This paper addresses the topic of determinism in contemporary microbiome research. I distinguish two types of deterministic claims about the microbiome, and I show evidence that both types of claims are present in the contemporary literature. First, the idea that the host genetics determines the composition of the microbiome which I call “host-microbiome determinism”. Second, the idea that the genetics of the holobiont (the individual unit composed by a host plus its microbiome) determines the expression (...) of certain phenotypic traits, which I call “microbiome-phenotype determinism”. Drawing on the stability of traits conception of individuality (Suárez in Hist Philos Life Sci 42:11, 2020) I argue that none of these deterministic hypotheses is grounded on our current knowledge of how the holobiont is transgenerationally assembled, nor how it expresses its phenotypic traits. (shrink)

We argue that microbiome research should be more reflective on the methods that it relies on to build its datasets due to the danger of facing a methodological problem which we call “epistemic misalignment.” An epistemic misalignment occurs when the method used to answer specific scientific questions does not track justified answers, due to the material constraints imposed by the very method. For example, relying on 16S rRNA to answer questions about the function of the microbiome generates epistemic (...) misalignments, due to the different temporal scales that 16S rRNA provides information about and the temporal scales that are required to know about the functionality of some microorganisms. We show how some of these exist in contemporary microbiome science and urge microbiome scientists to take some measures to avoid them, as they may question the credibility of the field as a whole. (shrink)

Humans’ indigenous microbes strongly influence organ functions in an age‐ and diet‐dependent manner, adding an important dimension to aging biology that remains poorly understood. Although age‐related differences in the gut microbiota composition correlate with age‐related loss of organ function and diseases, including inflammation and frailty, variation exists among the elderly, especially centenarians and people living in areas of extreme longevity. Studies using short‐lived as well as nonsenescent model organisms provide surprising functional insights into factors affecting aging and implicate attenuating effects (...) of microbes as well as a crucial role for certain transcription factors like forkhead box O. The unexpected beneficial effects of microbes on aged animals imply an even more complex interplay between the gut microbiome and the host. The microbiome constitutes the major interface between humans and the environment, is influenced by biosocial stressors and behaviors, and mediates effects on health and aging processes, while being moderated by sex and developmental stages. (shrink)

A distinction between different notions of “structure” and “function” is suggested for interpreting the overwhelming amount of data on microbiome structure and function. Sequence data, biochemical agents, interaction networks, taxonomic communities, and their dynamics can be linked to potential or actual biochemical activities, causal roles, and selected effects, respectively. This conceptual clarification has important methodological consequences for how to interpret existing data and approach open questions in contemporary microbiome research practice. In particular, the field will have to start (...) thinking about notions of function more directly. Also see the video abstract here https://youtu.be/j5pq5uGld1k. (shrink)

There has been a spurt in both fundamental and translational research that examines the underlying mechanisms of the human microbiome in psychiatric disorders. The personalized and dynamic features of the human microbiome suggest the potential of its manipulation for precision psychiatry in ways to improve mental health and avoid disease. However, findings in the field of microbiome also raise philosophical and ethical questions. From a philosophical point of view, they may yet be another attempt at providing a (...) biological cause for phenomena that ultimately cannot be so easily localized. From an ethical point of view, it is relevant that the human gut microbiome comprises data on the individual’s lifestyle, disease history, previous medications, and mental health. Massive datasets of microbiome sequences are collected to facilitate comparative studies to identify specific links between the microbiome and mental health. Although this emerging research domain may show promise for psychiatric patients, it is surrounded by ethical challenges regarding patient privacy, health risks, effects on personal identity, and concerns about responsibility. This narrative overview displays the roles and advances of microbiome research in psychiatry and discusses the philosophical and ethical implications of microbiome big data and microbiome-based interventions for psychiatric patients. We also investigate whether these issues are really “new,” or “old wine in new bottles.”. (shrink)

