Making Sense of Illness: Science, Society, and Disease

The social legitimacy of a disease concept affects the provision of health care, research funding, and insurance reimbursement. Using case studies, Robert Aronowitz shows that disease concepts do not have “some unadulterated biological core” (p. 171), but are based on “negotiations among the different parties with a stake in the outcome” (p. 1). His analysis differentiates “two competing ideal-typical notions of ill health” (p. 8): the ontological view, which became preeminent with the germ theory, maintains that diseases can be conceived independently of the patient; the older holistic perspective holds that diseases result from the interaction of the individual and the environment—a view that has been strengthened by etiological models for chronic disease.

Chronic fatigue syndrome and myalgic encephalitis are functional diseases without an agreed-upon etiology and pathophysiology. Both conditions became well known through media coverage and advocates in the medical and lay communities. They engendered controversy because they lacked conventional indicators and were used to justify occupational disability claims.

Ulcerative colitis became a “paradigmatic psychosomatic disease” (p. 39) because of the failure of somatic theories, the popularity of psychoanalysis, and ineffective treatment. The psychosomatic model waned in the 1960s due to corticosteroid therapy, the failure of psychotherapy, and the rise of gastroenterology, even though no conclusive research discredited it or justified alternative explanations.

Lyme disease resulted from a “subspecialty mind-set, condescending attitudes toward research done in earlier eras by foreign dermatologists, and a natural self-interest in discovering a new disease” (p. 179). Erythema chronicum migrans (ECM), described in Europe about 1910, is caused by a tick bite and produces a rash, joint pain, and other symptoms; about 1950 a spirochete was indicated as its cause, a thesis strengthened by the effectiveness of penicillin therapy. Early Lyme disease patients in Connecticut who saw dermatologists were diagnosed and treated successfully for ECM, while those who saw rheumatologists at Yale Medical School were diagnosed and treated unsuccessfully for juvenile arthritis. Spurred on by the media, lay demands, and munificent federal funding, American researchers who followed the Yale approach produced a superfluous new disease concept that is not accepted in Europe.

The shift from the patient-centered angina pectoris to the ontological coronary heart disease occurred in the 1930s. Previously angina pectoris, which is not always associated with coronary artery occlusion, was thought to be determined by both organic and personal factors. The discovery of coronary thrombosis led to the redefinition of angina pectoris and the exclusion of patients with chest pain but without obstructed coronary arteries.

The medical risk factor, which originated in the Framingham Heart Study using new diagnostic and statistical techniques, attempted to shift medicine from “monocausal, reductionist approaches regarding [chronic] disease to social and individual factors” (p. 112). This “unquestioned, implicit, ill-defined, and largely invisible framework for understanding disease” (pp. 111–12) has become increasingly ontological through claims for the “discrete, quantitative contribution of these factors” and the “tendency to view risk factors as diseases in their own right” (p. 112). Screening and treating risk factors provided physicians with an “economic incentive to support risk factor concepts and practices” (p. 127). Risk factors have “ignored sociocultural processes” (p. 134) like occupation and housing. The type A hypothesis holds that “excessive competitiveness and time urgency is a major risk factor” (p. 145) for coronary heart disease. It was accepted in the 1960s and 1970s, but because it was “not amenable to drugs or surgery and . . . difficult to define and measure” (pp. 158–59) it lost support from physicians and public health workers.

This overview cannot do justice to the many perceptive observations in this outstanding analysis of a fundamental issue in medicine. However, Aronowitz implies (unintentionally, I am sure) that the biological reductionist model accurately describes the etiology of many infectious diseases. This misconception has been corrected by René Dubos in books such as The World of René Dubos: A Collection of His Writings (1990).