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Epidemiology has been the principal discipline in preparing the grounds for the prevention of infectious diseases, several forms of cancer, and most cardiovascular diseases. However, it has contributed relatively little towards the understanding of causation and prevention of injuries. This chapter presents an approach for teaching general injury epidemiology, covering teaching and learning objectives, teaching contents, and assessing students' achievements.

Over the last fifty years, the hospital has been technologized, corporatized, and bureaucratized due to demographic, political, economic, and scientific developments. The demographic shift has led to the greying of the population, with an associated increase in chronic disease, resulting in hospitalized patients becoming sicker and more complex. Legislative changes such as the introduction of Medicare led to a surge in the number of hospitalizations of older individuals; the subsequent move to prospective payment led to shorter hospital stays—and increased reliance on the skilled nursing facility. A change in the economic climate produced consolidation, with the resulting growth of hospital chains and hospital systems. Scientific advances, fuelled in many cases by generous research grants from the National Institutes of Health, led to new, non-invasive imaging techniques such as computerized tomography and magnetic resonance imaging. Advances in biology and epidemiology led to new approaches to the hospital’s management of diseases as disparate as heart attacks and cancer.

The principles of design, conduct, analysis and reporting of clinical trials, including trials conducted for regulatory purposes, are sufficiently advanced that drugs and other therapeutic interventions can be put to fair tests that provide valid evidence of efficacy and safety. However, clinical research—especially research that can make a product a winner or a loser—is not a value-free human endeavor. The rosiglitazone story exemplifies how medical product manufacturers can manipulate regulatory evidence by designing trials to ensure certain answers are—or are not—obtained, how companies can try to intimidate scientists whose research yields unfavorable evidence about a product, and how ambiguous can be the evidence from clinical trials. Federally-mandated comparative effectiveness research does not generate evidence used in product regulation, but it generates evidence that has market implications. It therefore will always be at risk for the same kinds of manipulation observed in the rosiglitazone saga.

Epidemiological research is the cornerstone of public health. Frequently, it begins with a hypothesis, for which data is then collected and the hypothesis is proved or disproved. This chapter describes how people’s searches on commercial search engines can also be used to improve public health, not only because it provides useful data for studies that are based on a hypothesis, but because they can be used to create new hypotheses. This chapter details how algorithms can scour data to discover adverse effects of drugs, to identify possible risk factors for disease, and to rapidly alert health authorities when mass gatherings such as music festivals become the breeding ground for disease.

Schizophrenia research encompasses many different categories of observation: (a) genetic research, which examines variants in single base pairs, (b) cellular and applied neuroscience, including animal models, (c) clinical research representing a broad spectrum of patient-centered research, and (d) population-based epidemiology and health services research. Each field of research has a natural tendency to become more specialized and, as a consequence, more inward looking. Meta-research, the study of the process of research per se, shows that creativity tends to occur at the boundaries of disciplines and research areas. This chapter examines ways to facilitate this type of cross-disciplinary translational research. Examples are provided of collaborative scientific programs that have used clues from fields such as epidemiology and genetics, and these clues are explored via the prism of various neuroscience platforms. Published in the Strungmann Forum Reports Series.

The introduction lays out what we know about the social context of schizophrenia from the epidemiological literature: that risk of schizophrenia is particularly high for immigrants from predominantly dark-skinned countries to Europe; that risk increases with lower socioeconomic status at birth and even at parent’s birth; that risk increases with urban dwelling and seems to increase the longer time is spent in cities; that risk increases as ethnic density in the neighborhood declines. The chapter presents a history of the way schizophrenia has been understood in the United States, and the diagnostic complexities of serious psychotic disorder. It then discusses what ethnographers have observed so far about the social conditions which may shape the experience of psychosis: the local cultural interpretation of mental illness; the role and presence of the family; the structure of work; and the basic social environment. This becomes the ground for our case studies.

This chapter provides a critical overview of historical and contemporary approaches to preventing sexual violence. It also presents an overview of all chapters, outlining their contribution to the field and provide a clear message related to the coherence of the book.

Prevention is a seductive concept. It has a wide range of positive connotations largely derivable from the medical world. However, in order to prevent, it is important to locate the cause and have an accurate picture of the associated epidemiology of the problem. The purpose of this chapter is to examine the extent to which either of these factors are present in what is known about sexual violence and further to explore the extent to which what is known informs preventive strategies. Starting from the position that violence (against women) is 'an everyday experience this chapter will consider the ways in which strategies designed to prevent sexual violence actually deny the ordinariness of such, but rather rely on rendering it extra-ordinary in order to render such strategies justifiable. These practices of denial, by implication, also deny what is known about its causes and its epidemiology. As a result, such practices tent to serve the interests of the professionals engaged in then rather than those so afflicted by such violence

Since the Great Depression, schools and sports administrators had chosen to manage football’s financial risks by focusing primarily on improving insurance schemes. Large athletic insurance programs offered families and schools a greater degree of financial protection against the risk of football injuries. The development of these programs also influenced football injury epidemiology. Mid-century research using large scale insurance data pointed to the limitations of protective equipment in preventing injuries. Doctors and researchers’ efforts to “save football” in the face of this evidence represented a broad cultural investment in preserving the sport among the experts responsible for protecting youth health. By the early 1960s, the most influential sports and research organizations had zeroed in on setting standards for football helmets as the most important technological strategy needed to control the sport’s hazards.

