Popular understanding holds that genetic changes create cancer. James DeGregori uses evolutionary principles to propose a new way of thinking about cancer’s occurrence. Cancer is as much a disease of evolution as it is of mutation, one in which mutated cells outcompete healthy cells in the ecosystem of the body’s tissues. His theory ties cancer’s progression, or lack thereof, to evolved strategies to maximize reproductive success.

Through natural selection, humans evolved genetic programs to maintain bodily health for as long as necessary to increase the odds of passing on our genes—but not much longer. These mechanisms engender a tissue environment that favors normal stem cells over precancerous ones. Healthy tissues thwart cancer cells’ ability to outcompete their precancerous rivals. But as our tissues age or accumulate damage from exposures such as smoking, normal stem cells find themselves less optimized to their ecosystem. Cancer-causing mutations can now help cells adapt to these altered tissue environments, and thus outcompete normal cells. Just as changes in a species’ habitat favor the evolution of new species, changes in tissue environments favor the growth of cancerous cells.

DeGregori’s perspective goes far in explaining who gets cancer, when it appears, and why. While we cannot avoid mutations, it may be possible to sustain our tissues’ natural and effective system of defense, even in the face of aging or harmful exposures. For those interested in learning how cancers arise within the human body, the insights in Adaptive Oncogenesis offer a compelling perspective.

    In 1859 a Hungarian obstetrician named Ignaz Semmelweis, reflecting on his years as resident in the Vienna maternity clinic, wrote a graphic account of his attempt to diagnose and eliminate the then epidemic scourge of childbed fever.  The resulting Etiology triggered an immediate and international squall of protest from Semmelweis’s colleagues; today it is recognized as a pioneering classic of medical history.  Now, for the first time in many years, Codell Carter makes that classic available to the English-speaking reader in this vivid translation of the 1861 original, augmented by footnotes and an explanatory introduction.  For students and scholars of medical history and philosophy, obstetrics and women’s studies, the accessibility of this moving and revolutionary work, important both as an historical document and as a groundbreaking precursor of modern medical theory, is long overdue.
    Semmelweis’s exposure to the childbed fever was concurrent with his appointment to the Vienna maternity hospital in 1846.  Like many similar hospitals and clinics in the major cities of nineteenth-century Europe and America, where death rates from the illness sometimes climbed as high as 40 percent of admitted patients, the Viennese wards were ravaged by the fever.  Intensely troubled by the tragic and baffling loss of so many young mothers, Semmelweis sought answers.  The Etiology was testimony to his success.  Based on overwhelming personal evidence, it constituted a classic description of a disease, its causes, and its prevention.  It also allowed a necessary response to the obstetrician’s already vocal, rabid, and perhaps predictable critics.  For Semmelweis’s central thesis was a startling one - the fever, he correctly surmised, was caused not by epidemic or endemic influences but by unsterilized and thus often contaminated hands of the attending physicians themselves.
    Carter’s translation of this radical work, judiciously abridged and extensively footnoted, captures all the drama and impassioned conviction of the original.  Complementing this translation is a lucid introduction that places Semmelweis’s Etiology in historical perspective and clarifies its contemporary value.  That value, Carter argues, is considerable.  Important as a model of clinical analysis and as a chronicle of early nineteenth-century obstetrical practices, the Etiology is also a revolutionary polemic in its innovative doctrine of antisepsis and in its unique etiological explanation of disease.  As such its recognition and reclamation allows a crucial understanding, one that clarifies the roots and theory of modern medicine and ultimately redeems and important, resolute, pathfinder.

This book investigates the controversial claim by welfare critics that public assistance programs like Food Stamps and the National School Lunch programs contribute to obesity among the poor. The author synthesizes empirical evidence from an array of disciplines--anthropology, economics, epidemiology, medicine, nutrition science, marketing, psychology, public health, sociology, and urban planning--to test this claim and to test whether other causal processes are at work.

With a lucid presentation that makes it a model for applying research to questions of social policy, the book lays out the different hypotheses and the possible causal pathways within each. The four central chapters test whether "public assistance causes obesity," "obesity causes public assistance," "poverty causes both public assistance and obesity," and "Factor X causes both." The factors in the last category that may relate to both public assistance and obesity include stress, disability, and physical abuse.

Autism is a complex and incurable constellation of bizarre behaviors, impaired cognition, limited language, and most distressingly, a lack of responsiveness to other people, and it has been the center of impassioned debates for decades. What is it? What causes it? How can it be treated?

In The Science and Fiction of Autism, one of the country's leading experts in behavioral treatments approaches autism through the context of its controversies, showing where extraordinary and unfounded claims have falsely raised hopes, stirred fears, and ruined lives. Arguing that autism is an entirely biological disorder, however complex its neurological origins, Laura Schreibman lays waste to the beliefs that it is caused by "refrigerator mothers" or the MMR vaccine, as well as to the simplistic claims that it can be cured by a variety of unsubstantiated treatments.

Drawing from her own long clinical experience with autistic children and their parents, Schreibman arms her readers--students, educators, psychologists, and parents alike--with information and arguments to deal with the onslaught of good, bad, deficient, and irrelevant ideas about autism.

Twenty-Two Years presents the results of a unique longitudinal study of the first 22 years in the lives of more than 200 young people with varying degrees of mental retardation. By following their paths through available services, job histories, leisure activities, friendships, and marriages, the authors provide objective information about the quality of life of young people with mental retardation.

The book makes a unique contribution by determining what factors in childhood predict who will and who will not require mental retardation services and, for those who disappear from services, why some fare better than others. Most important, the results help answer a question that haunts parents: "What will happen when my child grows up?"

This study expands on an internationally acclaimed clinical and epidemiological study of children with mental retardation published in 1970. It provides prevalence rates by severity of mental retardation, gender, social class, and family stability, and shows how these change over time.

The authors confirm the central role of biomedical factors in the etiology of severe mental retardation. For the etiology of mild mental retardation, the book examines the relative contributions of biomedical and intergenerational genetic factors as well as psychosocial adversity. The book should be of interest to a broad range of clinicians, researchers, and students, as well as the families of people with mental retardation, and it will serve as a model for future epidemiological and follow-up research.