Breast cancer incidence in postmenopausal women using testosterone in addition to usual hormone therapy

OBJECTIVE: There is now convincing evidence that usual hormone therapy for ovarian failure increases the risk for breast cancer. We have previously shown that ovarian androgens normally protect mammary epithelial cells from excessive estrogenic stimulation, and therefore we hypothesized that the addition of testosterone to usual hormone therapy might protect women from breast cancer. DESIGN: This was a retrospective, observational study that followed 508 postmenopausal women receiving testosterone in addition to usual hormone therapy in South Australia. Breast cancer status was ascertained by mammography at the initiation of testosterone treatment and biannually thereafter. The average age at the start of follow-up was 56.4 years, and the mean duration of follow-up was 5.8 years. Breast cancer incidence in this group was compared with that of untreated women and women using usual hormone therapy reported in the medical literature and to age-specific local population rates. RESULTS: There were seven cases of invasive breast cancer in this population of testosterone users, for an incidence of 238 per 100,000 woman-years. The rate for estrogen/progestin and testosterone users was 293 per 100,000 woman-years--substantially less than women receiving estrogen/pro-gestin in the Women's Health Initiative study (380 per 100,000 woman-years) or in the "Million Women" Study (521 per 100,000 woman-years). The breast cancer rate in our testosterone users was closest to that reported for hormone therapy never-users in the latter study (283 per 100,000 woman-years), and their age-standardized rate was the same as for the general population in South Australia. CONCLUSIONS: These observations suggest that the addition of testosterone to conventional hormone therapy for postmenopausal women does not increase and may indeed reduce the hormone therapy-associated breast cancer risk-thereby returning the incidence to the normal rates observed in the general, untreated population.     

Prior hormone therapy and breast cancer risk in the Women's Health Initiative randomized trial of estrogen plus progestin

OBJECTIVES: To assess the extent to which prior hormone therapy modifies the breast cancer risk found with estrogen plus progestin (E+P) in the Women's Health Initiative (WHI) randomized trial. METHODS: Subgroup analyses of prior hormone use on invasive breast cancer incidence in 16,608 postmenopausal women in the WHI randomized trial of E+P over an average 5.6 years of follow-up. RESULTS: Small but statistically significant differences were found between prior HT users and non-users for most breast cancer risk factors but Gail risk scores were similar. Duration of E+P use within the trial (mean 4.4 years, S.D. 2.0) did not vary by prior use. Among 4311 prior users, the adjusted hazard ratio (HR) for E+P versus placebo was 1.96 (95% confidence interval [CI]: 1.17-3.27), significantly different (p=0.03) from that among 12,297 never users (HR 1.02; 95% CI: 0.77-1.36). The interaction between study arm and follow-up time was significant overall (p=0.01) and among never users (p=0.02) but not among prior users (p=0.10). The cumulative incidence over time for the E+P and placebo groups appeared to cross after about 3 years in prior users, and after about 5 years in women with no prior use. No interaction was found with duration (p=0.08) or recency of prior use (p=0.17). Prior hormone use significantly increased the E+P hazard ratio for larger, more advanced tumors. CONCLUSION: A safe interval for combined hormone use could not be reliably defined with these data. However, the significant increase in breast cancer risk in the trial overall after only 5.6 years of follow-up, initially concentrated in women with prior hormone exposure, but with increasing risk over time in women without prior exposure, suggests that durations only slightly longer than those in the WHI trial are associated with increased risk of breast cancer. Longer-term exposure and follow-up data are needed.     

