Archive for the ‘Female Health Issues’ Category

Is hormone replacement therapy safe or not?

Thursday, October 25th, 2012

It has taken a decade of research to arrive at a conclusion that is far from definitive: The evidence suggests it may help in the short term to manage  hot flashes and other symptoms of menopause in some younger, healthy women. But, taking it for long periods of time or later in menopause to help prevent certain chronic diseases isn’t recommended.

On Monday, the U.S. Preventive Services Task Force once again backed the idea that long-term use later in menopause is unwise when it released recommendations that said the increased health risks outweighed the benefits of using the treatment in that medical scenario.

That was not always the prevailing view in the medical community, however.

For years, it was common for women suffering from hot flashes, night sweats and other life-disrupting symptoms of menopause to go on hormone replacement therapy — typically a combination of estrogen and progesterone or progestin (a progesterone-like medication). That all changed in 2002, when the practice was halted by many after the landmark Women’s Health Initiative trial found that rates for breast cancer and stroke were higher in women on hormone replacement therapy compared to women who weren’t taking the treatment.

Although the study of more than 16,000 women reported some benefits, including lower rates of hip fractures and fewer cases of colon cancer, there were increases in heart disease, strokes and pulmonary embolisms (dangerous blood clots in the lungs) in women who took estrogen and progestin compared to women on placebo pills. The study, scheduled to run until 2005, was shut down early as a result.

“After 2002 and the Women’s Health Initiative study, people just stopped their hormone therapy. I think the study was an amazing study and gave us really good information, but you have to look at it in the time it was organized and developed, in early 2002, 2003,” said Dr. Anne Ford, associate professor of obstetrics and gynecology at Duke University School of Medicine.

Hormone replacement therapy formulations have since changed, and more recent research has teased out some groups of women who might benefit from the treatment, she added.

A Danish study of 1,000 women published earlier this month in BMJ suggested that women who began taking hormone replacement therapy early in menopause and who continued taking it for an average of 10 years cut their risk of having a heart attack, heart failure or dying without raising their risk for breast cancer or blood clots.

Two other recent reports also suggested that hormone replacement therapy holds benefits for some. One found that it was safe for the heart, and the other reported that it did not worsen memory in younger women.

“The new studies are well done and very important, since they address younger women,” said Dr. Judi Chervenak, a reproductive endocrinologist at Montefiore Medical Center in New York City.

Although the newer research does not necessarily negate the findings of the Women’s Health Initiative study, she said, it also does not have the power of that study in terms of how many women were followed. She said the new studies support that for some women — especially younger women without any health problems — hormone therapy might be a good option.

“Hormone therapy is no longer the arsenic it was once thought to be after the Women’s Health Initiative,” Chervenak said. A woman suffering from hot flashes, vaginal dryness or osteoporosis should discuss the pros and cons with her doctor, she said.

“They need to talk about family history of heart disease, blood clots and high cholesterol,” she explained. “For someone with very high triglycerides, for example, estrogen could adversely affect those levels.”

There are two issues at play, said Dr. Margery Gass, executive director of the North American Menopause Society.

“I want to get across the difference between taking something long term for prevention versus taking it short term when you’re younger and healthier to treat symptoms for a limited amount of time,” Gass said. “We recommend [hormone replacement therapy] as a viable option for treating menopausal symptoms in healthy women — in women not at high risk for blood clots, breast cancer and stroke.”

Gass said the newer research suggests that women should not be taking hormone therapy to prevent chronic diseases associated with aging.

That conclusion mirrors the latest opinion issued by the U.S. Preventive Services Task Force, an independent panel of experts in prevention and evidence-based medicine that makes screening recommendations for various conditions and diseases.

The panel’s review of 51 articles published since 2002 recommended that postmenopausal women, including those who have had a hysterectomy, not take estrogen alone to prevent chronic conditions.

The potential harms of hormone replacement therapy outweigh any possible disease-prevention benefits in these women, the task force said.

For women seeking non-drug options to manage the discomforts of menopause, Ford suggested exercise, such as yoga, and a healthy diet. Other strategies: Layer clothing, meditate, practice paced breathing (also called relaxation breathing), maintain a healthy weight and avoid smoking.

Ford said there is probably a lot to be learned by looking at different communities and cultures, too. “Ethnicity seems to play a role in how women manage menopause,” she noted.

Earlier research has shown that black and Hispanic women tend to enter menopause earlier than white women, and also tend to suffer more severe symptoms.

Good and Bad Estrogens?

