Hormones, Estrogen, and Menopause (Alternative Medicine Book 12)

Where to get it: May present estrogenic actions and is an herb for hot flashes, especially relevant in hot flashes leading to insomnia. May present estrogenic actions especially relevant in hot flashes, excessive sweating, heart palpitations, and panic, making it another great herb for menopause and natural remedy for hot flashes.

Has estrogenic effects on endometrial and breast cancer cells in vitro. Contains isoflavones similar to soy. Organic Red Clover Capsules. This North American native wildflower has long been used, and is widely currently used, for menopausal symptoms, including hot flashes, menstrual disorders including amenorrhea, and PMS. It is not clear whether black cohosh has an actual estrogen effect in the body or whether it mimics estrogen or works in an altogether different manner as a natural remedy for menopause.

Organic Black Cohosh Capsules. Is high in lignans phytoestrogens. Easy to include in the diet, flax reduces total and LDL cholesterol. An excellent adrenal support herb, licorice is soothing and anti-inflammatory and makes a good tier 3 corollary herb for menopause, but because it can cause water retention and high blood pressure, it should not be used long-term as a natural menopause supplement nor by those with hypertension.

Organic Licorice Root Capsules. The following herbs have traditionally been used to support progesterone-like effects in the body although neither directly increases progesterone. Further study and work with a phytotheraphy professional is needed. Contains the sterol saponin, which resembles progesterone but cannot be converted naturally by the body into progesterone.

Unclear whether internal natural wild yam herbal remedies taken for menopause can increase progesterone in the body; its action may lie in its influence on other endocrine organs or systems. Organic Wild Yam Tincture. This natural menopause supplement, can be taken long-term for anxiety associated with PMS or menopause, but is contraindicated in pregnancy.

Soy also contains the saponins that resemble progesterone, though soy is most commonly used to increase estrogen. Organic Vitex Chaste Tree Phytocapsules. When the endocrine system registers an emergency or a stressful situation, it responds with the self-protective symptoms including increased heartbeat, pupil dilation, redirection of blood and energy from the periphery to the heart, rapid breathing, and muscle contractions; afterward, the person experiences fatigue and confusion.

The hormone-secreting adrenals are already under excessive stress since the ovaries have ceased producing their fair share of estrogen and progesterone. Typical perimenopause symptoms such as hot flashes, rapid heart beat, vaginal dryness, sweating, rapid breathing, muscle aches, confusion or mental fog, and fatigue can often be explained by adrenal stress.

It makes sense to approach issues of perimenopause as if you were addressing adrenal insufficiency —with adrenal supportive and adaptogenic natural remedies for menopause and stress that nourish and tone the endocrine system. Also called Siberian ginseng, this herb is generally used for stamina and endurance and to support the immune system. It is an effective choice for menopausal women undergoing an extreme transition and feel exhausted or depleted, or who are at risk for contracting viral or bacterial infections. A number of recent studies have aroused concern over the effect of menopausal HT on breast tissue density.

In women not on HT, breast density has been found to be an independent risk factor for breast cancer Hormone therapy has been found to increase breast density, with the greatest increase in women on conjugated estrogen and progesterone Although an association between breast density and breast cancer has not been seen in women on HT, there has been some concern that mammograms may be less effective in women on HT with greater breast density. However, Rutter et al. Therefore, until this issue is better understood, it may be advisable for women to discontinue HT for two weeks before a mammogram exam, especially in the case of prior problematic mammograms.

Evidence suggests, however, that estrogen plus progestin may have an impact on breast cancer. This risk amounted to approximately 8 more women per 10, being diagnosed with breast cancer compared to those on placebo It is important to note, however, that the average age of women in this study was It is important to note though, that women taking estrogen only had a significantly lower increase in risk compared with women taking both an estrogen and progestogen.

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It is an important to recognize that this was an observational study only and hence has a larger potential area for error. Although there is some evidence that combination therapy may increase risk of breast cancer above that of estrogen alone, neither a protective, nor a detrimental effect has been demonstrated convincingly, particularly for younger, healthier women. One study interviewed nearly women with and without breast cancer and found a significant correlation between use of continuous combined replacement therapy and breast cancer However, the risks were higher in thin women than in heavier women which may confound the results.