Lessons to be learned from animal studies on hormones and the breast

The relation of hormone use by postmenopausal women to breast cancer risk has been controversial and unclear. A recent large randomized trial, the Women's Health Initiative (WHI) and a large observational study (Million Women Study) provided somewhat conflicting answers. The WHI found an increased incidence of breast cancer among women given hormone therapy (conjugated equine estrogen plus medroxyprogesterone acetate) but no increase in those given estrogen only therapy (conjugated equine estrogen alone). Whereas, the Million Women Study found an increased breast cancer risk among the estrogen plus progestin and the estrogen only users. This review brings comparative perspective to the issue of the effects of estrogen plus progestin versus estrogen only effects on breast cancer and is focused particularly on nonhuman primates. Although data from rodents is mixed, studies of monkeys suggest that estrogen only treatment has little or no effect on breast cell proliferation, and by inference, on breast cancer risk. On the other hand, data from both mouse and monkey studies strongly support the conclusion that the co-administration of a progestogen with an estrogen markedly increases breast cell proliferation and the potential for breast cancer promotion.     

Reduced breast cancer incidence in women treated with subcutaneous testosterone,or testosterone with anastrozole: A prospective,observational study

Objectives

There is evidence that androgens are breast protective and that testosterone therapy treats many symptoms of hormone deficiency in both pre and postmenopausal patients. However, unlike estrogen and progestins, there is a paucity of data regarding the incidence of breast cancer in women treated with testosterone therapy. This study was designed to investigate the incidence of breast cancer in women treated with subcutaneous testosterone therapy in the absence of systemic estrogen therapy.

Study design

This is a 5-year interim analysis of a 10-year, prospective, observational, IRB approved study investigating the incidence of breast cancer in women presenting with symptoms of hormone deficiency treated with subcutaneous testosterone (T) implants or, T combined with the aromatase inhibitor anastrozole (A), i.e., T + A implants. Breast cancer incidence was compared with that of historical controls reported in the literature, age specific Surveillance Epidemiology and End Results (SEER) incidence rates, and a representative, similar age group of our patients used as a ‘control’ group. The effect of adherence to T therapy was also evaluated.

Results

Since March 2008, 1268 pre and post menopausal women have been enrolled in the study and eligible for analysis. As of March 2013, there have been 8 cases of invasive breast cancer diagnosed in 5642 person-years of follow up for an incidence of 142 cases per 100 000 person-years, substantially less than the age-specific SEER incidence rates (293/100 000), placebo arm of Women's Health Initiative Study (300/100 000), never users of hormone therapy from the Million Women Study (325/100 000) and our control group (390/100 000). Unlike adherence to estrogen therapy, adherence to T therapy further decreased the incidence of breast cancer (73/100 000).

Conclusion

T and/or T + A, delivered subcutaneously as a pellet implant, reduced the incidence of breast cancer in pre and postmenopausal women. Evidence supports that breast cancer is preventable by maintaining a T to estrogen ratio in favor of T and, in particular, by the use of continuous T or, when indicated, T + A. This hormone therapy should be further investigated for the prevention and treatment of breast cancer.     

The Association Between the Socioeconomic Status and Thyroid Cancer Prevalence; Based on the Korean National Health and Nutrition Examination Survey 2010-2011

The incidence of thyroid cancer has recently increased in most industrialized countries, including Korea. To date, few studies have examined the association between thyroid cancer and socioeconomic status (SES). The current study was based on data collected from a total of 12,276 subjects (5,277 men and 6,999 women) by the Korean National Health and Nutrition Examination Survey (KNHANES) between 2010 and 2011. Univariate and multivariate logistic regression analysis revealed that older age (odds ration [OR], 1.03; 95% confidence interval [CI], 1.00-1.05), being female (OR, 8.16; 95%CI, 2.99-22.24), being overweight (OR, 1.04; 95%CI, 1.01-1.06), monthly household income (OR, 3.27; 95%CI, 1.16-9.20 for medium-highest household income vs lowest household income; OR, 3.30; 95%CI, 1.16-9.34 for highest household income vs lowest household income), educational level (OR, 2.74; 95%CI, 1.16-6.46 for 10-12 yr vs < 7 yr) and alcohol consumption (OR, 1.89; 95%CI 1.08-3.32) were significant risk factors for thyroid cancer. Our results indicate that the recent increase in thyroid cancer is attributable to better early detection rather than to any increase in actual prevalence.     

