On physicalism and Downward Causation in Developmental and Cancer Biology

The dominant position in Philosophy of Science contends that downward causation is an illusion. Instead, we argue that downward causation doesn't introduce vicious circles either in physics or in biology. We also question the metaphysical claim that "physical facts fix all the facts." Downward causation does not imply any contradiction if we reject the assumption of the completeness and the causal closure of the physical world that this assertion contains. We provide an argument for rejecting this assumption. Furthermore, this allows us to reconsider the concept of diachronic emergence.     

Causation and space-time

This paper considers the physical accounts of causation in terms of conserved quantities in the light of the theory of general relativity. As it is rather well-known among physicists, there are several difficulties with the notions of conservation and localization of the (gravitational) energy-momentum within general relativity. We first begin to review the so-called conserved quantity theory of causation mainly due to Dowe and Salmon, then we discuss some consequences of these difficulties for this physical account of causation. We argue that these difficulties are due to the fundamental nature of the space-time structure as described by GR, which the conserved quantity theory of causation does not account for.     

Causation and models of disease in epidemiology

Nineteenth-century medical advances were entwined with a conceptual innovation: the idea that many cases of disease which were previously thought to have diverse causes could be explained by the action of a single kind of cause, for example a certain bacterial or parasitic infestation. The focus of modern epidemiology, however, is on chronic non-communicable diseases, which frequently do not seem to be attributable to any single causal factor. This paper is an effort to resolve the resulting tension. The paper criticises the monocausal model of disease, so successful in the nineteenth century. It also argues that a multifactorial model of disease can only be satisfactory if it amounts to more than a mere rejection of the monocausal model. A third alternative, the contrastive model, is proposed and defended on the grounds that it links the notions of disease and of general explanation, while avoiding the philosophical naiveties and practical difficulties of the monocausal model.     

On Reciprocal Causation in the Evolutionary Process

Recent calls for a revision of standard evolutionary theory (SET) are based partly on arguments about the reciprocal causation. Reciprocal causation means that cause–effect relationships are bi-directional, as a cause could later become an effect and vice versa. Such dynamic cause-effect relationships raise questions about the distinction between proximate and ultimate causes, as originally formulated by Ernst Mayr. They have also motivated some biologists and philosophers to argue for an Extended Evolutionary Synthesis (EES). The EES will supposedly expand the scope of the Modern Synthesis (MS) and SET, which has been characterized as gene-centred, relying primarily on natural selection and largely neglecting reciprocal causation. Here, I critically examine these claims, with a special focus on the last conjecture. I conclude that reciprocal causation has long been recognized as important by naturalists, ecologists and evolutionary biologists working in the in the MS tradition, although it it could be explored even further. Numerous empirical examples of reciprocal causation in the form of positive and negative feedback are now well known from both natural and laboratory systems. Reciprocal causation have also been explicitly incorporated in mathematical models of coevolutionary arms races, frequency-dependent selection, eco-evolutionary dynamics and sexual selection. Such dynamic feedback were already recognized by Richard Levins and Richard Lewontin in their bok The Dialectical Biologist. Reciprocal causation and dynamic feedback might also be one of the few contributions of dialectical thinking and Marxist philosophy in evolutionary theory. I discuss some promising empirical and analytical tools to study reciprocal causation and the implications for the EES. Finally, I briefly discuss how quantitative genetics can be adapated to studies of reciprocal causation, constructive inheritance and phenotypic plasticity and suggest that the flexibility of this approach might have been underestimated by critics of contemporary evolutionary biology.     

Function and Causation of Social Signals in Lizards

SYNOPSIS. We describe here a multidisciplinary investigationof the stimuli and mechanisms controlling reproduction in thegreen anole lizard, Anolis carolinensis. Bothenvironmental andsocial stimuli that vary seasonally are used as proximate cuesto reproduction. In order for these ecological factors to initiatebreeding, they must be perceived and integrated in the centralnervous system. External and internal stimuli converge uponthe hypothalamus, the major neuroendocrine integrative areaof the brain, which, in turn, directly regulates pituitary andautonomic function. In addition to their role in reproduction,the gonadal hormones are important throughout the life of theorganism, acting both peripherally and centrally, to adapt theindividual to its environment. Thus, the environment, behavior,and physiology interact in complex ways to synchronize the socialand reproductive activities of individuals.     

Zooming in on Downward Causation

An attempt is made to identify a concept of ‘downward causation’ that will fit the claims of some recent writers and apply to interesting cases in biology and cognitive theory, but not to trivial cases. After noting some difficulties in achieving this task, it is proposed that in interesting cases commonly used to illustrate ‘downward causation’, (a) regularities hold between multiply realizable properties and (b) the explanation of the parallel regularity at the level of the realizing properties is non-trivial. It is argued that the relation between a realizable property and the property that realizes its effect in a particular case is not usefully regarded as a species of causation and that use of the concept of downward causation deflects our attention from our central explanatory tasks.