Also, it is possible that the use of cyclic therapy could provide the additional risk, and HT was generally given at higher doses that are rarely used today. One hypothesis to explain this observation is that HT may promote the development of slow-growing tumors or discourage the development of more aggressive tumors. It has also been posited that better screening of these women leads to lower mortality rates. The argument that menopausal HT should not be given to women who have a personal history of breast cancer may seem reasonable based on evidence that breast cancer is a hormone responsive tumor.

However, while women with a first-degree relative mother, sister, or daughter who has or had premenopausal breast cancer are at increased risk by virtue of their family history alone, their risk of breast cancer is not thought to be increased further by HT use. Eighty percent of women who develop breast cancer do not have a family history. This is supported by the findings of Rebbeck et al. HT use did not negate the observed reduction in cancer risk. Interestingly, studies of breast cancer survivors showed that women using HT had a lower risk of recurrence compared to survivors not using HT , Breast cancer incidence is thought to increase after hormone use and since WHI there has been much interest on the role of the progestin in combination with estrogen in contrast to the use of estrogen alone 13, 14, In general most studies that have shown a small increase have shown more of an effect with the combination 26 and nurse health and collaborative study.

This has led to speculation as to the role of progestin, and to the minimization of progestin use despite the well-recognized and significant risk of endometrial cancer with the use of unopposed estrogen. Some recent studies suggest the progesterone and dydrogesterone may be safer than other progestins but no randomized studies examine this question In general, some effect is seen with treatment duration and some studies show an effect although small.

WHI reported an increase in breast cancer risk in the combined therapy arm in subjects who had used hormones prior to enrollment but only after 5 years A later paper from the WHI study however suggested that the risk was higher in women who initiated therapy soon after menopause within 3 to 5 years However, in this study, a much larger group of women who were recently menopausal had been on HT and the effect was more pronounced in the less rigorous observational arm. In general the effect takes several years to appear and is small.

When hormones are discontinued the effect starts to decline within one year All of this confusing and contradictory data suggests that the combined HT may be acting as a promoter in susceptible women with undiagnosed subclinical cancer and the promoter effect may disappear with discontinuation of therapy. This may also explain the overall drop in breast cancer seen with the Seer Surveillance, Epidemiology and End Result cancer registries database report.

This report showed a drop in breast cancer rates after when women stopped hormone therapy after the WHI publications This effect has not been seen universally and the trend was actually seen prior to the reports. In fact there has been a drop in many different cancer rates, possibly due to earlier detection and earlier treatment However this effect was not seen in WHI.

Both combined hormone use and estrogen alone lead to denser breasts and more abnormal mammograms , This effect is rapidly reversible and stopping hormones 10 to 30 days before a mammography may decrease abnormalities requiring follow up One group of women who benefit from hormone therapy is the women with BRAC 1 and 2 mutations who undergo oophorectomy as prophylaxis.

Use of HT does not appear to place them at risk for the genetically determined breast cancer and will improve quality of life It will also prevent the effects of estrogen deprivation at a young age. The effects of stopping hormones are contradictory depending on the study. Breast cancer prognosis does not appear to be influenced by the high hormone levels during pregnancy, nor has oral contraceptive use been shown to increase breast cancer risk. These observations may allay some of the fear regarding the use of exogenous hormones after menopause.

Data on ovarian cancer has not shown a consistent risk with use of hormone therapy. There is possible weak association with long term at least 10 years of therapy but data are inconclusive for recommendations Its use does not adversely affect the risk of cancer in BRCA mutations Other studies too, including HERS and a meta-analysis of 15 case-controlled studies found no significant association In , 38, cases of endometrial cancer were diagnosed, and 6, women died of the disease. The mean age at diagnosis is 61 years, with most cases occurring in women 50 to 59 years old.

Estrogen alone causes endometrial hyperplasia and a two to three-fold increase in the risk of endometrial cancer. However, the addition of progestogen reduces this risk to lower levels than those seen in women not on HT , Thus, the addition of a progestational agent to postmenopausal estrogen therapy is now standard for women with an intact uterus.

While there have been some reports that the risk of endometrial cancer may be slightly increased even with the combined therapy, most studies have not confirmed this. Women in the WHI study on combined therapy showed no difference in endometrial cancer rates compared to women on placebo Recent research has focused on the use of lower doses of estrogen and a progestogen in HT to reduce the risk of endometrial cancer The dose of progestogen given depends on several factors, including the number of days given each month, the amount of estrogen given, the individual needs of the patient, and her ability to tolerate the medication.