Higher levels of central adiposity in healthy premenopausal women with family histories of premenopausal breast cancer

Research strongly suggests that lower overall adiposity and higher central adiposity are independent risk factors for premenopausal breast cancer in the general population. We aimed to test the possibility that these factors may contribute to familial risk of premenopausal breast cancer. A convenience sample of healthy women, ages 25–49, was recruited to yield three study groups: (1) Women with first‐degree family histories of premenopausal breast cancer, operationally defined as being diagnosed prior to age 50 (Group FH < 50, n = 39); (2) Women with first‐degree family histories of postmenopausal breast cancer, operationally defined as being diagnosed at age 50 or after (Group FH ≥ 50, n = 33); and (3) Women without a history of breast cancer in first‐degree relatives (Group FH?, n = 132). Multinomial logistic regression analyses, including possible confounders, waist circumference, and BMI, revealed a lower BMI among FH < 50 compared to either FH? (OR = 0.72; 95% CI = 0.59–0.87), or FH ≥ 50 women (OR = 0.75; 95% CI = 0.60–0.95), and higher waist circumferences in FH < 50 compared to either FH? (OR = 1.15; 95% CI = 1.06–1.25), or FH ≥ 50 women (OR = 1.16; 95% CI = 1.05–1.28). No group differences were seen for waist skinfold measures. These results support the possibility that differences in patterns of adiposity may contribute to familial risk of premenopausal breast cancer, and suggest the importance of conducting large scale, population‐based studies of the link between body size characteristics and familial breast cancer risk. Am. J. Hum. Biol., 2008. © 2007 Wiley‐Liss, Inc.     

Reduced breast cancer incidence in women treated with subcutaneous testosterone,or testosterone with anastrozole: A prospective,observational study

ObjectivesThere is evidence that androgens are breast protective and that testosterone therapy treats many symptoms of hormone deficiency in both pre and postmenopausal patients. However, unlike estrogen and progestins, there is a paucity of data regarding the incidence of breast cancer in women treated with testosterone therapy. This study was designed to investigate the incidence of breast cancer in women treated with subcutaneous testosterone therapy in the absence of systemic estrogen therapy.Study designThis is a 5-year interim analysis of a 10-year, prospective, observational, IRB approved study investigating the incidence of breast cancer in women presenting with symptoms of hormone deficiency treated with subcutaneous testosterone (T) implants or, T combined with the aromatase inhibitor anastrozole (A), i.e., T + A implants. Breast cancer incidence was compared with that of historical controls reported in the literature, age specific Surveillance Epidemiology and End Results (SEER) incidence rates, and a representative, similar age group of our patients used as a ‘control’ group. The effect of adherence to T therapy was also evaluated.ResultsSince March 2008, 1268 pre and post menopausal women have been enrolled in the study and eligible for analysis. As of March 2013, there have been 8 cases of invasive breast cancer diagnosed in 5642 person-years of follow up for an incidence of 142 cases per 100 000 person-years, substantially less than the age-specific SEER incidence rates (293/100 000), placebo arm of Women's Health Initiative Study (300/100 000), never users of hormone therapy from the Million Women Study (325/100 000) and our control group (390/100 000). Unlike adherence to estrogen therapy, adherence to T therapy further decreased the incidence of breast cancer (73/100 000).ConclusionT and/or T + A, delivered subcutaneously as a pellet implant, reduced the incidence of breast cancer in pre and postmenopausal women. Evidence supports that breast cancer is preventable by maintaining a T to estrogen ratio in favor of T and, in particular, by the use of continuous T or, when indicated, T + A. This hormone therapy should be further investigated for the prevention and treatment of breast cancer.     

Postmenopausal hormone therapy and breast cancer: What is the problem?