Thursday, March 3rd, 2011

There has been much talk about the role of estrogens in breast cancer risk. While cumulative estrogen exposure is the most critical breast cancer risk factor. The role of different metabolites of estrogen in cancer risk has increasingly been researched. In premenopausal women, the ovaries produce the estrogen estradiol (E2), which converts into estrone (E1), both of which must eventually be broken down and excreted from the body. This breakdown occurs primarily in the liver, and the excreted metabolites flow out in the bile or urine. Estradiol and estrone undergo this breakdown through a process called hydroxylation, an enzymatic activity in which the parent estrogen is transformed by the addition of a hydroxyl (OH) group at specific positions on estrogen’s molecular ring.{{{*}}}

Estrogen molecules are composed of carbon ring structures that are named numerically. Estradiol has 17 carbon atoms and can be hydroxylated at particular points on that ring. Considerable research has shown that major metabolites of estradiol and estrone are those hydroxylated at either the C-2 or the C-16 positions. Hydroxylated metabolites at the C-4 position also are present, but in lesser amounts. We might think of this process as parent estrogens (estradiol and estrone) begetting daughter estrogens (C-2, C-4, and C-16 hydroxyestrones and hydroxyestradiols).

The problem is, some of these are the proverbial good daughters and some are bad daughters. I’ll describe how the “bad” daughters can cause significant trouble.

What makes an estrogen good or bad? That has to do with the biological activity, or potency, of that estrogen. Estrogens are important in a host of cellular activities that affect growth and differentiation in various target cells. This is normal and beneficial, but too much estrogenic stimulation can have a negative effect. Therefore, properly metabolizing and excreting estrogens is crucial. This is how the daughter compounds differ substantially. If these estrogens are metabolized into the 2-hydroxylated estrone and estradiol, they lose much of their cell proliferative and estrogenic activity and are termed “good” estrogen metabolites. Studies show that when 2-hydroxylation increases, the body resists cancer, and that when 2-hydroxylation decreases, cancer risk increases.

However, the C-4 and C-16 hydroxylated estrone and estradiol metabolites are different from C-2 because these metabolites have more estrogenic activity than their mother compound.2 Research strongly suggests that women who metabolize a larger proportion of their estrogens down the C-16 pathway, as opposed to the C-2 pathway, have elevated breast cancer risk,3 and that the daughter estrogens metabolized down the C-16 route may be associated with direct genotoxic effects and carcinogenicity.4

Predicting Cancer Risks

In one recent large trial of 10,786 premenopausal women at the State University of New York at Buffalo, researchers found that those who went on to develop breast cancer had significantly less 2-hydroxyestrone and more 16-alphahydroxyestrone metabolites than women who did not. Following women for 5.5 years, they found that participants with increased levels of 2-hydroxyestrone had a 40 percent decrease in the occurrence of breast cancer.5

In a longer-term study on postmenopausal women, women with the highest C-2:C-16 ratio (a higher ratio means more C-2 and less C-16, proportionally) had 30 percent less risk of developing breast cancer than women with lower ratios.6 With this information, it would seem useful to discover what, if any, dietary or lifestyle modifications could guide estrogens down the C-2 pathway.

Estrogens are metabolized by a series of oxidizing enzymes in the cytochrome P450 family. These are the detoxification enzymes that break down all manner of drugs, hormones, and environmental toxins into generally less harmful metabolites. By closely studying this family of 30 or so enzymes, scientists have discovered how the parent estrogen compounds are modified in the C-2, C-4, or C-16 pathways. Researchers found that if particular enzymes within this family, namely cytochrome P450 1A1 and 1A2, are activated or stimulated, then more parent estrogens are metabolized into C-2-hydroxylated compounds.7 However, if cytochrome P450 3A4 and 1B1 are activated, then more C-4 and C-16 are produced8. The C-16-alpha version tends to damage DNA and cause abnormal cellular proliferation, while the C-2 metabolite has less estrogenic activity.1-3 If the proportion of C-16-alpha-hydroxyestrone can be decreased while the C-2-hydroxyestrone is increased—changing the ratio between the two—cancer risk could be reduced.

