Thursday, December 27, 2007

Hormonal Contraception: More Bad News

I'm on vacation but cannot resist posting this info. I advise my patients to go nonhormonal with contraception - condoms, rhythm method, IUD, or Fem Cap. Here's more data to add to the mounting pile of adverse effects associated with hormonal contraception! SG

Hormonal Contraception and Cervical Cancer Risk

Risk for cervical cancer increased in current users of hormonal contraception but declined after use stopped.

Cervical cancer risk is increased in current and recent users of hormonal contraception, but the effect’s duration has not been delineated. To quantitate this risk more precisely, investigators pooled data on 16,573 women with cervical cancer and 35,509 women without cervical cancer from 24 studies. Analyses were stratified by potential confounders (e.g., study site, time since last use, and type of contraceptive [oral or injectable; combined oral estrogen-progestogen or progestogen only]).

The risk for cervical cancer was higher in current users of combined oral contraceptives than in never users (relative risk, 1.9 with more than 5 years’ use). After cessation of use, the risk declined, equaling that of never users in 10 years. The increase in risk did not vary substantially with human papillomavirus status, although confidence intervals were wide because of limited numbers. Data were insufficient for fully comparable analyses of progestogen-only and injectable contraceptives.
Comment: Although this careful analysis confirms an increase in risk for cervical cancer among women using hormonal contraception, the finding should not dissuade clinicians from providing such contraception. The increased risk could reflect biologic interaction or confounding by sexual behavior: Women who use hormonal contraception are less likely to use barrier methods and so are more likely to be exposed to HPV, some types of which are documented cervical carcinogens. However, among women with oncogenic HPV infection, use of hormonal contraception has not been shown to affect the natural history of HPV-induced dysplasia (Journal Watch Women’s Health Feb 7 2006). Furthermore, hormonal contraception decreases parity, thereby reducing other causes of morbidity and mortality — especially in the developing world. Women choosing hormonal contraception can also be reassured that cytologic screening as well as HPV vaccination and testing are effective methods for preventing cervical cancer.

— Anna Wald, MD, MPH
Published in Journal Watch Women's Health December 20, 2007

Tuesday, December 25, 2007

Revisiting Hormone Therapy in Women

Happy Holidays. Here is a nice summary of the latest view, albeit conventional, from the Harvard Women's Health Watch, Dec 2007. SG

Harvard Women's Health Watch | December 2007

Revisiting hormone therapy’s risks and benefits

A more nuanced picture may emerge as researchers re-examine data from the government’s massive postmenopausal hormone trials.

Hormone therapy has long been the standard treatment for relieving menopausal symptoms: hot flashes, night sweats, and vaginal dryness. Until 2002, many clinicians were also recommending it long term to prevent chronic health problems, including heart disease, stroke, and osteoporosis. There was some evidence that estrogen might contribute to breast cancer, but except for women at especially high risk for that disease, cardiovascular disease was a more serious concern — a far greater cause of death and disability. For that reason, most health organizations recommended that postmenopausal women consider taking hormone therapy.

Then, in 2002, the hormonal approach to averting women’s later-life ills screeched to a halt. Researchers had to stop the Women’s Health Initiative (WHI) randomized trial of estrogen and progestin (in the form of Prempro) because the hormone combination was actually causing more heart attacks and strokes than a placebo, as well as more blood clots and breast cancer.

Two years later, the WHI’s trial of estrogen alone (Premarin), also ended early, after it became apparent that estrogen increased the rate of strokes and blood clots without conferring any benefits on the heart.

Although there were some benefits — fewer fractures in both trials and a reduced risk for colon cancer in the combined-hormone trial — they didn’t outweigh the risks. That left hormone therapy back where it started, as a short-term treatment for menopausal symptoms.

Impact and critique of the WHI

Hormone therapy is still the most effective treatment for hot flashes and night sweats. But the WHI results — and the associated media firestorm — left women worried and confused about even such short-term use. They were told to use hormones only for short periods and at low doses, and hormone therapy prescriptions plummeted. (One study reported a 75% drop between 2002 and 2006.) Yet menopausal women looking for symptom relief shouldn’t misinterpret the WHI findings. These studies were not about short-term management of menopausal symptoms. Moreover, the results aren’t above criticism. New questions have arisen as scientists try to reconcile the findings of earlier observational studies with those of the WHI — a randomized, placebo-controlled trial, considered the “gold standard” type of clinical investigation.

Some critics argue that the WHI results may not apply to the typical woman considering hormone therapy because most of the 27,347 participants were in their 60s and 70s — well past the perimenopausal transition and early menopause (the usual time for starting hormone therapy). Others say that the risks were overstated. Each year, for example, the women taking Prempro had only six more heart attacks per 10,000 than the women taking a placebo; among younger women, the difference was even less.

Because of these and other concerns, scientists have been re-examining the WHI data and undertaking new trials. Researchers are also reappraising earlier studies that suggested hormone therapy could prevent cardiovascular disease.

Some scientists now suggest that the cardiac risk and benefit of hormone therapy may depend on a woman’s age, particularly the age at which she starts taking hormones. This new hypothesis doesn’t change current recommendations (see chart), but it may reassure perimenopausal and newly menopausal women who are considering short-term hormone treatment for symptom relief.

Recommendations regarding hormone therapy (HT)* use



U.S. Preventive Services Task Force (USPSTF)**

Recommends against the routine use of HT to prevent chronic conditions in postmenopausal women.

North American Menopause Society

Moderate to severe vasomotor symptoms (hot flashes and night sweats) are the main use for systemic HT.

Food and Drug Administration

HT should be used at the lowest dose and for the shortest time needed to reach treatment goals, although it’s not known how low you should go to reduce the risk of serious side effects. When hormone therapy is prescribed only for vaginal symptoms, consider topical vaginal products.

