February 2013 Lunchtime Abstracts & Details

:::Why We Reason:  Intention-Alignment and the Genesis of Human Rationality
Andy Norman
Carnegie Mellon University, Dept. of Philosophy

Friday, February 8, 2013
12:05 pm, 817R Cathedral of Learning

Abstract:  Why do humans reason?  Many animals draw inferences, but in our prolific production and consumption of reason-giving performances, we appear unique. Mercier and Sperber (2011) propose that we view reasoning as having evolved to serve an argumentative function.  On this account, reasoning faculties emerged because the ability to produce persuasive arguments, and evaluate the arguments of others, provided a competitive advantage.  The evidence indicates that our reasoning propensities are indeed shaped by its social function, but Mercier & Sperber's account proves problematic on at least two counts.  First, the explanatory strategy fails because reasoning practices could not have predated reasoning propensities in a way that would have provided selective pressure for those propensities.  Hence, the origins of our reasoning faculties must be sought in another function.  Second, M&S characterize reasoning as a fundamentally competitive or strategic activity, when its primary function was—and remains—collaborative.  It is true that we reason competitively, but for the most part, reasoning functions to align intentions.  Typically, reasons are used to overwrite another's divergent belief with a convergent one, thereby facilitating collaboration between the reason-giver and the reason-taker.  Curiously, it makes sense to think of reason-giving as as a mostly communicative (but sometimes strategic) kind of "mind-writing."  In fact, the emergence of reasoning may have been the development that put humanity on the path to ultrasociality, language and culture.

:::The Genealogical Concept of Human Nature
Maria Kronfeldner
Center Visiting Fellow, Bielefeld U.

Tuesday, February 12, 2013
12:05 pm, 817R Cathedral of Learning

Abstract:  In contemporary philosophy of biology, the biological concept of human nature does not have a very good reputation: it is believed to be a ghost haunting us from long gone essentialist times, a ghost to be exorcised. The talk compares the much criticized essentialist concept of human nature with a purely nomological, an evolutionary and a genealogical concept of human nature. The latter is a development of David Hull’s minimalist concept of human nature and is here to stay, because it ‘carves nature’ at one of its important joints and performs an epistemic function in science that goes back to Greek antiquity, namely securing boundaries between fields of expertise. To look at this and further functions (e.g. related to the term’s ambiguity) helps to see why talk about human nature won’t go away, despite the fact that human nature is (according to the genealogical concept) reducible to a cluster of causal factors.

:::Russell meets Woodward - Three Objections to the Open Systems Argument
Alexander Reutlinger
Center Visiting Fellow, U. of Cologne

Tuesday, February 19, 2013
12:05 pm, 817R Cathedral of Learning

Abstract:  Several proponents of the interventionist theory of causation have recently argued for a Neo-Russellian account of causation. According to the Neo-Russellian account, the conjunction of the following three claims is true: (1) there are no fundamental physical causal facts (orthodox Russellian claim), (2) there are higher-level causal facts to which the special sciences refer (Neo-Russellian claim), and (3) higher-level causal facts metaphysically depend on fundamental physical facts (dependence claim). This talk discusses an argument for the Neo-Russellian account, which several interventionists advocate:  the open systems argument (Eagle 2007, Hitchcock 2007, Woodward 2007).  It is argued that the open systems argument is not sound.

:::Gene-Environment Interaction in the 21st Century: Its Rise, Its Fall, Its Rise?
James Tabery
U. Utah, Dept. of Philosophy

Tuesday, February 26, 2013
12:05 pm, 817R Cathedral of Learning

Abstract: At the turn of the 21st, Terrie Moffitt and Avshalom Caspi published a series of empirical papers on gene-environment interaction. These articles were published in premier scientific journals, and the results were hailed in major news outlets. One paper in particular, on the relationship between the serotonin transporter gene and exposure to stress in the development of clinical depression, has been replicated dozens of times and cited over 4000 times. A 2009 meta-analysis of those replications, however, was negative, suggesting that the original result may have just been due to chance. But then a 2011 meta-analysis came back positive, suggesting a confirmation of the original result. A commentary in Archives of General Psychiatry (which published the 2011 meta-analysis), worried, "The reader is therefore entitled to ask, 'What should I believe? Which explanation is true?'". And an article on the 2011 meta-analysis in the Los Angeles Times mocked, "Ah, the process of science. One week, oat bran is the font of eternal youth. The next week, it kills. It's not clear what these results mean. Or what next week might bring." I will situate this most recent debate over gene-environment interaction in the larger history of research on the phenomenon. That history reveals that there have been two quite distinct ways to understand interaction in terms of how to conceptualize it, how to investigate it, and how to weigh evidence for it. My thesis for this talk is that these competing understandings are playing out yet again in this 21st century debate over gene-environment interaction.