Breast Cancer Incidence Plateaued

Women and clinicians are regularly reminded about the threat of breast cancer by the media, advertisements, and the experiences of friends or family members who are fighting the disease. And there is good reason for breast cancer to be prominent in our consciousness: The breast is the leading site of cancer in US women (32% of all cancers); however, probably because of smoking, cancers of the lung and bronchus have surpassed cancer of the breast as causes of cancer death in women. Every year in the US, there are about 212,000 new cases of invasive breast cancer and 56,000 new cases of in situ breast cancer.

The good news is that since 1990, incidence of breast cancer has plateaued, increasing only in women older than age 50 years at a rate of about 0.4% per year, and has been limited to localized disease. Mortality rates also began to decline in the 1990s. The 5-year survival rate for localized breast cancer (about 60% of cases) has risen from 72% in the 1940s to 97%.1 This trend, which is expected to continue, is attributable to earlier diagnosis as a result of greater utilization of screening mammography and increased use of chemotherapy. For clinicians who care for postmenopausal women, breast cancer is a major focus because it is increasingly frequent with age. About 94% of all breast cancers occur in women older than age 40 years, versus 15% in those younger than age 50 years, and only 6.5% in women younger than age 40 years.

Impact of Androgens

Researchers who study the influence of hormones on behavior have the greatest difficulty in associating testosterone with any human behaviors whatsoever. They have injected all kinds of animals at all stages of development with synthetic testosterone to see how it affected their behavior. They have juggled the naturally occurring estrogens and androgens to see whether the role of receptors and sensitizers was more important than the action of the hormones themselves. Yet they still can not define any specific influence of testosterone on the behavior of the human male.

Research has long indicated that androgens, testosterone in particular, are linked not only with libido but with aggressiveness, particularly in the male. Animal research has been much more consistent in suggesting this hypothesis than human research has. However, the fact that sexual awakening in the adolescent is associated with rises in testosterone level, does link it to libidinal urges and possibly to aggression.

The testosterone levels of violent men have been measured time and again, and often, but not always, found to be higher than those in a control population. Violent sex offenders have been found, again not consistently, to have the highest testosterone levels of all. The effect of alcohol and drugs is variable; habitual use suppresses testosterone but occasional use can stimulate secretion, possibly as a feed-back effect of disinhibition.

This raises a further possibility that violent men are not violent because they have more testosterone to cope with, but that they have more testosterone because they are more violent. Traditional patterns of male activity might have developed because they stimulate the secretion of testosterone. If a woman can have an estrogen ‘high’, it seems likely that a man can have a testosterone ‘high’.

Effect of Estrogen plus Progestin on Quality of Life

In the recently published analysis of the effects of estrogen plus progestin on health-related quality of life (QOL) in the Women’s Health Initiative (WHI), the authors concluded that this therapy did not have a clinically meaningful effect.1 However, caution is warranted in interpreting the findings of this analysis. The study design has several limitations that diminish the strength and usefulness of its conclusions.

The main finding — that QOL was not significantly improved — was to be expected in this population. Symptomatic women were discouraged from participation, and vasomotor symptoms were reported by only 12% of the participants. Furthermore, it is unlikely that many women who had bothersome menopausal symptoms would volunteer for a study in which they had a 50% chance of receiving placebo for a prolonged time. Symptom relief is the most relevant factor for improvement of QOL with hormone therapy; therefore, women without symptoms are not likely to experience large improvements in their QOL. Nevertheless, even this older population showed improvements in sleep, physical functioning, and pain. Thus, it is possible that there was an effect on the QOL, but that the study was not designed to capture this information.

The more important question of effect on QOL in symptomatic women was addressed by a subgroup analysis of 574 women ages 50 to 54 years who reported moderate to severe vasomotor symptoms at baseline. Women in the estrogen and progestin group demonstrated a significant improvement of vasomotor symptoms (p < 0.001) and sleep quality (p=0.02), as compared to placebo. Despite this, improvement in QOL was not observed. This contradicts previous well-designed prospective trials.2 There are several limitations in this study’s design that may explain the failure of this analysis to detect an improvement in QOL. First, the primary objectives of the WHI did not include evaluation of the effect on QOL. The study, and particularly the subgroup, may not have had the power to detect a meaningful effect.

