Thursday, December 27, 2007
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
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.
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
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.
Thursday, December 20, 2007
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
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: www.shaklee.net/DrGottfried
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
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-
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
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.
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.
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
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
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
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
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
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. firstname.lastname@example.org
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. email@example.com
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.
Friday, November 23, 2007
Here's the link to the article:
Wednesday, November 21, 2007
STUDY RESULTS--Penn researchers use brain imaging to demonstrate how men and women cope differently under stress
**Findings have implications for identifying gender differences in mood disorders
PHILADELPHIA – According to a study that appears in the current issue of SCAN (Social Cognitive and Affective Neuroscience), researchers at the University of Pennsylvania School of Medicine discuss how men and women differ in their neural responses to psychological stress.
“We found that different parts of the brain activate with different spatial and temporal profiles for men and women when they are faced with performance-related stress,” says J.J. Wang, PhD, Assistant Professor or Radiology and Neurology, and lead author of the study.
These findings suggest that stress responses may be fundamentally different in each gender, sometimes characterized as “fight-or-flight” in men and “tend-and-befriend” in women. Evolutionarily, males may have had to confront a stressor either by overcoming or fleeing it, while women may have instead responded by nurturing offspring and affiliating with social groups that maximize the survival of the species in times of adversity. The “fight-or-flight” response is associated with the main stress hormone system that produces cortisol in the human body – the hypothalamic-pituitary-adrenal (HPA) axis.
Thirty-two healthy subjects – 16 females and 16 males – received fMRI (functional Magnetic Resonance Imaging) scans before, during and after they underwent a challenging arithmetic task (serial subtraction of 13 from a 4 digit number), under pressure. To increase the level of stress, the researchers frequently prompted participants for a faster performance and asked them to restart the task if they responded incorrectly. As a low stress control condition, participants were asked to count backward without pressure.
The researchers measured heart rate, cortisol levels (a stress hormone), subjects’ perceived stress levels throughout the experiments, and regional cerebral blood flow (CBF), which provides a marker of regional brain function. In men, it was found that stress was associated with increased CBF in the right prefrontal cortex and CBF reduction in the left orbitofrontal cortex. In women, the limbic system – a part of the brain primarily involved in emotion – was activated when they were under stress. Both men and women’s brain activation lasted beyond the stress task, but the lasting response in the female brain was stronger. The neural response among the men was associated with higher levels of cortisol, whereas women did not have as much association between brain activation to stress and cortisol changes.
“Women have twice the rate of depression and anxiety disorders compared to men,” notes Dr. Wang. “Knowing that women respond to stress by increasing activity in brain regions involved with emotion, and that these changes last longer than in men, may help us begin to explain the gender differences in the incidence of mood disorders.”
Sunday, November 18, 2007
Don't do it, Girlfriend!
While sometimes there is a time and a place for a birth control pill, this is not one of them.
Acne is usually due to an imbalance in the family of hormones called androgens, which include testosterone and DHEA among others. We think of androgens as "boy" hormones, but women have and need levels in their blood (although only about a tenth of those in men). We know that testosterone is crucial for women's maintenance of mood, sense of well-being and to see a decent response in the body to exercise. We're not talking Barry Bonds levels - we're talking testosterone and DHEA in balance such that it is not too high and not too low.
Many of us find more zits on our skin as we enter peri-menopause, which can feel like puberty in reverse. It's especially fun when you are sharing your anti-acne skin-care products with your kids.
What causes acne?
Step 1: stimulation of the oil-making (sebaceous) glands by testosterone.
Step 2: the pores get plugged and trap the oil inside. Bacteria grow in the trapped oil, causing the production of irritants.
Step 3: your immune system finds out. Like with most things in the body, this is good and bad news. Your army of immune cells fights the bacteria, and that renders the redness, swelling, pus-like fluid and later scarring. Pretty! This is the part we would all love to skip.
Most women notice that their acne is worse in the week before their period. We believe this is related to your testosterone peak at day nine but the mechanism is not well understood.