Side effects of progestogen can include anxiety, irritability, depressed mood, acne, bloating, fluid retention, headaches, breast tenderness, and bleeding problems. The inability to tolerate these effects is the main reason for poor compliance or discontinuation of HT. Despite being one of the major causes of cancer-related mortality in women, colon cancer is often overlooked by patients in their risk assessment of HT.

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In addition, reports from the WHI study showed that the combined estrogen plus progestin therapy was associated with a decrease in the incidence of colon cancer compared to women on placebo 6 fewer cases per 10, women on HT This was not found with estrogen alone At present; however, although the evidence that HT may be beneficial in reducing the risk of colon cancer should be considered, there is insufficient evidence to warrant recommending long-term HT solely for this purpose. The existence of estrogen receptors in the hippocampus, a part of the brain essential to learning and memory, has been known for some time.

Several mechanisms may account for the effects of estrogen on the brain. Firstly, estrogen increases levels of choline O-acetyl-transferase, the enzyme needed to synthesize acetylcholine, a neurotransmitter thought to be critical for memory Studies on healthy middle-aged and elderly postmenopausal women have supported the theory that estrogen may help to maintain aspects of cognitive function , Data also suggest that estrogen therapy may enhance short- and long-term memory , Additional effects of estrogen on neural function include: A recent review of clinical trials of hormone therapy suggest that there is a clear difference between the effects of estrogen therapy and estrogen plus progestin There is modest support for the beneficial effect of estrogen alone on verbal memory in women under 65, and possibly surgically menopausal, while a harmful effect is seen with estrogen plus progestin in women over Conjugated estrogen with medroxyprogesterone acetate may also have some detrimental effect on younger women.

Estrogen alone appears to be neutral in women over Thus the age of initiation of therapy and the use of progestins are important when evaluating possible effects on verbal memory At present there is no combination which appears to be neutral to verbal memory and there is suggestion of some harm even with micronized progesterone Hot flashes appear to relate to memory dysfunction, and some of the cognitive improvement on hormone therapy may relate to the treatment of the hot flashes For every five years after the age of 65, the prevalence of Alzheimer's disease doubles in the population.

As the population ages over the next 20 years, these numbers are expected to increase. According to epidemiologic evidence, there is reason to believe that estrogen deficiency may contribute to Alzheimer's disease. Low body weight is associated with low levels of circulating estrogens in postmenopausal women. Women who suffer from Alzheimer's disease tend to have lower body weights than women without the disorder Incidences of Alzheimer's disease are low or its expression is delayed in postmenopausal women with high levels of endogenous estrogenic steroids or those receiving long-term HT.

One explanation for estrogen's apparent protective effect may involve neurotransmission. Estrogen acts as a trophic factor for cholinergic neurons in vitro. Cholinergic depletion is the most prominent neurotransmitter deficit in Alzheimer's disease. However, while HT does show promise in preventing or delaying the onset of the disease, a recent study showed no benefit of either 0. Most likely, estrogen may merely delay the deterioration seen in Alzheimer's patients.

The effect of HT on different subtypes of dementia could not be determined because the number of cases was too small. It must be noted, however, that because the WHIMS participants were all 65 or older, these results may not apply to women who initiate HT at a younger age. The results of the Cache County Study serve to further confuse the issue. In this prospective study of incident dementia in older women mean age For current users with more than 10 years of therapy the HR was 0. Interestingly, in past users, reductions were present in all age groups and showed a duration effect HR 0.

The Nurses' Health Study showed a twofold increase in the risk of pulmonary embolism among postmenopausal women who were current estrogen users. The recent findings of the WHI study confirmed these findings for women on combined estrogen plus progestin therapy. Women on this treatment suffered 8 more pulmonary emboli per 10, than women on placebo Although estrogen use has been associated with an increase in the relative risk of venous thromboembolism VTE , the absolute risk remains low, as VTE occurs infrequently in this setting.

Women on combined estrogen-progestin therapy in the WHI study suffered 18 cases of more venous thromboembolism than women on placebo. It does, however, show that patients should be screened for a history of idiopathic thrombosis as this has been a consistent finding Some epidemiologic studies have found an increased risk of gallstones among women who use HT.