Research on the human microbiome has gen- erated a staggering amount of sequence data, revealing variation in microbial diversity at the community, species (or phylotype), and genomic levels. In order to make this complexity more manageable and easier to interpret, new units—the metagenome, core microbiome, and entero- type—have been introduced in the scientific literature. Here, I argue that analytical tools and exploratory statisti- cal methods, coupled with a translational imperative, are the primary drivers of this new ontology. By (...) reducing the dimensionality of variation in the human microbiome, these new units render it more tractable and easier to interpret, and hence serve an important heuristic role. Nonetheless, there are several reasons to be cautious about these new categories prematurely ‘‘hardening’’ into natural units: a lack of constraints on what can be sequenced metagenomically, freedom of choice in taxonomic level in defining a ‘‘core microbiome,’’ typological framing of some of the concepts, and possible reification of statistical constructs. Finally, lessons from the Human Genome Project have led to a translational imperative: a drive to derive results from the exploration of microbiome variation that can help to articulate the emerging paradigm of per- sonalized genomic medicine (PGM). There is a tension between the typologizing inherent in much of this research and the personal in PGM. (shrink)

It is becoming increasingly clear that most, if not all, animals and plants are associated with a diverse array of resident gut microbiota. This symbiosis is regulated by host-microbiome interactions which influence the development, homeostasis, adaptation and evolution of the host. Recent evidence indicated that these interactions can also affect the host germline and have a potential of supporting transgenerational effects, including inheritance of acquired characteristics. Taken together, the influence of gut bacteria on the host soma and germline could (...) potentially give rise to emergent phenotypes, which may be partially inherited by three distinguishable modes of transgenerational influence of gut bacteria: 1) “soma-to-soma” 2) “soma-to-germline” and 3) “soma-germline-soma”. Here, we discuss these possibilities in light of evidence supporting bacterial-mediated modes of transgenerational inheritance. All animals are consortiums of hosts and microbiota. Their interactions influence many aspects of the adaptation and evolution of the Holobiont. The host germline can also be affected which can give rise to new modes of transgenerational influence of gut bacteria: 1) “soma-to-soma” 2) “soma-to-germline,” and 3) “soma-germline-soma.”. (shrink)

Healthism and ableism intertwine through an imperative of normalcy and the ensuing devaluing of those who fail to meet societally dominant norms and expectations around “normal” health. This paper tracks the effect of that imperative of normalcy through current research into gut microbiome therapies, using therapies targeting fatness and autism as examples. The complexity of the gut microbiome ought to encourage us to rethink our conception of ourselves and our embeddedness in the world; instead, the microbiome is (...) transformed into one more tool for controlling unruly bodies and minds. (shrink)

Research on the human microbiome has generated a staggering amount of sequence data, revealing variation in microbial diversity at the community, species (or phylotype), and genomic levels. In order to make this complexity more manageable and easier to interpret, new units—the metagenome, core microbiome, and enterotype—have been introduced in the scientific literature. Here, I argue that analytical tools and exploratory statistical methods, coupled with a translational imperative, are the primary drivers of this new ontology. By reducing the dimensionality (...) of variation in the human microbiome, these new units render it more tractable and easier to interpret, and hence serve an important heuristic role. Nonetheless, there are several reasons to be cautious about these new categories prematurely ‘‘hardening’’ into natural units: a lack of constraints on what can be sequenced metagenomically, freedom of choice in taxonomic level in defining a ‘‘core microbiome,’’ typological framing of some of the concepts, and possible reification of statistical constructs. Finally, lessons from the Human Genome Project have led to a translational imperative: a drive to derive results from the exploration of microbiome variation that can help to articulate the emerging paradigm of personalized genomic medicine (PGM). There is a tension between the typologizing inherent in much of this research and the personal in PGM. (shrink)

The aim of the present paper is to explore whether seasonal outbreaks of infectious diseases may be linked to changes in host microbiomes. This is a very important issue, because one way to have more control over seasonal outbreaks is to understand the factors that underlie them. In this paper, I will evaluate the relevance of the microbiome as one of such factors. The paper is based on two pillars of reasoning. Firstly, on the idea that microbiomes play an (...) important role in their hosts’ defence against infectious diseases. Secondly, on the idea that microbiomes are not stable, but change seasonally. These two ideas are combined in order to argue that seasonal changes in a given microbiome may influence the functionality of the host's immune system and consequently make it easier for infectious agents to infect the host at certain times of year. I will argue that, while this is only a theoretical possibility, certain studies may back up such claims. Furthermore, I will show that this does not necessarily contradict other hypotheses aimed at explaining seasonal outbreaks; in fact, it may even enhance them. (shrink)