Second, the main instrument used to evaluate QOL was the RAND-36.1 Although a good measure of health-related functioning, it was not designed to assess variables relevant to QOL in postmenopausal women.3 For example, important domains, such as sexual function, are not addressed. The authors attempted to evaluate this variable by asking a single question with a four-point response scale: very unsatisfied, a little unsatisfied, somewhat satisfied, and very satisfied. This approach is clearly inadequate as a method for assessing change in such a complex aspect of human function. Nevertheless, the data in this subgroup revealed an improvement in the estrogen and progestin group that had borderline statistical significance (p=0.06). Thus, the RAND-36 was not designed to assess the “sense of well-being,” particularly in the postmenopausal population. Validated instruments such as the Utian Quality of Life Scale (UQOL) are available for this purpose, and should be utilized in future studies.3

Another weakness of this study was the high rate of drop-ins. Many women randomized to placebo initiated hormones. Symptomatic women were most likely to do this, which may have introduced bias toward the null hypothesis, thereby decreasing the likelihood of detecting an improvement in QOL.

In summary, it is incorrect to conclude, on the basis of this study, that estrogen plus progestin therapy does not improve QOL in women with vasomotor symptoms. Previous randomized controlled trials have provided evidence to the contrary. Furthermore, even in asymptomatic women this conclusion is questionable, as the study was not designed to evaluate QOL in postmenopausal women.

Postmenopausal Hormone Therapy and Breast Cancer

Holmberg and Anderson recently published a research letter in the journal Lancet regarding early cessation of the HABITS study,1 a Scandinavian trial designed to evaluate the risk of breast cancer recurrence in women with previously treated breast cancers who were given hormone therapy (HT) for relief of menopausal symptoms. The primary objective of the study was to investigate the safety of administering HT over a 2-year period for the treatment of menopause-related symptoms in women with a history of breast cancer; secondary goals included evaluation of quality-of-life issues and associated breast cancer mortality. The trial was directed only at women with climacteric symptoms; both perimenopausal and postmenopausal patients were eligible for enrollment. In terms of follow-up, study participants were to be evaluated at least twice yearly for the first 3 years, with a total of 5 years observation in all.

The study was terminated early because the results of an interim safety analysis indicated an unacceptable risk of breast cancer recurrence in women randomized to HT, compared to those randomized to “best symptomatic treatment without hormones.” After a median of 2.1 years, 26 women (14%) in the HT group and seven (4%) in the non-HT group had a new breast cancer event (local or distant recurrence or disease in the contralateral breast). These findings disagree with the results of previous studies that have found either a decreased or no increased risk of recurrence associated with HT use in breast cancer survivors.2-6 The HABITS investigators indicated that the hazard ratio of 3.5 (95% CI, 1.5-8.1) also differed significantly (p=0.02) from the unpublished, interim results of a similar trial among breast cancer survivors in Stockholm, Sweden, which found no increased risk of recurrence among HT users (RH=0.82, 95% CI 0.35-1.9)

As one of relatively few prospective randomized trials investigating the safety of HT use among breast cancer survivors, the early cessation of the HABITS study is important to note. Equally important to consider, however, are a number of limitations in the trial’s design. Primarily, the study is not double blinded or placebo controlled. Randomization occurred centrally, but the only categories used for data stratification were the participating research center, current use of tamoxifen, and history of HT use before cancer diagnosis (patients could have a history of HT use, but must not have been on HT for 3 months prior to randomization). In addition, while patients were randomized to either HT or “best symptomatic treatment without hormones,” the protocol was highly flexible, and decisions about the specific type of treatment were made by local practitioners. As a result, women in the HT group received varying types and doses of estrogen and progestin, and we do not know the impact of differing dose or preparation on the study results. The protocol recommends administration of “medium potency estrogen replacement (with or without progestins) therapy as it is commonly given in the environment where the patient lives and the clinician works” for those in the HT arm, although the term “medium potency”is not defined. Local vaginal hormone treatment was allowed in the control arm. Furthermore, it is difficult to assess the degree of adherence to other aspects of the study protocol; for example, some patients in the HT group received tibolone even though the investigators noted in their research letter that this therapy was not allowed. Similarly, the protocol recommended recent mammograms (within 3 months) for all patients before inclusion in the study, although no documentation is provided to confirm that this was done.