American College of Obstetricians and Gynecologists

Estrogens are the most effective treatment for menopausal vasomotor symptoms (hot flashes and night sweats). Their use (with or without a progestin) should be reassessed yearly. The lowest effective dose should be used for the shortest possible time to alleviate symptoms.

American Society for Reproductive Medicine

Low-dose estrogen is a valid option for many seeking short-term relief from menopausal symptoms. HT does not provide additional health benefits that would justify its use beyond the immediate relief of menopausal symptoms. HT is not indicated for the primary or secondary prevention of coronary artery disease events.

Canadian Task Force on Preventive Health Care

HT should not be used for the primary prevention of chronic diseases in postmenopausal women. To maintain heart health, women should use other preventive strategies, such as increased exercise, smoking cessation, and blood pressure control. There’s not enough evidence to make a recommendation on HT regarding stroke and death from stroke.

*HT refers to estrogen alone, or estrogen plus a progestin.

**The USPSTF did not consider the use of hormone therapy for managing menopausal symptoms.

Heart risk: Is it a matter of timing?

The lack of heart benefits in the WHI contradicts findings from observational studies, such as the Nurses’ Health Study, in which participants are followed for years but are not asked to take medications or do anything differently. In those studies, women have tended to start taking hormones closer to the onset of menopause. Researchers have observed that these women suffer fewer of the heart problems caused by atherosclerosis (for example, angina and heart attacks) than women who don’t take hormones.

The idea that hormone therapy might help protect women from atherosclerosis was biologically plausible. It’s long been recognized that women develop atherosclerosis-related heart problems at an older age than men — that is, after menopause and the decline in estrogen. And in animal studies, estrogen has been shown to slow the development of atherosclerosis.

So why might estrogen then increase the risk of heart disease in women who start taking it at an older age? Evidence indicates that estrogen can destabilize atherosclerotic plaques, the artery-clogging accumulations of cholesterol and debris that are a major source of heart disease. Estrogen appears to make plaques more vulnerable to rupture, which can result in a heart attack. Older women are more likely to have developed plaques. So for them, estrogen might do more harm than good. It may be that hormone therapy is good for the heart only during a fairly narrow window, when plaques are starting to form but are not fully developed.

Nurses’ Health Study researchers found some support for this hypothesis in 2006 in a study undertaken to shed light on the discrepancies between the WHI results and earlier research. They found a 30% reduction in risk for heart disease among women who began hormone therapy within about four years of menopause, but little or no cardiac benefit for women who started hormones either after age 60 or 10 or more years after menopause.

A reanalysis of the WHI data turned up similar evidence that timing may be a factor. Investigators reporting in the Journal of the American Medical Association (April 4, 2007) found no increased risk for heart disease among hormone users ages 50 to 59 and a suggestion of reduced risk among women who started hormone therapy within 10 years after menopause. Thereafter, the greater the gap between onset of menopause and start of hormone therapy, the greater the risk for heart disease, especially in those with a history of hot flashes and night sweats. Stroke remained a problem, regardless of time since menopause, for women receiving either estrogen alone or combined therapy. The risk for breast cancer rose after five years in women taking combined hormones, although not in those taking estrogen alone.

In an ancillary study, WHI investigators assessed coronary artery calcium, which is a marker for atherosclerosis, in 1,064 women ages 50 to 59 who’d had a hysterectomy before entering the WHI estrogen-only trial. The women took their study medications for an average of 7.4 years and then, a year after the trial ended, they underwent CT scans of the heart. Results, published in the June 21, 2007, issue of The New England Journal of Medicine, showed that the estrogen-takers had less calcified plaque in their arteries than the placebo takers, suggesting a reduced risk for future cardiovascular events. But it’s not known how long this benefit would have lasted — or whether it would have actually led to fewer heart attacks or strokes — if the women had continued taking estrogen. According to WHI investigator (and the study’s lead author) Dr. JoAnn Manson, these findings lend support to the idea that estrogen, when it’s started near menopause, may slow the early stages of plaque buildup. “But estrogen’s effects are complex, and it has other known risks,” Dr. Manson points out, so it “shouldn’t be used for the express purpose of preventing cardiovascular disease.” Also, this study did not include older women, so there’s no indication of whether age makes a difference in the way estrogen affects plaque buildup. Only a randomized trial can test the “timing” hypothesis, and until then it remains unproven.

What about breast cancer?

Initial results from the WHI’s estrogen-only trial indicated that estrogen alone reduced the risk for breast cancer by 23% over about seven years. The effect was not statistically significant (meaning that it could have been due to chance), but it was still surprising in light of the increased risk found in the combined-hormone trial after four years. So investigators decided to take a closer look. In a final report — published in the April 12, 2006, issue of the Journal of the American Medical Association — they concluded that the women taking estrogen alone were at no greater risk for breast cancer than those taking a placebo.

The difference in risk between estrogen alone versus combined estrogen and progestin is one of the unanswered questions about hormone therapy and breast cancer. In the WHI, the estrogen-only takers had undergone hysterectomy, which is different from natural menopause. Also, we don’t know yet whether the time when hormone therapy starts influences breast cancer risk in the way it does heart disease risk. WHI investigators will soon report on a follow-up study of women in the estrogen-plus-progestin trial who continued to have annual mammograms after stopping their study medications in 2002. This could shed light on how long it takes for breast cancer risk to return to normal after women stop taking combined hormone therapy.

In the meantime, several groups of researchers reported in 2007 that the rate of new breast cancers began to decline in 2003, the year hormone therapy prescriptions fell off sharply.

Selected resources

Hot Flashes, Hormones, and Your Health, by JoAnn E. Manson, M.D., and Shari S. Bassuk, Sc.D., McGraw Hill, 2007.