This chapter discusses the spread of diseases over contact networks between individuals and the methods used to model this process. The chapter begins with an introduction to the classic models of mathematical epidemiology, including the SI model, the SIR model, and the SIS model. Models for coinfection and competition between diseases are also discussed, as well as “complex contagion” models used to represent the spread of information. The remainder of the chapter deals with the behavior of these models on networks, where the behavior of spreading diseases depends strongly on network structure. It is shown that the SIR model maps to a bond percolation process on networks, allowing us to solve for static properties such as the total number of individuals infected in a disease outbreak. The case of the configuration model is developed in detail and the calculations are extended to competing diseases, coinfection, and complex contagion. Time-dependent behavior of diseases on networks is also studied using various differential equation approximations, including pair approximations and degree-based approximations.

Intellectual disability is the most common developmental disorder and the most handicapping of the disorders beginning in childhood. It ranks as first among chronic conditions that limit full participation in society. Epidemiologic approaches provide a basis for understanding the distribution and dynamics of health, disease, and disorder for persons with intellectual disability; epidemiology is the foundation of public health practice. Because it relies largely on statistical methods, accurate data and clear definitions are essential. The interpretation of epidemiologic information requires background knowledge of demography, social sciences, environmental science, and the clinical sciences. Although epidemiologic studies are essential in establishing prevalence, and in describing the demography of a disorder, the role of epidemiology is far more extensive than this. Epidemiology can teach us about the nature and scope of intellectual disability and associated general medical, behavioral, emotional, and psychiatric problems. In so doing, epidemiologic approaches may be combined with neurobiologic and psychosocial measures. Moreover, epidemiologic studies can disclose individual developmental trajectories and the influences that shape those trajectories. Some of these influences promote risk; others provide protection and promote resiliency in the individual. Finally, experimental approaches in epidemiology allow the study of causative processes, factors that influence the course of the disorder, and service needs. It is these more extensive uses of epidemiology that are called for in future research. Chapter 3 outlines the classification of intellectual disability. This chapter will discuss the use of definitions of intellectual disability in establishing its prevalence, factors affecting prevalence, variability in rates in the various states, demographic features including the impact of increasing life expectancy, associated physical, behavioral, and emotional impairments, and new research directions. Accurate estimates of the number of intellectually disabled individuals are required for planning purposes and to gain better knowledge of the impact of interventions. Studies of the prevalence and incidence of intellectual disability date back to at least 1811, when Napoleon ordered a census of “cretins” to be made in one of the Swiss cantons (Kanner, 1964). Although little information is available about how this census was used, many surveys have been carried out since that time.

It has become fashionable to start discussions of disease related to fibrous inorganic materials by referring to Pliny the Younger (A.D. 61-114), who commented in a letter on the sickness of slaves who worked with asbestos. His observation was forgotten, as evidenced by the fact that during the Middle Ages, Paracelsus (1493–1541) as well as Agricola (1494–1556) wrote extensively on “miner’s disease” without mentioning asbestos. Later, Zenker (1867) coined the word pneumo(no)coniosis to describe the diseases endemic to coal and iron miners. Differential diagnosis of the pulmonary disorders, tuberculosis, silicosis, pneumonia, and other lung disease was attempted thereafter, although the varieties were often confused even by experienced physicians. The industry that provided asbestos to modern society started at about this same time (in the 1870s). The first indication of pulmonary disorder in an asbestos worker came in an autopsy report of fibrosis by Dr. Montague- Murray at Charing Cross Hospital, London, in 1899–1900 (Peters and Peters, 1980). By 1902 asbestos was included in the list of dusts considered injurious by the Lady Inspector of Factories, Adelaide Anderson (Oliver, 1902). Auribault (1906) appears to have been the first to note high mortality in workers in an asbestos mill and weaving establishment, but he attributed their illness to calcium carbonate dust rather than asbestos. Scarpa (1908) believed the pulmonary disease of 30 asbestos workers was caused by tuberculosis, and Fahr (1914), who published the case of a female asbestos worker who died of “pleuro-pneumonia . . . with a large number of crystals in pulmonary tissue of a peculiar nature,” was clearly somewhat mystified at the presence of nonbiological materials. It was Cooke (1924, 1927, 1929) who first defined asbestos as a specific etiologic agent in pulmonary fibrosis. He described extensive fibrosis with thickened pleura and adhesions to the chest wall and pericardium in asbestos workers and noted the presence of abundant mineral matter (“curious bodies”), but also tubercular lesions. The term asbestosis was used in the 1927 publication. Pancoast and Pendergrass (1925) argued that the fibrosis seen in asbestos workers was a result of ad-mixed silica and an expression of “asbestosilicosis,” signifying uncertain etiology of the observed symptoms, a view that survivied into the 1930s (Lynch and Smith, 1935).