In this paper, I will conduct three interrelated analyses. First, I will develop an analysis of various concepts in the history of biology that used to refer to individual-level phenomena but were then reinterpreted by the Modern Synthesis in terms of populations. Second, a similar situation can be found in contemporary evolutionary theory. While different approaches reflect on the causal role of developing organisms in evolution, proponents of the Modern Synthesis refrain from any substantial change by reinterpreting and explaining individual-level phenomena from a population perspective. Finally, I will approach these historical and contemporary debates by arguing for the statistical reading of natural selection, which holds that explanations by natural selection are statistical. My main conclusion is that the historical conceptual reinterpretations belong to a new explanatory strategy developed by the Modern Synthesis based on population thinking. Adopting the statistical point of view has three advantages for the issues discussed in this paper. First, understanding historical conceptual change as part of an explanatory shift fits with the emergence of population biology as a discipline that employs statistical methods. Second, concerning current debates in evolutionary biology, the statisticalist reading can validate the goal of both sides of the dispute. It ascribes an invaluable role to the population statistical explanation of the MS and also commends the study of developmental and organismal causes of adaptive evolution. Finally, the division of explanatory roles in evolutionary biology, embarrassed by statisticalism, can be related to the different interpretations that important biological concepts have undergone throughout history and contemporary biology, i.e., that the division of explanatory roles allows for a division of conceptual interpretations.

The concept of "progress" in evolutionary theory and its relationship to a putative notion of "Progress" in a global, normatively loaded sense of "change for the better" have been the subject of debate since Darwin admonished himself in a marginal note to avoid using the terms 'higher' and 'lower.' While an increase in some kind of complexity in the natural world might seem self-evident, efforts to explicate this trend meet notorious philosophical difficulties. Numerous historians pin the Modern Synthesis as a pivotal moment in this history; Michael Ruse even provocatively hypothesizes that Ernst Mayr and other "architects" of the Synthesis worked actively to eliminate Progress from evolutionary biology's scientific purview. I evaluate these claims here with a textual analysis of the journals Evolution and Proceedings of the Royal Society B (a corpus of 27,762 documents), using a dynamic topic modeling approach to track the fate of the term 'progress' across the Modern Synthesis. The claim that this term declines in importance for evolutionary theorizing over this period can, indeed, be supported; more tentative evidence is also provided that the discussion of 'progress' is largely absent from the British context, emphasizing the role of American paleontology in the rise and fall of 'progress' in 20th-century evolutionary biology.

Edvard August Vainio was a world-renowned Finnish lichenologist. In Finland, however, he was a controversial person due to his strong pro-Finnish political views. Equally disputed was his opinion that systematics should be based on evolutionary theory and phylogenetic thinking. Vainio was familiar with the ideas of the early German phylogeneticists-especially those of Carl Wilhelm von Nägeli - and, applying them, aimed to create an exact method for building a natural classification of lichens already at the end of the nineteenth century. In this respect, Vainio was a true pioneer, as no actual phylogenetic method had yet been developed. In the general spirit of the time, Vainio focused on finding the ancestors of species and other taxa by comparing primitive and derived features of homologous characters. However, Vainio already understood the concept of sister groups in 1880, the identification of which is the basis of all modern phylogenetic research. Nevertheless, the distinctive method developed by Vainio was not so much focused on the construction of a phylogenetic tree, but on revealing the origin of species through the differentiation and fixation of their polymorphic variation. Indeed, Vainio's species concept is surprisingly similar to the phylogenetic species concepts presented a hundred years later. Although in many ways progressive, Vainio's views did not influence the development of phylogenetics more widely, but his discussions are nevertheless a valuable source to understanding the early development of phylogenetic theory.

