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This chapter discusses the link between exogenous hormones and cancer. It focuses on estrogen and progesterone effects on tissues of the breast, endometrium, uterine cervix, ovary, and colon. All measures of association (odds ratios (ORs), relative risks (RRs), and hazard ratios (HRs)) for oral contraceptives (OCs) include women who never used OCs as the referent group. Similarly, associations for hormone therapy reflect no menopausal hormone use as the referent group.

Cases illustrating variables that arise in the health care of women who are HIV positive or have AIDS, women with breast or gynecological cancer, and the use of hormone replacement therapy for treatment of menopausal symptoms are presented. For each topic, empirical and theoretical factors are discussed from an “egalitarian perspective” that imputes privileged status to the standpoint of women as patients.

This chapter discusses the different methods of systematic therapy, with stress on the importance of chemotherapy, hormone therapy, and biological therapy in palliative care. Systemic therapy is advantageous compared to local treatment such as surgery and radiotherapy because of its ability to deliver tumouridical therapy throughout the body so that all sites are exposed to therapy. However, it can increase exposure of normal tissues to tumour cells. While this puts a negative light on the efficacy of systemic therapy for the alleviation and palliation of cancer, the chapter affirms that systemic therapy can play a major role in palliation by employing drugs that have limited toxicity and considerable efficacy. Those drugs that are significant in systemic therapy and in palliation are discussed in the chapter, together with the methods and administration of chemotherapy and hormone therapy, the management of patients undergoing chemotherapy, and the biological agents that can be used in the management of diseases.

Endometrial cancer occurs mostly after the menopause and has an excellent prognosis. The age-standardized incidence varies at least ten-fold across countries, suggesting the strong influence of modifiable risk factors. Risk reduction is conferred by current smoking, past oral contraceptive use, childbearing, lower weight and, tentatively, physical activity. The most compelling evidence that hormones determine the risk of endometrial cancer comes from studies of hormone therapy following menopause. Use of estrogens alone for ten years or more increases the risk about ten-fold. This excess risk may be counteracted substantially by combined use of estrogens and progestins. Hence, it should be possible to prevent a substantial fraction of all endometrial cancers through modification of lifestyle, maintaining normal weight, optimal use of oral contraceptives and postmenopausal hormones.

Chapter 8 analyzes how people's health has been harmed—or helped—depending on epidemiologic theory employed. For “harm,” case examples are: (1) hormone therapy, cardiovascular disease, and breast cancer, with iatrogenic disease resulting from biomedical disregard for social determinants of health; (2) peptic ulcers, H. pylori, and allergies, contrasting psychosocial and biomedical extremes; (3) diabetes and Indigenous health, tracing theorizing from “thrifty genes” and racialized disease to reckoning with the transgenerational biological embodiment of social and ecological injustice; and (4) the impact of curtailing and depoliticizing relevant timeframes for analyzing temporal trends in health inequities. For “help,” they are: (a) improving public health surveillance systems; (b) exposing discrimination as a determinant of health inequities; and (c) new national policies and global recommendations to promote health equity. Looking ahead, the chapter argues that the science of epidemiology can be improved by consciously embracing, developing, and debating epidemiologic theories of disease distribution.

The job of scientists is to try to distinguish what is true from what is false by means of observation and experiment. That job has been made difficult by some philosophers of science who appear to give academic respectability to relativist, and even postmodernist, postures. This chapter suggests that the contributions of philosophers to causal understanding have been unhelpful. It puts the case for randomised studies as the safest guarantee of the reliability of scientific evidence. It uses the case of hormone replacement therapy to illustrate the importance of randomisation, and the case of processed meat and cancer to illustrate the problems that arise in the absence of randomised tests. Finally, it discusses the opposition to randomisation that has come from some philosophers of science.

This chapter explains the influence of sex hormones on hemispheric asymmetry and interhemispheric integration. It shows that sex hormones are important modulators of performance asymmetries and that this reveals an intraindividual variation in addition to interindividual variation. The chapter argues that sex hormones have powerful neuromodulatory properties which dynamically change the functional brain organization and cognitive behavior, not only during prenatal development but throughout life. It suggests that a stable hormonal environment with low sex-hormone levels promotes a stable interhemispheric integration, and also reveals that hormone therapy improves intrahemispheric performance at a processing stage critical for the manifestation of across-field advantage. The chapter establishes the potential origin and the true extent of sex differences in functional brain organization and cognitive abilities.

This chapter reviews the factors at each stage of life that affect timing of the menopause, common urogenital disorders and the decision to have a hysterectomy, and the level of symptomatology experienced during the menopause transition and the decision to take hormone replacement therapy (HRT). In particular, it considers whether developmental processes or early life experiences influence these outcomes in addition to genetic and adult social and biological factors.

