Chronic obstructive pulmonary disease (COPD) is a major health care problem. Formerly mainly a disease of men, women are increasingly frequently afflicted. In many of these patients, exercise intolerance is the chief complaint. Few effective therapies are available. In recent years, dysfunction of the muscles of ambulation has been identified as a source of a portion of the exercise intolerance these patients experience, and this dysfunction has been shown to be, at least in part, remediable. Mechanisms inducing muscle dysfunction include disuse atrophy, malnutrition, low levels of anabolic steroids, and myopathy from corticosteroid use. Endurance exercise training has been conclusively demonstrated to improve exercise tolerance in COPD. Recent studies suggest that strength training is beneficial as well. A new frontier of therapy for muscle dysfunction in COPD is the use of anabolic hormones. Testosterone supplementation has been shown to increase muscle mass and strength in both hypogonadal and eugonadal healthy men. Low-dose testosterone supplementation is being considered for use in postmenopausal women. Though short-term administration of testosterone in moderate doses seems to be well tolerated in both men and women, further studies are required before safety and effectiveness can be established for routine use in COPD patients.

Skeletal muscle dysfunction in chronic obstructive pulmonary disease.

Background: Levels of endogenous hormones have been associated with the risk of breast cancer among postmenopausal women Little research, however, has investigated the association between hormone levels and tumor receptor status or invasive versus in situ tumor status Nor has the relation between breast cancer risk and postmenopausal progesterone levels been investigated We prospectively investigated these relations in a case-control study nested within the Nurses' Health Study Methods: Blood samples were prospectively collected during 1989 and 1990 Among eligible postmenopausal women, 322 cases of breast cancer (264 invasive, 41 in situ, 153 estrogen receptor [ER]-positive and progesterone receptor [PR]-positive [ER + /PR + ], and 39 ER-negative and PR-negative [ER - /PR - ] disease) were reported through June 30, 1998 For each case subject, two control subjects (n = 643) were matched on age and blood collection (by month and time of day) Endogenous hormone levels were measured in blood plasma We used conditional and unconditional logistic regression analyses to assess associations and to control for established breast cancer risk factors Results: We observed a statistically significant direct association between breast cancer risk and the level of both estrogens and androgens, but we did not find any (by year) statistically significant associations between this risk and the level of progesterone or sex hormone binding globulin When we restricted the analysis to case subjects with ER + /PR + tumors and compared the highest with the lowest fourths of plasma hormone concentration, we observed an increased risk of breast cancer associated with estradiol (relative risk [RR] = 33, 95% confidence interval [CI] = 20 to 54), testosterone (RR = 20, 95% CI = 12 to 34), androstenedione (RR = 25, 95% CI = 14 to 43), and dehydroepiandrosterone sulfate (RR = 23, 95% CI = 13 to 41) In addition, all hormones tended to be associated most strongly with in situ disease Conclusion: Circulating levels of sex steroid hormones may be most strongly associated with risk of ER + / PR + breast tumors

https://www.hormonebalance.org/images/documents/Missner%2004%20E,%20A,%20Pr%20B%20Ca%20risk%20JNCI.pdf

Endogenous Estrogen, Androgen, and Progesterone Concentrations and Breast Cancer Risk Among Postmenopausal Women

Background. Contrasting etiologic hypotheses about the role of endogenous sex steroids in breast cancer development among premenopausal women implicate ovarian androgen excess and progesterone deficiency, estrogen excess, estrogen and progesterone excess, and both an excess or lack of adrenal androgens (dehydroepiandrosterone [DHEA] or its sulfate [DHEAS]) as risk factors. We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort to examine associations among premenopausal serum concentrations of sex steroids and subsequent breast cancer risk. Methods: Levels of DHEAS, (Delta 4-)androstenedione, testosterone, and sex hormone binding globulin (SHBG) were measured in single prediagnostic serum samples from 370 premenopausal women who subsequently developed breast cancer (case patients) and from 726 matched cancer-free control subjects. Levels of progesterone, estrone, and estradiol were also measured for the 285 case patients and 555 matched control subjects who had provided information about the day of menstrual cycle at blood donation. Conditional logistic regression models were used to estimate relative risks of breast cancer by quartiles of hormone concentrations. All statistical tests were two-sided. Results: Increased risks of breast cancer were associated with elevated serum concentrations of testosterone (odds ratio [OR] for highest versus lowest quartile = 1.73, 95% confidence interval [CI] = 1.16 to 2.57; P-trend =.01), androstenedione (OR for highest versus lowest quartile = 1.569 95% CI = 1.05 to 2.32; P-trend =.01), and DHEAS (OR for highest versus lowest quartile = 1.48, 95% CI = 1.02 to 2.14; P-trend =.10) but not SHBG. Elevated serum progesterone concentrations were associated with a statistically significant reduction in breast cancer risk (OR for highest versus lowest quartile = 0.61, 95% CI = 0.38 to 0.98; P-trend =.06). The absolute risk of breast cancer for women younger than 40 followed up for 10 years was estimated at 2.6% for those in the highest quartile of serum testosterone versus 1.5% for those in the lowest quartile; for the highest and lowest quartiles of progesterone, these estimates were 1.7% and 2.6%, respectively. Breast cancer risk was not statistically significantly associated with serum levels

/pdf/serum-sex-steroids-in-premenopausal-women-and-breast-cancer-59jds6a850.pdf

Serum Sex Steroids in Premenopausal Women and Breast Cancer Risk Within the European Prospective Investigation into Cancer and Nutrition (EPIC)