What do we mean when we talk about epigenetic harm? This paper presents a multidimensional view of epigenetic harm. It is a plea to take a step back from discussions of epigenetic responsibility distributions prevalent in ELSA literature on epigenetics. Instead, it urges researchers to take a closer look at the normative role played by the concept of epigenetic harm. It starts out by showing that the ways in which the object of epigenetic responsibility has already been conceptualized are all related to 'epigenetic harm': something negative that happens in which epigenetic mechanisms play a role, or rather something that needs to be avoided. Epigenetic harm is then characterized as a bridging concept between relatively neutral findings on epigenetics on the one side, and potential ethical and societal implications of those findings, primarily in terms of responsibility ascriptions and distributions, on the other. The paper proposes that a sufficiently nuanced account of epigenetic harm should include at least three dimensions. The dimension of causation alone leads to an overly narrow understanding of harm, and a wrong understanding of this dimension might prompt researchers to support an excessively simplistic epigenetic determinism. It is argued that a multidimensional analysis of epigenetic harm is less vulnerable to this threat and more reflective of the various kinds of harm that may be experienced by the subjects of epigenetic alterations. The paper applies insights from disability studies and feminist philosophy to draw attention to two other dimensions of epigenetic harm, namely lived experiences and relationality. The paper concludes by exploring what a shift towards a multidimensional approach to epigenetic harm might mean for epigenetic research and responsibility ascriptions by formulating some concrete implications.

The present article examines the material, epistemological, and social dimensions of late nineteenth-century anti-cholera serum controversies that unfolded in Tokyo and Berlin. It seeks to shed light on the conflicting values embedded in the construction of scientific evidence during the transnational exploration of bacteriology as an effective response to controlling epidemics. Driven by Japanese health authorities' initiatives, Japanese bacteriologist Kitasato Shibasaburo participated in the elaboration of bacteriological research oriented toward therapeutic application during his stay in Berlin. This work coincided with the rise of a controversy over anti-cholera serum in relation to the animal experiments conducted by Richard Pfeiffer, a German bacteriologist. After presenting a series of animal experiments and certain clinical cases conducted in Germany, France, and Egypt in the context of the controversies, the article analyzes a therapeutic trial conducted by Kitasato in Japan during an 1895 cholera epidemic. His strategy, bringing new data to the transnational debate through an intensive investment of resources in the trial, provoked criticism from his Japanese and German colleagues. These critics questioned Kitasato's method and pointed out the low social value of this experimental serum therapy, performed in highly equipped conditions. Through this case study, the present article highlights: a) a strong tension between transnational research interactions among bacteriologists and local medical practices during public health campaigns against epidemics at the turn of the twentieth century; b) the importance of analyzing the interconnected effects of local, national and transnational frameworks of medical science when examining the increasingly intertwined relationships between laboratory science and clinical medicine.

"The Strategy of Model Building in Population Biology" published by Richard Levins in 1966 has been cited over 2500 times. For a paper concerned with modeling approaches in population biology a surprisingly large part of the attention. The Strategy received comes from history and philosophy of biology, and specifically from accounts on model and model formulation. The Strategy is an unusual paper; it presents neither new data nor a new formal model; at times it reads like a manifesto for some modeling approach, without specifying which broader program that approach intends to support. When these peculiarities of The Strategy are even mentioned, the philosophical literature tends to explain them away by invoking Levins' Marxist commitments. In contrast, I argue that those peculiarities can be explained by examining the programmatic purpose of the paper; starting from his doctoral work, Levins was trying to establish a research program meant to account for the relations between fitness and environment in different terms than the prevalent lock-and-key view. My paper brings that program back to the discussion, explains its relation to competing approaches and examines Levins' approach to modeling in light of that context.

We present a case study of two scientific perspectives on the phenomenon of nerve signal propagation, a bio-electric and a thermodynamic perspective, and compare this case with two accounts of scientific perspectivism: those of Michela Massimi and Juha Saatsi, respectively. We demonstrate that the interaction between the bio-electric perspective and the thermodynamic perspective can be captured in Saatsi's terms of progress in explanatory understanding. Using insights from our case study, we argue that both the epistemic and pragmatic dimensions of scientific understanding are important for increasing explanatory understanding of phenomena. The epistemic dimension of understanding is important for increasing the number of actually answered what-if-things-had-been-different questions about a phenomenon, the pragmatic dimension for pointing out the potentially answerable what-if questions that have been overlooked or purposefully neglected thus far. Exposing the limitations of the acquired understanding within a particular perspective can be achieved by criticizing the assumptions that have been adopted to make models of the perspective intelligible, but that are considered problematic from a rival perspective.