A compelling case can be made for estrogen’s role in maintaining synaptic health in the context of cognitive aging. This chapter first reviews clinical literature pertinent to estrogenic actions on cognition in menopausal women. Next, the authors provide a comprehensive summary of recent investigations in aging rhesus monkeys, which have emerged as a particularly powerful model for the study of synaptic and cognitive effects of both natural and surgical menopause. In particular, we focus on hippocampal and dorsolateral prefrontal cortex neurons and circuits that degenerate in normal aging and Alzheimer’s disease. The responsiveness of these brain regions to estrogen and implications for their related memory systems are discussed. Finally, the chapter highlights work that needs to be done to more fully understand the molecular basis for the complex interplay between menopause, aging, and vulnerability to Alzheimer’s disease in higher cognitive function and synaptic health.

Before 2002, hormone therapy (HT) was commonly prescribed to restore naturally diminishing hormonal levels during and after menopause. HT was also thought to prevent many health conditions faced by menopausal women, including osteoporosis, heart disease, cancer, and dementia. Support for these claims came primarily from epidemiological studies and basic research suggesting biological plausibility. Women now live a third of their life beyond ovarian function cessation. Given that cognitive impairment and dementia increase with age, increasing life expectancy may result in greater public health consequences. This chapter reviews the potential risks and benefits of HT, with a focus on cognitive function. It also discusses the implications of menopausal HT on cognitive impairment and dementia prevention, diagnosis, and treatment for aging women.

An effort to mitigate the cumbersome physiological, cognitive, and psychological changes that naturally occur during the menopausal transition has been ongoing for decades. Discrepant findings of symptom presentation and mediation across translational models and among human studies have perplexed researchers for years. Specifically, as an understanding of the role of estrogenic signaling in processes underlying cognition and emotion regulation evolved, researchers speculated that exogenous hormonal therapy might modify disease/symptom onset and course. This chapter describes the variable methodological approaches that likely led to disparities in the literature around hormone therapy use, particularly as it pertains to manipulating symptom onset and course of Alzheimer’s pathology. The authors expound upon current recommendations for exogenous hormone therapy use in aging women and how researchers arrived at these conclusions. Finally, we describe remaining questions regarding hormone therapy use and its long-term impact on cognition and mood, Alzheimer’s disease biomarkers, vascular functioning, and genomic variables.

There are three services that a palliative care team may be specifically involved with: the pain clinic, radiotherapy, and medical oncology. This chapter reviews the contribution of these services to the care of patients with advanced cancer. The pain clinic and oncology services have an important role in treating pain and other symptoms of advanced cancer. Obviously, the role of the palliative care team can overlap with these services. There is the potential for misunderstanding and conflict; although such services may feel threatened by a palliative care team, the problem is not one-sided. If palliative care team members have not worked in a pain clinic or oncology ward, they may be ignorant of the benefits these services can offer. The chapter also considers the available techniques, hormone and chemotherapy, and working with oncology services.

This chapter describes a half-century of research and debate over the synthesis of exogenous hormones for oral contraception and replacement therapy, together with associated risks of heart disease and cancers. Two current methodologies and their limitations are discussed: controlled randomized trials designed to pick up short-term effects of exogenous hormone preparations by comparing a representative sample population taking a new drug with a sample taking a placebo; and observational epidemiology which tracks large cohorts over longer periods. There has been a recurring failure to specify populations at risk accurately or at least agree on adequate procedures for doing so. Differing institutional interests have led to different base populations being used for estimation, and hence to continuing disagreements over appropriate trial criteria. The choice of population models becomes a material factor that may allow biomedical products with significant counter-indications to go on being prescribed, despite evidence of risk to individual women.

Over the last decade, several large-scale randomized trials have reported results that disagreed substantially with the motivating observational studies on the value of various chronic disease–prevention strategies. One high-profile example of these discrepancies was related to postmenopausal hormone therapy (HT) use and its effects on cardiovascular disease and cancer. The Women’s Health Initiative (WHI), a National Heart, Lung, and Blood Institute–sponsored program, was designed to test three interventions for the prevention of chronic diseases in postmenopausal women, each of which was motivated by a decade or more of analytic epidemiology. Specifically, the trials were testing the potential for HT to prevent coronary heart disease (CHD), a low-fat eating pattern to reduce breast and colorectal cancer incidence, and calcium and vitamin D supplements to prevent hip fractures. Over 68,000 postmenopausal women were randomized to one, two, or all three randomized clinical trial (CT) components between 1993 and 1998 at 40 U.S. clinical centers (Anderson et al., 2003a). The HT component consisted of two parallel trials testing the effects of conjugated equine estrogens alone (E-alone) among women with prior hysterectomy and the effect of combined estrogen plus progestin therapy (E+P), in this case conjugated equine estrogens plus medroxyprogesterone acetate, among women with an intact uterus, on the incidence of CHD and overall health. In 2002, the randomized trial of E+P was stopped early, based on an assessment of risks exceeding benefits for chronic disease prevention, raising concerns among millions of menopausal women and their care providers about their use of these medicines. The trial confirmed the benefit of HT for fracture-risk reduction but the expected benefit for CHD, the primary study end point, was not observed. Rather, the trial results documented increased risks of CHD, stroke, venous thromboembolism (VTE), and breast cancer with combined hormones (Writing Group for the Women’s Health Initiative Investigators, 2002). Approximately 18 months later, the E-alone trial was also stopped, based on the finding of an adverse effect on stroke rates and the likelihood that the study would not confirm the CHD-prevention hypothesis.