If have "bumps" as my older daughter calls them and are reading this post, it is likely that the standard approaches have not cleared your skin. Good news here: treatments aimed at the hormonal cause often work when standard ones have not.
One specific type of hormonal imbalance associated with acne that deserves mention is the poorly-named polycystic ovarian syndrome or PCOS, a common disorder in reproductive-aged women. One of the main symptoms of PCOS is testosterone-induced skin and hair changes, which include acne, hirsuitism (increased facial and/or body hair) and sometimes scalp hair loss or thinning. Other symptoms are irregular periods or anovulatory (no ovulation to the rest of us) cycles, difficulty controlling weight and metabolic changes such as insulin resistance. Female acne can be a sign of PCOS. If you have some of these additional symptoms, consider getting evaluated for PCOS.
On the other hand, many women with hormonal acne have just simple acne, nothing else, and benefit from a hormonal assessment (usually saliva or blood testing), and balancing of any existing hormonal disorders with bioidenticals. While it is true that a birth control pill will lower your testosterone and make your skin more clear, it also lowers your libido and may have long-term risks associated with synthetic hormones.
Many of you know that I am a follower of Nourishing Traditions, the way of eating that is based on the work of Weston Price and I believe helps us restore hormone balance and keep our kids healthy. Below is a fervent call to ask you to help our crusade to save raw milk in California from a new bill that will remove it from our grocery shelves. Please take a few moments like I have to write or email the Governor or just read about the health benefits of raw milk. Below is a letter from Kris Brewer who brought this important fight to my attention. If you want to read more about raw milk and its many positive effects, check out:
Hello friends et al,
I am disturbed by recently passed legislation that, effective January 2008, will eliminate consumer access to raw organic milk. My family and I drink this daily and since we started drinking it, my youngest has ceased having terrible asthma, and my husband's hands and feet no longer ache from rheumatoid arthritis! As many of you know, there are many benefits to consuming raw milk and many health problems linked to drinking pasteurized milk.
I am working actively to get the word out to help fight/reverse this legislation which was passed in secret without the input of the small, organic raw dairy farmers or consumers. I am in touch with Colette Cassidy, of Claravale Dairy (small, 55 cows, supplying clean raw milk for 80 years) about the crisis at hand and gathering information from various sources. I want to strongly encourage people to speak up and act NOW before we can no longer get this milk in the stores. Below are some important links on this-
Thanks for your timely reading, acting and passing this on to others.
Kris Richardson Brewer
Representing Bay Area Raw Milk Consumers
HERE IS AN EXCERPT OF THE LATEST UPDATE FROM MARK MCAFEE (President of Organic Pastures Dairy)--
"In California, raw milk is a sacred food. The consumption of raw milk is an intentional act and not done by error or mistake. Consumption of raw milk is a freedom preserved by longstanding California Food and Agriculture Code #35928 (F). This venerable raw milk law makes restriction of California raw milk illegal. Our arguments stand on solid ground. Even though the CDFA has promised full cooperation, it is still early in this process and many turns lay ahead. Look for updates on this historic showdown, and keep supporting the struggle to protect your fundamental right to eat any whole, unprocessed, natural food of your choosing. In another secret legislative process earlier this year, you lost your right to buy truly raw almonds at the grocery store. Let this not be the year we also lose raw milk! "
My husband and I were reading the New York Times this morning, which is to say that we were getting about one minute of focused concentration before our toddler would need us. We felt that much of our mounting alarm and wish for expeditious intervention to lessen climate change was reflected in a new document (check it out at nytimes.com/dotearth) called the Synthesis Report of the United Nations Intergovernmental Panel on Climate Change.
What inspired me about the article on page 3 of the front sections were the following:
1. The synthesis report was approved by 130 nations. That's not easy when you are aware of the science involved.
2. It is personal -- the cost of action is less than the cost of inaction, to paraphrase Jeff Sachs of Columbia University's Earth Institute. We need to get rid of our two cars (and just keep the Prius), we need to make our homes energy-efficient, we need to walk and bike when we can, we need to think carefully about our consumption and it's effect on climate change, we need to figure out how best to model this for our kids and encourage them to join us on the path of earth stewardship. We need to find ways to integrate social justice into the movement so it's not just the upper classes who are able to afford to "green" their homes, lives and closets.
