Stefan Linquist

Research on patients with damage to ventromedial frontal cortices suggests a key role for emotions in practical decision making. This field of investigation is often associated with Antonio Damasio’s Somatic Marker Hypothesis—a putative account of the mechanism through which autonomic tags guide decision making in typical individuals. Here we discuss two questionable assumptions—or ‘myths’—surrounding the direction and interpretation of this research. First, it is often assumed that there is a single somatic marker hypothesis. As others have noted, however, Damasio’s ‘hypothesis’ admits of multiple interpretations (Dunn et al. [2006]; Colombetti [2008]). Our analysis builds upon this point by characterizing decision making as a multi-stage process and identifying the various potential roles for somatic markers. The second myth is that the available evidence suggests a role for somatic markers in the core stages of decision making, that is, during the generation, deliberation, or evaluation of candidate options. On the contrary, we suggest that somatic markers most likely have a peripheral role, in the recognition of decision points, or in the motivation of action. This conclusion is based on an examination of the past twenty-five years of research conducted by Damasio and colleagues, focusing in particular on some early experiments that have been largely neglected by the critical literature. 1 Introduction2 What is the Somatic Marker Model?3 Multiple Somatic Marker Hypotheses3.1 Are somatic markers necessary for practical decision making?3.2 Speed, accuracy, or both?3.3 At which of the five stages of decision making are somatic markers engaged?4 Anecdotal Evidence Suggests a Peripheral Role for Somatic Markers4.1 Chronic indecisiveness4.2 Extreme impulsiveness4.3 Enhanced decision making in the lab4.4 Lack of motivation. 5 Early Experiments Suggest that VMF Damage Leaves Core Processes Intact5.1 The evocative images study5.2 Five problem solving tasks6 Recent Experiments Fail to Discriminate among Alternate Versions of SMH7 Conclusion

A promising recent development in molecular biology involves viewing the genome as a miniecosystem, where genetic elements are compared to organisms and the surrounding cellular and genomic structures are regarded as the local environment. Here we critically evaluate the prospects of Ecological Neutral Theory, a popular model in ecology, as it applies at the genomic level. This assessment requires an overview of the controversy surrounding neutral models in community ecology. In particular, we discuss the limitations of using ENT both as an explanation of community dynamics and as a null hypothesis. We then analyze a case study in which ENT has been applied to genomic data. Our central finding is that genetic elements do not conform to the requirements of ENT once its assumptions and limitations are made explicit. We further compare this genome-level application of ENT to two other, more familiar approaches in genomics that rely on neutral mechanisms: Kimura’s Molecular Neutral Theory and Lynch’s Mutational Hazard Model. Interestingly, this comparison reveals that there are two distinct concepts of neutrality associated with these models which we dub ‘fitness-neutrality’ and ‘competitive neutrality’. This distinction helps to clarify the various roles for neutral models in genomics, for example, in explaining the evolution of genome size.

Considerable variation exists not only in the kinds of transposable elements (TEs) occurring within the genomes of different species, but also in their abundance and distribution. Noting a similarity to the assortment of organisms among ecosystems, some researchers have called for an ecological approach to the study of transposon dynamics. However, there are several ways to adopt such an approach, and it is sometimes unclear what an ecological perspective will add to the existing co-evolutionary framework for explaining transposon-host interactions. This review aims to clarify the conceptual foundations of transposon ecology in order to evaluate its explanatory prospects. We begin by identifying three unanswered questions regarding the abundance and distribution of TEs that potentially call for an ecological explanation. We then offer an operational distinction between evolutionary and ecological approaches to these questions. By determining the amount of variance in transposon abundance and distribution that is explained by ecological and evolutionary factors, respectively, it is possible empirically to assess the prospects for each of these explanatory frameworks. To illustrate how this methodology applies to a concrete example, we analyzed whole-genome data for one set of distantly related mammals and another more closely related group of arthropods. Our expectation was that ecological factors are most informative for explaining differences among individual TE lineages, rather than TE families, and for explaining their distribution among closely related as opposed to distantly related host genomes. We found that, in these data sets, ecological factors do in fact explain most of the variation in TE abundance and distribution among TE lineages across less distantly related host organisms. Evolutionary factors were not significant at these levels. However, the explanatory roles of evolution and ecology become inverted at the level of TE families or among more distantly related genomes. Not only does this example demonstrate the utility of our distinction between ecological and evolutionary perspectives, it further suggests an appropriate explanatory domain for the burgeoning discipline of transposon ecology. The fact that ecological processes appear to be impacting TE lineages over relatively short time scales further raises the possibility that transposons might serve as useful model systems for testing more general hypotheses in ecology.

The culture of honour hypothesis offers a compelling example of how human psychology differentially adapts to pastoral and horticultural environments. However, there is disagreement over whether this pattern is best explained by a memetic, evolutionary psychological, dual inheritance, or niche construction model. I argue that this disagreement stems from two shortcomings: lack of clarity about the theoretical commitments of these models and inadequate comparative data for testing them. To resolve the first problem, I offer a theoretical framework for deriving competing predictions from each of the four models. In particular, this involves a novel interpretation of the difference between dual inheritance theory and cultural niche construction. I then illustrate a strategy for testing their predictions using data from the Human Relations Area File. Empirical results suggest that the aggressive psychological phenotype typically associated with honour culture is more common among pastoral societies than among horticultural societies. Theoretical considerations suggest that this pattern is best explained as a case of cultural niche construction

Lawton’s contingency thesis states that there are no useful generalizations at the level of ecological communities because these systems are especially prone to contingent historical events. I argue that this influential thesis has been grounded on the wrong kind of evidence. CT is best understood in Woodward’s terms as a claim about the instability of certain causal dependencies across different background conditions. A recent distinction between evolution and ecology reveals what an adequate test of Lawton’s thesis would look like. To date, CT remains untested. But developments in genome and molecular ecology point in a promising direction.