IJE vol.33 no.4 © International Epidemiological Association 2004; all rights reserved.
Book Review |
The Rise of Causal Concepts of Disease: Case Histories. Codell Carter K. Aldershot UK: Ashgate Publishing, 2003, pp. 248, (HB) £55.00 ISBN: 0-7546-0678-3.
The aetiological standpoint
What causes ill health? The answer for any particular disease or health problem is inevitably controversial. For example, is our current obesity epidemic caused by declining international food prices, itself a function of technological innovation and tax subsidies? Or have we engineered physical activity out of our communities? What about the role of permissive parenting? Marketing phenomena such as super-sizing? Gluttony? Where we look for answers and change often depends on one's day job. Bench researchers focus their attention on gene–environment interactions while community activists are likely to stress the role of fast food franchises and limited access to nutritious foods in poor neighbourhoods.
In so many modern aetiological controversies, giving prominence to one cause over another is often a deeply political choice. This is true because causality is linked to who or what we hold to be responsible for ill health. Claims about causality also shape how resources and status are allocated to particular types of research, institutions, disciplines, and careers. While the best fit with scientific evidence should ideally rule, in so many contemporary health problems the data constrains but does not resolve debate.
If you add to this already volatile mix, contemporary ‘culture war’ debates over the objectivity, status, and authority of science, you get K Codell Carter's stubbornly old-fashioned history of causal ideas in medicine, The Rise of Causal Concepts of Disease. Carter celebrates the intellectual achievements of 19th century bacteriologists to the near exclusion of anything else. He wants to correct the misguided efforts of social historians and others who have not emphasized enough the enduring accomplishments of medical science. In so doing, he hopes to shore up the status and importance of biomedical research from the hordes of post-modernists and misguided social critics who look to society as both the cause and remedy for ill health.
Carter recounts what he considers to be the major accomplishment of 19th century Western medical science—the ascendancy of the ‘aetiological standpoint.’ ‘Between about 1830 and 1880,’ Carter explains:
medicine reorganized itself around the concept of universal necessary causes. Robert Koch referred to the new way of thinking as the etiological standpoint. ... Recharacterizing diseases in terms of necessary causes was a major advance that made possible coherent explanations of disease phenomenon as well as systematic treatment and prophylaxis.The substance of the ‘aetiological standpoint’ is that diseases are uniquely caused by specific bacterial species and need a set of agreed upon rules and procedures for proving causal relationships, such as the requirement that scientists grow putative disease causing agents on artificial media and be able to elicit disease by inoculating microbes into previously healthy laboratory animals (crucial heuristics that in part constitute Koch's postulates).
Carter shows how some 19th century bacteriologists hoped their insights would displace existing aetiological understandings of disease that stressed individual variation, constitution, miasmas, and social location. Friedrich Jakob Henle in 1844 caricatured the received aetiological thinking about disease by comparing them to a physicist who taught ‘that bodies fall because boards or beams are removed, because ropes or cables break, or because of openings, or so forth’ rather than appealing to Newton's laws of mechanics. Both Carter and his favourite 19th century scientists argue that the simplifying assumptions that constitute the aetiological standpoint were necessary to impose order on chaos, parallel to theoretical accomplishments in the more exact sciences.
Carter unquestioningly accepts these particular 19th century bacteriologists' self-understanding and self-promotion and their caricatures of any and all disease concepts besides the ascendant germ theory. As a result, Carter ignores the social and clinical meaningfulness of constitutional medicine, traditional therapeutics, and social and environmental explanations of disease in their actual historical context and obscures the many continuities with our own era's disease situation and aetiological debates. While Carter acknowledges that clinical knowledge was often lost or de-emphasized by the ensuing tautologous definitions of new diseases (for example, the new disease tuberculosis, defined as whatever consequences might arise from infection with the causative mycobacteria, replaced the clinical syndrome of consumption), he does not let it dampen his narrative of progress.