Is it hot in here? Or is it me? by Pat Wingert and Barbara Kantrowitz, Workman Publishing, 2006.

What it means

Women in early menopause with troublesome hot flashes or night sweats can take short-term hormone therapy without increasing their risk for heart disease. Hormone therapy should be taken only for symptoms and, like any drug, for the shortest time possible and at the lowest effective dose (although we don’t know whether lower doses are actually safer). Studies suggest that estrogen patches may be less likely to cause blood clots in the legs than oral estrogen. For some women, the major menopausal complaint is vaginal dryness, which may persist for many years. Low-dose vaginal estrogen is an effective treatment for this symptom with negligible systemic effects.

When it comes to prevention, hormone therapy reduces the chances of fractures and colon cancer. Whether its adverse effect on the heart is related to timing still needs more study. But you can reduce these risks in other ways without increasing your odds for breast cancer, blood clots, and stroke. Avoid tobacco; exercise at least 30 minutes a day; adopt a healthy eating plan; and control your blood pressure, cholesterol, and blood sugar — with medications, if necessary. Be sure to get adequate calcium (1,200 milligrams per day) and vitamin D (800 to 1,000 IU per day). And if you’re at high risk for osteoporosis, there are many medications to choose from that curb bone loss.

Sunday, December 23, 2007

Treatment for Vaginal Dryness

We know that one quarter of women at or past menopause note vaginal thinning, irritation, decreased sexual response or dryness, and seek medical attention for it. I find the numbers are actually much higher if you ask women routinely. I'm a big fan of natural lubricants first, and if that doesn't work, try a tiny dose of natural estriol vaginal cream. I like estriol because you usually need less of it than the other forms of estradiol. It is by prescription, and needs to be formulated by a reliable compounding pharmacy. The good news is that it takes about 2 weeks to re-estrogenize the tissues, and it also prevents bladder infections. Remember that pre-menopausal women can have thiss too -- especially thin women who don't have much estrogen on board. Below are some guidelines, published by the North American Menopause Society.

New Guidelines Issued for Treatment of Vaginal Atrophy
News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD

May 15, 2007 — The North American Menopause Society (NAMS) has issued a 2007 position statement about the treatment of vaginal atrophy with local vaginal estrogen. The guidelines, which are published in the May-June issue of Menopause, state that therapy should be guided by clinician and patient preference.

Using the general principles established for evidence-based guidelines, NAMS convened a panel of clinicians and researchers with expertise in genitourinary disease to review, synthesize, and interpret the current evidence on vaginal estrogen therapy for vaginal atrophy, develop conclusions, and make recommendations. The advice of this expert panel was used to assist the NAMS Board of Trustees in publishing this position statement.

"Although hot flashes typically accompany the loss of ovarian estrogen production at menopause, they usually abate over time regardless of whether estrogen therapy is used," Editorial Board Chair Gloria A. Bachmann, MD, said in a news release. "In contrast, vaginal symptoms (eg, vaginal dryness, vulvovaginal irritation and itching, and painful intercourse) are usually progressive and unlikely to resolve spontaneously. Left untreated, vaginal atrophy can result in years of discomfort, with a significant impact on quality of life."

About 10% to 40% of postmenopausal women have symptoms related to vaginal atrophy, most of whom require treatment. However, only about 25% of symptomatic women seek medical attention.

The therapeutic standard for moderate to severe vaginal atrophy is estrogen therapy, administered either vaginally at a low dose or systemically. There has been a relative lack of randomized controlled trials performed to date, but they have shown that low-dose, local vaginal estrogen delivery is effective and well tolerated for treating vaginal atrophy.

In North America, US Food and Drug Administration–approved treatments of vaginal atrophy symptoms that offer localized vaginal delivery of estrogen include cream, tablet, and ring formulations. These products are associated with fewer adverse effects than systemic estrogen. At the doses recommended in labeling, all of the low-dose vaginal estrogen products approved in the United States for treatment of vaginal atrophy are equally effective. The choice of treatment should therefore be individualized based on clinical experience and patient preference.

In general, creams may be associated with more adverse effects than ring or tablet formulations, perhaps because there is more potential for women to apply higher-than-recommended dosing with cream. However, a Cochrane review reported no significant differences among the delivery methods in terms of hyperplasia, endometrial thickness, or the proportion of women with adverse events. The most commonly reported adverse effects associated with vaginal estrogen therapy are vaginal bleeding and breast pain, with nausea and perineal pain reported less frequently.

When low-dose estrogen is administered locally for vaginal atrophy, progestogen is generally not indicated. Data are insufficient to recommend annual endometrial surveillance in asymptomatic women using vaginal estrogen therapy.

Vaginal estrogen therapy should be continued as long as women continue to have distressing symptoms. Management of vaginal atrophy is similar for the group of women without a cancer history and for women treated for non–hormone-dependent cancer. However, for women with a history of hormone-dependent cancer, management recommendations are individualized and vary based on each woman's preference in consultation with her oncologist.

Specific recommendations are as follows:

The primary goals of vaginal atrophy management are symptom relief and reversal of atrophic anatomic changes.

For women with vaginal atrophy, first-line treatments include nonhormonal vaginal lubricants and moisturizers.

Symptomatic vaginal atrophy that does not respond to nonhormonal vaginal lubricants and moisturizers may require prescription therapy.

Randomized controlled trials in postmenopausal women are limited. However, they have demonstrated that low-dose, local, prescription vaginal estrogen delivery is effective and well tolerated for treating vaginal atrophy while limiting systemic absorption.