Nutrition And Estrogen

Epidemiological studies suggest the protective effects of soy protein on breast cancer rates in Asian countries where soy is a dietary mainstay.9 While soy protein is a complex mixture of nutrients and phytochemicals, it appears that part of its benefit is related to the isoflavones genistein and daidzein. Studies suggest that they change the way estrogens are metabolized, therefore changing the C-2:C-16 ratio. In studies on both pre- and postmenopausal women, it has been shown that isoflavones increase the beneficial C-2-hydroxyestrone at the expense of the C-16-hydroxyestrone, therefore increasing the C-2:C-16 ratio.10,11

It appears that isoflavones found in other plants might also have beneficial effects. Kudzu (Pueraria lobata), a vine found in the southern United States, contains unique isoflavones. It was found that one of kudzu’s isoflavones—puerarin—induced cytochrome P450 enzymes 1A1 and 1A2, among others, which pushed estrogen through the beneficial C-2-hydroxylation metabolic pathway.12

Lignans found in fiber-rich foods such as seeds and grains, and in particularly high concentrations in flaxseeds, contain phytochemicals that, when acted upon by bacteria in the gut, are converted to the metabolites called enterolactone and enterodiol, which appear to have similar effects as isoflavones. Researchers have demonstrated in animal and cell studies that lignans have chemoprotective effects, and they may influence estrogen production and metabolism.13,14 Studies also have shown that women with breast cancer, or at risk for breast cancer, have low excretion levels of urinary lignans. In cell-culture studies, lignans have been shown to inhibit estrogen-sensitive breast cancer cell proliferation.13 When flax was supplemented at five and 10 grams per day for three seven-week periods in a group of 28 postmenopausal women, the levels of C-2 hydroxyestrone increased in the urine, which increased the ratio of C-2:C-16.14 This suggests that flax may have a beneficial effect on estrogen metabolism.

The Phytonutrient I3C

The results of epidemiological studies on cruciferous and mustard family vegetables (Brassica genus)—including bok choy, broccoli, brussels sprouts, cabbage, cauliflower, kale, kohlrabi, mustard, rutabaga, and turnip—suggest that diets high in these vegetables lower the breast cancer rate. Increasing the amount of cruciferous vegetables in the diet can increase the C-2: C-16-estrogen ratio.15The vegetables’ phytochemicals seem to have a specific estrogen-modulating effect, and indole-3-carbinol (I3C) may be the most important phytonutrient in this regard.

Eating broccoli, kale, or other crucifers releases I3C, which is transported to the stomach. I3C is not the only indole formed16 but is probably the most important and well studied.

In the stomach, I3C is converted into many active compounds, one of which is diindolylmethane (DIM). Although DIM appears to be one important metabolite of I3C, most of the past and ongoing studies are performed on I3C itself. This is because I3C breaks down into a number of indole products, aside from DIM, which also may have estrogen-modulating activity.17,18 Cell-culture studies and human clinical trials have shown that I3C at doses of 200­400 mg/day can influence estrogen metabolism and promote formation of 2-OH-estrone, and therefore may be useful in breast cancer prevention.19,20 Current U.S. research studies are under way on I3C and women at increased risk for breast cancer.21

There is some controversy with I3C and when it should be administered. Most studies with I3C suggest it is best used as a preventive agent for women at high risk. Supplementing with I3C after cancer is present is less clear as far as benefit, as animal studies have been conflicting on this issue.22,23