Observational studies provide evidence that breast cancer risk is increased with long-term oral use of postmenopausal estrogen replacement therapy (ET). Various large cohort studies have shown that the addition of a progestogen in combined hormone replacement therapy (EPT) increases this risk further. Prospective, randomized controlled trials have confirmed this for the continuous combined regimen. So, why not tell our patients, “Stop using ET and EPT, it is dangerous to your health!”? The answer is: there are too many problems to allow such an oversimplified, definite statement. What is the problem? There is more than one!The problems are as follows:

• •There are many observational studies, but these are not consistent in their results.
• •Relative risk increases, if any, are small and thus often statistically non-significant.
• •Observational studies have inherent biases that cannot be corrected for; therefore evidence should come from randomized clinical trials (RCTs).
• •There are no RCTs that provide evidence as to the breast cancer risk with ET, compared to EPT in the same study population.
• •In the three large RCTs available, the populations studied are: not representative, too old and without climacteric complaints, and therefore lacking any indication for postmenopausal hormone therapy (HT).
• •The data obtained thus far do not apply to non-oral routes, neglect the difference in progestogens, and do not address tibolone, a valuable alternative to classical HT in Europe.
• •And finally, are these epidemiological findings biologically plausible? Can estrogens cause breast cancer and why then does the Women's Health Initiative (WHI) RCT not find this? And how can the addition of a progestogen increase the ET risk further as progestogens are pro-apoptotic and down-regulate estrogen receptors as well as local estrogen biosynthesis?

In conclusion, we have a problem as we cannot formulate any general advice that holds for the majority of European postmenopausal women due to lack of consistency, lack of biological plausibility, and lack of relevance of randomized clinical trial data to our daily practical work.So, we have a problem and not a firm basis for undisputable statements.     

Population attributable risk of modifiable risk factors associated with invasive breast cancer in women aged 45–69 years in Queensland,Australia

ObjectivesTo quantify the population attributable risk of key modifiable risk factors associated with breast cancer incidence in Queensland, Australia.Study designPopulation attributable fractions (PAFs) for high body mass index (BMI), use of hormone replacement therapy (HRT), alcohol consumption and inadequate physical activity were calculated, using prevalence data from a representative survey of women attending mammographic screening at BreastScreen Queensland in 2008 and relative risk estimates sourced from published literature. Attributable cancers were calculated using ‘underlying’ breast cancer incidence data for 2008 based on Poisson regression models, adjusting for the inflation of incidence due to the effects of mammographic screening.Main outcome measuresAttributable burden of breast cancer due to high body mass index (BMI), use of hormone replacement therapy (HRT), alcohol consumption and inadequate physical activity.ResultsIn Queensland women aged 45–69 years, an estimated 12.1% (95% CI: 11.6–12.5%) of invasive breast cancers were attributable to high BMI in post-menopausal women who have never used HRT; 2.8% (95% CI: 2.7–2.9%) to alcohol consumption; 7.6% (95% CI: 7.4–7.9%) to inadequate physical activity in post-menopausal women and 6.2% (95% CI: 5.5–7.0%) to current use of HRT after stratification by BMI and type of HRT used. Combined, just over one quarter (26.0%; 95% CI: 25.4–26.6%) of all invasive breast cancers in Queensland women aged 45–69 years in 2008 were attributable to these modifiable risk factors.ConclusionsThere is benefit in targeting prevention strategies to modify lifestyle behaviours around BMI, physical activity, HRT use and alcohol consumption, as a reduction in these risk factors could decrease invasive breast cancer incidence in the Queensland population.     

Glutathione S-transferase M1 status and breast cancer risk: a meta-analysis

It is not yet clear whether Glutathione S-transferase M1 (GSTM1) polymorphisms affect the risk of breast cancer. The aim of this study is to provide a comprehensive meta-analysis of all the available, published case-control studies on the extent of the possible association between GSTM1 polymorphisms and susceptibility to breast cancer. Twenty case-control studies on GSTM1 and breast cancer were identified using both PUBMED and a manual search. Meta-analysis was conducted by the Peto method. Subgroup analyses were undertaken, in order to explore the relationship between effect sizes and the study characteristics. The overall odds ratio (OR) was found to be 1.06 (95% CI, 0.99-1.14). The OR for post-menopausal women with GSTM1 deficiency was determined to be 1.19 (95% CI, 1.05-1.34). In populations with a low frequency of GSTM1 deficiency, a greater increase was observed (OR, 1.20; 95% CI, 1.08-1.34). Furthermore, the highest associations were found in post-menopausal women with a low frequency of GSTM1 deficiency (OR, 1.44; 95% CI, 1.20-1.73). The fact that GSTM1 deficiency is not rare in the general population implies that the attributable risk for breast cancer could be sizable. Further studies focusing on the structure of haplotype blocks of GSTM1 are required in order to find a specific haplotype with a predisposing breast cancer susceptibility allele.     