Estrogen has been shown to increase cholesterol saturation of bile, alter bile acid composition, and decrease bile flow.

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Each of these effects can enhance gallstone formation. Data from the Nurses' Health Study 54, postmenopausal women monitored for eight years showed that current HT users were more likely to have undergone cholecystectomy than nonusers relative risk, 2. This risk tends to increase with long-term therapy and with high doses of estrogen Because many women gain weight as they age, a common fear is that HT will exacerbate this problem. However, this is unconfirmed by prospective studies. Attention to diet with reduced fat intake and regular aerobic exercise for weight maintenance should be recommended to all postmenopausal women.

Data from WHI also showed an attenuation of increases in weight seen with age in the combined hormone treated arm This suggests there may be some beneficial effect to HT on the normal increases that are seen in postmenopausal women and that the effect may protect against the increase in central obesity seen in hypoestrogenic menopausal women.

A decrease in the incidence of diabetes, and lower insulin levels suggestive of better insulin sensitivity may be related to this attenuated weight gain. Some studies have shown a small reduction in the incidence of this eye disorder among users of HT , It is thought that skin may be an important target organ for reproductive hormones. In postmenopausal women, dermal collagen decreases, and skin becomes thinner.

Applying estrogen cream to the skin after menopause improves the external appearance of facial skin. In addition, systemic HT increases dermal collagen and limits age-related skin extensibility. To date, of the eleven clinical trials that examined the effect of HT on collagen levels, only one failed to demonstrate efficacy Furthermore, results from a recent study indicates that estrogen also increases skin thickness HT has also been shown to accelerate cutaneous wound healing, both microscopically and macroscopically, in postmenopausal women This study also showed delayed repair of acute incisional wounds in ovariectomized young female rodents; the delay was reversed by the topical application of estrogen.

The risk of tooth loss increases after menopause.

Osteoporosis, as well as estrogen deficiency, could both be contributing to this effect. Data from the Nurses' Health Study indicate that the risk of tooth loss may be decreased in women with a history of estrogen therapy Several treatments have recently become available and have FDA approval for relief of vasomotor symptoms. A progestin is not necessary as this combination offers endometrial safety , Another SERM ospemifene has been approved for the treatment of postmenopausal vulvovaginal atrophy Another treatment consists of a Swedish pollen extract femal, which has been shown to be effective in a small study for a composite of menopausal symptoms including vasomotor symptoms, fatigue and quality of life Over the years, doses of estrogen in hormone therapy have been decreasing: Today, a CE dose of 0.

The goal of hormone therapy is to reduce menopausal symptoms e. Use of the lowest clinically effective dose of HT for relief of menopause-related symptoms and for prevention of osteoporosis is now recommended. The benefit-risk ratio of hormone therapy for each woman is influenced by the severity of her menopausal symptoms and their impact on quality of life, her current age, age at menopause, time since menopause, cause of menopause, and baseline disease risks.

Generally appropriate indications include also treatment or prevention of osteoporosis in women who are not candidates for or cannot tolerate other osteoporosis therapies including bisphosphonates or teriparatide. Absolute contraindications for systemic HT include hormone-related cancer, active liver disease, history of hormone-induced venous thromboembolism, history of pulmonary embolism not caused by trauma, vaginal bleeding of unknown etiology, and pregnancy.

Relative contraindications include chronic liver disease, severe hypertriglyceridemia, endometriosis, history of endometrial cancer, history of breast cancer, coronary artery disease. Guidelines for hormone use are reviewed in the statement of the North American Menopause Society and recently by the Endocrine Society Considerable confusion has developed as a result of the numerous transdermal preparations which have appeared on the market.

The effective dose depends on the delivery rate and the surface area applied so that there is much variation in terms of estradiol delivered to the blood stream. The following charts attempt to present equivalent doses. Lower doses take longer weeks for effective relief, and it is important to individualize therapy. Most preparations take a full 12 weeks for maximum effect although standard therapy provides relief sooner weeks. There is also much debate as to the safety of oral vs.

One study suggests that venous thromboembolism may be lower with transdermal products, but the doses compared were not equivalent Another study shows a decreased risk of stroke in women on transdermal preparations with higher doses of both oral and transdermal estrogen showing significant effect One study suggests progesterone may be associated with a lower risk of breast cancer than progestins but this again awaits further study These preparations offer no advantage over regulated and tested preparations approved by the FDA, and their risk is equivalent to commercial compounds.