Low-dose vaginal estrogen products approved in the United States for treating vaginal atrophy include estradiol vaginal cream, conjugated estrogens vaginal cream, the estradiol vaginal ring, and the estradiol hemihydrate vaginal tablet. These are equally effective at the doses recommended in labeling, so specific choice depends on clinical experience and patient preference.

When low-dose estrogen is administered locally for vaginal atrophy, progestogen is generally not indicated.

Closer surveillance may be required for women at high risk for endometrial cancer, those using a higher dose of vaginal estrogen therapy, or those with symptoms such as spotting or breakthrough bleeding. Evidence is insufficient to recommend annual endometrial surveillance in asymptomatic women using vaginal estrogen therapy.

Vaginal estrogen therapy should be continued for as long as women have distressing symptoms.

For women treated for non–hormone-dependent cancer, management of vaginal atrophy is similar to that for women without a cancer history, but for those with a history of hormone-dependent cancer, management recommendations should be based on each woman's preference and the advice of her oncologist.
"Overall, subjective improvement occurs in 80% to 90% of women treated with local vaginal estrogen," the authors conclude. "Vaginal atrophy unresponsive to estrogen may be due to undiagnosed dermatitis/dermatosis or vulvodynia, so treatment failure warrants future evaluation and careful examination."

Novo Nordisk supported the development of this position statement through an unrestricted educational grant. Members of the Editorial Board have disclosed various financial relationships with Berlex, Duramed, Johnson & Johnson, Pfizer, Roche, Wyeth, Paladin Labs Canada, Wyeth Canada, Procter & Gamble, and/or Merck.

Menopause. 2007;14:357-369.

Thursday, December 20, 2007

PMS & Your Nervous System

Check out this article on PMS. It describes new data on how women with PMS have decreased autonomic nervous system activity. This makes sense as I love yoga as a first line therapy, which can remedy this. 5HTP and correcting estrogen dominance also do this. SG

Bad PMS May Mean A Depressed Nervous System

ScienceDaily (Dec. 20, 2007) — For some women premenstrual syndrome (PMS) is a minor monthly annoyance, but for others, more severe symptoms seriously disrupt their lives. However despite the number of women affected, science has yet to offer a full explanation or universal treatment. Now intriguing new findings published in the online open access journal BioPsychoSocial Medicine suggest not only that PMS is tied to decreased nerve activity each month, but also that those with extreme symptoms may have a permanently depressed nervous system.

A team of Japanese researchers led by Tamaki Matsumoto from the International Buddhist University in Osaka investigated whether the activity of the autonomic nervous system, which plays a vital role in equilibrium within the human body, changed during the menstrual cycle. The team measured heart rate variability and hormone levels and used questionnaires to evaluate physical, emotional and behavioural symptoms accompanying 62 women's menstrual cycles.

For the parameters Matsumoto's team was testing, the control group with little or no menstrual symptoms did not vary during the month. However women suffering from PMS saw results reflecting autonomic and parasympathetic nerve activity decrease significantly in the late luteal phase, which precedes menstruation. Those with the most marked symptoms (known as premenstrual dysphoric disorder) had lower rates of nerve activity than the other groups during the entire menstrual cycle.

"Our findings indicate that the occurrence of premenstrual symptomatology could be attributable to an altered functioning of the autonomic nervous system in the symptomatic late luteal phase," says Matsumoto. For women with PMDD, findings indicate that sympathovagal activity was altered even in the follicular phase. Matsumoto asks: "Does this imply that women with lower autonomic function regardless of the menstrual cycle are vulnerable to more severe premenstrual disorders? At the moment, the underlying biomechanisms of PMS remain enigmatic."

PMS comprises myriad non-specific physical, emotional, behavioural, and cognitive symptoms that occur in the days prior to menstruation and is nearly omnipresent in women of reproductive age from all cultures and socio-economic levels. The most prevalent symptoms include: irritability, mood lability, depression, anxiety, impulsivity, feelings of "loss of control," fatigue, decreased concentration, abdominal bloating, fluid retention, breast swelling, and general aches.

Friday, December 14, 2007

Xenoestrogens, Killing Us Softly

I love the wry yet educational voice of the following author. It's about the 700+ known xenoestrogens that are creating estrogen dominance in us, and perhaps contributing to our epidemic of breast cancer. I found the following article, Killing Her Softly, on a Yahoo Natural Hormone usergroup as well as other places. I don't know the author- let me know if you do. I plead with you to green your home, life, health and planet. The least expensive way I've discovered is with Shaklee products and have decided to set up a website for you to have access to this (see end of article for more information). Other options are to use certified organic products for the home, the face, the body -- especially makeup and sunscreen. And drink from a stainless steel bottle. Get one from Whole Foods or REI. SG

