Medscape women's health最新文献

Objective: The aims of this study were to examine the relation between life satisfaction and the menopausal transition, identify factors predictive or associated with life satisfaction, and determine the relation between life satisfaction and other health outcomes.

Research design and methods: This is a prospective population-based study of 438 middle-aged Australian-born women followed for 6 years after baseline measures. Retention rate at 6 years was 90% (n = 395). Two self-reported measures of life satisfaction (Life Satisfaction Index-Z scale [LSI-Z] and Satisfaction with Life Scale [SWLS]) were used in year 6. Positive and negative affect scales and questions about satisfaction with work and daily living were also used. Sociodemographic variables were measured at baseline, and attitudes toward menopause and aging were documented at years 2 and 5, respectively. Other explanatory variables, including symptoms, health, stress, life events, sexual functioning, and lifestyle were measured in year 6.

Results: Women overwhelmingly endorsed positive responses to life satisfaction questions. The LSI-Z and the SWLS were highly correlated with each other (r = 0.70), with the mood scales, and with responses to questions about satisfaction with work and daily living. The LSI-Z and SWLS were not related to menopausal status, hormone levels (follicle-stimulating hormone, estradiol), age, body mass index, hot flushes, hormone replacement therapy, sexual interest, employment status, type of profession, children at home, alcohol, chronic conditions, surgery, premenstrual complaints, life events (major or secondary), and social support. Stepwise multiple regression found that life satisfaction was predicted by earlier attitudes and was positively associated with feelings for partner and exercise and negatively associated with daily hassles, interpersonal stress, dysphoric symptoms, and current smoking.

Conclusions: Life satisfaction was closely related to mood, predicted by earlier attitudes, and affected by relationship to partner, stress, and lifestyle. Life satisfaction was unrelated to menopause status, hormone levels, or hormone replacement therapy.

The concern that postmenopausal hormone replacement therapy (HRT) may cause cancer of the breast has generated much research in epidemiology, endocrinology, and tumor cell biology. The recognition that naturally occurring 17beta-estradiol is a weak genotoxic and mutagenic carcinogen provides a plausible background for the association of breast cancer with HRT. However, because of the small anticipated effect and several confounding factors, the epidemiology of this association is complex. The consensus at this writing is that long-term HRT (>10 years) is associated with an increased risk of breast cancer, which, on average, is equivalent to the risk associated with delaying menopause for the same period of time. The particular risk depends on the duration and probably the dose to which the individual woman is exposed, as well as on a number of predisposing environmental and genetic factors. One clinical implication of the data reviewed here is that the dosage of HRT chosen should be the lowest that produces the desired effect. The use of HRT in women with a history of breast cancer is also addressed. Low-dose estrogen together with a selective estrogen receptor modulator to protect the breast may be a treatment option for women with severe symptoms of estrogen deficiency.

Breast cancer remains a common and devastating disease that affects approximately 180,000 women and results in more than 43,000 deaths annually in the United States. Although only 10% of patients have overt metastatic disease at the time of diagnosis, as many as one third of those who present with lymph node-negative disease and half of those who present with lymph node-positive disease eventually develop metastatic breast cancer. With few exceptions, metastatic breast cancer is largely incurable, and the median duration of survival remains 18 to 24 months. Over the past 3 decades, both laboratory and clinical efforts to increase survival have focused on dose intensity in chemotherapy regimens.

Several important questions emerge from the study of gender differences in schizophrenia: Why does schizophrenia begin later in women? Why is outcome superior in women, at least in the first 15 years after onset? What causes sex differences in symptoms? What can gender differences teach us about the etiology of schizophrenia? Do men and women require substantially different treatments? What interventions during pregnancy and after childbirth ensure optimal health for the children of mothers with schizophrenia? Although complete answers may not yet be forthcoming, it is important to define the questions and keep them in mind when delivering services to women suffering from this severe, persistent mental illness.

Premenstrual syndrome (PMS), a common disorder in women, refers to physical and/or mood symptoms that appear predictably during the latter half of the menstrual cycle, last until menses begin, and are absent during the early part of the menstrual cycle. A diagnosis of PMS requires that the symptoms be severe enough to affect a woman's ability to function at home or in the workplace or in her relationships with others. Diagnostic assessment entails a thorough medical and psychiatric history and prospective daily ratings. Disorders such as major depression, anxiety, hypothyroidism, and diabetes must be excluded before a diagnosis of PMS can be considered. Treatment strategies include either eliminating the hormonal cycle associated with ovulation or treating the symptom(s) causing the most distress to the patient. Medical therapies are available for both treatment approaches but should be initiated only after behavioral measures have failed; the physician must also carefully weigh the severity of symptoms against the potential for adverse effects of treatment.

In just 3 years, striking new advances have been made in understanding the molecular mechanisms that govern the crosstalk between osteoblasts/stromal cells and hemopoietic osteoclast precursor cells that leads to osteoclastogenesis. Led first by the discovery of osteoprotegerin (OPG), a naturally occurring protein with potent osteoclastogenesis inhibitory activity, rapid progress was made to the isolation of RANKL, a transmembrane ligand expressed on osteoblasts/stromal cells, that binds to RANK, a transmembrane receptor on hemopoietic osteoclast precursor cells. The interaction of RANK and RANKL initiates a signaling and gene expression cascade that results in differentiation and maturation of osteoclast precursor cells to active osteoclasts capable of resorbing bone. Osteoprotegerin acts as a decoy receptor; it binds to RANKL and blocks its interaction with RANK, thus inhibiting osteoclast development. Many of the calciotropic hormones and cytokines, including vitamin D3, parathyroid hormone, prostaglandin E2 and interleukin-11, appear to stimulate osteoclastogenesis through the dual action of inhibiting production of OPG and stimulating production of RANKL. Estrogen, on the other hand, appears to inhibit production of RANKL and RANKL-stimulated osteoclastogenesis. Recently, the results of the first clinical trial with OPG supported its potential as a therapeutic agent for osteoporosis. The new understanding provided by the RANK/RANKL/OPG paradigm for both differentiation and activation of osteoclasts has had tremendous impact on the field of bone biology and has opened new avenues for development of possible treatments of diseases characterized by excessive bone resorption.