The brevity of the published report from the safety analyses on which termination of the trial was based leaves many additional questions unanswered:

Patients with a history of previously treated in situ, stage 1 or stage 2 breast cancer were eligible for the trial, but we are not provided with the numbers of patients in each stage in either HT or non-HT arms of the study. Patients whose tumors were estrogen receptor positive, receptor negative, or receptor status unknown were enrolled in the trial, although we do not know how many women in each of these groups were included in the HT and non-HT arms. An individual patient could also be included if she had four or fewer positive nodes, if nodal status was known. There is no documentation regarding the number of patients in whom nodal involvement was investigated, or the percentage of patients in whom data concerning the presence of positive nodes was lacking. At baseline, the HT population included 5% more patients with positive nodes than those randomized to the non-HT group. From this incomplete information, we cannot accurately assess if the arms of the study are equivalent for comparison, as there is no correction for the most important risk factors, stage and node status. Clearly, the patient with four positive nodes carries a worse prognosis than the patient with only one positive node.

The purpose of the trial was to investigate whether treatment of menopausal symptoms with HT was safe in women with a previously treated breast cancer, but the degree to which patients were symptomatic is not specified. We do not know the number of patients who were menopausal versus postmenopausal, or the length of time that elapsed since last menses. The study includes women up to 75 years of age-how many of these older women had menopausal symptoms?

It was anticipated that analysis would require enrollment of 250 to 300 patients per year, for a total population of 1300 participants. Only 381 patients were enrolled in the trial from its initiation in May 1997 until May 2002. The HABITS protocol was then amended to include collaboration with the Stockholm trial to pool data for safety and final analyses. Only 434 patients were enrolled by September 2003, and the study was discontinued in December 2003. Interestingly, only 79% of enrolled patients were included in the data analysis, as the other 21% did not have at least one follow-up examination. Information regarding compliance with follow-up is not given. The investigators recommended clinical mammograms every 12 to 24 months or participation in screening, although no information about adherence to these guidelines is provided. Thus, we cannot tell if there is a difference in compliance with imaging follow-up between the two arms.

The impact of duration of treatment and compliance with assigned therapy is unknown as well. The authors indicate that 18% of the patients assigned to the non-HT group received HT. In addition, we do not know the duration of therapy in those randomized to the HT group. Although the authors state that all participants diagnosed with recurrences in the HT group took hormones, 19% were not currently receiving HT when the cancer was discovered. It is also unknown if the patients treated with tamoxifen were compliant with its use, and if tamoxifen use affected the recurrence rate.

The follow-up period of 2.1 years is very short and information regarding the timing of breast cancer recurrence is not provided. Certainly, we know that when breast cancer is diagnosed it has been in the breast for up to 10 years or longer; thus, it is likely that the study patients with cancer recurrence or contralateral breast cancer had unrecognized disease at the time of initial randomization. Long-term follow-up of recurrence incidence in the non-HT group will be required before conclusions can be made regarding the potential role of HT as a promoter.

Testosterone and Agression

Children, old people and women are all short of testosterone. Even ten years ago, testosterone was a word not often heard; nowadays the presence of testosterone in the environment is often remarked on. When the stands at the football ground are packed with vociferating fans it is described as a testosterone storm. When a driver kills another driver who cut him up at a corner, he does it in a blind testosterone rage.

Aggression is part of the currency exchanged in all masculine dealings. Male biochemistry and masculine enculturation interact to generate a threatening climate in which men, particularly young men, choose to live dangerously. Adrenaline is a drug which the violent man supplies of himself to himself. The flooding of fight-or-flight chemicals into the bloodstream is pure pleasure; many of our entertainments consist in little other than the deliberate stimulation of terror.

Television programme-maker Paul Kozminsky described some people as thinking of child abuse ‘as something bestial – out of too much testosterone’. By invoking testosterone a man can abdicate responsibility for his own behavior.

People who don’t appreciate excitement, who can see no more point in going on the big dipper than in wilding or ram-raiding, who cannot watch films which are little more than realistic representations of people being tortured, blown up, mown down, cut in half or simply terrified, are pathetic. Our culture now depicts much more elaborate violence in more media more often than it did thirty years ago.

ERT for Menopausal Women With History of Breast Cancer

Women with a history of breast cancer have been advised to avoid estrogen replacement therapy (ERT). A reassessment of this approach has been initiated by several authors and clinical reports to date have not supported this tenet. The only prospective randomized trial reported to date is that of Vassilopoulou-Sellin et al. The authors conducted a prospective clinical trial to assess the safety and efficacy of prolonged ERT in a group of menopausal women with localized (Stage I or II) breast carcinoma and a minimum disease-free interval of 2 years, if the estrogen receptor (ER) was negative, or 10 years if the ER status is unknown. For 5 years, the authors followed 77 trial participants and 222 other women with clinical and prognostic characteristics comparable to those of the trial participants. Overall, 56 women were on ERT, and 243 women were not on ERT. Patient and disease characteristics, such as tumor size, number of lymph nodes involved, ER status, menopausal status, and disease-free interval were comparable for women who were on ERT and women who were not on ERT. Two of the 56 women on ERT (3.6%) developed a contralateral, new breast carcinoma. In the group that was not on ERT, 33 of the 243 women (13.5%) developed new or recurrent breast carcinoma. There were no differences in the development of other carcinomas with respect to ERT. Thus, ERT did not compromise disease-free survival in select patients who were treated previously for localized breast carcinoma.