In 1899, the first cases of plague were recognised in Paraguay and a few months later in Buenos Aires as part of the third plague pandemic. In the first decades of the twentieth century, plague slowly advanced towards the Argentinian hinterland. In this paper we focus on the production of scientific knowledge about plague in Argentina, where a core of bacteriologists emerged early on. We show how they not only played a central role in the complex process of plague recognition and intervention, but also influenced the scientific development of bacteriology in Argentina and potentially in South America. We argue that bacteriology became a key tool in articulating the promises of modern science with political and economic interests, allowing the Argentinian government to extend its territorial control over Buenos Aires and the hinterland. This can be seen in two different configurations of the plague as an epistemic and political object in Argentina. In the first period, from 1899 to 1910, plague was a problem linked to the ports. In this section of the article, we show how plague became an important issue in the development of bacteriology in Argentina, how this research contributed to new intervention measures and, in some cases, developed innovative ideas about serotherapeutic treatments and the characteristics of the disease. In the second period, from the mid-1910s until the 1940s, research in Argentina provided new evidence of the 'rural' nature of plague, a process in deep dialogue with research on plague among peri-domestic and wild rodents carried out in other parts of the Americas, Europe and Africa. This article thus aims to contribute to a history of bacteriology that highlights the role of non-European centres, like Argentina, in the production and circulation of bacteriological knowledge.

This article's jumping-off point is the highly incisive but often-ignored claim by the French doctor, Louis-Jacques Tanon, in 1922 that rats acted as plague reservoirs in Paris; in other words, that they harboured the plague bacillus but were refractory to it. This claim partially reframed the fight against this disease in the French capital in the 1920s, which became more centred on surveilling the plague reservoir rather than on destroying rats. Drawing upon Tanon's hypothesis, this article explores the emergence, evolution, and several iterations of the idea of disease reservoirs in the early twentieth century. On the one hand, it describes the crafting of a range of ideas with which Tanon was directly or indirectly dialoguing, namely, that rats could present a stage called chronic plague, which was especially developed in India; and that human populations, especially children, acted as sources or reservoirs of malaria in Sierra Leone and Algeria. On the other hand, this article shows how Tanon created original reasoning by combining and reformulating some of these ideas and applying them to Paris. Thus, this article contributes to the early history of reasoning in terms of disease reservoirs, as well as presenting a more dynamic history of microbiology by showing how concepts crafted in the "Rest" found their place in Europe.

Adverse childhood experiences (ACEs) have become a topic of public and scientific attention. ACEs denote a range of negative experiences in early life, from sexual abuse to emotional neglect, that are thought to impact health over the life course. The term was coined in the CDC-Kaiser ACE Study, an epidemiological study that surveyed 17,421 adults about ACEs and correlated the responses with participants' current health records. Shortly after the study was published in 1998, the US CDC deemed ACEs an important public health target; however, it is only recently that ACEs feature prominently in scientific and public discourses. We contend that this rise in popularity is linked to the adoption of epigenetic explanations for how ACEs affect health. Based on a literature analysis, we trace the evolution of explanatory frameworks for ACEs-from coping behaviors to allostatic load to epigenetics-and analyze how each of these explanations not only reconsiders the mechanisms by which ACEs affect health, but also who should be held responsible for addressing ACEs and how. Epigenetics provides distinctly different discursive possibilities than previous frameworks: firstly, it offers one distinct molecular mechanism for how ACEs work, lending "molecular credibility" to epidemiological findings; secondly, it raises the possibility of reversing the negative effects of ACEs on the biological level. This epigenetic articulation makes ACEs attractive for new actors in science and society. Particularly, it facilitates novel interdisciplinary collaborations and attracts actors in health advocacy who are interested in non-deterministic readings of ACEs that counteract stigma and support positive health interventions and healing.