The dual role of microbial communities as either beneficial/functional or harmful/pathogenic involves two issues concerning causality in physiology and medicine, etiology of disease, and the notion of function in biology. Causal explanation formulated by the germ theory of disease and the Koch postulates connects the existence of a specifically identified microbe to disease by the isolation and identification of a pathogen from an organism with the disease and the successful infection of a healthy individual. Similarly, microbiome research in medicine (...) centers on taxonomic composition in correlation with physiological conditions and germ-free mice experimentations to establish causal connections. However, because the microbiome is an ecological community, it lacks the specificity of identification assumed in the germ theory. Furthermore, the ecological aspects within and between microbiomes such as background conditions, microbial interactions, and interdependence, are treated as confounding. Looking at ecological studies, the causal explanations are less specific regarding complex systems with their processes of interactions. This article makes the following two points: One is that microbiome causality in the host should be understood similarly to the microbiome causality in an ecosystem. The second is that if considering a microbiome’s causality in the host as an ecosystem, its etiological explanation needs to be revisited to include a heterogeneous and mutual notion of interactions. Finally, according to the second point, the notion of function in ecology with its relevant notion of causality should be considered accordingly. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s (...) postulates are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s (...) postulates are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

. Early microbiome research found numerous associations between microbial community patterns and host physiological states. These findings hinted at community-level explanations. “Top-down” experiments, working with whole communities, strengthened these explanatory expectations. Now, “bottom-up” mechanism-seeking approaches are dissecting communities to focus on specific microbes carrying out particular biochemical activities. To understand the interplay between methodological and explanatory scales, we examine claims of “dysbiosis,” when host illness is proposed as the consequence of a community state. Our analysis concludes with general observations (...) about how methodologies relate to explanations, and the implications for microbiome research. (shrink)

The microbiome has become one of the most recognizable research subjects and presences in the headlines of news and scientific articles published in almost every biological science area in the last few years. The steady decline in the price of DNA sequencing has enabled metagenomics, community analysis and genome sequencing to enter routine research in microbiology and biotechnology laboratories all around the world. The already open access to national and international databases that include nucleotide (including full genomes) and protein (...) sequences such as GenBank or EMBL-Bank and a multitude of free bioinformatic software resources accessible online, along with the international efforts towards open science publication and open data, allow the possibility of the microbiome and microbiota to be envisaged as a potential data and material resource for new media art projects especially for artists interested in biological processes. Recent results on the creation of synthetic life that are already testing the boundaries of life could be another approach for the creative exploration of microbiology and microbial processes from the artistic point of view. This article will attempt to uncover and reflect on the potential for further exploration of this resource. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s (...) postulates are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

This essay, written by a biologist, a microbial ecologist, a biological anthropologist, and an anthropologist‐historian, examines tensions and translations in microbiome research on animals in the laboratory and field. The authors trace how research questions and findings in the laboratory are extrapolated into the field and vice versa, and the shifting evidentiary standards that these research settings require. Showing how complexities of microbiomes challenge traditional standards of causation, the authors contend that these challenges require new approaches to inferences used (...) in ecology, anthropology, and history. As social scientists incorporate investigations of microbial life into their human studies, microbiome researchers venture into field settings to develop mechanistic understandings about the functions of complex microbial communities. These efforts generate new possibilities for cross‐fertilizations and inference frameworks to interpret microbiome findings. Microbiome research should integrate multiple scales, levels of variability, and other disciplinary approaches to tackle questions spanning conditions from the laboratory to the field. (shrink)

Multicellular organisms contain numerous symbiotic microorganisms, collectively called microbiomes. Recently, microbiomic research has shown that these microorganisms are responsible for the proper functioning of many of the systems of multicellular organisms. This has inclined some scholars to argue that it is about time to reconceptualise the organism and to develop a concept that would place the greatest emphasis on the vital role of microorganisms in the life of plants and animals. We believe that, unfortunately, there is a problem with this (...) suggestion, since there is no such thing as a universal concept of the organism which could constitute a basis for all biological sciences. Rather, the opposite is true: numerous alternative definitions exist. Therefore, comprehending how microbiomics is changing our understanding of organisms may be a very complex matter. In this paper we will demonstrate that this pluralism proves that claims about a change in our understanding of organisms can be treated as both true and untrue. Mainly, we assert that the existing concepts differ substantially, and that only some of them have to be reconsidered in order to incorporate the discoveries of microbiomics, while others are already flexible enough to do so. Taking into account the plurality of conceptualisations within different branches of modern biology, we will conduct our discussion using the developmental and the cooperation–conflict concepts of the organism. Then we will explain our results by referring to the recent philosophical debate on the nature of the concept of the organism within biology. (shrink)