Carter sees revolution, new paradigm, in his story of the rise of the aetiological standpoint.
There was no transition (i.e. between older notions of remote causes and the germ theories he is writing about)—there could be none: one either accepted new etiological definitions or one did not. As with any true revolution in science, the change is all or nothing.
Although he does not explore the actual social mechanisms by which this aetiological revolution came about, he suggests that the revolutionaries did not win solely on evidence and brilliance. Carter notes that:
where rational persuasion fails, the only alternative is conversion, and converting opponents to the bacterial theory required successes, that were ‘supernatural’ in the sense of being outside what could reasonably have been expected within the framework of traditional medicine. To achieve conversion, bacteriologists required, not mere evidence, but something akin to miracles.But Carter does not explore how this revolution actually happened and quotes like this serve only as rhetorical cover for his attacks on other historical accounts of this act of persuasion, such as Bruno Latour's and Gerry Geison's books on similar terrain, that he derides as postmodernist cant. Carter is not really interested in exploring how these ideas were sold and how people were persuaded to believe in universal and necessary causes. His reliance on published scientific articles makes such an exploration impossible.
In this and other ways, The Rise of Causal Concepts of Disease has a culture war feel but I doubt many readers will be engaged by Carter's baiting. Few people will accept Carter's simplistic and partisan view of the goals of medicine. ‘‘The final hope and aim of medical science is the establishment of monogenic disease entities (quoting F Knaupl Taylor).’ It can't be made clearer than that.’ He criticizes less-reductionist formulations such as Bill Bynum's as being
influenced by one brand of postmodernism—the French disease—historians have become suspicious of anything that smacks of rationality, so scientific theories are marginalized.And later:
As a result, we know less about the nature and origin of the medical theories that affect our lives than about, say, eighteenth century quackery or the average income of general practitioners in Victorian England. And that, I think, is an abrogation of responsibility.
Carter's history is strictly of the ‘history of ideas’ variety, derived from the published writings of medical researchers we now believe to have made important contributions. Carter is aware of how out of fashion such text-based, intellectual history is to historians of medicine and how uninteresting his myopic focus on universal, necessary, and sufficient causes will be to philosophers:
Honestly speaking, I suspect that any philosopher who happens to read this book will find the philosophy nearly empty, and I already know that many historians regard my history as blind.Carter nevertheless views his work as a corrective to contemporary historians' ‘precious little interest in scientific theories.’
Universal and necessary causes in their wider historical context
The stories Carter tells of the ascendant theory of specific, universal, and necessary causes is not only a kind of ‘cherry picking’ of a few tidy and dramatic links from a much more complex causal chain, it is also a biased picture of older and contemporaneous aetiological ideas. Carter celebrates the 19th century victory of causal definitions of disease over traditional, pre-germ theories of disease, labelling them ‘Chimbuki’ medicine because disease is attributed to immorality, as is presumably the case in contemporary non-Western cultures. This crude characterization of multiple pre-bacteriological approaches to disease reveals the author's ignorance of the many continuities between traditional and modern concepts of disease, including the very incomplete banishing of morality from our own disease concepts.
Carter puts too much emphasis on a narrow set of developments in bacteriology, ignoring more important ideas even within the intellectual history of medicine. He ignores the long historiographic tradition (from Knud Faber to Osweii Temkin to Charles Rosenberg) that has recognized and explicated an enduring tension between holistic views of illness that stress individual idiosyncrasy and constitution, on the one hand, and ontological views of illness that stress disease as specific entity. From this wider and richer perspective, late 19th century microbiologists aetiological standpoints are one particular exemplar of the ‘ontological’ programme arising incrementally from older notions, fuelled by much larger social, technological, and economic changes. This older ontological tradition can be seen in clinical accounts of specific disease entities in earlier eras and is part of a fabric of assumptions that underlie surgical practices before the ascendancy of germ theory. From this vantage point, the kind of aetiological specificity that Carter celebrates is but one way among many of constituting disease specificity.