  1. Bradlow HL, et al. 2-hydroxyestrone: the ‘good’ estrogen. J Endocrinol 1996;150 Suppl:S259-65.
  2. Gupta M, et al. Estrogenic and antiestrogenic activities of 16 alpha- and 2-hydroxy metabolites of 17 beta-estradiol in MCF-7 and T47D human breast cancer cells. J Steroid Biochem Mol Biol 1998;67(5-6):413-9.
  3. Kabat GC, et al. Urinary estrogen metabolites and breast cancer: a case-control study. Cancer Epidemiol Biomarkers Prev 1997;6(7):505-9.
  4. Bolton JL, et al. Role of quinoids in estrogen carcinogenesis. Chem Res Toxicol 1998;11(10):1113-27.
  5. Muti P, et al. Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16 alpha-hydroxyestrone ratio in premenopausal and postmenopausal women. Epidemiology 2000;11(6):635-40.
  6. Meilahn EN, et al. Do urinary oestrogen metabolites predict breast cancer? Guernsey III cohort follow-up. Br J Cancer 1998;78(9):1250-5.
  7. Bradlow HL, et al. Multifunctional aspects of the action of indole-3-carbinol as an antitumor agent. Ann NY Acad Sci 1999;889:204-13.
  8. Huang Z, et al. 16-alpha-hydroxylation of estrone by human cytochrome P4503A4/5. Carcinogenesis 1998;19(5):867-72.
  9. Vincent A, Fitzpatrick LA. Soy isoflavones: are they useful in menopause? Mayo Clin Proc 2000;75(11):1174-84.
  10. Xu X, et al. Effects of soy isoflavones on estrogen and phytoestrogen metabolism in premenopausal women. Cancer Epidemiol Biomarkers Prev 1998;7(12):1101-8.
  11. Xu X, et al. Soy consumption alters endogenous estrogen metabolism in postmenopausal women. Cancer Epidemiol Biomarkers Prev 2000;9(8):781-6.
  12. Guerra MC, et al. Comparison between Chinese medical herb Pueraria lobata crude extract and its main isoflavone puerarin antioxidant properties and effects on rat liver CYP-cataly-sed drug metabolism. Life Sci 2000;67(24):2997-3006.
  13. Mousavi Y, Adlercreutz H. Enterolactone and estradiol inhibit each other’s proliferative effect on MCF-7 breast cancer cells in culture. J Steroid Biochem Mol Biol 1992;41(3-8):615-9.
  14. Haggans CJ, et al. Effect of flaxseed consumption on urinary estrogen metabolites in postmenopausal women. Nutr Cancer 1999;33(2):188-95.
  15. Fowke JH, et al. Brassica vegetable consumption shifts estrogen metabolism in healthy postmenopausal women. Cancer Epidemiol Biomarkers Prev 2000;9(8):773-9.
  16. Stephenson PU, et al. Modulation of cytochrome P4501A1 activity by ascorbigen in murine hepatoma cells. Biochem Pharmacol 1999;58(7):1145-53.
  17. Liu H, et al. Indolo[3,2-b]carbazole: a dietary-derived factor that exhibits both antiestrogenic and estrogenic activity. J Natl Cancer Inst 1994;1758-65.
  18. Wong GY, et al. Dose-ranging study of indole-3-carbinol for breast cancer prevention. J Cell Biochem Suppl 1997;29:111-6.
  19. Telang NT, et al. Inhibition of proliferation and modulation of estradiol metabolism: novel mechanisms for breast cancer prevention by the phytochemical indole-3-carbinol. Proc Soc Exp Biol Med 1997;216(2):246-52.
  20. Michnovicz JJ, et al. Changes in levels of urinary estrogen metabolites after oral indole-3- carbinol treatment in humans. J Natl Cancer Inst 1997;89(10):718-23.
  21. Osborne MP. Chemoprevention of breast cancer. Surg Clin North Am 1999;79(5):1207-21.
  22. Bailey GS, et al. Enhancement of carcinogenesis by the natural anticarcinogen indole-3-carbinol. J Natl Canc Inst 1987 May;78(5):931-4.
  23. Xu M, et al. Post-initiation effects of chlorophyllin and indole-3-carbinol in rats given 1,2-dimethylhydrazine or 2-amino-3-methyl-imidazo[4,5-f]quinoline. Carcinogenesis 2001;22:309-14.

WHI studies in perspective

Monday, February 14th, 2011

First, let’s take a deeper look at the Women’s Health Initiative (WHI) studies that change the medical perspective of menopausal hormone therapy (MHT) and drop the use of hormones significantly.

The menopausal hormone therapy clinical trial had two parts. The first involved 16,608 postmenopausal women with a uterus who took either estrogen plus-progestin therapy or a placebo. (The added progestin protects women against uterine cancer.) These were the first randomized placebo controlled trials for MHT. The past trials were all observational studies.

The second involved 10,739 women who had had a hysterectomy and took estrogen alone or a placebo. (A placebo is a substance that looks like the real drug but has no biologic effect.)

The estrogen-plus-progestin trial used 0.625 milligrams of conjugated equine estrogens taken daily plus 2.5 milligrams of medroxyprogesterone acetate (PremproTM) taken daily. The estrogen-alone trial used 0.625 milligrams of conjugated equine estrogens (PremarinTM) taken daily.

Prempro and Premarin were chosen for two key reasons: They contain the most commonly prescribed forms of estrogen-alone and combined therapies in the United States, and, in several observational studies, these drugs appeared to benefit women’s health.

Women in the trials were aged 50 to 79—their average age at enrollment was about 64 for both trials. They enrolled in the studies between 1993 and 1998.Their health was carefully monitored by an independent panel, called the Data and Safety Monitoring Board (DSMB).{{{*}}}

Both hormone studies were to have continued until 2005, but were stopped early. The estrogen plus-protestin study was halted in July 2002, and the estrogen-alone study at the end of February 2004.