Microbiome science asserts humans are made up of more microbial cells and genes than human ones, and that each person harbors their own unique microbial population. Human microbiome studies gesture toward the post-racial aspirations of personalized medicine—characterizing states of human health and illness microbially. By viewing humans as “supraorganisms” made up of millions of microbial partners, some microbiome science seems to disrupt binding historical categories often grounded in racist biology, allowing interspeciality to supersede race. But inevitably, unexamined (...) categories of race and ethnicity surface in a myriad of studies on microbiota. This paper approaches race as a ghost variable across microbiome research and asks, what is race doing in studies of the microbiome? Why is it there, and how is it functioning? I examine this research to argue that social scientists must work with biological scientists to help put microbial differences into perspective—to investigate how microbiomes and race are entangled embodiments of the social, environmental, and biological. Ultimately, transdisciplinary collaboration is required to address racial health disparities in microbiome research without reifying race as a straightforward biological or social designation. (shrink)

Human microbiome research has revealed that legions of bacteria, viruses, and fungi live on our skin and within the cavities of our bodies. New knowledge from these recent studies shows that humans are superorganisms and that the microbiome is indispensible to our lives and our health. This volume explores some of the science on the human microbiome and considers the ethical, legal, and social concerns that are raised by this research.

I propose a T‐cell receptor (TcR)‐based mechanism by which immunity mediates both “genetic self” and “microbial self” thereby, connecting microbiome disease with autoimmunity. The hypothesis is based on simple principles. First, TcR are selected to avoid strong cross‐reactivity with “self,” resulting in selection for a TcR repertoire mimicking “genetic self.” Second, evolution has selected for a “microbial self” that mimics “genetic self” so as to share tolerance. In consequence, our TcR repertoire also mimics microbiome antigenicity, providing a novel (...) mechanism for modulating tolerance to it. Also, the microbiome mimics the TcR repertoire, acting as a secondary immune system. I call this TcR‐microbiome mimicry “holoimmunity” to denote immune tolerance to the “holobiont self.” Logically, microbiome‐host mimicry means that autoimmunity directed at host antigens will also attack components of the microbiome, and conversely, an immunological attack on the microbiome may cross‐react with host antigens producing “holoautoimmunity.”. (shrink)

Animals and plants are metaorganisms and associate with microbes that affect their physiology, stress tolerance, and fitness. Here the hypothesis that alteration of the microbiome may constitute a fast‐response mechanism to environmental change is examined. This is supported by recent reciprocal transplant experiments with reef corals, which have shown that their microbiome adapts to thermally variable habitats and changes over time when transplanted into different environments. Further, inoculation of corals with beneficial bacteria increases their stress tolerance. But corals (...) differ in their ability to flexibly associate with different bacteria. How scales of microbiome flexibility may reflect different metaorganism adaptation mechanisms is discussed and future directions for research are pinpointed. It is posited that microbiome flexibility is a broad phenomenon that contributes to the ability of organisms to respond to environmental change. Importantly, adapting with microbial help may provide an alternate route to organismal adaptation that facilitates rapid responses. (shrink)

With the advancement of human microbiome research, it is inevitable that a growing number of biobanks will include a collection of microbiota specimens to characterize the microbial communities that inhabit the human body and explore the relationships between the microbiota and their human hosts. Biobanks of human microbiota and their associated genetic information may become a valuable health resource. But, this area of research also presents ethical and social problems, some of which are distinct from those faced by biobanks (...) that store human tissue samples. This paper examines four core issues which are considered highly relevant to microbiome biobanking: the nature of human microbiome samples and how different understandings have an impact on benefit/risk evaluation, privacy, informed consent, and returning the result to participants. We argue that these issues should be addressed early on in microbiome research projects and also call for adjusting or developing new governance mechanism to better accommodate these changes. (shrink)

