I want to combine two hitherto largely independent research projects, scientific understanding and mechanistic explanations. Understanding is not only achieved by answering why-questions, that is, by providing scientific explanations, but also by answering what-questions, that is, by providing what I call scientific descriptions. Based on this distinction, I develop three forms of understanding: understanding-what, understanding-why, and understanding-how. I argue that understanding-how is a particularly deep form of understanding, because it is based on mechanistic explanations, which answer why something happens in (...) virtue of what it is made of. I apply the three forms of understanding to two case studies: first, to the historical development of thermodynamics and, second, to the differences between the Clausius and the Boltzmann entropy in explaining thermodynamic processes. (shrink)

Side effects are ubiquitous in medicine and they often play a role in treatment decisions for patients and clinicians alike. Philosophers and health researchers often use side effects to illustrate issues with contemporary medical research and practice. However, technical definitions of ‘side effect’ differ among health authorities. Thus, determining the side effects of an intervention can differ depending on whose definition we assume. Here I review some of the common definitions of side effect and highlight their issues. In response, I (...) offer an account of side effects as jointly (i) unintended and (ii) effects due to the causal capacities or invariances of an intervention. I discuss (i) by examining the intentions or reasons behind therapeutic interventions, and I discuss (ii) by appealing to a manipulationist model of causation. The analysis here highlights that side effects are conceptually distinct from related outcomes like adverse events, adverse drug reactions, and placebo effects. The analysis also allows for reflection on the utility of ‘side effect’ as a technical term in medical research and practice. (shrink)

Nursing scholars continuously refine nursing knowledge and the philosophical foundations of nursing practice. They advance nursing knowledge by creating new knowledge and weighing the relevance of developments in cognate sciences. Nurse philosophers go further by providing epistemological and ontological arguments for explanations of nursing phenomena. In this article, I engage with Bender's arguments about why mechanisms should have more primacy as carriers of nursing knowledge. Despite the careful scholarship involved, Bender's arguments need to be more convincing. Accordingly, this article encourages (...) debate about Bender's arguments for reorientating nursing science to mechanisms. I begin by suggesting that the claim that the theory‐practice divide can be overcome by reorientating to mechanisms is acceptable only if we accept Bender's depiction of the challenge. Then I question the ontology Bender relies on to justify reorientating nursing science. After that, I argue that mechanisms in models that parallel analytical sociology undermine the kind of nursing science Bender advocates. I illustrate my arguments with a social mechanism thought experiment. Then I explain why Bender's arguments cannot escape the received view of science or inform emancipatory nursing action without theory. Finally, I mention some caveats and implications for nursing science. (shrink)

This work addresses biological explanations and aims to provide a philosophical account which brings together logical-procedural and historical-processual aspects when considering molecular pathways. It is argued that, having molecular features as explananda, a particular non-classical logical language – Zsyntax – can be used to formally represent, in terms of logical theorems, types of molecular processes, and to grasp how we get from one molecular interaction to another, hence explaining why a given outcome occurs. Expressing types of molecular biology processes in (...) terms of the Zsyntax language allows us to represent causal interactions by taking into account their context-sensitivity, and amounts to partly reviving the spirit of the so-called received view of explanation – which aimed to capture scientific explanatory accounts in terms of their logical structure and their appealing to nomological relations. Such a partial revival is pursued by invoking here non-classical deductions and empirical generalisations, which are called to provide the epistemic norms to explain the behavior of molecular pathways. (shrink)

Following an analysis of the state of investigations and clinical outcomes in the Alzheimer's research field, I argue that the widely-accepted 'amyloid cascade' mechanistic explanation of Alzheimer's disease appears to be fundamentally incomplete. In this context, I propose that a framework termed 'principled mechanism' (PM) can help with remedying this problem. First, using a series of five 'tests', PM systematically compares different components of a given mechanistic explanation against a paradigmatic set of criteria, and hints at various ways of making (...) the mechanistic explanation more 'complete'. These steps will be demonstrated using the amyloid explanation, and its missing or problematic mechanistic elements will be highlighted. Second, PM makes an appeal for the discovery and application of 'biological principles' (BPs), which approximate ceteris paribus laws and are operative at the level of a biological cell. As such, although thermodynamic, evolutionary, ecological and other laws or principles from chemistry and the broader life sciences could inform them, BPs should be considered ontologically unique. BPs could augment different facets of the mechanistic explanation but also allow further independent nomological explanation of the phenomenon. Whilst this overall strategy can be complementary to certain 'New Mechanist' approaches, an important distinction of the PM framework is its equal attention to the explanatory utility of biological principles. Lastly, I detail two hypothetical BPs, and show how they could each inform and improve the potentially incomplete mechanistic aspects of the amyloid explanation and also how they could provide independent explanations of the cellular features associated with Alzheimer's disease. (shrink)