The two WHI studies’ findings should not be compared directly.  Women in the estrogen-alone study began the trial with a higher risk for cardiovascular disease than those in the estrogen-plus-progestin study.  They were more likely to have such heart disease risk factors as high blood pressure, high blood cholesterol, diabetes, and obesity.

Here are the main findings:

Estrogen Plus Progestin

With 5.2 years of followup.  For every 10,000 women each year, estrogen plus progestin (combination therapy) use compared with a placebo on average resulted in:

Increased risk for

Breast cancer

  • 26 percent increased risk—8 more cases (38 cases on combination therapy and 30 on placebo)


  • 41 percent increased risk—8 more cases (29 cases on combination therapy and 21 on placebo)

Heart attack

  • 29 percent increased risk—7 more cases (37 cases on combination therapy and 30 on placebo)

Blood clots (legs, lungs)

  • Doubled rates—18 more cases (34 cases on combination therapy and 16 on placebo)

Increased benefits

Colorectal Cancer

  • 37 percent less risk—6 fewer cases (10 cases on combination therapy and 16 on placebo)


  • 37 percent fewer hip fractures—5 fewer cases (10 on combination therapy and 15 on placebo

No difference


Total cancer case

Estrogen Alone

With 6.8 years of followup.  For every 10,000 women each year, estrogen-alone use compared with a placebo on average

resulted in:

Increased risk for


  • 39 percent increase in strokes—12 more strokes (44 cases in those on estrogen alone and 32 in those on placebo)

Venous thrombosis (blood clot, usually in a deep vein of legs)

  • About a 47 percent higher risk—6 more cases (21 cases in those on estrogen alone and 15 in those on placebo.) An increased risk of pulmonary embolism (blood clots in the lungs) was not statistically significant. There were 13 cases in those on estrogen alone and 10 in those on placebo.

No difference in risk (neither increased nor decreased) or of uncertain effect

Coronary heart disease

  • No significant difference—5 fewer cases (49 cases in those on estrogen alone and 54 in those on placebo).  During the first 2 years of use, the risk was slightly increased for estrogen alone, but it appeared to diminish over time.

Colorectal/total cancer

  • No significant difference—1 more case for colorectal cancer and 7 fewer cases for total cancer (for colorectal cancer, 17 cases with estrogen alone and 16 with placebo; for total cancer, 103 cases in those on estrogen alone and 110 in those on placebo.)

Deaths (all or specific cause)

  • No significant difference—3 more deaths (for all deaths, 81 in those on estrogen alone and 78 in those on placebo)

Breast cancer

  • Uncertain effect—7 fewer cases (26 cases in those on estrogen alone and 33 in those on placebo).  This finding was not statistically significant.

Increased benefit

Bone fractures

  • 39 percent fewer hip fractures—6 fewer cases (11 cases in those on estrogen alone and 17 cases in those on placebo)

These findings are best summarized in this diagram:

U.S. Food and Drug Administration (FDA) Approved Use of Menopausal Hormone Therapy

  • Menopausal hormone therapy products are effective for treating moderate-to-severe hot flashes and night sweats, moderate-to-severe hot flashes and night sweats moderate-to-server vaginal dryness and prevention of osteoporosis associated with menopause, but carry serious risks. Therefore post-menopausal women who use or are considering using estrogen or estrogen with progestin treatment should discuss with their health care providers whether the benefits outweigh the risks.
  • If these products are prescribed solely for vaginal symptoms, health care providers are advised to consider the use of topical vaginal products (gel or cream applied locally).
  • If menopausal hormone therapy is used for osteoporosis, the risks for osteoporosis must outweigh the risk of estrogen or estrogen with progestin. Health care providers are encouraged to consider other treatments before providing menopausal hormone therapy for osteoporosis.
  • Menopausal hormone therapy has never been approved for the prevention of cognitive disorders such as Alzheimer’s disease or memory loss. In fact, the WHI found that women treated with menopausal hormone therapy have a greater risk of developing dementia.
  • Menopausal hormone therapy should be used at the lowest doses for the shortest duration to reach treatment goals, although it is not known at what doses there may be less risk of serious side effects.