'Obesity' has, for decades, been a subject of intense scientific and public interest, and remains a key target for postgenomic science. I examine the emergence of determinism in research into 'obesity' in the postgenomic field of metabolomics. I argue that determinism appears in metabolomics research in two ways: firstly, fragmentation and narrow construal of the environment is evident in metabolomics studies on weight loss interventions, resulting in particular features of the environment (notably, dietary intake) having outsized influence while the wider social environment is neglected. Secondly, studies aiming to characterize the metabolic signature of 'obesity' are guided by a commitment to a deterministic connection between 'obesity' and dysfunction, leading to a neglect or distortion of metabolic heterogeneity across individuals regardless of body size.

Barbara McClintock (1902-1992), the renowned American maize geneticist, received the 1983 Nobel Prize "for her discovery of mobile genetic elements," becoming the seventh woman scientist to receive a Nobel Prize. However, Nathaniel Comfort points out that McClintock viewed her primary contribution as the elucidation of control systems, rather than the discovery of mobile elements. McClintock's interest in control systems dates back to the 1940s, and this paper investigates her 1961 conversation with François Jacob and Jacques Monod, where she sought to shape the interpretation of her work by drawing parallels between maize control systems and a bacterial system they had recently discovered. Despite McClintock's efforts, Jacob and Monod rejected her parallels and suggested that her contribution was limited to mobile elements. Through an examination of their published papers, I argue that Jacob and Monod's rejection stemmed from their failure to fully comprehend maize control systems. Disciplinary discrepancy helps explain Jacob and Monod's lack of comprehension: they were molecular geneticists working on bacteria, while McClintock was a classical geneticist studying maize. I further argue that gender played a role, as McClintock experienced the Matilda effect-the under-recognition of her contribution, reinforced by the reactions of two male geneticists, and ironically, by the award of the Nobel Prize. Control systems, stemming from McClintock's reverence for organisms, embodied what Evelyn Fox Keller defines as "gender-neutral science." This divergent view of science provides insight into why Jacob and Monod failed to grasp McClintock's work in 1961.

Comparative to the commonplace focus onto developments in mathematics and physics, the life sciences appear to have received relatively sparse attention within the early history of analytic philosophy. This paper addresses two related aspects of this phenomenon. On the one hand, it asks: to the extent that the significance of the life sciences was indeed downplayed by early analytic philosophers, why was this the case? An answer to this question may be found in Bertrand Russell's 1914 discussions of the relation between biology and philosophy. Contrary to received views of the history of analytic philosophy, Russell presented his own 'logical atomism' in opposition not only to British Idealism, but also to 'evolutionism'. On the other hand, I will question whether this purported neglect of the life sciences does indeed accurately characterise the history of analytic philosophy. In answering this, I turn first to Susan Stebbing's criticisms of Russell's overlooking of biology, her influence on J.H. Woodger, and her critical discussion of T.H. Huxley's and C.H. Waddington's application of evolutionary views to philosophical questions. I then discuss the case of Moritz Schlick, whose evolutionist philosophy has been overlooked within recent debates concerning Logical Empiricism's relation to the philosophy of biology.

Drawing on institutional historical records, interviews and student theses, this article charts the intersection of hospital acquired illness, the emergence of antimicrobial resistance (AMR), environments of armed conflict, and larger questions of social governance in the specific case of the American University of Beirut Medical Center (AUBMC) in Lebanon. Taking a methodological cue from approaches in contemporary scientific work that understand non-clinical settings as a fundamental aspect of the history and development of AMR, we treat the hospital as not just nested in a set of social and environmental contexts, but frequently housing within itself elements of social and environmental history. AMR in Lebanon differs in important ways from the settings in which global protocols for infection control or rubrics for risk factor identification for resistant nosocomial outbreaks were originally generated. While such differences are all too often depicted as failures of low and middle-income countries (LMIC) to maintain universal standards, the historical question before us is quite the reverse: how have the putatively universal rubrics of AMR and hospital infection control failed to take account of social and environmental conditions that clearly matter deeply in the evolution and spread of resistance? Focusing on conditions of war as an organized chaos in which social, environmental and clinical factors shift dramatically, on the social and political topography of patient transfer, and on a missing "meso" level of AMR surveillance between the local and global settings, we show how a multisectoral One Health approach to AMR could be enriched by an answering multisectoral methodology in history, particularly one that unsettles a canonical focus on the story of AMR in the Euro-American context.