Additionally, observational studies reported by DiSaia, O’Meara, and Peters have supported this same conclusion. O’Meara assembled data from 2,755 women ages 35 to 74 years who were diagnosed with incident invasive breast cancer while they were enrolled in a large health maintenance organization from 1977 to 1994. Pharmacy data identified 174 users of hormone replacement therapy (HRT) after diagnosis. Each HRT user was matched to four randomly selected non-users of HRT with similar age, disease stage, and year of diagnosis. The rate of breast cancer recurrence was 17 per 1,000 person-years in women who used HRT after diagnosis and 30 per 1,000 person-years in non-users (adjusted relative risk for users, compared with non-users was equivalent to 0.50; 95% confidence interval was 0.30-0.85). Total mortality rates were 16 per 1,000 person-years in the HRT users and 30 per 1,000 person-years in the non-users.

DiSaia et al reported on 125 women who were breast cancer survivors with and without positive nodes, both ER positive and ER negative, who elected to take ERT or HRT. These patients were matched to 362 control patients from the same population base with the approximate ratio of four controls to one patient taking ERT or HRT. The risk of death was lower among the HRT survivors; odds ratio 0.28 (95% Cl 0.11-0.71). This analysis also did not suggest an adverse outcome with HRT use.

Peters interviewed 607 breast cancer survivors concerning ERT usage. Sixty-four patients indicated they had received some form of ERT after their breast cancer diagnosis. Eight patients were excluded because they had used only vaginal cream ERT. The remaining 56 received ERT as conjugated estrogens, an estradiol patch, or birth control pills. The median follow-up from diagnosis was 12.8 years and the median time on ERT since diagnosis was 6.4 years. One local recurrence and one contralateral breast cancer occurred during the follow-up period at 13.5 and 9.6 years respectively. There were no breast cancer deaths. The author also concluded that the use of ERT in a cohort of breast cancer survivors with tumors of generally good prognosis was not associated with increased breast cancer events compared with non-ERT users, even after a long follow-up period.

The question then remains as to whether all patients who have had breast cancer should be denied the benefits of estrogen replacement therapy. This is particularly relevant in the patient who has serious quality of life issues before her. At present, therapy with ERT/HRT is indicated in the management of quality of life issues, using lowest possible dose of hormone for shortest duration of time possible. Is it appropriate to deny a woman the option of taking replacement therapy for relief of her symptoms when there is no clinical evidence that it adversely affects outcome?

Testosterone: Use and Pharmaceutical Forms

The original intention of testosterone were the treatment of males who have too little or no natural endogenous testosterone production with hypogonadism. Appropriate use for this purpose is legitimate hormone replacement therapy which maintains serum testosterone levels in the normal range.

Many other applications of testosterone includes the following:

  • Infertility
  • Lack of libido
  • Erectile dysfunction
  • Osteoporosis
  • Penile enlargement
  • Height growth
  • Bone marrow stimulation
  • Reversal of anemia
  • Appetite stimulation

Testosterone is often used by athletes to improve their performance. In men, however, a slight increase in testosterone levels can have great effects on their physical shape. Anabolic steroids (testosterone is one of them) have been taken to enhance muscle development, strength and endurance. After a series of scandals and publicity in the 1980s such as Ben Jonhson’s improved performance at the 1988 Summer Olympics, anabolic steroids were designated as “controlled substance.” In the former Eastern Germany even women used it so they would have superior physical abilities to their competitors. The noticeable side effects that took an impact on those women are extensive growth of facial hair and outer look that was man-like.

The different pharmaceutical forms of testosterone for human administration are currently available. Among them are:

  • Injectable (such as testosterone cypionate/testosterone enanthate in oil),
  • Oral Andriol,
  • Bucall Striant,
  • Transdermal skin patches and transdermal creams,
  • Gels Androgel and Testim,
  • Roll on and Nasal Sprays.