Killing Her Softly… When the alarm rings she slowly gets out of bed, turns on the shower and under the steady stream of warm water, she gently scrubs her body with Ammonia, Formaldehyde and Phenol. Next, she shampoos her tinted hair with mutagenic DEA and Sodium Lauryl Sulfate. Rinsing the shampoo, she applies more mutagenic DEA & Propylene Glycol and lets it penetrate while she pops the top on the shaving cream and shaves her legs with A-Pinene. The shower finished, she towel dries and spreads on an even coat of Contaminant, Polycyclic Aromatic Hydrocarbons (PHAs) and a dusting of an Asbestos Substance over her skin. She sprays the scented Aluminum under her arms, brushes her teeth with FD&C Blue#1 & Resorcinol, Saccharin, and Fluoride. Then she rinses and gargles with Ethanol and Phenol Alcohol. She combs setting gel through her hair then blows it dry and sprays it with polyvinylpyrrolidine (PVP). Sitting at her vanity, she carefully applies a thin film of Phenol Carbolic Acid, Dioxin and Propylene Glycol, over her face to reduce the fine lines. Today, she'll wear foundation and a little FD&C Red #3. And, better add some eye-Iron Oxide for today is a special meeting and a little Toxic and Mutagenic Ascorbyl Palmitate to line her lids and a stroke of Bacteria & Polyvinylpyrrolide (PVP) to her lashes. A dab of Benzo-A-Pyrene and Benzo-B-Fluroanthene to color her lips, a spritz of her favorite scent, Toluene and Benzaldehyde, and a little Carcinogenic Nitrosamine, NMPABAO on her face arms and legs to block the suns rays and she is set for the day. She looks radiant and healthy.. but her looks are killing her! If you are wondering if these poisons are being absorbed through her skin go cut open a clove of garlic and rub it on the bottom of your foot and see how long it takes to taste it in your mouth.. about 3 seconds! What have these product brands exposed her to in a matter of minutes? Read on to learn about what it is that we are really putting on and in our bodies every day. *Bar Soap has a pH of 9, which removes the protective acid mantle of the skin making it more alkaline and therefore, more vulnerable to penetration. It also contains ammonia, formaldehyde and phenol, known carcinogens and triclocarbans. *Shampoo contains cocamide DEA, which is associated with carcinogenic nitrosamines and sodium lauryl sulfate, a known mutagen. *Hair Tint contains quaternium-15, which releases carcinogenic formaldehyde and the carcinogen, phenylenediamine. *Conditioner contains DEA & Propylene Glycol both known mutagenic carcinogens *Shaving Cream contains a-pinene, a chemical that damages the immune system. *Body Lotion contains mineral oil, which, as a cosmetic grade petroleum product, includes the contaminant polycyclic aromatic hydrocarbons (PHAs) known as xenoestrogens that can mimic estrogen in the body. *Dusting Powder contains talc, a substance like asbestos. When talc was combined with a common air pollutant, benzo(a)pyrene, it induced tumors in 80% of the animals tested. Many scientists believe talc should be placed on the "known carcinogens" list. *Deodorant has aluminum, which is being tested in connection to Alzheimers. *Toothpaste contains saccharin and FD&C Blue#1, which are carcinogens. It also contains resorcinol, which can cause a blood disorder (methemoglobinemia), convulsions and death. Fluoride is also a known carcinogen. *Mouthwash contains 27% ethanol, which is suspected of causing esophageal cancer. It also contains phenol, which can cause fatal poisonings through skin absorption. *Hair Spray contains polyvinylpyrrolidine (PVP) and reports show that it may cause harm if the particles are inhaled. Modest intravenous doses fed to rats caused tumors. *Skin Moisturizer contains phenol carbolic acid, which can cause circulatory collapse, paralysis, convulsions, coma and death as a result of respiratory failure. It also contains PEG-40, which contains dangerous levels of dioxin and propylene glycol, which studies show can negatively alter brain waves and cause liver and kidney disorders. *Blush contains FD&C Red #3, which caused human breast cells to grow, mimics the effect of natural estrogen at the molecular level and damages the genetic material of human breast cells. *Eye shadow contains iron oxide, which is a suspected carcinogen, teratogen or toxin. *Eyeliner, contains ascorbyl palmitate, and studies suggest that the palmitates are to be considered carcinogenic, mutagenic, or toxic. *Mascara may be contaminated with bacteria.It also contains polyvinylpyrrolide (PVP), a carcinogen. *Lipstick contains paraffin, which is a mixture of hydrocarbons and is derived from petroleum. It is known to be contaminated with the carcinogens, benzo-a-pyrene and benzo-b-fluroanthene. *Perfume contains toluene, a suspected potent carcinogen that was found in every fragrance tested, and benzaldehyde, which is a central nervous system depressant that may cause kidney damage. *Sunscreen contains padimate O and the preservative, BNPD, which together create the carcinogenic nitrosamine, NMPABAO. To green your home cleaning products with the world's first and best biodegradable, natural cleaner, to replace your soaps and shampoos and toxic makeup, and to find a healthy way to support your health with supplements, visit my website:

Estrogen improves skin

In case you are wondering if I am an estrogen junkie, the answer is yes, but estrogen in balance. We know that excessive estrogen increases stroke, and synthetic estrogen with synthetic progesterone increases breast cancer and heart disease. But it also improves bones, prevents fractures, helps mood and libido, and now... improves skin! We all knew that but it's good to have a randomized controlled trial prove it.... SG

Sator PG, Sator MO, Schmidt JB, et al. A prospective,
randomized, double-blind, placebo-controlled study on
the influence of a hormone replacement therapy on skin
aging in postmenopausal women. Climacteric 2007;
10:320-334. Level of evidence: I.

Menopausal hormone therapy (HT) has a positive
effect on skin in postmenopausal women,
according to a prospective, randomized, double-
blind, placebo-controlled study that examined the
effect of treatment with Femoston for 7 months.
The trial included 40 women between ages 44
and 55 (mean age, 51.3 y). The mean duration of
amenorrhea was 46.6 months in the HT group
and 39 months in the placebo group. The women
received the HT, a combination of 2 mg 17β-
estradiol/10 dydrogesterone, for seven 28-day

Women in the study visited the blinded
investigators at screening, randomization, weeks
7 and 13 of treatment, and weeks 1 to 3 after
treatment. Skin properties were measured by
noninvasive measures. Skin elasticity, skin
surface lipids, skin hydration, and skin thickness
were measured at time of randomization, week
13 of treatment, and at 1 to 3 weeks after
treatment. Instruments used to measure skin
properties included the Sebumeter, the
Corneometer, and high-frequency ultrasound. In
addition, a clinical dermatological exam of skin
status was performed. After 7 months of HT,
there were significant improvements in skin
elasticity, skin hydration, and skin thickness. The
dermatological exam was in concordance with
these results.