Microbiome research shows that human health is foundationally intertwined with the ecology of microbial communities living on and in our bodies. This challenges the categorical separation of organisms from environments that has been central to biomedicine, and questions the boundaries between them. Biomedicine is left with an empirical problem: how to understand causal pathways between host health, microbiota and environment? We propose a conceptual tool – environmentality – to think through this problem. Environmentality is the state or quality of (...) being an environment for something else in a particular context: a fully perspectival proposition. Its power lies partly in what Isabelle Stengers has called the efficacy of the word itself, contrasting the dominant sense of the word environment as something both external and fixed. Through three case studies, we argue that environmentality can help think about the causality of microbiota vis-a-vis host health in a processual, relational and situated manner, across scales and temporalities. We situate this intervention within historical trajectories of thought in biomedicine, focusing on the challenge microbiome research poses to an aperspectival body. We argue that addressing entanglements between microbial and human lives requires that the environment is brought into the clinic, thus shortening the conceptual gap between medicine and public health. (shrink)

Therapeutic translations of the microbiome-gut-brain (MGB) axis are reconstructing the educational subject in a manner amenable to Foucauldian analysis. Yet, at the same time, under the sway of MGB research social scientists are taking a biosocial turn that threatens the integrity of Foucault’s historicizing philosophical project. Meeting that challenge head-on, this article argues that the MGB axis augments the neurobiological constitution of the educational subject by means of a dietetic mode of subjectivation. Absent a pedagogical element, there is a (...) hollowness to critical academics’ claims that holobiontic self-conceptions springing from the axis can elicit a resistant subjectivity. Though wild pedagogies might inform a resistant tactics of the self, contemporary self-technologies are – as Foucault has taught us – a pale shadow of the ancient Greek conception of dietetics as an holistic, embodied and ensouled practice. At the intersection between the disciplinary apparatuses of criminology and education, therefore, the MGB-driven biosocial turn unambiguously reinforces the social control function of schooling. (shrink)

The human microbiome is the bacteria, viruses, and fungi that cover our skin, line our intestines, and flourish in our body cavities. Work on the human microbiome is new, but it is quickly becoming a leading area of biomedical research. What scientists are learning about humans and our microbiomes could change medical practice by introducing new treatment modalities. This new knowledge redefines us as superorganisms comprised of the human body and the collection of microbes that inhabit it and (...) reveals how much we are a part of our environment. The understanding that microbes are not only beneficial but sometimes necessary for survival recasts our interaction with microbes from adversarial to neighborly. This volume explores some of the science that makes human microbiome research possible. It then considers ethical, legal, and social concerns raised by microbiome research. Chapters explore issues related to personal identity, property rights, and privacy. The authors reflect on how human microbiome research challenges reigning views on public health and research ethics. They also address the need for thoughtful policies and procedures to guide the use of the biobanked human samples required for advancing this new domain of research. In the course of these explorations, they introduce examples from the history of biomedical science and recent legal cases that shed light on the issues and inform the policy recommendations they offer at the end of each topic's discussion.This volume is the product of an NIH Human Microbiome Project grant. It represents three years of conversations focused on consensus formation by the twenty-seven members of the interdisciplinary Microbiome Working Group. (shrink)

This paper brings feminist public health ethics and feminist analytic tools to bear on mainstream medical research. Specifically, it uses these approaches to call attention to several problems associated with “The Placenta Harbors a Unique Microbiome,” a recent study published in Science Translational Medicine. We point out the potential negative consequences these problems have for both women’s health and their autonomy.Our paper has two parts. We begin by discussing the study, which examines the composition of the placental microbiome, (...) that is to say, the communities of microorganisms that live in the placenta. Among other things, this study considers two different relations: a correlation.. (shrink)