Risk of Breast Cancer with Combined EPT

Baseline incidence of invasive breast cancers in non-HRT users is 32/1000 between ages 50 and 65 years. Baseline incidence of endometrial cancers in non-HRT users is 5/1000 between ages 50 and 64 years.

The excess risk of breast cancer with long-term use (10 years) of 19/1000 EPT and 5/1000 for ET alone can be compared with the excess risk of endometrial cancer after 10 years use of ET alone of 10/1000. Ten years of EPT is estimated to result in no increased risk of endometrial cancer.

Since the Million Women study shows a greater risk of breast cancer with combined EPT, women and their physicians will need to weigh the possibility that the increased risk of breast cancer caused by the addition of a progestogen is greater than the risk of endometrial cancer with estrogen only. If this is correct, the logical conclusion may be that women should be advised to take estrogen alone for hormonal therapy, even if they have a uterus and that screening be instituted for endometrial cancer. This possibility would need extensive discussion before making a general recommendation. Other options include using progestogen delivery systems that allow a local progestogen effect at the uterus.

Because this is an observational study, it has potential for error. According to Utian and colleagues6, the major weakness is that the study took only a snapshot of hormone therapy use at the time of entry into the study, when women had their every third year mammogram. No further information was obtained about changes in hormones, route, dose, or discontinuation.

In conclusion, the Million Women Study serves as a large observational study that confirms the WHI findings of a small increase in absolute risk of breast cancer with EPT therapy, and confirms prior observational studies of a smaller increase in absolute risk of breast cancer with ET. These findings are important to convey to women making decisions about initiation or continuation of hormone therapy. The findings do not change current recommendations to use hormones primarily for menopausal symptom relief, vulvovaginal atrophy, and quality of life issues in symptomatic menopausal women with natural, premature, or surgically induced menopause.

They support current recommendations from the North American Menopause Society (NAMS)7, American College of Obstetrics and Gynecology (ACOG),8 and the Food and Drug Administration (FDA)9,10 to use the lowest, most effective dose for the shortest period of time.

Hormone Therapy and Osteoporosis

The effects of estrogen deficiency on the skeletal system have been clearly established for more than 60 years. The molecular mechanisms accounting for estrogen-related bone loss have been known for a decade or longer, and the benefits of estrogen on the skeleton have been recognized for half a century. The adverse consequences of estrogen depletion and benefits of estrogen replacement have been reported by every clinical study evaluating estrogen use in the postmenopausal woman.

The benefits of estrogen therapy in the prevention of osteoporotic fractures were most recently confirmed in the largest clinical trial to date, the Women’s Health Initiative (WHI) (Cauley et al 2003, 1729-38). This study clearly demonstrates that therapy with continuous combined hormone therapy (0.625 mg conjugated equine estrogen + 2.5 mg medroxyprogesterone acetate ([CEE/MPA]) significantly decreases the risk of osteoporosis-related hip fractures and all other osteoporosis-related fractures in postmenopausal women. Despite these results, the authors concluded

“When considering the effects of hormone therapy on other important disease outcomes in a global index there was no benefit, even in women considered to be at high risk of fracture.” This conclusion is based on an analysis of stratification of fracture risk against the global index.

The statistics report the hazard ratio (HR) for the global index was not statistically significant for women in the lowest third (HR 1.20; 95% confidence interval [CI] 0.93-1.58) and upper third (HR 1.03 (95% CI 0.88-1.24) of the fracture risk scale (see below). The hazard ratio was statistically significant only for those patients in the middle third of the fracture risk scale (HR 1.23; 95% CI 1.04-1.46). The full text of the article states: “The interaction between treatment effect and summary fracture risk on the global index was not significant (p=0.54).Thus, there was no evidence of a net benefit, even in women at highest risk of fracture.” I readily admit to not understanding this sophisticated analysis but I believe that the data could equally well be reported that there was no evidence of net harm in those women at highest risk of fracture.

The global index was incorporated into the WHI as an overall measure of estrogen + progestin’s benefit vs. risk, which the investigators believe to be more significant than the evaluation of mortality alone. To my knowledge this innovative approach has not been used in other clinical trials, and has not been validated in any model. The WHI fracture risk scale is based on a validated model published by Black et al, which identified 20 different risk factors associated with fracture (Black 2001, 519-528). The differences between the WHI fracture risk assessment model and that described by Black et al are not trivial (e.g., the WHI did not include measurements of the hip bone mineral density for all patients, and did not assess peak adult height just to mention two items). The WHI fracture risk assessment model, like the global index, has not been validated. Thus, the conclusions based on the current WHI study are the result of an analysis of two nonvalidated models.