Comment. The condition of the skin is one of the
most visible signs of aging and has been
especially important to women’s sense of
attractiveness. Ingestion or topical application of
hormones is not a new strategy for inhibiting
aging. Estrogen and progesterone were common
cosmetic additives until laws prohibited the
inclusion of ingredients that altered the structure
and function of the skin.1 The presence of
hormone receptors in the skin and the dermal
benefits of HT are well documented, primarily in
European studies.2-6 No doubt the results of this
study will be of interest to the growing sector of
the population that spends millions of dollars on
Botox therapy, cosmetic surgery, and antiaging
skin moisturizers—results of the successful
marketing of “looking younger” in the twenty-
first century.

This study by Sator et al reports the findings of a
small European study of the influence of an oral
HT preparation, Femoston (not marketed in the
United States), on aging skin. All 40 participants
were reported to have medically indicated
reasons for taking HT. Three women in each
group withdrew or were lost to follow-up, with a
resulting sample size of 34 women. The paper
includes numerous tables with detailed results of
multiple statistical comparisons between baseline
measures and comparable assessments at 3
months and 7 months post initiation of therapy.

Although there are numerous statistically
significant findings, the clinical significance,
given the small sample size, is not apparent. With
so many comparisons reported, there is a greater
chance of there being spurious statistically
significant findings. One important finding,
however, was that the skin benefits were more
pronounced in women who initiated HT close to
the date of their final menses. The authors note
that the success of the therapy is likely to be
directly related to the timing of initiation and
duration of treatment. Possible harmful side
effects of HT were not noted. The short duration
of the intervention (7 mo) is also a limitation. A
variety of questions about prescribing HT for
cosmetic or quality of life reasons were raised.

Both the US Food and Drug Administration
(FDA) and NAMS have clearly indicated that
until reliable evidence proves otherwise, we must
assume that the risks and benefits of all systemic
estrogens are the same. Clearly, women who are
prescribed HT for medically indicated reasons
may experience positive skin effects. But
prescribing systemic HT for the express reason of
skin benefits is not warranted. Local estrogen
therapies provide clear benefits to vaginal and
vulvar tissue. And, for women with extremely
dry, inelastic, and poorly hydrated skin, HT
would be the treatment of choice for improving
their quality of life. However, larger, double-
blinded, well-controlled studies of topical
therapies are needed before HT as an antiaging
skin therapy can be considered.

Catherine L. Juve, PhD, MPH, WHNP, RN
Professor, School of Nursing
University of Minnesota
Minneapolis, MN
Member, NAMS Professional Education Committee
1. Draelos ZD. Topical and oral estrogens revisited for
antiaging purposes. Fertil Steril 2005;84:291-292.
2. Patriarca MT, Goldman KZ, Dos Santos JM, et al.
Effects of topical estradiol on the facial skin collagen of
postmenopausal women under oral hormone therapy: a
pilot study. Eur J Obstet Gynecol Reprod Biol 2007;
3. Hall G, Phillips TJ. Estrogen and skin: the effects of
estrogen, menopause, and hormone replacement therapy
on the skin. J Am Acad Dermatol 2005;53:555-568.
4. Holzer G, Riegler E, Hönigsmann H, Farokhnia S,
Schmidt JB. Effects and side-effects of 2% progesterone
cream on the skin of peri- and postmenopausal women:
results from a double-blind, vehicle-controlled, randomized
study. Br J Dermatol 2005;153:626-634.
5. Brincat MP, Baron YM, Galea R. Estrogens and the
skin. Climacteric 2005;8:110-123.
6. Naftolin F. Prevention during the menopause is critical
for good health: skin studies support protracted hormone
therapy. Fertil Steril 2005;84:293-294.

Fibroids - Say "No" to the Knife!

This is an article I posted in my Zaadz blog last year. We have to be careful not to jump ship too fast in favor of hysterectomy for fibroids. Read on....
Over the past week, I've had 3 women suffering severely from fibroids in my yoga classes and practice, so I want to share some thoughts. Some background: Half of women have fibroids or benign tumors of the uterus which are made of muscle fibers. They range in size from little pellets to enormous fruit sizes (plums to grapefruits). Some women have one big one, other women have multiple fibroids of various sizes. We don't understand what causes them, but know there is a genetic link. We also know, fortunately, that 99.9% are benign or not cancer. They can be painful, very annoying, and can cause hemorrhaging, especially if they are located beneath on the surface or near the surface of the uterine lining. These are called submucosal fibroids as they are beneath the mucosal layer of the lining. The best news is that they shrink 30-50% in menopause. Personally, I have 2 fibroid friends in my uterus, both about 3cm in size. They increase my bleeding with my cycle and my discomfort. Many women get so fearful about the bleeding and pain that they rush along with their gynecologists to hysterectomy. For some women, a tiny minority, this is life-saving. For most, it is unnecessary. There are many other alternatives. A major cause of increased pain and bleeding is inflammation. There are two main causes of inflammation: first, hormone imbalance (usually estrogen dominance, or not enough progesterone in from age 35-50 years); and second, food intolerances/allergies. Common allergens are wheat, soy, dairy and citrus. An anti-inflammatory diet can often reduce blood flow and pain by 40% and help with hormone balance. Often over-the-counter progesterone cream, or prescription bioidentical progesterone cream, can help with hormone imbalance -- although I recommend following both protocols under the direction of a knowledgeable physician. Two great sources of information include Andy Weil's book Healthy Aging, and Suzanne Somers' new book, Ageless. One other important cause of fibroid symptoms is exposure to xenohormones, or environmental sources of endocrine disruptors that often cause estrogen dominance. Many women don't realize that their non-organic food, shampoo, cosmetics and air pollutants are exposing them to the 700+ agents that act like estrogen. To read more about this, I recommend Dr. John Lee's books, especially What Your Doctor May Not Tell You about Premenopause or What Your Doctor May Not Tell You about Breast Cancer. Sometimes a small change in diet, and/or adding progesterone cream or other bioidentical hormones, can help significantly with fibroid symptoms. If that doesn't work and the bleeding or pain are serious, other alternatives from minor out-patient surgery to remove the fibroids through the uterus (works best for heavy bleeding) or through the abdomen (ask about laparoscopic-assisted as this reduces your pain and speeds recovery). Another alternative, which cures 70-80% is uterine artery embolization. Seek a world-class center with lots of experience. The purpose is to plug the blood vessels that feed your fibroids by going through a large blood vessel in your groin. Not sure how you feel about Condy Rice, but she had this procedure done recently. Like most integrative medicine, you must find the path that works for you. This is best done by consulting your community and finding a great physician with whom you can freely share your hopes and fears, and particularly your preferences. Birth control pills, possibly lupron (or medical castration) followed by hysterectomy is what I was conventionally trained to offer, yet I found it to be unsatisfying. Find the right path for you. This information is general in nature and is not intended as medical advice. Anyone wishing to actively use this information for personal health improvement is advised and urged to consult with the qualified health care provider of their choice before attempting to use the information. Consult with your DOCTOR. Comments on this site do not apply to any person in particular.

