Grant Ramsey

This article argues that a core area of the philosophy of biology—the philosophy of fitness—has for decades rested on fundamental conceptual and mathematical errors. These errors have been leveraged to support the position in the philosophy of biology known as statisticalism, which holds that biological fitness does not cause evolution, but is merely a kind of statistical summary of evolutionary outcomes. This is opposed to causalism, which holds that fitness is based on (causally efficacious) probabilistic propensities, a position known as the propensity interpretation of fitness. The error I focus on is the idea that fitness depends on population size, n, and because population size is not a causal quantity, fitness cannot be causal. In this paper, I show that fitness is not dependent on n and therefore a central critique of the propensity interpretation of fitness is ill founded.

Behavioral innovativeness—the propensity of an individual organism or higher group to innovate—is frequently invoked as a measurable trait allowing for cross-species comparisons. Individuals or species are often regarded as more innovative or less innovative than others, implying that we can rank order the degree of innovativeness along a single dimension. This paper defends a novel multidimensional understanding of behavioral innovativeness in which innovativeness can be modulated with respect to the generation and capitalization of opportunities, as well as the effectiveness and depth of the innovative behaviors. Besides innovation being multidimensional, it is also multilevel. Here we show how innovativeness at one level (such as the species level) does not automatically translate to innovativeness at another (such as the organism level) and discuss why this matters for cross-species comparisons.

The definition of tool use has long been debated, especially beyond humans. Recent work argues that the phenomena included within tool use are so broad and varied that there is little hope of using the category for scientific generalizations, explanations, and predictions about the evolution, ecology, and psychology of tool users. One response to this argument has been the development of tooling as a replacement for tool use. In this article, we analyze the tool use and tooling frameworks. Identifying advantages and limitations in each, we offer a synthetic approach that suggests promising avenues for future research.

Niche construction is the process of organisms changing themselves or their environment—or their relationship with their environment—in ways that affect the evolutionary trajectory of their population. These evolutionary trajectory changes are traditionally understood to be triggered by changes in selection pressures. Niche construction thus necessarily involves organisms altering selection pressures. In this paper, we argue that changes in selection pressures is not the only way organisms can influence the evolutionary futures of their population. We propose that organisms can also affect drift probabilities, and that such changes should be considered niche construction. Drift probabilities can be modulated by altering population size or by affecting driftability (individual variance in possible reproductive outcomes). We consider both and provide examples of how niche construction can stabilize, increase, or dampen drift probabilities. Finally, we revisit and broaden the traditional definition of niche construction. We hold that organismic activities that modify drift probabilities should count as niche construction, even if selection pressures remain unaltered.

Theoretical frameworks concerning cell fate typically center on proximate causes to explain how cells know what type they are meant to become. While major advances in cell fate theory have been achieved by these mechanism-focused frameworks, there are some aspects of cell decision-making that require an evolutionary interpretation. While mechanistic biologists sometimes turn to evolutionary theory to gain insights about cell fate (cancer is a good example), it is not entirely clear in cell fate theory what insights evolutionary theory can add, and why in some cases it is required for understanding cell fate. In this perspective we draw on our work on cellular mortality to illustrate how evolutionary theory provides an explanation for death being selected as one of the potential cell fates. Using our hypothesis for why some microbes in a community choose death as their fate, we suggest that some insights in cell fate theory are inaccessible to a theoretical framework that focuses solely on proximate causes.

Proponents of the extended evolutionary synthesis have argued that there are explanatory gaps in evolutionary biology that cannot be bridged by standard evolutionary theory. In this paper, we consider what sort of explanatory gaps they are referring to. We outline three possibilities: data-based gaps, implementation-based gaps, and framework-based gaps. We then examine the purported evolutionary gaps and attempt to classify them using this taxonomy. From there we reconsider the significance of the gaps and what they imply for the proposed need for an extended evolutionary synthesis.

The chin, a distinguishing feature of Homo sapiens, has sparked ongoing debates regarding its evolutionary origins and adaptive significance. We contend that these controversies stem from a fundamental disagreement about what constitutes a well-defined biological trait, a problem that has received insufficient attention despite its recognized importance in biology. In this paper, we leverage paleoanthropological research on the human chin to investigate the general issue of character or trait identification. First, we examine four accounts of the human chin from the existing literature: the mandibular differential growth byproduct, the bony prominence, the inverted T-relief, and the symphyseal angle. We then generalize from these accounts and propose a three-stage framework for the process of character identification: description, detection, and justification. We use this framework to reinterpret the four accounts, elucidating key points of contention surrounding the chin as well as other morphological characters. We show that debates over the chin carry broad and important biological implications that extend beyond this trait and that are not mere semantic issues of definition.