Claims that they are safer are misleading particularly since they have not been studied and one of the estrogens used, estriol, has no safety or efficacy data.

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In general initiation of treatment of the symptomatic newly menopausal women will provide benefit which greatly outweighs risk and provides protection from bone loss. Older women who continue to be symptomatic may. Although the decision to treat menopausal women rests on individualized risk vs. In general, hormone treatment is being used for symptoms. These include vasomotor symptoms and vulvovaginal atrophy. There are, however, a variety of symptoms which make up the menopausal syndrome and are not strictly classified as vasomotor or vulvovaginal symptoms and are distressing to the patient and may also be a consideration for treatment Some patients can endure two hot flashes a day while others who are in stressful or public jobs cannot.

Patients are usually uncomfortable and distressed by more than two hot flashes per day. In particular the patient who wakes at night two or more times and suffers from sleep deprivation is usually in need of treatment. Patients suffering from five to seven hot flashes a day are experiencing moderate to severe symptoms and should be offered treatment.

The physician should help the patient make a quality of life decision and advise these patients on the low risks associated with treatment particularly for a few years. Some patients may be experiencing bone loss and hormone therapy is ideal for this type of patient. Some of the estrogens on the market are also approved for prevention of osteoporosis and data shows they are very effective and prevent fractures.

A patient on hormone therapy does not need a second drug for prevention of bone loss. If bone loss is occurring on hormone therapy a secondary cause should be searched for such as vitamin D deficiency, over treatment with thyroid hormone or hyperparathyroidism. Patients with mood issue may have problems with progestins and micronized progesterone or a vaginal delivery system may be better tolerated. Estrogens should be started first and a progestin added after a few weeks.

Patients with migraines also have special tolerability issues and fluctuations of hormone levels which may be triggering the headaches may persist or be aggravated initially by hormone treatment. A transdermal patch may be the best option and a progestin should be started after a trial of treatment with estrogen. The issue of duration of hormone treatment will arise. Two to five years is usual. The small risk of breast cancer is also important to review with the patient. This risk surfaces after 5 years of use and did not surface at all with estrogen alone therapy after 7 seven years.

This interval does not apply to patients with premature menopause who have been shown to be at risk for osteoporosis and premature heart disease if they are not replaced. All patients need a yearly mammogram and the increase in density can be avoided by stopping hormones for two weeks prior to the mammogram if she can tolerate it.

Some patients stay on hormone therapy long term because of mood or other issues or they are in the unfortunate 10 percent who continue to suffer form vasomotor symptoms or cannot tolerate other drugs for osteoporosis. Patients with severe mood issues may require antidepressants. Recent data has shown the efficacy of low doses for vasomotor symptoms and many are available. However the patient with severe symptoms may prefer a standard dose which may be lowered after 6 months when symptoms are well controlled.

Lastly, vaginal estrogens are an excellent option for patients with symptoms of vaginal atrophy and do not have the risks associated with systemic use. In particular, recurrent urinary tract infections and or vulvovaginitis are a hallmark of genitourinary estrogen deficiency which can be easily relieved or prevented with the use of vaginal estrogen. Treatment with hormone therapy is very individualized and quality of like may be greatly improved its use.

When therapy is discontinued, a return of symptoms is common although generally in a milder form. Unfortunately there is little data to guide the physician but many clinicians slowly taper doses over several months. When assessing risk vs. The normal menopause transition. Clinical observations on the use of an ovarian hormone: Am J Med Sci. Overview of estrogen replacement therapy: Proc Soc Exp Biol Med. Postmenopausal estrogen for treatment of hot flashes: Steroid and gonadotropin levels in women during the peri-menopausal years. Factors associated with age at natural menopause in a multiethnic sample of midlife women.

Vasomotor flushes in menopausal women. Am J Obstet Gynecol. Options for hormone therapy in women who have had a hysterectomy. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. Global consensus statement on menopausal hormone therapy. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Hormone replacement therapy and risk of breast cancer: Postmenopausal hormone therapy and mortality.

Postmenopausal hormone use and secondary prevention of coronary events in the nurses' health study. Prospective study of exogenous hormones and risk of pulmonary embolism in women. Bone mineral density changes during the menopause transition in a multiethnic cohort of women.