"Micro" estrogen doses effective for hot flashes

I always say go as low as you can with estrogen dosing, and this is an article proving the wisdom and efficacy of "quarter-dose" estrogen therapy. That is, quarter of the standard dosing. The commentary is by the North American Menopause Society (, a conventional but solid organization. We always want to be guided by Level 1 evidence -- meaning randomized controlled trials, as this is the way we can make sure we are safe with how we dose hormones. This is an important new study to integrate into your thinking about whether to use estrogen after menopause. Healthy holidays, SG

Microdose of transdermal
17β-estradiol effectively relieves hot flashes

Bachmann GA, Schaefers M, Uddin A, Utian WH. Lowest effective transdermal 17β-estradiol dose for relief of hot
flushes in postmenopausal women: a randomized controlled trial. Obstet Gynecol 2007;110:771-779. Level of evidence: I.

A microdose of 17β-estradiol relieves hot flashes
in a significant proportion of postmenopausal
women, found this randomized, double-blind,
placebo-controlled, multicenter trial that
compared a low-dose 2.2 mg 17β-estradiol/0.69
mg levonorgestrel combination transdermal patch
with a microdose 1.0 mg 17β-estradiol
transdermal patch with a placebo patch in healthy
postmenopausal women in 48 centers in the
United States. A total of 425 postmenopausal
women aged 40 years and older (mean age, 52.7
y) were enrolled who had at least 7 moderate or
severe hot flashes per day or at least 50 per week.
The study measured the mean changes from
baseline in frequency and severity of hot flashes
with hormone therapy (HT) compared with
placebo at weeks 4 and 12 of treatment, as well as
the proportion of responders with at least 75% and
90% reduction in frequency of moderate and
severe hot flashes.

Of the total, 145 women received the 17β-
estradiol/levonorgestrel patch, which delivered
0.023 mg/day and 0.0075 mg/day of the drugs,
respectively. There were 147 women who
received the estradiol-only patch, which
delivered 0.014 mg/day of the drug. Placebo
was given to 133 women. The mean weekly
frequency of hot flashes at baseline was similar
for the three groups, as were the mean daily
severity scores.

At week 12, the mean frequency of hot flashes
was significantly reduced in the low-dose group
(–51.80; P < 0.001) and microdose group
(–38.46; P < 0.001) compared with placebo.
Reductions in severity scores for hot flashes
were equally significant in the low-dose and
microdose groups compared with the placebo
group. Reductions in frequency of hot flashes
were larger with the low-dose combination, but
41% of women in the microdose 17β-estradiol
group had a 75% or greater reduction in
frequency of hot flashes from baseline at week
12, and 35% had a 90% reduction in frequency.
In this group, the mean reduction in moderate
and severe hot flashes was 70% after 4 weeks of
treatment and 90% after 8 weeks. The time
frame for the onset of efficacy was similar in the
low-dose 17β-estradiol group. To treat with the
lowest effective dose, the findings support the
notion of starting treatment for hot flashes at the
microdose and then adjusting the dosage upward
if symptom relief is not achieved after 8 weeks.

Comment. In their paper, Bachmann et al report a
significant lowering of hot flashes (at least 7/d or
50/wk) with a microdose of transdermal estradiol
(a patch delivering 0.014 mg/d) with maximum
efficacy at 8 weeks. This is the lowest dose yet
that shows efficacy for hot flashes and suggests
that there is no threshold minimal dose as was
once previously believed. This dose is also known
to protect bone.

The time required to achieve maximum effect is 8
weeks, however, and for some women this may be
unacceptably long. But some patients respond
more quickly so an acceptable reduction may be
seen earlier.

Recent findings about standard-dose HT have
been reassuring, but use of the lowest effective
dose of any medication is an important goal of
clinical practice, presumably because lower doses
are associated with fewer side effects and are
more likely safer.1 Current guidelines around the
world unanimously recommend the use of the
lowest effective dose of HT.