Another continuity Carter misses is the social meaning of debates about disease mechanisms. Carter's discussion of 19th century British proto-epidemiologist William Farr is brought up to illustrate the way causes of disease were conflated with causes of death prior to the rise of the aetiological standpoint. But Carter misses the political significance of Farr's attribution of death in early 19th century England to causes such as starvation. Farr, according to historian Chris Hamlin (who Carter chides), was engaged in a debate with Edwin Chadwick about the role of market solutions for social welfare and health issues. Accepting starvation as a cause of death had little to do with biological mechanisms per se but whether a political and economic system could be held responsible for illness and death, a question at the heart of modern concerns about racial, ethnic, and income-related health disparities.
Impact on health?
Carter also fails to make the case that the revolution he sees in causal thinking was complete and has had a lasting impact in all areas of medicine. He ignores the great amount of historical scholarship on the pidgin-like and halting ways that early bacteriological insights were assimilated with traditional medical and public health practices. Nineteenth century smallpox inoculation and vaccination were often performed along with traditional therapeutics such as bleeding and leaching and many public health measures—sanitary reforms and individual hygiene—that one might imagine were rationalized by belief in necessary and sufficient germs were often understood as impacting the miasmatic origins of disease.
Carter merely asserts that the putative theoretical revolution in understanding causality had a leading role in subsequent health improvements in western societies. ‘By contrast (to the possible evasion of disease through indirect measures),’ Carter writes, ‘if we somehow block invasion of the tuberculosis bacillus, we avoid the disease altogether—end of story, no matter what one breaths or eats or drinks.’ In contrast to this assertion, historians and demographers have convincingly shown the decline of tuberculosis mortality in the Western world since the late 19th century had everything to do with non-specific socio-economic advancement and arguably little with rational, self-conscious attempts to interrupt the transmission of the tuberculosis germ.
Looking to our present disease situation, the quest for necessary and sufficient causes of disease is not only chimerical but often a diversion from the kinds of population-level interventions that are likely to significantly improve the world's health. And on a purely mechanistic level, this quest has often led to ‘simplifying assumptions’ that fly in the face of disease realities. We have witnessed in the recent past a costly and largely unsuccessful search for the viral aetiology of cancer that was unconstrained by ‘facts’ about cancer's actual distribution in societies. In the more immediate present, we invest heavily in identifying genetic causes for diseases such as tobacco abuse and drug addiction, whose distribution within and between societies is patterned along socio-economic lines.
Modern epidemiologists and others concerned with disease aetiology have also generally eschewed the deterministic causal reasoning embodied in the ‘quest for universal necessary causes,’ instead relying on, however uncomfortably, multi-level, multi-factorial, and probabilistic models of health and disease. Even in the era of AIDS, which only with considerable myopia can be understood as universally and necessarily caused by a retrovirus (a view that obscures the role of social determinants such as poverty, globalization, gender inequality, substance abuse, etc., let alone biological factors associated with transmission and immunity), medical researchers have found few such necessary and sufficient causes for most of our leading health problems.
As an ideal-type, the modern quest for necessary and sufficient causes that Carter celebrates also represents a particular set of interests within the structural economy of scientific research and clinical and public health efforts—one which rewards particular styles of research programmes (e.g. molecular biology) and institutions (basis science in research universities) and not others (e.g. the social determinants of population health studied by social scientists or interventions within the domain of social work, social welfare, and economic policy). It is not so much that I or anyone can predict with any exactitude which lines of research will lead to significant health benefits or the most elegant aetiological insights, but we can safely say that it is wrong to put all or even most of our eggs in a single, reductionist basket. I would not doubt for a moment that universal, necessary causes, one for each disease, permit the easiest consensus and are inherently persuasive. But that does not privilege them as being right or the most strategic points of intervention in disease.
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