Abstract
After half a century of cognitive revolution we remain far from agreement about what cognition is and what cognition does. It was once thought that these questions could wait until the data were in. Today there is a mountain of data, but no way of making sense of it. The time for tackling the fundamental issues has arrived. The biogenic approach to cognition is introduced not as a solution but as a means of approaching the issues. The traditional, and still predominant, methodological stance in cognitive inquiry is what I call the anthropogenic approach: assume human cognition as the paradigm and work ‘down’ to a more general explanatory concept. The biogenic approach, on the other hand, starts with the facts of biology as the basis for theorizing and works ‘up’ to the human case by asking psychological questions as if they were biological questions. Biogenic explanations of cognition are currently clustered around two main frameworks for understanding biology: self-organizing complex systems and autopoiesis. The paper describes the frameworks and infers from them ten empirical principles—the biogenic ‘family traits’—that constitute constraints on biogenic theorizing. Because the anthropogenic approach to cognition is not constrained empirically to the same degree, I argue that the biogenic approach is superior for approaching a general theory of cognition as a natural phenomenon.
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Notes
‘Anthropogenic’ is an adjective long used in plant ecology to refer to plants introduced by humans; it increasingly refers to climate change associated with human activity. ‘Biogenic’ is used in geology to refer to the origins of certain rock strata. Limestone is biogenic, for example, because its origin is material that once formed part of living organisms. I am indebted to Jon Opie for suggesting that I devise neologisms for this distinction and to my husband, Richard Bradshaw, for finding them.
An example: “As our species designation—sapiens—suggests, the defining attribute of human beings is an unparalleled cognitive ability. We think differently from all other creatures on earth, and we can share those thoughts with one another in ways that no other species even approaches. In comparison, the rest of our biology is almost incidental” (Deacon 1997).
Biosemiotics should not be conflated with biosemantics, with which it is congenial but not identical. Biosemantics is Millikan’s relentlessly biological rendering of intentionality within the content of ongoing anthropogenic debates (Millikan 1989). Biosemiotics, by contrast, is grounded in Jacob von Uexküll’s biological theory of meaning, Piercean sign theory and contemporary molecular biology—its leading advocates are, in fact, biologists—and does not engage with analytic philosophical debates.
Whereas some thinkers (e.g., Matthen and Levy 1986) are comfortable ascribing intentionality to macromolecules, others (e.g., Rosenberg 1986) strongly oppose such attribution.
Erwin Schrödinger is commonly credited with pointing out the peculiarity of organisms relative to the laws of classical thermodynamics, which ultimately led to the development of nonclassical elaborations such as dissipative structures. In reality, the German theoretical biologist Ludwig von Bertalanffy proposed the idea of a thermodynamically open system in 1940, which forced physicists (and chemists such as Prigogine) to take note. Ironically, Bertalanffy proposed the open system concept as a counter to metaphysical vitalism, only to have his own general system theory tarred with the vitalist brush by reductionists such as Jacques Monod.
‘True equilibrium’ here refers to thermodynamic equilibrium, or total molecular disorder, which is death for a living system. The phonemic similarity but conceptual antonymity of thermodynamic equilibrium and metabolic balance maintained by homeostasis, which is often referred to in terms of equilibrium, is an unfortunate fact of interdisciplinary history and is an object lesson in the problems of overlapping terminologies.
Homeostasis is defined as “the regulation by an organism of the chemical composition of its body fluids and other aspects of its internal environment so that physiological processes can proceed at optimum rates. It involves monitoring changes in the external and internal environments by means of receptors and adjusting the composition of the body fluids accordingly; excretion and (osmotic) regulation are important in this process” (Martin and Hine 2000). Two examples of homeostatic regulation are the acid-base balance and body temperature.
Kringelbach points out that relatively slow metabolic processes, in humans at least, means that internal system changes do not swiftly track food intake, thus regulation of eating behaviour requires “sophisticated [neural] mechanisms to learn to predict in advance when a meal should be initiated and terminated” (2004, p 808).
For this reason Kringelbach suggests that food intake in nonhuman mammals may provide good model systems for investigating the neurobiology of phenomenal experience.
Another gap relates to organisms’ “limited autonomy from local energy potentials” and their ability to “vary their rate of energy consumption independently of variations in local gradients” (Barham 1996). This is possible because organisms have their own on-board energy supply in the form of adenosine triphosphate (ATP). It is a biological system’s “ability to use low-energy fluxes from a distal source in order to detect high-energy potentials before it becomes thermodynamically coupled with them” that is the odd trick, according to Barham (p 239). This capacity is contingent upon the system’s ability to “distinguish between those conditions external to itself that will support its continued oscillation, and those which will not” (p 238). Under starvation conditions, for example, certain species of bacteria will sporulate, a process that induces dramatic, global changes in cell state such that the organism can hunker down indefinitely until conditions improve (Marahiel and Zuber 1999). Sporulation is highly energy intensive and, in some cases, irreversible to the extent that the bacterium cannot ‘change its mind’ halfway through the process. The sporulation option, therefore, involves a calculated risk regarding the extent to which conditions will support “continued oscillation”.
This section is a summary of a longer, more detailed presentation in Lyon (2004). Please note that Maturana has consistently declined to characterize as a ‘theory’ the framework he developed in partnership with Varela and others, and indeed it has been criticized for not being a proper theory (see especially Scheper and Scheper 1996). But as autopoiesis constitutes a coherent conceptual structure that provides explanations and makes predictions, ‘theory’ is an appropriate label, in my view.
It is beyond the scope of this paper to show how autopoietic theory accounts for complex cognitive phenomena such as language use. Suffice to say that the theory recently has proven as influential in disciplines related to education, business systems, management and nursing as it has in relation to cognition.
Maturana and Varela in their early work resiled from using the word ‘environment’ on the basis that it was observer-dependent and encompassed a broader view than which the system itself was capable. The observer/system distinction is critical to the autopoietic model.
Robert Rosen came to a similar conclusion regarding ‘state determinism’ in his biological rendering of dynamical systems theory. “In a nutshell, a system which is both (thermodynamically) open and autonomous...must have the property that the flows from environment to system, and from system to environment, are determined by what is inside the system” (Rosen 2000).
I have niggling doubts about this claim. If a shark eats a fish, autopoiesis will cease and the fish will die. Granted, the cessation of autopoiesis is the immediate cause of death, but surely the shark is more than a mere ‘trigger’ for change.
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Acknowledgements
I would like to thank Jon Opie for his invaluable help in developing the anthropogenic/biogenic distinction, and to two anonymous reviewers whose comments greatly improved the paper.
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Lyon, P. The biogenic approach to cognition. Cogn Process 7, 11–29 (2006). https://doi.org/10.1007/s10339-005-0016-8
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DOI: https://doi.org/10.1007/s10339-005-0016-8