Lower HT doses, when used with adequate doses
of progestogen, have an excellent endometrial
safety profile and in some studies less breast pain.
Surprisingly, in this study breast pain did not
differ between the groups. Microdoses were
associated with less bleeding but the lower dose
was combined with a progestin and only lasted 12
weeks, making comparisons difficult. Some have
suggested that ultralow or microdose estrogen
may not require regular progestogen or that lower
progestogen doses might be safe because little to
no endometrial stimulation is expected at these
doses. The lack of uterine-related consequences of
unopposed ultralow-dose estrogen was
demonstrated in a study of nonhysterectomized
postmenopausal women, aged 60 to 80 years,
receiving unopposed transdermal estradiol (14
μg/d). Compared with placebo, women receiving

estrogen had similar rates of endometrial
hyperplasia, endometrial proliferation, and
vaginal bleeding over the course of 2 years of

The effect of lower estrogen and/or progestogen
doses on breast cancer risk in HT users is
unclear and there is little evidence at this time to
address this important clinical issue. Recent
evidence suggests that ultralow-dose HT has a
neutral effect on mammographic breast density,
which may be a predictor of breast cancer and
make mammographic reading more difficult.3

Overall, low- and ultralow-dose formulations
are increasingly becoming the first choice for
the initial management of menopause-related
symptoms, particularly as women pass from
their most symptomatic phase or, as the authors
point out, wish to restart therapy. Ultralow-dose
regimens may be especially attractive for
relieving menopause-related symptoms as well
as for prevention of bone loss. These factors and
the improved tolerability profile compared with
standard-dose regimens impart a favorable
benefit-risk profile and suggest an important
role for the lowest dose HT regimens in and
postmenopausal management.

Michelle P. Warren, MD
Professor of Medicine and Ob/Gyn
Medical Director, Center for Menopause, Hormone
Disorders, and Women’s Health
Wyeth-Ayerst Professor of Women’s Health
Columbia University
New York, NY
Member, NAMS Professional Education Committee
Member, NAMS Board of Trustees

1. Ettinger B. Personal perspective on low-dosage
estrogen therapy for postmenopausal women. Menopause
2. Johnson SR, Ettinger B, Macer JL, Ensrud KE, Quan J,
Grady D. Uterine and vaginal effects of unopposed
ultralow-dose transdermal estradiol. Obstet Gynecol
3. Boyd NF, Rommens JM, Vogt K, et al. Mammo-
graphic breast density as an intermediate phenotype for
breast cancer. Lancet Oncol 2005;6:798-808.

Thursday, December 13, 2007

Hear Better with Hormones

Here are some recent articles showing that women on hormone therapy have better hearing than women who do not take hormones. What?! This is part of my crusade to make sure women are careful to get a nuanced view of whether they would benefit from hormones, rather than the over-simplified view that all hormones are bad. Hormones, taken at the lowest doses and preferably bioidentical, can be safe and life-altering. They've been proven to help mood, libido, vasomotor symptoms, and now HEARING!

Acta Otolaryngol. 2007 Feb;127(2):149-55. Hearing in women at menopause. Prevalence of hearing loss, audiometric configuration and relation to hormone replacement therapy. Hederstierna C, Hultcrantz M, Collins A.

Department of Audiology, Karolinska University Hospital, Stockholm, Sweden.

CONCLUSION. Hormone replacement therapy (HRT) may have a protective effect on hearing impairment in postmenopausal women. New guidelines for classification of audiometric configuration in age-related hearing loss are suggested. OBJECTIVES. To describe prevalence of hearing loss and audiometric configuration in a group of middle-aged women with respect to menopausal stage and HRT. SUBJECTS AND METHODS. A total of 143 women around menopause were sampled through the Swedish population register. The mean hearing threshold levels were compared according to menopausal status. The audiograms in the 57 women with hearing loss were classified according to audiometric configuration. RESULTS. In all, 57 women (40%) had any kind of hearing loss; 42 had very minute hearing loss; 15 had a 4FA (average of thresholds at 0.5, 1, 2, and 4 kHz) of at least 20-39 dB HL in at least one ear. Two of these had a 4FA of 40-69 dB HL in at least one ear. The most common configurations were: gently sloping (47%), steeply sloping (14%), and high-frequency U-shaped (14%). The postmenopausal women who were not on HRT had poorer hearing mainly at 2 and 3 kHz, compared with pre- and perimenopausal women, and postmenopausal women on HRT.

Acta Otolaryngol. 2006 Jan;126(1):10-4. Estrogen and hearing: a summary of recent investigations.
Hultcrantz M, Simonoska R, Stenberg AE.

Department of Otorhinolaryngology, Karolinska University Hospital, Stockholm, Sweden.

Is the female sex steroid estrogen the key to preserved hearing in the aging human? This question remains unanswered, but hearing loss is more profound in elderly males than females. There are also well-known sex differences in the auditory brainstem response (ABR), i.e. women have shorter latencies than men. Moreover, menopausal women who are administered hormone replacement therapy have slightly better hearing than those who are not, and women with Turner's syndrome (45,X), who are biologically estrogen-deficient, show longer ABR latencies and early presbyacusis. These findings are also supported by animal experiments. When boosted with estrogen or testosterone the non-reproductive female midshipman fish alters its inner ear auditory mechanism so that it can hear the male's hum-like call. If estrogen receptor beta is knocked out in mice, severe progressive hearing loss occurs, leading to early deafness. In apparent contradiction to these findings, there have been case reports suggesting that hormone replacement therapy and oral contraceptive use can lead to hearing loss, but of another type, namely acute sudden deafness. Such contradictory aspects of the action of estrogen are commonly found and may spring from the fact that there are two estrogen receptors, alpha and beta, both of which are present in the inner ear of mice, rats and humans. Knowing how sex steroids can alter hearing ability may give important clues as to how estrogen can preserve hearing in humans. In this review we present a summary of current knowledge about hearing and estrogen.

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I'm an organic gynecologist, yoga teacher + writer. I earn a living partnering with women to get them vital and self-realized again. We're born that way, but often fall off the path. Let's take your lousy mood and fatigue, and transform it into something sacred and useful.