3. Achim Steiner - head of the UN Environment Program - wants this message sent to individuals and not just world leaders: "What we need is a new ethic in which every person changes lifestyle, attitude and behavior."
My husband and I have been paying a lot of attention to "greening" our lives over the five years we've been together. He regularly uses a tool he invented from his developer days -- a "Life Balance Sheet" as a way of benchmarking his place in the world and how he's contributing to the triple bottom line of green. We are deep in the design of a deep-green remodel of a small bungalow in our hometown of Rockridge here in Oakland. We are trying to be mindful of our mutual tendencies to be overachieving and under-relaxed, and how this affects our health, connection and our kids. This is my corner - the intersection of health and green. We are lessening our carbon footprint, although some experiments are more successful than others.
Meanwhile, the UN report pumps up the urgency. I would love to hear from other moms, yoginis and fellow warriors who have figured out how to lessen the carbon footprint of driving our beautiful kids many miles to the glorious schools we've chosen for them. I've found carpooling to be much harder to pull off than it should be -- perhaps again getting to Mr. Steiner's comment about us needing a new ethic of lifestyle, attitude and behavior, so that driving our kids to school is less about our individual needs, schedule and convenience, and more about modeling for our kids our willingness to try new things to do our part in reducing climate change.
Get inspired, do your part. Walk the talk. Tell us about it. Namaste and blessings, SG.
Friday, November 16, 2007
We have more data now on the ongoing body of work on whether the synthetic hormones in birth control pills cause breast cancer. You'll notice in my other blog a recent study showing an increased risk (http://menopause.zaadz.com/blog/2006/12/the_pill_linked_to_premenopausal_breast_cancer). In the spirit of unbiased opinion -- here is a recent study showing no increased risk, although remember that The Pill is proven to lessen libido.
Do Oral Contraceptives Affect Risk for Death from Breast Cancer?
OC use had neither a beneficial nor a harmful effect on breast cancer mortality.
The relation between oral contraceptive (OC) use and breast cancer risk remains under constant surveillance. To study the effects of OC use on risk for death from breast cancer, investigators analyzed cancer registry data from the Surveillance, Epidemiology, and End Results Program in conjunction with linked data from the population-based, case-control Cancer and Steroid Hormone (CASH) study. Fifteen-year survival was assessed in 4292 women who had been diagnosed with breast cancer and who were interviewed about reproductive contraceptive and disease history, family history, and personal characteristics and behaviors during the CASH study (conducted from 1980 through 1982).
During the 15-year follow-up, 1473 of the women died from breast cancer; 80% survived for 5 years, 70% for 10 years, and 64% for 15 years. Compared with women who had never used OCs, the relative risk for death from breast cancer in ever-users was less than 1.0 (adjusted hazard ratio, 0.94; 95% confidence interval, 0.83–1.06). Neither duration of use nor age at first use affected the risk for death from breast cancer. Adjusted analysis showed that stage of disease at diagnosis did not affect the relation between breast cancer mortality and time since first and last use of OCs. Women who were currently using OCs at diagnosis had a statistically insignificant adjusted HR of 0.90.
Comment: These researchers did not address the association between oral contraceptive use and breast cancer diagnosis but rather the effect of OCs on breast cancer mortality. One limitation of the study is that it did not take into account estrogen- or progesterone-receptor status or the presence of BRCA mutations or HER2/neu _expression. Nonetheless, these results provide reassurance that prior use of OCs is not associated with increased mortality from breast cancer.
— Sandra Ann Carson, MD
Published in Journal Watch Women's Health November 15, 2007
Wingo PA et al. Oral contraceptives and the risk of death from breast cancer. Obstet Gynecol 2007 Oct; 110:793.
