bradlow et al. 1985). The metabolite 16-hydroxyestrone has several unique chemical and biological properties that explain its involvement in this disease. As an alpha-hydroxyl ketone, it is capable of binding tightly to amines, and with molecular rearrangement (Miyairi et al. 1995), this estrogen may form covalent linkages with estrogen receptors (Swaneck et al. 1988), nuclear histone proteins (Yu et al. 1985), and DNA. Because of this covalent linkage to estrogen receptors, 16-hydroxyestrone shows persistent biological activity (Lustig et al. 1989).

In addition to the persistence in estrogenic activity, it was recently established that16-hydroxyestrone, unlike estradiol or estriol, possesses both carcinogenic initiator and promoter activities in normal mammary epithelial cells (Telang et al. 1992). In proliferation assays, 16-hydroxyestrone had activity comparable to that observed for the mutagen dimethylbenzanthracene (DMBA) (unlike estradiol and estriol, both of which showed only minimal responses). In a mutagenic assay measuring unscheduled DNA repair, this metabolite was likewise considerably more potent than estrone, estradiol, and estriol. In addition, 16-hydroxyestrone is the only estrogen that has been shown to be directly mutagenic in the standard Ames test, causing gene alterations in two of five cell lines tested (Arts et al. 1990).

The levels of 16-hydroxyestrone are relatively stable and change relatively less than 2-hydroxyestrone in response to lifestyle and dietary changes. Fortunately, most factors that dramatically induce 2-hydroxylation of estrogens will reduce circulating levels of 16-hydroxy-estrone, because these metabolic pathways compete for the same substrate. Because of its potency, even small changes in the levels of 16-hydroxyestrone may have significant consequences.

Numerous studies have demonstrated that altered metabolism of 2- and/or 16-hydroxyestrone are associated with breast cancer and risk for this disease. In nearly all instances, the expression of both metabolites was altered such that decreased 2-hydroxylation and increased 16-hydroxylation of estrone were associated with increased risk. In these cases, the ratio of 2/16 was by far the most significant predictor for breast cancer risk. The power of this unique variable suggests that (just as in the case of LDL vs. HDL cholesterol) the kind of estrogen a woman has is relatively more important than the amount of each or the total. The diagnostic power of this ratio may derive from the fact that nearly every genetic, lifestyle, and dietary positive risk factor for breast cancer decreases levels of 2-hydroxyestrone and/or increases 16-hydroxyestrone. The ratio of 2/16, then, is a unique variable that may express the total or combined risk of breast cancer due to diverse factors.

Six observational human clinical studies have found a decreased urinary or serum 2/16 ratio in established cases of postmenopausal breast cancer (Fleisher et al. 1996; Kabat et al. 1997; Coker et al. 1997; Ho et al. 1998; Meilahn et al. 1998; Dupont et al. 2000). While one study (Ursin et al. 1999) found no reduction in the ratio, "breast cancer" samples in that study had been taken from essentially disease-free women 8 years after diagnosis of breast cancer. By contrast, in a case-controlled study of 101 women initially presenting with abnormal breast masses, researchers found a ten-fold higher risk of breast cancer in women with below average urinary 2/16 (Ho et al. 1998). A more recent prospective study of 60 women undergoing surgery for suspected breast cancer found a two- to three-fold reduction in urinary and serum 2/16 in women with metastatic breast cancer as compared to women with benign breast disease (Ursin et al. 1999). One prospective trial showed an average of 15% greater urinary 16-hydroxy-estrone at baseline in 102 women who subsequently developed breast cancer over a 12- to 19-year follow up period (Meilahn et al. 1998).

The 2/16 ratio has also been correlated to two other estrogen-sensitive tumors: HPV-related recurrent respiratory papillomatosis (Auborn et al. 1998; Rosen et al. 1998) and cervical dysplasia (Sepkovic et al 1995). In each setting, a lowered ratio correlated to increasing disease severity.

It is possible that elevated 16-hydroxyestrone and decreased 2-hydroxyestrone are epiphenomena, concurrent with breast cancer but not causative. It is also possible that both 4-hydroxyestrone and 16-hydroxy-estrone are produced by the same enzymes (Shou et al. 1997), in which case they might be interchangeable, i.e., the 2/16 ratio and the 2/4 ratio might yield the same information.