Here are my comments:

  1. It is a fact that the incidence of breast cancers among post-menopausal women has declined since the decline of the use of MHT in the early 2000s especially those with positive estrogen receptors which is the majority of breast cancers.
  2. There has also been an increase in bio-identical hormone replacement such as the use of phytoestrogens and micronized natural progesterone during the same period. Many experts criticized the use of equine conjugated estrogens and synthetic progestin in the WHI trials. Could this contribute to the higher risks of breast cancer, stroke and clots? There are studies, mainly animal studies, that confirmed the differences of synthetic and natural female hormones on estrogen receptor bindings and their physiological effects. Could the type of hormones account for the adverse risks?
  3. New insights from more studies and follow up of the WHI studies:
    • Could progestin mediates the CHD risk when the 2 studies were compared? E+P has higher risk than E alone. It is also interesting to note that in this group of women ,those on statins have beneficial efforts for risk of CHD when taking together with the hormones.
    • Could progestin mediates risk of breast and colorectal cancers?  E+P has higher risk of invasive breast cancer vs P alone where there is no difference to placebo. The reverse is true for colorectal cancers, E+P reduces CRC while E alone shows no difference, could progesterone confers lower risk to colorectal cancer?
    • It is important to get the perspective right in terms of the added risk from MHT. The attributable risk which is the difference of the risk from the MHT over the prevalence of these risks in the studied population is what should be looked at. In these 2 groups of patient average age of 63 years, the overall number of major disease events was low only 1 in 300 major outcomes per year i.e. one third of 1 percent. E+P added less than one tenth of 1 percent to that rate. If you compare these risks to other risk factors for breast cancers, late menopause, obesity, lifetime alcohol excess and lack of exercise, the risks related to MHT are smaller compared to these other factors. The same is true for the E alone study.
    • Timing of MHT since menopause is also important. The risk for example to CHD is higher the longer the start of MHT from menopause e.g. more than 20 years as compared to the benefits rather than harm from CHD in the group that starts MHT early in menopause i.e. less than 10 years from start of menopause. This was the same observation for E alone and the E+P studies. The theory proposed for this difference is the “estrogen gap” theory. In premenopausal period, endogenous estrogens protect the arterial lining from plagues. If there was an interval immediate post menopausal when estrogens are not replaced, the theory proposes that there will be no benefit due to estrogen resistance or gap. The arterial wall will no longer respond to estrogen due to the gap period. In fact, animal studies show that if estrogen is given when estrogen resistance developed, the plague progression could be worst.  This was confirmed from coronary calcium score studies in early menopausal women where estrogen and progestin use has less calcium score as compared to placebo.

My recommendations:

Is MHT still a rational choice – Yes, but it depends on the profile of the woman who is looking for treatment.

Women with symptoms of MHT early menopause especially vasomotor symptoms, estrogen alone seem better than the combined E+P in terms of risk. But 60% of women have a uterus. Here one could consider milder progesterone. The FDA’s position is that there is no evidence to justify the use of bioidentical hormones. We will cover this in another post. The methods of delivery e.g. transdermal do not seem to change the risk situations in MHT.

Vasomotor symptom relief:

There are definite benefits for those with vasomotor symptoms. What is not included in this analysis is the sleep disturbances associated with menopausal. These could be very debilitating and estrogen has helped with these sleep disturbances.

I would therefore recommend hormonal replacement for early menopausal patient – low dose estrogen and transdermal is preferred for patients with vasomotor symptoms such as hot flashes, night sweats and sleep disturbances. Natural progesterone such as micronized progesterone would be my preference. Usually the symptoms improved within 2 weeks of treatment. After second month of unopposed estrogen, cyclic micronized progesterone should be initiated. I would then review the continuation after 1 year of treatment. Some cases might need up to 2 years of replacement to settle the vasomotor symptoms.

The use of MHT in prevention of CHD, breast cancer and dementia needs further evaluation in robust clinical studies. MHT is definitely beneficial for osteoporosis. However, there are other options (see future post). I would not recommend its use until we fully understand the mechanisms of the hormones in driving some of these risks with further research.

Female health issues

Saturday, February 12th, 2011

After a long sabbatical leave pursuing my Masters program in Human Nutrition at the University of Bridgeport, I am back. Some patients have requested me to provide updated information on female health issues especially hormonal issues. Some of the questions commonly raised are – do we need hormonal replacement during menopause? Is menopause a natural progression of aging and therefore should not be tempered with? What is the current thinking on menopausal hormonal replacement? Are there different types of estrogen metabolites – some are carcinogenic and some useful? How do I know if I am suffering from hormonal imbalance? What is estrogen dominance and progesterone deficiency and what do these mean in layman terms? We will embark on the journey to explore all these interesting questions that might have a bearing on your wellness in the silvering years.