Original article (Subscription may be required)
Medline abstract (Free)
Monday, November 12, 2007
Here are some new studies on natural therapies for menopause symptoms as well as bacterial vaginosis (BV), with commentary from Toni Hudson, ND.
Black Cohosh, with or without St. John's wort and menopause symptomsBriese V, Stammwitz U, Friede M, Henneicke-von Zepelin H. Black cohosh with or without St. John's wort for symptom-specific climacteric treatment-Results of a large-scale, controlled, observational study. Maturitas 2007; 57(4):405-414.
6141 women at 1287 outpatient gynecology offices were treated with recommended doses of Remifemin (an isopropanol extract of black cohosh), 1 cap bid, or Remifemin in combination with St. Johns wort, 1 or 2 tablets bid, at the discretion of the clinician.
Treatment responses were assessed using the menopause rating scale (MRS), an established standard symptom rating scale for evaluating menopausal symptoms. The primary effectiveness variable was the change in the MRS subscore of psychological symptoms (including depressive mood, nervousness, irritability, impaired performance and memory) from baseline to month three.
Of the enrolled women, 3027 received the black cohosh only, and 3114 received the black cohosh/St. John's wort combination. During the study, 244 women changed treatment from monotherapy to the combination product, and 87 women changed from the combination product to monotherapy.
The differences in baseline symptoms between the two treatment groups indicate different indications for use. Prior to treatment, the women receiving the combination therapy had significantly worse psychological symptoms than those in the black cohosh only group. The symptoms in both groups were mostly mild to moderate and mostly included hot flushes, sleep disorders, nervousness and depressive mood, which were moderate in severity.
The symptom scores improved in both groups. The changes in the psychological symptoms were greater in the combination therapy group than in the black cohosh only group at months 3 and 6. With both treatments, the greatest effects were seen with hot flashes and night sweats. Improvements in symptoms were evident at month 3, and were greater at month 6.
Both treatments were very well tolerated. The rate of adverse events related to the treatments was very small, at 0.16% or 10 cases. Seven cases were in the black cohosh only group and three were in the combination group.
Commentary: The results from this large study support the effectiveness of black cohosh preparations alone or in combination with St. John's wort for relief of common menopausal symptoms such as hot flushes, nightsweats and psychological symptoms. The combination of the two herbs appears to be the best approach for menopausal symptoms that include depressive moods, nervousness, irritability, and impaired memory.
Soy nuts and menopause symptoms
Welty F, Lee K, Lew N, et al. The association between soy nut consumption and decreased menopausal symptoms. J Women's Health 2007;16(3):361-369
Sixty postmenopausal women were randomized in a crossover trail to either a therapeutic lifestyle changes (TLC) diet alone or a similar TLC diet which included one-half cup soy nuts containing 25 grams of soy protein and 101 mg of isoflavones, divided into 3-4 doses throughout the day. For each 8-week time period, study subjects recorded the number of hot flashes.
In women with more than 4.5 hot flashes per day, the TLC diet plus soy nuts was associated with a 45% decrease in hot flashes, when compared to the TLC diet alone. With treatment, there were 4.1 hot flashes per day in the TLC plus soy nut group vs. 7.5 hot flashes per day in the TLC diet alone group. Soy nuts were also associated with a significant improvement in other menopausal quality of life issues including psychosocial symptoms.
Diet and the presence of bacterial vaginosis (BV) was studied in a subset of 1521 women, 86% of whom were African American, from the Longitudinal Study of Vaginal Flora. Women were assessed at baseline and quarterly for one year for up to 5 visits. Vaginal flora was evaluated by Gram stain according to Nugent criteria. The Nugent score is derived from estimating the relative proportions of bacterial morphotypes to give a score between 0 and 10. A score of <4>6 is bacterial vaginosis. BV was defined as a Nugent score > 7 while severe BV was defined as a Nugent score of > 9 and with vaginal pH of > 5. At each visit, patients also completed a questionnaire and had a standard pelvic exam. Dietary analysis was conducted by the Block Dietary Data Systems, which analyzes for energy, nutrients, and various vitamin and mineral intakes.