Claims that our species is an “evolutionary success” typically do not feature prominently in academic articles. However, they do seem to be a recurring trope in science popularization. Why do we seem to be attracted to viewing human evolution through the lense of “success”? In this chapter we discuss how evolutionary success has both causal-descriptive and ethical-normative components, and how its ethical status is ambiguous, with possible hints of anthropocentrism. We also place the concept of “success” in a wider context of biological thought, contrasting it with two other value-laden concepts: evolutionary progress and human uniqueness. Claiming the human species to be an evolutionary success is ostensibly grounded in metrics such as the dominance or the size of the human population, but often goes beyond this, suggesting that humans are a unique species or the pinnacle of evolutionary progress.

The developmental properties of organisms play important roles in the generation of variation necessary for evolutionary change. But how can individual development steer the course of evolution? To answer this question, we introduce developmental channeling as a disposition of individual organisms that shapes their possible developmental trajectories and evolutionary dappling as an evolutionary outcome in which the space of possible organismic forms is dappled—it is only partially filled. We then trace out the implications of the channeling-dappling framework for contemporary debates in the philosophy of evolution, including evolvability, reciprocal causation, and the extended evolutionary synthesis.

During the battle of Iwo Jima in June 1944, Private First Class Jackylin Harold Lucas and three other U.S. Marines came under attack while making their way along a ravine. Upon seeing two grenades thrown near the soldiers, Lucas dove onto one grenade and pulled the other under his body, saving his companions from serious injury or death. Lucas survived, but his injuries were so grave that his companions left him for dead. Lucas’s act was one of spectacular and nearly suicidal altruism. What does such an act show us about our nature and the human capacity for good and evil? Perhaps it offers a window onto our true nature—a nature ultimately good, though susceptible to corrupting influences. Or perhaps it seems extraordinary precisely because we are greedy and violent by nature but can, in rare instances, rise above those instincts. Questions about what human nature is and how we can learn about it are difficult to answer. They are difficult not just because humans are complex creatures whose behavior is deeply embedded in the cultural environment that they are a part of, but also because it is not obvious what a concept of human nature is supposed to do or what it is for. The concept of human nature is often used as a normative concept, one that can serve as a guide to action, showing us how we ought to behave. Less commonplace is an approach that seeks a descriptive account of human nature, one that characterizes what humans do and are disposed to do. I argue in this essay that the normative and descriptive approaches are at odds and that we should not expect a single concept of human nature to play both roles. Furthermore, there are deep problems with normative accounts. They often ignore or contradict the contemporary scientific worldview, and they often merely reflect biases about how we ought to be and what we ought to do. Human nature in this sense becomes politicized and serves in arguments about the moral status of issues like homosexuality, abortion, or biomedical enhancement. Because of the problems inherent in normative notions of human nature, I offer a descriptive alternative. My alternative attempts to align the scientific study of the human with human nature.

Human nature is frequently evoked to characterize our species and describe how it differs from others. But how should we understand this concept? What is the nature of a species? Some take our nature to be an essence and argue that because humans lack an essence, they also lack a nature. Others argue for non-essentialist ways of understanding human nature, which usually aim to provide criteria for sorting human traits into one of two bins, the one belonging to our nature and the other outside our nature. This Element argues that both the essentialist and trait bin approaches are misguided. Instead, the author develops a trait cluster account of human nature, which holds that human nature is based on the distribution of our traits over our (actual and possible) life histories. One benefit of this account is that it aligns human nature with the human sciences, rendering the central concern of the human sciences to be the study of human nature.

Organismal death is foundational to the evolution of life, and many biological concepts such as natural selection and life history strategy are so fashioned only because individuals are mortal. Organisms, irrespective of their organization, are composed of basic functional units—cells—and it is our understanding of cell death that lies at the heart of most general explanatory frameworks for organismal mortality. Cell death can be exogenous, arising from transmissible diseases, predation, or other misfortunes, but there are also endogenous forms of death that are sometimes the result of adaptive evolution. These endogenous forms of death—often labeled programmed cell death, PCD—originated in the earliest cells and are maintained across the tree of life. Here, we consider two problematic issues related to PCD (and cell mortality generally). First, we trace the original discoveries of cell death from the nineteenth century and place current conceptions of PCD in their historical context. Revisions of our understanding of PCD demand a reassessment of its origin. Our second aim is thus to structure the proposed origin explanations of PCD into coherent arguments. In our analysis we argue for the evolutionary concept of PCD and the viral defense-immunity hypothesis for the origin of PCD. We suggest that this framework offers a plausible account of PCD early in the history of life, and also provides an epistemic basis for the future development of a general evolutionary account of mortality.