Breast cancer risk with postmenopausal hormonal treatment

This review was designed to determine from the best evidence whether there is an association between postmenopausal hormonal treatment and breast cancer risk. Also, if there is an association, does it vary according to duration and cessation of use, type of regimen, type of hormonal product or route of administration; whether there is a differential effect on risk of lobular and ductal cancer; and whether hormone treatment is associated with breast cancers that have better prognostic factors? Data sources for the review included Medline, the Cochrane Database of Systematic Reviews (Cochrane Library, 2005) and reference lists in the identified citations. Eligible citations addressed invasive breast cancer risk among postmenopausal women and involved use of the estrogen products with or without progestin that are used as treatment for menopausal symptoms. Abstracted data were demographic groupings, categories of hormone use, categories of breast cancer, two-by-two tables of exposure and outcome and adjusted odds ratios, relative risks (RRs) or hazard rates. Average estimates of risk were weighted by the inverse variance method, or if heterogeneous, using a random effects model. The average risk of invasive breast cancer with estrogen use was 0.79 [95% confidence interval (95% CI) = 0.61-1.02] in four randomized trials involving 12 643 women. The average breast cancer risk with estrogen-progestin use was 1.24 (95% CI = 1.03-1.50) in four randomized trials involving 19 756 women. The average risks reported in recent epidemiological studies were higher: 1.18 (95% CI = 1.01-1.38) with current use of estrogen alone and 1.70 (95% CI = 1.36-2.17) with current use of estrogen-progestin. The association of breast cancer with current use was stronger than the association with ever use, which includes past use. For past use, the increased breast cancer risk diminished soon after discontinuing hormones and normalized within 5 years. Reasonably adequate data do not show that breast cancer risk varies significantly with different types of estrogen or progestin preparations, lower dosages or different routes of administration, although there is a small difference between sequential and continuous progestin regimens. Epidemiological studies indicate that estrogen-progestin use increases risk of lobular more than ductal breast cancer, but the number of studies and cases of lobular cancer remains limited. Among important prognostic factors, the stage and grade in breast cancers associated with hormone use [corrected] do not differ significantly from those in non-users, but breast cancers in estrogen-progestin users are significantly more likely to be estrogen receptor (ER) positive. In conclusion, valid evidence from randomized controlled trials (RCTs) indicates that breast cancer risk is increased with estrogen-progestin use more than with estrogen alone. Epidemiological evidence involving more than 1.5 million women agrees broadly with the trial findings. Although new studies are unlikely to alter the key findings about overall breast cancer risk, research is needed, however, to determine the role of progestin, evaluate the risk of lobular cancer and delineate effects of hormone use on receptor presence, prognosis and mortality in breast cancer.     

Rationale for using raloxifene to prevent both osteoporosis and breast cancer in postmenopausal women