In their paper “How Causal are Microbiomes? A Comparison with the Helicobacter pylori Explanation of Ulcers,” Lynch, Parke, and O’Malley successfully argue that certain causal attributions made to the microbiome have not satisfied Koch’s postulates nor the interventionist framework. However, their argument involves an implicit assumption that cases such as H. pylori are sufficiently similar to cases involving the microbiome, such that causal attributions to both should be evaluated according to the same causal framework. Our commentary targets this (...) assumption. First, we introduce the historical circumstances that led to the formulation of Koch’s postulates in order to differentiate the case of the microbiome from that of infectious bacteria. Then, we introduce the concept of the holobiont, the idea that hosts and their symbionts should be conceptualized as a metaphysical and biological unit. Finally, using the holobiont concept, we argue that Koch’s postulates and the interventionist framework are ill-equipped to handle the microbiome. We conclude by suggesting that a revision of what counts as microbiological causality within the holobiont is justified. (shrink)

We identify the significance and typical requirements of developmental analyses of the microbiome-gut-brain in parents, offspring, and parent-offspring relations, which have particular importance for neurobehavioral outcomes in mammalian species, including humans. We call for a focus on behavioral measures of social-emotional function. Methodological approaches to interpreting relations between the microbiota and behavior are discussed.

The microbiota-gut-brain axis field is at an exciting stage, but the most recent developments in microbiota research still have to find their way into MGB studies. Here we outline the standards for microbiome data generation, the appropriate statistical techniques, and the covariates that should be included in MGB studies to optimize discovery and translation to clinical applications.

This article reformulates Stephan Helmreich´s the ¨microbiomisation of race¨ as the historiality of otherness in the foundations of human microbiome science. Through the lens of my ethnographic fieldwork of a transnational community of microbiome scientists that conducted a landmark human microbiome research on indigenous microbes and its affiliated and first personalised microbiome initiative, the American Gut Project, I follow and trace the key actors, experimental systems and onto-epistemic claims in the emergence of human microbiome science (...) a decade ago. In doing so, I show the links between the reinscription of race, comparative research on the microbial genetic variation of human populations and the remining of bioprospected data for personalised medicine. In these unpredictable research movements, the microbiome of non-Western peoples and territories is much more than a side project or a specific approach within the field: it constitutes the nucleus of its experimental system, opening towards subsequent and cumulative research processes and knowledge production in human microbiome science. The article demonstrates that while human microbiome science is articulated upon the microbial ‘makeup’ of non-wester(nised) communities, societies, and locales, its results and therapeutics are only applicable to medical conditions affecting rich nations (i.e., inflammatory, autoimmune, and metabolic diseases). My reformulation of ¨microbiomisation of race¨ as the condition of possibility of human microbiome science reveals that its individual dimension is sustained by microbial DNA data from human populations through bioprospecting practices and gains meaning through personalised medicine initiatives, informal online networks of pseudoscientific and commodified microbial-related evidence. (shrink)

Much microbiota-gut-brain research focuses on the causal role of microbiomes as a whole, rather than their component parts: microbes. Hooks et al. find these whole-community explanations inadequate; however, they do not provide suggestions for better explanations. By appealing to proportionality – a criterion that can be used to develop more appropriate causal explanations – more accurate causal claims can be made.

It has become increasingly clear that there is a vast array of microorganisms on and in the human body, known collectively as the human microbiome. Our microbiomes are extraordinarily complex, and this complexity has been linked to human health and well-being. Given the complexity and importance of our microbiomes, we struggle with how to think about them. There is a long list of competing metaphors that we use to refer to our microbiomes, including as an “organ” containing our “second (...) genome,” as a “symbiont” in the human “holobiont,” and as an ecological “community” in the human “ecosystem,” among others. Each of these makes different assumptions about the fundamental biology of the human-microbe system, with important implications for how we choose to study microbiomes, and the therapies we envision for correcting microbiome-linked disorders. We believe that it is time to move beyond metaphors, and we propose a scientifically pluralist approach that focuses on characterizing fundamental biological properties of microbiomes such as heritability, transmission mode, rates of dispersal rates, and strength of local selection. Such an approach will allow us to break out of the confines of narrow conceptual frameworks, and to guide the exploration of our complexity as chimeric beings. (shrink)

Graphical AbstractMicrobiome research attributes to whole microbiomes a causal role in the occurrence of different health outcomes. I argue, following some distinctions about causal relationships and explanations made within a philosophical account of causation, the “interventionist account,” that such claims need more scrutiny.