What does it mean for our species—or for any species—to be successful? Human Success: Evolutionary Origins and Ethical Implications examines the concept of human success from a variety of disciplinary perspectives, with contributions from leading paleobiologists, anthropologists, geologists, philosophers of science, and ethicists. It tells the tale of how the human species grew in success-linked metrics, such as population size and geographical range, and how it came to dominate ecological systems across the globe. It explores how culture, technology, and creativity have contributed to human success. However, there is a darker side of human success, as has become apparent in a world affected by climate change and the destruction of biodiversity. This leads us to ask whether the human species can really be called successful, and what our future success will look like in terms of our bodies, minds, morals, and our place in the universe. The essays in this book probe us to reflect on what has led to our apparent evolutionary success—and, most important, what this success implies for the future of our species.

Adaptationism is often taken to be the thesis that most traits are adaptations. In order to assess this thesis, it seems we must be able to establish either an exhaustive set of all traits or a representative sample of this set. Either task requires a more systematic and principled way of individuating traits than is currently available. Moreover, different trait individuation criteria can make adaptationism turn out true or false. For instance, individuation based on natural selection may render adaptationism true, but may do so by presupposing adaptationism. In this paper, we show how adaptationism depends on trait individuation and that the latter is an open and unsolved problem.

Conceptions of human nature fall under two broad categories, trait bin accounts and trait cluster accounts. Trait bin accounts take there to be a special bin of traits, one composed of all and only those traits constituting our nature. For those arguing for a trait bin account of human nature, the challenge is to articulate what it is that marks a trait as being in or outside of the bin. For some, the bin is filled by the traits essential to being human. Others, such as Machery in his contribution to this volume, offer a non-essentialist trait bin conception of human nature. In this chapter, I argue that trait bin approaches to human nature are misguided, that there is no good way of dividing human traits into those that are a part of our nature and those that are not. Instead, I argue for a trait cluster account, which sees human nature not as a special bin of traits, but as the relationship among traits. Under this account, human nature lies in the patterns of trait expression within and across human life histories. This account does a superior job characterizing what humans are like and aligning human nature with the human sciences.

Millions of scientific articles are published each year, making it difficult to stay abreast of advances within even the smallest subdisciplines. Traditional approaches to the study of science, such as the history and philosophy of science, involve closely reading a relatively small set of journal articles. And yet many questions benefit from casting a wider net: Is most scientific change gradual or revolutionary? What are the key sources of scientific novelty? Over the past several decades, a massive effort to digitize the academic literature and equip computers with algorithms that can distantly read and analyze a digital database has taken us one step closer to answering these questions. The Dynamics of Science brings together a diverse array of contributors to examine the largely unexplored computational frontiers of history and philosophy of science. Together, they reveal how tools and data from automated textual analysis, or machine "reading," combined with methods and models from game theory and cultural evolutionary theory, can begin to answer fundamental questions about the nature and history of science.

Programmed cell death (PCD) in unicellular organisms is in some instances an altruistic trait. When the beneficiaries are clones or close kin, kin selection theory may be used to explain the evolution of the trait, and when the trait evolves in groups of distantly related individuals, group or multilevel selection theory is invoked. In mixed microbial communities, the benefits are also available to unrelated taxa. But the evolutionary ecology of PCD in communities is poorly understood. Few hypotheses have been offered concerning the community role of PCD despite its far-reaching effects. The hypothesis we consider here is that PCD is a black queen. The Black Queen Hypothesis (BQH) outlines how public goods arising from a leaky function are exploited by other taxa in the community. Black Queen (BQ) traits are essential for community survival, but only some members bear the cost of possessing them, while others lose the trait In addition, BQ traits have been defined in terms of adaptive gene loss, and it is unknown whether this has occurred for PCD. Our conclusion is that PCD fulfils the two most important criteria of a BQ (leakiness and costliness), but that more empirical data are needed for assessing the remaining two criteria. In addition, we hold that for viewing PCD as a BQ, the original BQH needs to include social traits. Thus, despite some empirical and conceptual shortcomings, the BQH provides a helpful avenue for investigating PCD in microbial communities.

