There is necessarily speculation in reconstructing "The Prehistoric Baseline" of our earliest human ancestors, but Barrett and Armelagos suggest that, "having examined the protective role of nutrition against human infections today, we could infer the same protective role in our ancestors". Foraging and hunting probably brought rich, if uncertain, diets (as well as exposure to wild animals and their pathogens); small groups regularly changing location would have been less vulnerable to acute disease outbreaks and environmental sources; and a generally egalitarian distribution of resources would have made groups less vulnerable.
Along with agriculture, the Neolithic Revolution saw the First Epidemiological Transition, with "The Domestication of Pathogens" and "the first major rises of acute infectious diseases in the human species". Barrett and Armelagos explain some of the ways we can know about the health of dead people and populations, but the bioarchaeology is circumstantial and alternative interpretations are possible. So they consider the evidence for decreasing nutritional diversity and quality, permanent settlements with increasing population density, pathogens derived from domesticated animals, and political centralisation. They also touch here on the "far from even" exchange of pathogens between New and Old Worlds, looking at immunological theories but suggesting that the disproportionate effect on the New World was partly the result of concomitant "violence, subjugation, and forced displacement".
Starting in the mid-19th century in industrialising parts of Europe, the Second Epidemiological Transition brought a rapid decline in mortality baselines. "Why Germ Theory Didn't Matter" describes key medical advances (and Germ Theory) and public health improvements (and the Sanitary Reform Movement). It then presents the McKeown Thesis, which argues that these, though they contributed, came too late to be responsible for population growth starting in the UK in the mid-17th century, and instead identifies improved nutrition as the primary determinant in the decline of infection-related mortality; criticisms of this hypothesis are also examined.
The developing world is not following in the footsteps of the industrialised world, however, but is experiencing "The Worst of Both Worlds", with a rising incidence of the chronic diseases of modernity alongside persistence of acute infectious diseases. An increasingly important role is being played by syndemics, interactions between multiple diseases that exacerbate the negative effects of one or more disease. Mortality declines have largely been driven by advances in medicine and antibiotic use; in contrast economic growth has been patchy and often very unevenly distributed, while the demographics of many countries have left large ageing populations living in poverty.
In "New Diseases, Raw and Cooked", Barrett and Armelagos turn to the current Third Transition and the rise of "a single, global disease ecology". Taking the Hong Kong SARS outbreak in 2003 as a starting point, they touch on bushmeat and wild birds and viral chatter (when a zoonotic pathogen can transfer from animal to human hosts but not yet between humans), but emphasise the role of commercial poultry and industrial meat production. And they explain how "plague, cholera, and the 1918 influenza pandemic illustrate the complex dynamics of virulence and transmissibility": contrasting Attenuation and Virulence Hypotheses may apply in different circumstances.
In "Inevitable Resistance" Barrett and Armelagos survey the mechanisms of antibiotic resistance (and its persistence) in pathogens, but again centre human concerns, "acknowledging the importance of pathogens while stressing their evolution in response to human activities: the ways we feed ourselves, the ways we populate and live together, and the ways we relate to each other for better and worse". Key topics here include prophylactic use and patient compliance, commercial agriculture, and the hot-housing of multi-resistant strains in vulnerable populations. Historical "soil" and "seed" ideas have given way to an almost exclusive focus on the latter: "the majority of medical research (public and private) has been devoted to the molecular characteristics of pathogens rather than the states of human hosts and their surrounding environments".
A conclusion tackles three myths: "that emerging infections are a new phenomena", "that emerging and re-emerging infections are primarily natural or spontaneous phenomena", and "that the disease determinants of our past are qualitatively different from those of the present". And, reiterating earlier conclusions, it suggests their implications for policies and programs: "if we understand the common and long-standing determinants of many infections and other health problems, then we can organize our health efforts around these fewer, upstream determinants instead of dealing with many more downstream consequences after they have already occurred."
With just 115 pages of text, albeit in a relatively small font on large pages, An Unnatural History of Emerging Infections is quite focused. It is nicely written and cogently argued, and I would have enjoyed seeing it fleshed out at greater length. Its core ideas are important and need to be widely disseminated, to help medical professionals and biomedical researchers look beyond the borders of their disciplines, but also to improve popular understanding and inform social policy.
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