Breast cancer incidence rates are high in societies with a Western lifestyle characterized by low levels of physical activity, and by an energy-dense diet rich in total and saturated fat and refined carbohydrates. Epidemiologic studies, so far mostly on postmenopausal women, have shown that breast cancer risk is increased in hyperandrogenic women, with decreased levels of plasma sex-hormone binding globulin, and with increased levels of testosterone and of free estrogens. This paper describes the role of hyperinsulinemia as a physiologic link between nutritional lifestyle factors, obesity, and the development of a hyperandrogenic endocrine profile, and reviews evidence that may or may not support the theory that chronic hyperinsulinemia is an underlying cause of breast cancer. An hypothesis is presented, stipulating that breast cancer risk is increased not only in hyperandrogenic postmenopausal women, but also in premenopausal women with mild hyperandrogenism and normal (ovulatory) menstrual cycles. The author suggests further investigation as to whether there is a positive association between risk of breast cancer before menopause and subclinical forms of the polycystic ovary syndrome (PCOS), and to what extent diet and physical activity during childhood, by modulating the degree of insulin resistance during adolescence, may or may not be determinants of a PCO-like hyperandrogenic endocrine profile persisting into adulthood.

Nutrition, hormones, and breast cancer: Is insulin the missing link?

We evaluated the reproducibility of plasma hormone levels over time in 79 healthy postmenopausal women, ages 51-69 years at baseline, who were not using postmenopausal hormones. Three blood samples were collected between 1989 and 1992 from each of these women. We assessed plasma levels of estradiol, free estradiol, percentage of free estradiol, bioavailable estradiol, percentage of bioavailable estradiol, estrone, estrone sulfate, sex hormone-binding globulin (SHBG), androstenedione, testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and prolactin at each of three sample collections. The means and SD for each of the plasma estrogens, SHBG, and prolactin were similar at each collection. For the androgens, plasma levels tended to decrease over time consistent with an aging effect; decreases with increasing age were statistically significant for androstenedione, dehydroepiandrosterone, and dehydroepiandrosterone sulfate. Intraclass correlation coefficients (ICCs) ranged from 0.92 (95% confidence interval = 0.89-0.95) for SHBG to 0.53 (95% confidence interval = 0.43-0.69) for prolactin. Most correlations were at least 0.70. The ICCs did not vary by age or time since menopause. Women who changed weight over the course of the study tended to have lower ICCs for a number of the hormones, although these differences were not statistically significant. These data indicate that, for most of these plasma hormones, a single measurement can reliably categorize average levels over at least a 3-year period in postmenopausal women.

/pdf/reproducibility-of-plasma-hormone-levels-in-postmenopausal-36o7w0vkja.pdf

Reproducibility of plasma hormone levels in postmenopausal women over a 2-3-year period.

We investigated the role of androgens in premenopausal breast cancer by comparing serum testosterone, dihydrotestosterone, androstenedione, dehydroepiandrosterone sulfate, progesterone, sex-hormone-binding globulin-binding capacity, and urinary testosterone and androstanediol in 63 women with breast adenocarcinoma and 70 healthy controls of similar age. With variables dichotomized at the 75th percentile, the age-adjusted relative risk was 3.4 (95% confidence interval, 1.6–7.3) for high versus low levels of serum testosterone, 2.1 (0.9–4.8) for urinary testosterone, and 2.5 (1.1–5.9) for serum dihydrotestosterone. We observed no differences in other hormones. The strength of the associations changed markedly with increasing time to the onset of the next menses. The risk for testosterone and dihydrotestosterone, which was negligible in women with onset within 5 days of sampling, increased progressively to nearly 10-fold higher than in unstratified data in women with onset 10 days or more after sampling. This study provides arguments in favor of a role for increased androgenic activity in premenopausal breast cancer. It also suggests that unknown factors related to cycle length may be important in modulating the strength of the association with testosterone. The results are discussed also in reference to possible biases and inadequacies in study design.

https://cancerres.aacrjournals.org/content/canres/49/2/471.full.pdf

Androgens and Breast Cancer in Premenopausal Women

In this paper we present a study of the diurnal variation of testosterone (T) and estradiol (E2) in women, carried out as part of the design of a prospective study on the hormonal and nutritional etiology of breast cancer. Blood samples were obtained 5 times on the same day, in the morning and early afternoon, from 23 women aged between 25 and 63 yr. Twelve were sampled within the first days following daylight-saving time (SUMTI) introduction. In postmenopause, T mean values decreased from 08:00 h to 15:00 h and the effect of blood drawing time was statistically significant (p < 0.01), with no significant effects of SUMTI. For E2 mean values, no significant effect was found for either blood drawing time or SUMTI. In premeno-pause, T mean values decreased from morning to afternoon (p < 0.01 ), while no effect of SUMTI was found. A significant decrease was observed for E2 during the day (p < 0.01), with no significant influence of SUMTI. These results indicate that diurnal variation of T and E2 are such, that one must not neglect the possible effects of timing procedures on hormonal measurements, when hormonal hypotheses are tested in comparative studies on cancer etiology.

Diurnal variation of testosterone and estradiol: a source of bias in comparative studies on breast cancer

Repeated serum and urinary androgen measurements in premenopausal and postmenopausal women

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Androgens and Breast Cancer in Premenopausal Women

Diurnal variation of testosterone and estradiol: a source of bias in comparative studies on breast cancer

Repeated serum and urinary androgen measurements in premenopausal and postmenopausal women