The validity and utility of the proximate-ultimate distinction in biology have recently been under debate. Opponents of the distinction argue that it rules out individual-level organismic processes from evolutionary explanations, thereby leading to an unfounded separation between organismic (developmental, behavioral, etc.) causation and evolutionary causation. Proponents of the proximate-ultimate distinction, on the other hand, argue that it serves an important epistemological role in forming different kinds of explanation-seeking questions in biology. In this paper we offer an interpretation the proximate-ultimate distinction not only as a means of forming explanation-seeking questions, but also as a distinction that can help highlight the way in which individual-level organismic processes can be evolutionary causes. We do this by interpreting the distinction between proximate and ultimate causes as a distinction between structuring and triggering causes.

The levels of selection debate is generally taken to be a debate about how natural selection can occur at the various levels of biological organization. In this paper, we argue that questions about levels of selection should be analyzed separately from questions about levels of organization. In the deflationary proposal we defend, all that is necessary for multilevel selection is that there are cases in which particles are nested in collectives, and that both the collectives and the particles that compose them each separately undergo natural selection. We argue that adopting this deflationary account helps to disentangle the levels of selection and the levels of organization, and thereby contributes to advancing the levels of selection debate.

Guilt poses a unique evolutionary problem. Unlike other dysphoric emotions, it is not immediately clear what its adaptive significance is. One can imagine thriving despite or even because of a lack of guilt. In this article, we review solutions offered by Scott James, Richard Joyce, and Robert Frank and show that although their solutions have merit, none adequately solves the puzzle. We offer an alternative solution, one that emphasizes the role of empathy and posttransgression behavior in the evolution of guilt. Our solution, we contend, offers a better account of why guilt evolved to play its distinctive social role.

A major debate in the philosophy of biology centers on the question of how we should understand the causal structure of natural selection. This debate is polarized into the causal and statistical positions. The main arguments from the statistical side are that a causal construal of the theory of natural selection's central concept, fitness, either (i) leads to inaccurate predictions about population dynamics, or (ii) leads to an incoherent set of causal commitments. In this essay, I argue that neither the predictive inaccuracy nor the incoherency arguments successfully undermine the causal account of fitness. 1 Introduction2 The Importance of Trait Fitness3 Trait Fitness is not a Silver Bullet4 The Fundamental Incoherency Argument5 Car Racing and Trait Fitness Reversals6 Population Subdivisions and Evolution7 The STP and the Argument for the Incoherency of the Causal Account of Fitness8 Conclusions.

Culture in humans connotes tradition, norms, ritual, technology, and social learning, but also cultural events like operas or gallery openings. Culture is in part about what we do, but also sometimes about what we ought to do. Human culture is inextricably intertwined with language and much of what we learn and transmit to others comes through written or spoken language. Given the complexities of human culture, it might seem that we are the only species that exhibits culture. How, then, are we to make sense of culture in animals? The study of animal culture is a booming research area. Culture is said to occur in a wide range of vertebrates from our close kin, chimpanzees and orangutans, to more distant relatives like rats and whales. Could these studies be misleading in that they are not actually studying culture but simply misapplying the term ‘culture’? Or is what is labeled culture in animals at the core of human culture, so that although human culture is more elaborate than animal culture, it is different in degree, not kind? While it is certainly easy to intentionally define culture in a way that makes it unique to humans, because of the growing field of animal culture, it would be most useful to attempt to offer a definition of culture that makes sense of how it is used by psychologists, biologists, anthropologists, and others who use the term culture in studies of animal behavior. The challenge is to produce a concept that is broad enough to be able to apply across humans and animals, but not be so anemic that it cannot do justice to human culture. Because of this, I will here construct a definition of animal culture and draw out some of its implications.

In this paper, we distinguish two different approaches to cultural evolution. One approach is meme-centered, the other organism-centered. We argue that in situations in which the meme- and organism-centered approaches are competing alternatives, the organism-centered approach is in many ways superior. Furthermore, the organism-centered approach can go a long way toward understanding the evolution of institutions. Although the organism-centered approach is preferable for a broad class of situations, we do leave room for super-organismic (group based) or sub-organismic (meme-based) explanations of some cultural phenomena.