The prevalence of BV was 41.8% and severe BV, 14.9%. Both BV and severe BV were significantly more prevalent in African-Americans than in Caucasians.
After adjusting for demographic and behavioral variables, total energy intake was 50% higher in those with BV, yet still only marginally associated with BV. Only total fat intake was significantly associated with BV. Total fat, saturated fat and monounsaturated fat intakes were significantly associated with severe BV. Protein intake was significantly inversely associated with severe BV.
There were significant inverse associations between severe BV and the intakes of folate, vitamin E and calcium. When the 17.6% of women who had persistent BV were compared with the 15.2% who had remitting BV, none of the macro- or micronutrients was significantly associated with the overall incidence of BV
Commentary: This was the first study that I have seen that has evaluated the relationship between BV and total nutritional intake. In this study, total fat intake was a significant predictor of BV. The risk of severe BV was more than twice as high in women who were in the highest quartile of intakes of total fat, saturated fat and monounsaturated fat.
Previous studies that looked at the relationship between BV and specific micronutrients such as vitamins C and A have shown no significant association. In the current study, the most striking finding was the relationship between dietary fat and BV. The mechanism for this is unclear but a high fat intake, especially saturated fat, may alter vaginal microflora and increase vaginal pH, which would then increase the risk of BV. Another possible mechanism may be explored by looking at the role that high fat intake has on intestinal mucosa. We have other evidence that high fat intake modulates immune function in the intestinal mucosa. It is plausible then that high dietary fat intake may affect the mucosal immune system in other parts of the body, such as the vagina, and by doing so, may increase the risk of BV.
May 2006, Vol. 2, No. 3, Pages 459-477
Testosterone and libido in surgically and naturally menopausal women
Jeanne L Alexander 1, Lorraine Dennerstein 2, Henry Burger 3 & Alessandra Graziottin 4,5,6
1Kaiser Permanente Medical Group of Northern California Psychiatry Women’s Health, Kaiser Permanente Medical Group, 1700 Shattuck Avenue, Suite 329, Berkeley, CA 94709, USA. firstname.lastname@example.org
2Office for Gender and Health, Department of Psychiatry, The University of Melbourne, 4th Floor, 766 Elizabeth Street, Melbourne, VIC 3010, Australia. email@example.com
3Prince Henry's Institute of Medical Research, Monash Medical Center, Clayton, VIC, Australia. firstname.lastname@example.org
4Center of Gynecology and Medical Sexology, Hospital San Raffaele Resnati, Milan, Italy
5Department of Obstetric and Gynecology, University of Florence and Parma, Italy
6Post-graduate Course in Sexual Medicine, University of Florence, Italy.
† Author for correspondence
The assessment and then treatment of a change in libido, or a change in the desire to partake in sexual activity, during the menopausal transition and beyond has been a challenging and elusive area of clinical research. This is partly due to the multidimensional nature of female sexuality, the difficulties of measuring testosterone in women in a reliable and accurate manner, and the complexity of the neurobiology and neurobehavior of female sexual desire. In addition, there is a lack of evidence for diagnostic specificity of low free testosterone levels for the symptom of low libido in women for whom there are no confounding interpersonal or psychological factors; although, in the symptomatic population of surgically or naturally menopausal women, a low level of free testosterone often accompanies a complaint of reduced desire/libido. The randomized clinical trial research on testosterone replacement for naturally and/or surgically menopausal women with sexual dysfunction has been criticized for a high placebo response rate, supraphysiological replacement levels of testosterone, the perception of modest clinical outcome when measuring objective data such as the frequency of sexual intercourse relative to placebo, and the unknown safety of long-term testosterone replacement in the estrogen-replete surgically or naturally menopausal woman. A careful review of current evidence from randomized, controlled trials lends support to the value of the replacement of testosterone in the estrogen-replete menopausal woman for whom libido and desire has declined. The issue of long-term safety remains to be answered.
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