Host-microbiome interactions (HMIs) are critical for the modulation of biological processes and are associated with several diseases, and extensive HMI studies have generated large amounts of data. We propose that the logical representation of the knowledge derived from these data and the standardized representation of experimental variables and processes can foster integration of data and reproducibility of experiments and thereby further HMI knowledge discovery. A community-based Ontology of Host-Microbiome Interactions (OHMI) was developed following the OBO Foundry principles. OHMI (...) leverages established ontologies to create logically structured representations of microbiomes, microbial taxonomy, host species, host anatomical entities, and HMIs under different conditions and associated study protocols and types of data analysis and experimental results. (shrink)

Human evolution has been punctuated by climate anomalies, structuring environments, deadly infections, and altering landscapes. How well humans adapted to these new circumstances had direct effects on fitness and survival. Here, how the gut microbiome could have contributed to human evolutionary success through contributions to host nutritional buffering and infectious disease resistance is reviewed. How changes in human genetics, diet, disease exposure, and social environments almost certainly altered microbial community composition is also explored. Emerging research points to the (...) class='Hi'>microbiome as a key player in host responses to environmental change. Therefore, the reciprocal interactions between humans and their microbes are likely to have shaped human patterns of local adaptation throughout our shared evolutionary history. Recent alterations in human lifestyle, however, are altering human microbiomes in unprecedented ways. The consequences of interrupted host–microbe relationships for human adaptive potential in the future are unknown. (shrink)

A holobiont is a composite organism consisting of a host together with its microbiome, such as a coral with its zooxanthellae. To explain the often intimate integration between hosts and their microbiomes, some investigators contend that selection operates on holobionts as a unit and view the microbiome’s genes as extending the host’s nuclear genome to jointly comprise a hologenome. Because vertical transmission of microbiomes is uncommon, other investigators contend that holobiont selection cannot be effective because a holobiont’s (...) class='Hi'>microbiome is an acquired condition rather than an inherited trait. This disagreement invites a simple mathematical model to see how holobiont selection might operate and to assess its plausibility as an evolutionary force. This paper presents two variants of such a model. In one variant, juvenile hosts obtain microbiomes from their parents (vertical transmission). In the other variant, microbiomes of juvenile hosts are assembled from source pools containing the combined microbiomes of all parents (horizontal transmission). According to both variants, holobiont selection indeed causes evolutionary change in holobiont traits. Therefore, holobiont selection is plausibly an effective evolutionary force with either mode of microbiome transmission. The modeling employs two distinct concepts of inheritance, depending on the mode of microbiome transmission: collective inheritance whereby juveniles inherit a sample of the collected genomes from all parents, as contrasted with lineal inheritance whereby juveniles inherit the genomes from only their own parents. A distinction between collective and lineal inheritance also features in theories of multilevel selection. (shrink)

Explaining the behaviour of ecosystems is one of the key challenges for the biological sciences. Since 2000, new-mechanicism has been the main model to account for the nature of scientific explanation in biology. The universality of the new-mechanist view in biology has been however put into question due to the existence of explanations that account for some biological phenomena in terms of their mathematical properties (mathematical explanations). Supporters of mathematical explanation have argued that the explanation of the behaviour of ecosystems (...) is usually provided in terms of their mathematical properties, and not in mechanistic terms. They have intensively studied the explanation of the properties of ecosystems that behave following the rules of a non-random network. However, no attention has been devoted to the study of the nature of the explanation in those that form a random network. In this paper, we cover that gap by analysing the explanation of the stability behaviour of the microbiome recently elaborated by Coyte and colleagues, to determine whether it fits with the model of explanation suggested by the new-mechanist or by the defenders of mathematical explanation. Our analysis of this case study supports three theses: (1) that the explanation is not given solely in terms of mechanisms, as the new-mechanists understand the concept; (2) that the mathematical properties that describe the system play an essential explanatory role, but they do not exhaust the explanation; (3) that a non-previously identified appeal to the type of interactions that the entities in the network can exhibit, as well as their abundance, is also necessary for Coyte and colleagues’ account to be fully explanatory. From the combination of these three theses we argue for the necessity of an integrative pluralist view of the nature of behaviour explanation when this is given by appealing to the existence of a random network. (shrink)