The dynamics of epiphytic bryophyte communities following natural and human disturbance have rarely been quantified. We describe the response of bryophyte communities on bigleaf maple trees in Olympia, Washington, following their experimental removal. Approximately 8% of the exposed area was recolonized by bryophytes 1 year after clearing, and 27% after 3 years. Lateral encroachment from bryophytes on the sides of the 20-cm-long plots accounted for 75% of this recolonization, with growth from residual plant parts or aerially dispersed diaspores accounting for the remaining 25%. Though it was not possible to distinguish between the latter two sources of cover, the number of clear de novo colonization events over the course of the year was low. Disturbance appeared to reduce bryophyte diversity at this successional stage, as alpha and gamma diversity remained low after 1 year and had not recovered after 3 years. Reflecting the preponderance of lateral encroachment as the mechanism for recolonization, disturbance size may significantly affect the time needed to recolonize disturbed branch substrates. In addition to contributing to ecologists' understanding of processes of succession, these experiments may help to develop sustainable practices for moss-harvesting in the Pacific Northwest.Key words: succession, bryophytes, epiphytes, Acer macrophyllum, recolonization, canopy studies.

There are three related criteria that a concept of fitness should be able to meet: it should render the principle of natural selection non-tautologous and it should be explanatory and predictive. I argue that for fitness to be able to fulfill these criteria, it cannot be a property that changes over the course of an individual's life. Rather, I introduce a fitness concept--Block Fitness--and argue that an individual's genes and environment fix its fitness in such a way that each individual's fitness has a fixed value over its lifetime.

There is clearly a plurality of forms of altruism. Classically, biological altruism is distinguished from psychological altruism. Recent discussions of altruism have attempted to distinguish even more forms of altruism. I will focus on three altruism concepts, biological altruism, psychological altruism, and helping altruism. The questions I am concerned with here are, first, how should we understand these concepts? and second, what relationship do these concepts bear to one another? In particular, is there an essence to altruism that unifies these concepts? I suggest that while there is no essence to altruism, this does not mean that the array of altruism concepts is completely disunified. Instead, I propose we place all the concepts into a common framework-an altruism space-that could lead to new questions about how this space can be filled.

Niche construction theory concerns how organisms can change selection pressures by altering the feature–factor relationship between themselves and their environment. These alterations are standardly understood to be brought about through two kinds of organism–environment interaction: perturbative and relocational niche construction. We argue that a reconceptualization is needed on the grounds that if a niche is understood as the feature–factor relationship, then there are three fundamental ways in which organisms can engage in niche construction: constitutive, relational, and external niche construction. We further motivate our reconceptualization by showing some examples of organismic activities that fall outside of the current categorization of niche construction, but nonetheless should be included. We end by discussing two objections to niche construction and show how our reconceptualization helps to undercut these objections. 1Introduction2Niche Construction Theory 2.1The standard account of niche construction2.2Two problems with the standard account of niche construction3Three Kinds of Niche Construction 3.1Constitutive niche construction3.2Relational niche construction3.3External niche construction4Conceptual Improvement on Niche Construction Theory 4.1Constitutive niche construction4.2Relational niche construction4.3External niche construction5The Status of Niche Construction Theory within Evolutionary Theory 5.1Is niche construction a helpful addition to evolutionary theory?5.2Is niche construction an evolutionary process?6Conclusion

"Correlation is not causation" is one of the mantras of the sciences—a cautionary warning especially to fields like epidemiology and pharmacology where the seduction of compelling correlations naturally leads to causal hypotheses. The standard view from the epistemology of causation is that to tell whether one correlated variable is causing the other, one needs to intervene on the system—the best sort of intervention being a trial that is both randomized and controlled. In this paper, we argue that some purely correlational data contains information that allows us to draw causal inferences: statistical noise. Methods for extracting causal knowledge from noise provide us with an alternative to randomized controlled trials that allows us to reach causal conclusions from purely correlational data.

In multicellular organisms, cells are frequently programmed to die. This makes good sense: cells that fail to, or are no longer playing important roles are eliminated. From the cell’s perspective, this also makes sense, since somatic cells in multicellular organisms require the cooperation of clonal relatives. In unicellular organisms, however, programmed cell death poses a difficult and unresolved evolutionary problem. The empirical evidence for PCD in diverse microbial taxa has spurred debates about what precisely PCD means in the case of unicellular organisms. In this article, we survey the concepts of PCD in the literature and the selective pressures associated with its evolution. We show that definitions of PCD have been almost entirely mechanistic and fail to separate questions concerning what PCD fundamentally is from questions about the kinds of mechanisms that realize PCD. We conclude that an evolutionary definition is best able to distinguish PCD from closely related phenomena. Specifically, we define “true” PCD as an adaptation for death triggered by abiotic or biotic environmental stresses. True PCD is thus not only an evolutionary product but must also have been a target of selection. Apparent PCD resulting from pleiotropy, genetic drift, or trade-offs is not true PCD. We call this “ersatz PCD.”