Philosophy

This paper examines constraints and their role in scientific explanation. In influential work, Lange (2018) suggests that constraints are non-causal and that they provide non-causal explanations. While Lange mainly focuses on examples from physics, this paper explores constraints from other fields, including neuroscience, physiology, and the social sciences. I argue that these cases involve constraints that are causal and that provide a unique type of causal explanation. This paper clarifies what it means for a factor to be a constraint, when such constraints are causal, and how they figure in scientific explanation.

The proximal-distal model of disease causation is often used to capture how social causes influ-ence health outcomes. This model serves as a conceptual framework for many analyses of “social determinants of health”—it does so by locating social factors as “distal” causes, which are up- stream of “proximal” biology. In a rich and influential paper, Krieger criticizes this model for being inaccurate and confused, and suggests that we “abandon the deeply confused language of the terms proximal and distal” (Krieger 2008). While we agree with many of Krieger’s criticisms, we examine different weaknesses of this model and argue that it has important strengths. We examine three causal scenarios to show how social and biological causes interrelate in various ways, which are only partly captured by this model. In particular, we show how social factors can play three types of causal roles: they can be distal causes, parallel causes, and proximal causes. We argue that— instead of eliminating “proximal” and “distal” causal terminology—accurate use of these terms is not only possible, but instrumental in capturing how social causes influence health and disease.

A fundamental goal of research in neuroscience is to uncover the causal structure of the brain. This focus on causation makes sense, because causal information can provide explanations of brain function and identify reliable targets with which to understand cognitive function and prevent or change neurological conditions and psychiatric disorders. In this research, one of the most frequently used causal concepts is ‘mechanism’ — this is seen in the literature and language of the field, in grant and funding inquiries that specify what research is supported, and in journal guidelines on which contributions are considered for publication. In these contexts, mechanisms are commonly tied to expressions of the main aims of the field and cited as the ‘fundamental’, ‘foundational’ and/or ‘basic’ unit for understanding the brain. Despite its common usage and perceived importance, mechanism is used in different ways that are rarely distinguished. Given that this concept is defined in different ways throughout the field — and that there is often no clarification of which definition is intended — there remains a marked ambiguity about the fundamental goals, orientation and principles of the field. Here we provide an overview of causation and mechanism from the perspectives of neuroscience and philosophy of science, in order to address these challenges.

This thesis addresses the active controversy regarding the nature and role of informational concepts as applied to the biological sciences { in particular, the relationship between statistical or correlational information on one hand and meaningful, semantic, intentional information on the other. It first develops a set of basic conceptual
tools that can be applied to any, or at least most, putative cases of information processing in biological systems. This framework shows that, contrary to popular belief, we can make sense of biological information in the former, statistical sense, without it trivially applying to any and all physical processes that take place in living things.
I then demonstrate the utility of this framework by applying its tools to specfic information-related controversies: the concept of innateness, and information versus influence in animal communication. These chapters demonstrate that these issues can be clarified with the tools previously developed. I also discuss the notion of primitive content - the simplest form of biological phenomenon that can reasonably be said to be contentful. This issue serves as a biological basis for future research
regarding the ongoing philosophical problem of relating the physical to the mental.

Jacques Monod (1971) argued that certain molecular processes rely critically on the property of ​ chemical arbitrariness​, which he claimed allows those processes to "transcend the laws of chemistry". It seems natural, as some philosophers have done, to interpret this in modal terms: a biological relationship is chemically arbitrary if it is possible, within the constraints of chemical "law", for that relationship to have been otherwise than it is. But while modality is certainly important for understanding chemical arbitrariness, understanding its biological role also requires an account of the concrete causal-functional features that distinguish arbitrary from non-arbitrary phenomena. In this paper I elaborate on this under-emphasised aspect by offering a general account of these features: arbitrary relations are instantiated by mechanisms that involve molecular ​ adapters​ , which causally couple two properties or processes which would otherwise be uncorrelated. More specifically, adapters work by acting as ​ intermediate rather than ​ cooperating​ causes.

Binding specificity​ is a centrally important concept in molecular biology, yet it has received little philosophical attention. Here I aim to remedy this by analyzing binding specificity as a causal property. I focus on the concept's role in drug design, where it is highly prized and hence directly studied: From a causal perspective, understanding why binding specificity is a valuable property of drugs contributes to an understanding of causal selection​ ーof how and why scientists distinguish between causes, not just causes from non-causes. In particular, the specificity of drugs is precisely what underwrites their value as experimental interventions on biological processes.