The complexity of the human mind and its interaction with the environment is one of the main epistemological debates throughout history. Recent ideas, framed as the 4E perspective to cognition, highlight that human experience depends causally on both cerebral and extracranial processes, but also is embedded in a particular sociomaterial context and is a product of historical accumulation of trajectory changes throughout life. Accordingly, the human microbiome is one of the most intriguing actors modulating brain function and physiology. Here, (...) we present the 4E approach to the Human Microbiome for understanding mental processes from a broader perspective, encompassing one's body physiology and environment throughout their lifespan, interconnected by microbiome community structure and dynamics. We review evidence supporting the approach theoretically and motivates the study of the global set of microbial ecosystem networks encountered by a person across their lifetime (from skin to gut to natural and built environments). We furthermore trace future empirical implementation of the approach. We finally discuss novel research opportunities and clinical interventions aimed toward developing low‐cost/high‐benefit integrative and personalized bio‐psycho‐socio‐environmental treatments for mental health and including the brain‐gut‐microbiome axis. (shrink)

Recent research about the microbiome points to a picture in which we, humans, are ‘living through’ nature, and nature itself is living in us. Our bodies are hosting—and depend on—the multiple species that constitute human microbiota. This article will discuss current research on the microbiome through the ideas of Japanese ecologist Imanishi Kinji (1902–1992). First, some of Imanishi’s key ideas regarding the world of living beings and multispecies societies are presented. Second, seven types of relationships concerning the human (...) microbiome, human beings, and the environment are explored. Third, inspired by Imanishi’s work, this paper develops the idea of dynamic, porous, and complex multispecies societies in which different living beings or species are codependent on others, including microbiota and human beings. (shrink)

Lynch et al., in an article in this issue, argue that an entire microbiome is rarely, if ever, the right target of analysis for causal explanations in microbiome research. They argue, using interventionist criteria of proportionality, specificity and stability, for restricting causal claims to the smallest subset of microbes—a causal core—that generate the effect of interest. A further question remains: what kind of interactions generate a consortium of microbes that can operate as causal agents in this manner? Here (...) I introduce two possible kinds of such consortia: ‘trojan horses’ and ‘syntrophic’ individuals. (shrink)

Lynch et al., in an article in this issue, argue that an entire microbiome is rarely, if ever, the right target of analysis for causal explanations in microbiome research. They argue, using interventionist criteria of proportionality, specificity and stability, for restricting causal claims to the smallest subset of microbes—a causal core—that generate the effect of interest. A further question remains: what kind of interactions generate a consortium of microbes that can operate as causal agents in this manner? Here (...) I introduce two possible kinds of such consortia: ‘trojan horses’ and ‘syntrophic’ individuals. (shrink)

The human microbiome has become one of the dominant biomedical frameworks of the contemporary moment that may be understood to be post-Pasteurian. The recognitions the human microbiome opens up for thinking about the biological self and the individual have ontological and epistemological ramifications for considering what and who the human being is. As this article illustrates, the microbiopolitics of the human microbiome challenges the immunitarian Pasteurian model in which the organismic self shores itself up and defends itself (...) against a microbial non-self or other. Instead, this theory presents the human organism as comprised of multiple ecosystems and as a multitude, suggesting that the thanatopolitical attempts to wipe out microbial others (evident in the overuse and misuse of antibiotics, for example) are giving way to an affirmative microbiopolitics grounded in generative multispecies relationality. This article sets out to make the case for this affirmative microbiopolitics. (shrink)

The human intestines are constantly under the influence of numerous pathological factors: enteropathogenic microorganisms, food antigens, physico‐chemical stress associated with digestion and bacterial metabolism, therefore it must be provided with a system of protection against adverse impact. Recent studies have shown that Paneth cells play a crucial role in maintaining homeostasis of the small intestines. Paneth cells perform many vital functions aimed at maintaining a homeostatic balance between normal microbiota, infectious pathogens and the human body, regulate the qualitative composition and (...) number of intestinal microorganisms, prevent the introduction of potentially pathogenic species, and protect stem cells from damage. Paneth cells take part in adaptive and protective‐inflammatory reactions. Paneth cells maintain dynamic balance between microbial populations, and the macroorganism, preventing the development of intestinal infections and cancer. They play a crucial role in gastrointestinal homeostasis and may be key factors in the etiopathological progression of intestinal diseases. (shrink)