The urinary 2/16 assay has been thoroughly studied and demonstrates good precision and accuracy (Klug et al. 1994), as well as good short- and long-term stability (Michaud et al. 1999; Chen et al. 1999). Only a random spot urine is required for the urine assay (Westerlind et al. 1999).

With respect to breast cancer, a considerable body of in vitro and in vivo evidence points to a protective role for 2-hydroxyestrone and a harmful role for 16-hydroxyestrone. Postmenopausal women should consider measurement of their urinary and/or serum 2/16 ratio, aiming for values greater than 2 and 0.6, respectively. Ratios that are greater than these are associated with at least a threefold reduction in breast cancer risk relative to the population at large. Interventions that might alter this ratio favorably include simple dietary and lifestyle modifications, including weight loss, exercise, and consumption of Brassica family vegetables as well as isoflavone-enriched soy products, flaxseed, fish oil, and supplemental indole-3-carbinol (and possibly its dimer, di-indolylmethane (DIM)) (Haggans et al. 1999; Lu et al. 2000).

While the role of these metabolites in premenopausal women is still under active investigation, preliminary evidence suggests that 2/16 is also altered in younger women with breast cancer. Certainly, premenopausal women at established increased risk of breast cancer (e.g., by family history) may also benefit from interventions that favorably alter the 2/16 ratio.

The urinary 2/16 a estrogen metabolite ratio test measures the ratio of 2-hydroxy- to 16-hydroxy-estrone (2/16) in a random urine sample. It requires only one urine specimen and the results come with an interpretation, and recommendations such as consuming indole-3-carbinol and eating more cruciferous vegetables if levels of the "bad" estrogen metabolite (16 a-hydroxyestrone) are too high or if levels of the "good" estrogen metabolite (2-hydroxyestrone) are too low. Two studies indicate that the optimal time to measure the 2/16a ratio is in the follicular or preovulatory phase of the menstrual cycle (Rosen et al. 1998; Haggans et al. 1999).

To inquire about this simple urine test, call (800) 208-3444.

What Are Your Options IF You Have Breast Cancer?

Currently, the decision to initiate hormone replacement therapy if you are a breast cancer survivor is risky. It is especially important that you know whether your breast cancer is estrogen receptor positive or progesterone receptor positive and to also know your hydroxyestrone ratio. If your cancer was hormone receptor positive or your ratio of estrone is unfavorable, it is not advisable to start hormone therapy initially. If the hydroxyestrone ratio is unfavorable, it can be altered by modifications in diet and by other measures previously discussed. Then, estriol therapy would be the safest choice of estrogen replacement if your tumor was not receptor positive.

If you are not receptor positive, consult your oncologist about the current recommendations for hormone replacement therapy and proceed with great caution. If you are having symptoms of menopause, there are other options that may relieve postmenopausal symptoms. Two prospective, randomized, placebo-controlled trials found that selective serotonin reuptake inhibitors reduced hot flashes by 50-60% and improved insomnia and sexual libido (Stearns et al. 2002). The authors stated that selective serotonin re-uptake inhibitor drugs such as Paxil® or Zoloft® should be considered as a first-line nonhormonal pharmacologic therapy for women with menopausal symptoms. Another, less compelling study suggested that 800 IU of vitamin E lessened the hot flashes of menopause, but the effect was modest, with only a small improvement over placebo (Pritchard 2001).

The use of megestrol acetate, an oral progesterone, can also be considered when other methods of relieving symptoms are not an option and if the tumor was not progesterone receptor positive. A placebo-controlled hot-flash trial found that a low dose of megestrol acetate reduced hot flashes by 80% compared to placebo in patients on hormone deprivation therapy for breast cancer. Numerous studies support the use of this form of progesterone to relieve hot flashes in these circumstances. Your oncologist should be consulted before using this therapy (Loprinzi et al. 1994; Quella et al. 1998; Bertelli et al. 2002).

Continued . . .


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