This chapter discusses the pros and cons of using estrogen and cognition-enhancing drugs in treating neuropsychiatric conditions, and presents health risks related to a decrease in estrogen levels in middle-age women, including Alzheimer’s disease, depression, and cognitive impairment. The use of hormone-replacement therapy for women during and after menopause, whose estrogen levels were low, was questioned following the Women’s Health Initiative report of risks and benefits of estrogen replacement. The chapter presents studies on the use of cognition-enhancing drugs by healthy, older individuals. The use of amphetamines to enhance cognition in older people is discussed along with its drawback of being addictive. The chapter discusses the positive effect of caffeine on improving cognition and its impact on the pathology of Alzheimer’s disease.

Over the past three decades, the media has bombarded the public with a seemingly endless array of risks, from the familiar to the exotic: hormone replacement therapy, anthrax, mad cow disease, SARS, West Nile virus, radon, vaccine-associated autism, childhood obesity, medical errors, secondhand smoke, lead, asbestos, even HIV in the porn industry. A drumbeat of risks to worry about, big and small, with new studies often contradicting earlier ones and creating further confusion. It's gotten so bad that some people feel like they're taking their lives in their hands just trying to order a meal at a restaurant. “Will it be the mad cow beef, the hormone chicken, or the mercury fish?” asks an imperious waiter in one of my favorite cartoons from the Washington Post. “Urn ... I think I'll go with the vegetarian dish,” the hesitant diner responds. “Pesticide or hepatitis?” the waiter asks. The diner, growing ever more fearful, asks for water. The waiter persists: “Point source, or agricultural runoff?” Perhaps it's time for the media to become part of the solution rather than continuing to be part of the problem. Ideally, science journalists could lead the way toward improved risk coverage that moves beyond case-by-case alarms—and easy hype—to a more consistent, balanced approach that puts the hazard du jour in broader perspective. The challenge is to create stories with chiaroscuro, painting in more subtle shades of gray rather than extremes of black and white. Too often, as my late Washington Post colleague Victor Cohn once said, journalists (and their editors) gravitate toward stories at either extreme, emphasizing either “no hope” or “new hope.” Unfortunately, today's “new hope” often becomes tomorrow's “no hope” (which is a good reason for avoiding words like “breakthrough” or “cure” in the first place). Hormone replacement therapy (HRT) is a classic example of this yo-yo coverage. In the '60s and '70s, the media helped overpromote hormones as wonder drugs for women, promising everlasting youth as well as a cure for hot flashes. Concerns rose, however, with reports of possible links to cancers of the breast and uterus. Later, when the uterine cancer risk was shown to return to normal by adding an additional hormone, the publicity about HRT became mostly positive again, emphasizing its potential to protect against bone loss and heart disease.

abstract

This task assesses the following clinical skills: • Patient safety • Communication with patients and their relatives • Information gathering • Applied clinical knowledge You are a ST4 doctor working in an infertility clinic. A couple who were referred to the clinic by their GP have returned for review. She has had oligomenorrhoea for the past year. She does not report headaches, visual disturbance, galactorrhoea or hyperandrogenism, she has been trying to conceive for two years. Her partner had an orchidopexy at the age of two. The assessor will ask you some questions and then give you the results of their investigations. You will be asked to explain the results and next steps to the patient. You have 10 minutes for this task (+ 2mins initial reading time). Please check that candidate and actor have read instructions. Ask the candidate what investigations they would like to organize for this patient and her partner. Give them the results of investigations (if asked for): Pregnancy test—ve LH 45, FSH 40, E2 120 (day two of cycle) PRL—200 TSH—1.2 Testosterone—0.8 USS—NAD HSG—Patent tubes Rubella immune Chlamydia swabs—ve Smear—ve Semen analysis—10m/ ml, 32% motility, 3% normal forms Ask them if they want to arrange any further investigations. Expect candidate to ask to repeat gonadotrophins more than a month after initial measurement in order to confirm the diagnosis of Premature Ovarian Insufficiency (POI). They should also repeat the semen analysis. Tell them that repeat gonadotrophins were again elevated—FSH 35, LH 20, E2 120. Repeat semen analysis was 15m/ ml, 34% motile, with 4% normal forms. Ask the candidate to explain these results to the patient and explain next steps, including further investigation and treatment options. They should then recommend that further investigations are arranged including karyotype, an auto-immune screen, lupus anticoagulant and vitamin B12 levels to try and identify a cause for the POI. Treatment options should include the role of hormone replacement therapy and oocyte donation with IVF. Observe consultation skills including the candidate’s ability to break bad news. Record your overall clinical impression of the candidate for each domain (i.e. pass, borderline, or fail).