J Clin Endocrinol Metab. The impact of hormone therapy on health-related quality of life: Breast cancer and hormone-replacement therapy in the Million Women Study. Methods and baseline cardiovascular data from the Early versus Late Intervention Trial with Estradiol testing the menopausal hormone timing hypothesis. Risk for new onset of depression during the menopausal transition: Effect of hormone replacement therapy on cardiovascular events in recently postmenopausal women: Freeman EW, Sherif K.

Prevalence of hot flushes and night sweats around the world: Management of menopausal symptoms. Ann N Y Acad Sci. Commonly used types of postmenopausal estrogen for treatment of hot flashes: Relief of vasomotor symptoms and vaginal atrophy with lower doses of conjugated equine estrogens and medroxyprogesterone acetate. Comparison of Alora estradiol matrix transdermal delivery system with oral conjugated equine estrogen therapy in relieving menopausal symptoms. Psychosocial and socioeconomic burden of vasomotor symptoms in menopause: Health Qual Life Outcomes. Symptoms during the perimenopause: Effects of REM sleep and ambient temperature on hot flash-induced sleep disturbance.

Effects of estrogens on sleep and psychological state of hypogonadal women. Depression and its influence on reproductive endocrine and menstrual cycle markers associated with perimenopause: Psychologic distress and natural menopause: Am J Public Health. Depressive symptoms during the menopausal transition: Hormones and menopausal status as predictors of depression in women in transition to menopause. Predictors of first lifetime episodes of major depression in midlife women.

A longitudinal analysis of the association between menopause and depression. Results from the Massachusetts Women's Health Study. A population-based study of depressed mood in middle-aged, Australian-born women. A longitudinal evaluation of the relationship between reproductive status and mood in perimenopausal women. Sex hormones and mood in the perimenopause. Female psychopathologic profile during menopausal transition: Vasomotor symptoms are associated with depression in perimenopausal women seeking primary care. Depressed mood during the menopausal transition and early postmenopause: A cross-sectional evaluation of perimenopausal depression.

Factors associated with early menopause. Efficacy of estradiol for the treatment of depressive disorders in perimenopausal women: Lack of efficacy of estradiol for depression in postmenopausal women: Panay N, Studd J. Progestogen intolerance and compliance with hormone replacement therapy in menopausal women. Sex steroids and affect in the surgical menopause: Affective changes with estrogen and androgen replacement therapy in surgically menopausal women.

A study of European womens' experience of the problems of urogenital ageing and its management.

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Vulvar transepidermal water loss TEWL decay curves. Effect of occlusion, delipidation, and age. Advances in the treatment of menopausal symptoms. Womens Health Lond Engl. Treatment of atrophic vaginitis with topical conjugated equine estrogens in postmenopausal Asian women. Efficacy of low-dose estradiol vaginal tablets in the treatment of atrophic vaginitis: Low-dose vaginal estrogens or vaginal moisturizer in breast cancer survivors with urogenital atrophy: Treatment of urogenital atrophy with low-dose estradiol: Management of symptomatic vulvovaginal atrophy: The role of androgen in the maintenance of sexual functioning in oophorectomized women.

Lifetime risks of hip, Colles', or vertebral fracture and coronary heart disease among white postmenopausal women. Hormonal determinants and disorders of peak bone mass in children. Rates of bone loss in the appendicular and axial skeletons of women. Evidence of substantial vertebral bone loss before menopause. Characterization of perimenopausal bone loss: J Bone Miner Res.

Questions and answers for estrogen and estrogen with progestin therapies for postmenopausal women updated http: A practical guide to prescribing estrogen replacement therapy. Int J Fertil Menopausal Stud. The report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: Prevalence of Vitamin D inadequacy among postmenopausal North American women receiving osteoporosis therapy. Menopause and risk factors for coronary heart disease. Risk of recurrent coronary events in relation to use and recent initiation of postmenopausal hormone therapy. Initiation of hormone replacement therapy after acute myocardial infarction is associated with more cardiac events during follow-up.

J Am Coll Cardiol. Estrogen in the prevention of atherosclerosis. A randomized, double-blind, placebo-controlled trial. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. Estrogen therapy and coronary-artery calcification. Benefits and risks of postmenopausal hormone therapy when it is initiated soon after menopause. Banks E, Canfell K.