The global index, once validated, may indeed be an appropriate approach to look at overall benefits and risks of CEE/MPA. It becomes less appropriate when looking at individual outcomes. For example, there is abundant documentation of the devastation resulting from hip fracture including excess mortality in the first year, long-term morbidity and nursing home placement for those who survive the first year, the impact on the family of the affected patient, and the overall cost to the health care system. How can these serious complications be given equal weight to pulmonary embolism, which fortunately is fatal in only a small proportion of cases and is not associated with the long-term morbidity and health care costs that approach those of hip fracture? It is possible to perform a quality of life or cost analyses of each of the adverse outcomes included in the global index and take a very different approach to a benefit-risk analysis.

The above concerns notwithstanding, the WHI investigators have missed an important opportunity to add to our knowledge base. Epidemiologic studies have indicated that those patients who are at greatest risk for breast cancer are the least likely to develop osteoporosis and vice versa. None of the several articles documenting this (including at least two by one of the coauthors of this WHI paper) is cited in this manuscript! There appears to be little doubt that the skeleton is an estrogen-dependent tissue, as is the breast. It is not surprising that those at lowest risk for fracture (possibly determined by higher lifetime estrogen exposure) are also at greatest risk for breast cancer (by the same mechanism). What we should have learned from the WHI investigators is whether this relationship is true in their study population as well. 8102 women were assigned to placebo, and one-third of these were assigned to the low-fracture risk group. We are told that their annualized incidence of fractures was 1.3%, half the incidence seen in women assigned to the high-fracture risk group (2.7%). What was the breast cancer incidence in these groups in the placebo arm? There certainly was as much or more data available in this study than in any of the previous reports relating osteoporosis protection and increased breast cancer risk. If breast cancer did not contribute to the HR of the global index, then which adverse outcomes were noted in those on HT? We cannot ascertain that important question from this WHI manuscript.

Finally, there is a crucial element missing from the WHI, particularly as it relates to the skeleton. The most rapid postmenopausal bone loss occurs during the first 5 years, slowing down substantially thereafter. The WHI population included only 16% to 17% of women who were within 5 years postmenopause (there was no need to include these patients because the benefits of estrogen in the early menopause have been repeatedly demonstrated in numerous controlled clinical trials). Women using estrogen for management of the menopause do not need other medications for skeletal protection. This beneficial effect only lasts as long as the patient continues estrogen therapy; bone density and fracture risk are back at baseline within 1 year of discontinuing the hormone.

In clinical practice, we have known for decades that women tend to take a holiday from estrogen whenever a prescription runs out and do not refill the prescription if her menopausal symptoms do not recur. This long predates WHI and should not change post-WHI. Most women did not and do not take estrogen for as long as five years postmenopause. However, there has always been a substantial minority of women who do not tolerate this estrogen-free period, and quickly experience a recurrence of symptoms leading to the reinstitution of estrogen therapy.

In conclusion, I believe the following statements can be made:

* Estrogen + progestin is now the only osteoporosis therapy documented to decrease fracture occurrence even in women not specifically selected as being at increased risk of fracture.

* The benefits of estrogen in controlling the symptoms of menopause are not questioned as a result of the WHI study findings.

* Patients will be receiving skeletal protection as long as they use estrogen +/- progestin for control of menopausal symptoms.

* Other effective therapies that can protect the postmenopausal patient from fracture are available once she no longer experiences symptoms of menopause.

Hormones and Postmenopausal Health

Menopause-related estrogen loss is associated with symptoms that can have a negative impact on a woman’s sense of well-being and her daily activities. In addition, menopausal women are at an increased risk for developing osteoporosis. Therefore, for some menopausal women, hormone therapy (HT, administered as either unopposed estrogen or estrogen plus progestin) may be a therapeutic option.

Recent media accounts of the findings from the HT trials of the Women’s Health Initiative (WHI) have increased women’s concerns about using hormones for relief from menopausal symptoms and have heightened the need for clinicians to take a more individualized approach to counseling their menopausal patients.

CME program, Scientific Update on Hormones and Postmenopausal Health, is designed to assist clinicians in providing their patients with accurate information and individualized counseling about menopausal health issues and HT. This slide series allows physicians to earn a maximum of 1 category 1 credit per presentation toward the American Medical Association’s Physician’s Recognition Award (AMA-PRA) through the University of Wisconsin Medical School.