Both osteoporosis with fracture and breast cancer are important health issues for postmenopausal women. It is well known that estrogen and estrogen receptors (ERs) play an important role in the pathogenesis of both diseases. In past decades, hormone therapy (HT), mainly estrogen plus progestin (EPT), has been frequently used for the purpose of preventing and treating postmenopausal osteoporosis because of its efficacy, but it also contributes to a significant increase in breast cancer. Currently, there is a dilemma regarding the use of estrogen for postmenopausal women. Fortunately, an increasing understanding of the action of estrogen has led ultimately to the design of new drugs that work by virtue of their interaction with the ER; these drugs have come to be known as selective estrogen receptor modulators (SERMs), and are not only effective in preventing osteoporosis and managing those with osteoporosis, but also in decreasing the incidence of breast cancer. Among these SERMs, raloxifene may be the most attractive agent based on the evidence from five recent large trials (Multiple Outcomes of Raloxifene Evaluation [MORE], Continuing Outcomes Relevant to Evista [CORE], Raloxifene Use for the Heart [RUTH], Study of Tamoxifen and Raloxifene [STAR], and Evista Versus Alendronate [EVA]). The former three trials showed that raloxifene not only decreases the incidence of osteoporosis-associated fractures, but also has efficacy in breast cancer prevention. The head-to-head comparison with the anti-fracture agent alendronate (EVA trial) and the chemoprevention agent tamoxifen (STAR trial) further confirmed that raloxifene is a better choice. We concluded that since there is an absence of a therapeutic effect on relieving climacteric symptoms and there is the presence of a potential risk of thromboembolism in the use of raloxifene, this drug can be prescribed for clear indications, such as the management of osteoporosis, the prevention of fracture, and decreasing the incidence of invasive breast cancer, with careful monitoring for thromboembolism. It is reasonable to use raloxifene as an appropriate medicine that targets climacteric symptom-free postmenopausal women because of its overall favorable risk-benefit safety profile using the global index proposed by the Women's Health Initiation (WHI).     

Postmenopausal hormone drugs and breast and colon cancer: Nordic countries 1995-2005

Objectives

The purpose of this study was to utilize the variation in the level and timing of the change in postmenopausal hormone therapy (HT) use between the Nordic countries to assess the population-level impact of decline in HT use on the breast and colon cancer incidences.

Methods

Nationwide HT-sales data in defined daily doses (DDDs) per 1000 inhabitant in 1995–2005 in Finland, Iceland, Norway and Sweden were obtained from drug control authorities. Breast and colon cancer incidence data by 5-year age-groups were obtained from the National Cancer Registers. By time series analysis we estimated in each age-group and country how much a change in HT-sales changes cancer incidence.

Results

The decline of HT-sales varied; the decline from the highest sales was 61% in Sweden, 51% in Norway, 43% in Iceland and 25% in Finland. With the exception of Finland, the breast cancer incidence increased from 1995 to the year following the year with maximum HT-sales and decreased after that year. In the model combining countries and years, changes in HT-sales predicted the change in breast cancer incidence, an average 7% for each 10 DDD units of HT-sales. No clear association between HT-sales and colon cancer incidence was found.

Conclusions

The time and country specific data suggest, that on the population level, a notable drop from high level of HT use somewhat decreases breast cancer incidence or breaks its increasing trends. The suggested protective effect of HT for colon cancer was not seen.     

The effect of the duration of progestin use on the occurrence of endometrial cancer in postmenopausal women.

OBJECTIVE: Women who have ever used estrogen replacement therapy (ERT), even at a low dose, have an increased incidence of endometrial cancer. The addition of a progestin to ERT reduces the incidence of endometrial cancer. The duration of progestin administration is more important than the dose. DESIGN: A MEDLINE review of the literature was performed using the search terms endometrial cancer, epidemiology, and hormone replacement therapy (HRT). RESULTS: Women who have ever used ERT have an increased incidence of endometrial cancer. The use of HRT for more than 5 years, with a progestin use of <10 days per cycle, has a relative risk = 1.8. Continuous combined HRT, or sequential or cyclic HRT with >10 days of progestin per cycle, appears to decrease the incidence of endometrial cancer to that found in nonusers of HRT. CONCLUSIONS: The use of HRT in postmenopausal women with a uterus reduces the incidence of endometrial cancer. The duration of progestin administration should be 14 days or more per cycle based on recent epidemiologic data.     

