We Can Think Ourselves into a Plague
The materialist answers, funny you mention it, but, yes, you can. A few minds thought through the ideas that produced the airplane and perhaps soon enough the personal jet pack with smart phone dock and coffee maker.
The dialectical materialist would modify science’s self-congratulations with the observation it’s taken many generations’ labor to produce the surplus permitting a few their deep thinking. Ingenuity is itself a social object.
And yet, despite, or perhaps because of, that backing, we can think ourselves into era-specific traps. Among these include animal and plant diseases that rope-a-dope us into a frustration we feel obliged by our lords and masters to fail to understand.
“It’s not only this concrete problem—big companies controlling, through money donations, universities,” philosopher Slavoj Zizek complains,
It’s something more fundamental going on. It’s a well-organized…campaign to turn us scientists, human or natural, into ‘experts’. The idea is, we have a problem—let’s say oil spill in Louisiana—oh, we need experts to tell us how to contain it. We have a public disorder, demonstrations; we need psychologists and so on. This is not thinking. What universities should do is not serve as experts to those in power who define the problems. We should redefine and question the problems themselves. Is this the right perception of the problem? Is this really the problem? We should ask much more fundamental questions.
Problematics, much less their solutions, are capital-driven. Beware the questions with which one bothers, scientist.
Given the nature of newly emerging and re-emerging pathogens, interdisciplinarity, following pathogens across epistemological domains, shifts front and center. We might otherwise confuse cheap logistical advances against disease for strategic victories.
But interdisciplinarity’s pursuit beyond lip service is contradicted by capitalism’s prime directives. The puzzle of the pathogens, already a haze, is obscured by the machinations of funding and reputation–the mechanisms by which capital disciplines science.
Capital also attempts to discipline pathogens. But the little buggers routinely violate protocol.
To their great credit, vaccines, pharmaceuticals and modern public health policies have been successful in addressing a wide array of diseases. The smallpox and polio vaccines work and have driven the former to extinction and the latter to widespread extirpation. Clean water marginalizes cholera.
In falling to what are now standard health practices, these pathogens show themselves to embody the very reductionism used to defeat them. Their biologies are indeed the sum of their parts. In understanding the molecular properties of the viruses and their proximate means of transmission, Zizek’s experts have been able to deliver stunning epidemiological victories for humans and their livestock alike.
But not all pathogens appear so cooperative. HIV, tuberculosis, malaria and influenza, among others, killing millions, confound even the most concerted efforts. Lab, field and modeling efforts, powered now by industrial computing, appear presently inadequate to the task of rolling back these scourges. Interventions are faltering.
The more intransient diseases are intrinsically holistic in nature. They are capable of using interactions at one level of biocultural organization to evolve out from underneath interventions directed at them from another. They operate across fluctuating swaths of time and space and host range.
So vaccines and pills alone are rarely decisive. Indeed, in some parameter spaces such interventions can exacerbate outbreaks (e.g., here and here). That is to say, taking a step back, modeling, or scientific epistemology more broadly, may have helped cause the evolution of such holistic diseases. We may be guilty of more than a failure of imagination. We may have had a role in selecting for such pathogens in the first place.
An example. In unpublished work Hal Stern and I attempted to use a molecular constraint to predict where a human-specific bird flu might emerge. We used a nucleotide substitution bias in favor of uracil previously shown in the polymerase loci of a variety of influenza serotypes to identify localities that may host strains of influenza A (H5N1) closer to a human-specific infection. The more the uracil, the greater the human specificity. There is a possibility areas hosting H5N1 polymerase of the greatest uracil may act as sources for more human-specific strains.
The details of the methodology matter little here. What the results might mean, however, is critical to our larger point.
Statistical significance may arise from truly adaptive changes in uracil content in space and time. It may also arise in part from an imbalance in the data imposed by sampling bias toward human cases and/or poultry of economic importance. Such sampling bias may also arise, however, from the very nature of epidemiological spread.
Panzootic dynamics undermine the kinds of factorial design upon which much science depends. Many pathogens spread out-of-phase across multiple geographic fronts and, as in the case of H5N1, by way of different host species. The resulting anisotropic distributions punch holes into the factorial coverage and for some factor combinations reduce statistical power. We may have a lot of geese infected in the Chinese province of Guangxi in 2006, for instance, but none elsewhere.
In addition, sampling resolution producing irregular geographical spacing reduces statistical power by decreasing the effective sample sizes of pairs of localities at a variety of proximities. The irregular spacing arises in part from H5N1’s spatial spread itself.
We need to recognize, then, that the evolution and spread of the more successful pathogens are defined by uneven spatiotemporal dynamics that in many ways allow them to elude our efforts at discovering the nature of their spread. As a result we are less able to easily propose interventions for control or extirpation.
In other words, in a world in which viruses and bacteria evolve in response to humanity’s multifaceted infrastructure—including our science—our epistemological and epidemiological intractabilities may be in fundamental ways one and the same. Some pathogens evolve into population states in which we cannot easily think.
Redemption is possible. Behind new efforts is a perspective that attempts to better match the dynamics of the holistic pathogens that bring about mortality and misery in animals and humans alike.
We can model such pathogens across the scales and processes over which they themselves operate. Modeling panzootics must include making large leaps cross scale and discipline. New concepts and objects must be defined. Econolandscapes. Cultural virology. Is influenza’s demic selection mitigated or facilitated by economies of scale? Do traditional SIR models oversimplify human impact on pathogen evolution by defining sociality in terms of density dependence alone?
These kinds of questions emphasize Richard Levins’s point what variables we include in our models is often a social decision. What we choose to make internal or external to these models, including which data to concatenate, can have a significant impact on their success.
It seems a true health interdisciplinarity means moving away from the kinds of expertise the powerful shop for in the marketplace of ideas. Whistling to the muzak.