Hormone therapy risks and benefits--The Women's Health Initiative findings and the postmenopausal estrogen timing hypothesis. Coronary heart disease in postmenopausal recipients of estrogen plus progestin therapy: Ann Intern Med; 4: Coronary heart disease and menopause management: Latest Data from the Elite Trial. Health risks and benefits 3 years after stopping randomized treatment with estrogen and progestin.

Endothelial function, but not carotid intima-media thickness, is affected early in menopause and is associated with severity of hot flushes. J Clin Endocrinol Metab;95 3: Are changes in cardiovascular disease risk factors in midlife women due to chronological aging or to the menopausal transition?

Effects of estrogen replacement on the progression of coronary-artery atherosclerosis. The effects of estradiol on blood lipids and lipoproteins in postmenopausal women. Angina and normal coronary arteries in women: Beneficial effect of oestrogen on exercise-induced myocardial ischaemia in women with coronary artery disease. Pulsatility index in internal carotid artery in relation to transdermal oestradiol and time since menopause. A clinical trial of estrogen-replacement therapy after ischemic stroke.

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The lifetime risk of developing breast cancer. J Natl Cancer Inst. Conjugated equine oestrogen and breast cancer incidence and mortality in postmenopausal women with hysterectomy: Prior hormone therapy and breast cancer risk in the Women's Health Initiative randomized trial of estrogen plus progestin. Effects of menopausal hormonal therapy on occult breast tumors. J Steroid Biochem Mol Biol. Influence of estrogen plus progestin on breast cancer and mammography in healthy postmenopausal women: Breast cancer and hormone replacement therapy: The role of hormone replacement therapy in the risk for breast cancer and total mortality in women with a family history of breast cancer.

Hormone replacement therapy and risk of breast cancer with a favorable histology: Clinical and biologic prognostic factors in breast cancer diagnosed during postmenopausal hormone replacement therapy. Prognosis after breast cancer diagnosis in women exposed to estrogen and estrogen-progestogen replacement therapy. Mammographic densities and breast cancer risk. Effects of estrogen and estrogen-progestin on mammographic parenchymal density. Changes in breast density associated with initiation, discontinuation, and continuing use of hormone replacement therapy. Effect of hormone replacement therapy on breast cancer risk: Low biologic aggressiveness in breast cancer in women using hormone replacement therapy.

Breast cancer risk after bilateral prophylactic oophorectomy in BRCA1 mutation carriers. Hormone replacement therapy after a diagnosis of breast cancer: Hormone replacement therapy after a diagnosis of breast cancer in relation to recurrence and mortality.

Estrogen-progestagen menopausal hormone therapy and breast cancer: The decrease in breast-cancer incidence in in the United States. CA Cancer J Clin. Relationship between menopausal hormone therapy and risk of ductal, lobular, and ductal-lobular breast carcinomas. Cancer Epidemiol Biomarkers Prev.

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Effects of conjugated equine estrogens on breast cancer and mammography screening in postmenopausal women with hysterectomy. Short-term cessation of hormone replacement therapy and improvement of mammographic specificity. Oral contraceptives, salpingo-oophorectomy and hormone replacement therapy in BRCA mutation carriers. Menopausal hormone therapy and health outcomes during the intervention and extended poststopping phases of the Women's Health Initiative randomized trials. Hormone therapy for the prevention of chronic conditions in postmenopausal women: Preventive Services Task Force.

Effects of estrogen plus progestin on gynecologic cancers and associated diagnostic procedures: Noncardiovascular disease outcomes during 6. A meta-analysis of estrogen replacement therapy and risk of epithelial ovarian cancer. Cancer incidence and mortality in women receiving estrogen and estrogen-progestin replacement therapy--long-term follow-up of a Swedish cohort. Endometrial effects of lower doses of conjugated equine estrogens and medroxyprogesterone acetate: The cholinergic hypothesis of geriatric memory dysfunction.

Estrogen improves psychological function in asymptomatic postmenopausal women. Estrogen use and verbal memory in healthy postmenopausal women. Estrogen effects on cognition in menopausal women. Estrogen replacement therapy and longitudinal decline in visual memory. A possible protective effect? Neuroprotection against oxidative stress by estrogens: The mitogen-activated protein kinase pathway mediates estrogen neuroprotection after glutamate toxicity in primary cortical neurons.