Attitudes towards and level of information on perimenopausal and postmenopausal hormone replacement therapy among Norwegian women

In order to investigate women's attitudes towards and level of information on perimenopausal and postmenopausal hormone replacement therapy (HRT) 1019 women over 17 years of age constituting a representative sample of the Norwegian female population were interviewed in 1990 as part of a monthly national opinion poll (response rate 96.5%). Women's magazines proved to be the most important source of information on hormone therapy. Only in the over-45 age group were doctors mentioned frequently as information sources. A high self-assessed information level was associated with a positive attitude towards hormone therapy. Those who had obtained information from a doctor were more positive than those who had not. More than half of those who expressed an opinion believed that hormone therapy increased the risk of heart infarction, stroke, breast cancer and cancer in general. There was a strong association between a negative attitude, towards using hormones and belief in an increased risk of serious disease. The women were more positive towards the use of HRT for the prevention of osteoporosis and for postmenopausal urogenital complaints than for the alleviation of climacteric symptoms.     

Population attributable risk of modifiable risk factors associated with invasive breast cancer in women aged 45–69 years in Queensland,Australia

Objectives

To quantify the population attributable risk of key modifiable risk factors associated with breast cancer incidence in Queensland, Australia.

Study design

Population attributable fractions (PAFs) for high body mass index (BMI), use of hormone replacement therapy (HRT), alcohol consumption and inadequate physical activity were calculated, using prevalence data from a representative survey of women attending mammographic screening at BreastScreen Queensland in 2008 and relative risk estimates sourced from published literature. Attributable cancers were calculated using ‘underlying’ breast cancer incidence data for 2008 based on Poisson regression models, adjusting for the inflation of incidence due to the effects of mammographic screening.

Main outcome measures

Attributable burden of breast cancer due to high body mass index (BMI), use of hormone replacement therapy (HRT), alcohol consumption and inadequate physical activity.

Results

In Queensland women aged 45–69 years, an estimated 12.1% (95% CI: 11.6–12.5%) of invasive breast cancers were attributable to high BMI in post-menopausal women who have never used HRT; 2.8% (95% CI: 2.7–2.9%) to alcohol consumption; 7.6% (95% CI: 7.4–7.9%) to inadequate physical activity in post-menopausal women and 6.2% (95% CI: 5.5–7.0%) to current use of HRT after stratification by BMI and type of HRT used. Combined, just over one quarter (26.0%; 95% CI: 25.4–26.6%) of all invasive breast cancers in Queensland women aged 45–69 years in 2008 were attributable to these modifiable risk factors.

Conclusions

There is benefit in targeting prevention strategies to modify lifestyle behaviours around BMI, physical activity, HRT use and alcohol consumption, as a reduction in these risk factors could decrease invasive breast cancer incidence in the Queensland population.     

Tibolone: clinical recommendations and practical guidelines. A report of the International Tibolone Consensus Group

An international multidisciplinary panel of experts in the management of the menopause met at the 4th Amsterdam Menopause Symposium in October 2004 to determine the specific place of tibolone, a synthetic steroid with a unique clinical profile, within the wide range of currently available postmenopausal therapy options. The consensus was that tibolone is a valuable treatment option for women with climacteric complaints. As well as relieving vasomotor symptoms, tibolone has positive effects on sexual well-being and mood, and improves vaginal atrophy and urogenital symptoms. Prevention of bone loss with tibolone is comparable to that seen with estrogen therapy (ET) and estrogen/progestogen therapy (EPT). As tibolone rarely causes endometrial proliferation, no additional progestogen is required. It also has good tolerability, being associated with a low incidence of vaginal bleeding and of breast pain. Tibolone does not increase mammographic density. Absolute numbers of women at increased risk for breast cancer are estimated to be low or absent with both tibolone and ET, and the risk with tibolone should be significantly lower than that with EPT. Tibolone might therefore be preferable to EPT in certain women who have not been hysterectomised. Based on the evidence available, the panel proposed a number of subgroups of postmenopausal women with vasomotor symptoms in whom tibolone might have added value; these included women with sexual dysfunction, mood disorders, fibroids and urogenital complaints, as well as those with breast tenderness or high mammographic breast density with EPT use.