Bio-ontologies are digital frameworks for handling biological and biomedical data. They consist of theoretical entities and relations with explicitly defined logical structures and precise definitions, whose purpose is to provide a shared language for representing information to be distributed and integrated across diverse scientific contexts. It is tempting to view bio-ontologies as clear and formal expressions of a scientific community's ontological commitments about their domain of inquiry, and to view their integration as tantamount to the metaphysical unification of science that some philosophers have envisaged. However, I argue that the local, practical, social and technological factors that influence their design prevent us from straightforwardly reading metaphysical conclusions from them. I discuss these complications and suggest how they can be overcome, revealing more general lessons for the development of a well-founded scientific metaphysics.

Binding specificity is a centrally important concept in molecular biology, yet it has received little philosophical attention. Here I aim to remedy this by analyzing binding specificity as a causal property. I focus on the concept’s role in drug design, where it is highly prized and hence directly studied. From a causal perspective, understanding why binding specificity is a valuable property of drugs contributes to an understanding of causal selection—of how and why scientists distinguish between causes, not just causes from noncauses. In particular, the specificity of drugs is precisely what underwrites their value as experimental interventions on biological processes.

We argue that there is a interesting connection between the old problem of the Speckled Hen and an argument that can be traced from Russell to Armstrong to Putnam that we call the “gradation argument.” Both arguments have been used to show that there is no “Highest Common Factor” between appearances we judge the same – no such thing as “real” sensations. But, we argue, both only impugn the assumption of epistemic certainty regarding introspective reports.

In his (2010) contribution to the Oberlin Colloquium in Philosophy—an early draft
of the first chapter of his book, Know How --Jason Stanley explores in more depth the Rylean arguments for antiintellectualism that Stanley and Williamson consider and reject in their influential (2001) paper. In particular, he concentrates his efforts on versions of the regress argument that appear in Ryle’s The Concept of Mind, arguing that there is no regress that intellectualism is committed to that Rylean anti-intellectualism isn’t. I want to here suggest that there might be.

This paper brings together two recent developments in the theory of epistemic justification: practical conditions on justification, and infinitism (the view that
justification is a matter of having an infinite series of non-repeating reasons). Pragmatic principles can be used to argue that, if we’re looking for an ‘objective’ theory of the structure of justification – a theory that applies to all subjects independently of their practical context – infinitism stands the only chance at being the correct theory.

The book is an exploration of the extent of our obligations to engage with arguments that we know ahead-of-time are unsound.  The primary conclusion of the book is that the obligation is quite limited.  If someone offers you an argument that the Holocaust didn’t occur or that homosexuality is a disability, there is no obligation to read the argument through or figure out what’s wrong with it.  On the contrary, in standard situations, you shouldn’t engage with such arguments open-mindedly and sometimes should not engage with them at all.  This is so even though it can be difficult to detect the errors in some arguments.  You can be fooled by unsound arguments; even though they’re unsound, each step might seem compelling and you might not be able to figure out what’s wrong with them.  Still, even if you can’t figure out what’s wrong with them, you can know that they’re bad arguments.  If so, you shouldn’t engage with them open-mindedly and sometimes shouldn’t engage with them at all.   
    The book has two parts.  The first part is epistemological.  I argue that you can know that controversial views are true, even if you can’t figure out what’s wrong with arguments against those views.  One way this can happen is if you’re an amateur regarding the kind of argument offered against you.  So, if you don’t have particularly solid expertise in history, this can give you license to ignore arguments that the Holocaust didn’t occur that are based on historical data, even if you can’t figure out what’s wrong with them.  That’s because, given your inadequate historical knowledge, you shouldn’t expect to be able to figure out what’s wrong with such arguments, even if they’re unsound.  (I also, in the first part of the book, offer a theory of open-mindedness: you’re open-minded toward an argument only if you’re willing to reduce your confidence in response to the argument if you can’t figure out what’s wrong with it and find each step compelling.) 
    In the second part of the book I apply the conclusions of the first part to the ethics of engagement in argumentation.  After going through some arguments that there is an obligation to engage with salient counterarguments, I argue in subsequent chapters that there is often no such obligation.  Sometimes, rather, there is a positive obligation not to engage – when you know the arguments are unsound.  You shouldn’t engage open-mindedly, because if you know the argument is unsound, you shouldn’t be willing to reduce your confidence in response to the argument (because to do so would be to be willing to reduce confidence in response to an argument that you know either has false premises or invalid steps, and that’s not a good thing to do).  And you sometimes shouldn’t engage even closed-mindedly, because to do so is either problematically deceptive (if you represent yourself as open-minded) or hostile and ineffective (if you represent yourself as closed-minded).  In the final chapter of Part II I argue that there is an obligation not to invite problematic speakers to campus (that is, speakers who you know will wrongly speak against marginalized groups or speakers who you know have wrongly harmed others and haven’t repented).

We argue that knowledge doesn't require any of truth, justification, or belief. This is so for four primary reasons. First, each of the three conditions has been subject to convincing counterexamples. In addition, the resultant account explains the value of knowledge, manifests important theoretical virtues (in particular, simplicity), and avoids commitment to skepticism.