The diagnosis of childhood schizophrenia was widely employed in the U.S. from the 1930s to the late 1970s. In this paper I will provide a history of the diagnosis. Some of the earliest publications on childhood schizophrenia outlined the notion that childhood schizophrenia had different types. I will outline the development of these types, outlining differing symptoms and causes associated with various types. I outline how different types of childhood schizophrenia were demarcated from one another primarily on age of onset and the type of psychosis which was believed to be present. I will outline how various child psychiatrists viewed the types of childhood schizophrenia posited by other child psychiatrists. I will outline the process of abandoning childhood schizophrenia. I use my history to challenge what I believe are misconceptions about childhood schizophrenia. Also, I will use my history to draw lessons for thinking about modern notions of autism. It shows potential problems around formulating psychiatric diagnoses around causes and how compromises might be needed to prevent those problems. Additionally, childhood schizophrenia shows that psychiatrists could formulate subtypes that are not based upon functioning levels and that we can conceive of subtypes as dynamic whereby someone can change which subtype they exhibit over time.

Cell biologists, including those seeking molecular mechanistic explanations of cellular phenomena, frequently rely on experimental strategies focused on identifying the cellular context relevant to their investigations. We suggest that such practices can be understood as a guided decomposition strategy, where molecular explanations of phenomena are defined in relation to natural contextual (cell) boundaries. This "top-down" strategy contrasts with "bottom-up" reductionist approaches where well-defined molecular structures and activities are orphaned by their displacement from actual biological functions. We focus on the central role of microscopic imaging in cell biology to uncover possible constraints on the system. We show how identified constraints are used heuristically to limit possible mechanistic explanations to those that are biologically meaningful. Historical examples of this process described here include discovery of the mechanism of oxidative phosphorylation in mitochondria, molecular explanation of the first steps in protein secretion, and identification of molecular motors. We suggest that these instances are examples of a form of downward causation or, more specifically, constraining relations, where higher-level structures and variables delimit and enable lower-level system states. The guided decomposition strategy in our historical cases illustrates the irreducibility of experimentally identified constraints in explaining biological activities of cells. Rather than viewing decomposition and recomposition as separate epistemic activities, we contend that they need to be iteratively integrated to account for the ontological complexity of multi-level systems.

Since the completion of the Human Genome Project (HGP), biomedical sciences have moved away from a gene-centred view and towards a multi-factorial one in which environment, broadly speaking, plays a central role in the determination of human health and disease. Environmental exposures have been shown to be highly prevalent in disease causation. They are considered as complementary to genetic factors in the etiology of diseases, hence the introduction of the concept of the "exposome" as encompassing the totality of human environmental exposures, from conception onwards (Wild in Cancer Epidemiol Biomark Prev 14:1847-1850, 2005), and the launch of the Human Exposome Project (HEP) which aims to complement the HGP. At first sight, and seen as complementary to the genome, the exposome could thus appear as contributing to the rise of novel postgenomic deterministic narratives which place the environment at their core. Is this really the case? If so, what sort of determinism is at work in exposomics research? Is it a case of environmental determinism, and if so, in what sense? Or is it a new sort of deterministic view? In this paper, we first show that causal narratives in exposomics are still very similar to gene-centred deterministic narratives. They correspond to a form of Laplacian determinism and, above all, to what Claude Bernard called the "determinism of a phenomenon". Second, we introduce the notion of "reversed heuristic determinism" to characterize the specific deterministic narratives present in exposomics. Indeed, the accepted sorts of external environmental exposures conceived as being at the origins of diseases are determined, methodologically speaking, by their identifiable internal and biological markers. We conclude by highlighting the most relevant implications of the presence of this heuristic determinism in exposomics research.