In this paper we take the making of the field of "developmental origins of health and disease" (DOHaD) around 1990 as a unique opportunity to understand scientists' constructions of the fetal environment through the second half of the twentieth century. DOHaD, previously known as "fetal origins of adult disease" and "fetal programming", is an interdisciplinary field that has been hailed widely for highlighting the importance of the early developmental environment – from periconception to weaning – for health in later life and risk of predilection to disease. Through bringing together molecular, experimental animal, theoretical evolutionary, clinical and epidemiological research, it has produced knowledge that has decisively influenced clinical practice as well as public health interventions. Yet at the same time this breadth has created a tension. Reductionist models of early developmental environment used in experimental fields clashed with the broader perspectives inherent in clinical medicine and epidemiology. Efforts to translate DOHaD knowledge into global health interventions – using the catchy rubric of "the first 1000 days" – came with specific ideas about parenting and motherhood, which paid little attention to historical and cultural dimensions of a given context. 

We will show that this tension did not simply appear later in the course of the recent expansion of DOHaD, and in relation to criticisms of social scientists, or difficulties related to creating and implementing globally applicable policies. Rather, it has been inherent from the outset, as DOHaD combined two traditions of fetal research. One relates to fetal physiology that for several decades studied the fetus in the laboratory conditions. In the research programme that centred on the notion of an "autonomous fetus", the environment was of secondary importance. By contrast, the other tradition was forged within social medicine (via environmental epidemiology) and linked common congenital malformations with environmental conditions during development. Starting in 1989, we go back several decades to understand the trajectories of these traditions in the socio-political environment of the UK since World War Two.

Addressing the so-called 'obesity epidemic' has been a subject of intense interest in the public health and biomedical literature for several decades. It is therefore no surprise that obesity has emerged as a key target for postgenomic research, with various fields, including epigenetics, microbiome research, and metabolomics, carrying out studies into its causes and consequences.

We have seen a shift in thinking about metabolism (Landecker 2011): instead of conceiving of the body simply as a machine that processes inputs and outputs, metabolism has become conceptualised as an interface, regulator, or mediator. Correspondingly, food becomes understood as environment. I argue we see the 'molecularisation of the environment' (Landecker 2010) and 'molecularisation of biography and milieu' (Niewohner 2011) recurring and deepening within postgenomic understandings of obesity, including in the emerging field of metabolomics. Metabolomics aims to characterise the dynamic human metabolome by using a variety of methods to measure the small molecules within the body, circulating as a result of both gene expression, as well as microbiota activity, and a range of environmental factors. Researchers in this field have aimed to stratify environments into 'exposotypes', tried to identify a 'metabolic signature' of obesity, and promised revolutionary steps towards precision or personalised medicine. 

I explore the deterministic narratives that arise within metabolomics research on obesity, and closely related fields. This is clearly evident in research surrounding the effect of the maternal metabolism on the developing foetus, part of a paradigm which emphasises the importance of the in utero environment for health outcomes across the life course. However, it also emerges in less remarked-upon ways: in the construction of the 'obesogenic' microbiome and its metabolic effects, in the kinds of environmental interventions that these studies rely on, and in the deterministic connection between fat bodies and disease. 

I then argue that this apparent environmental determinism has ambivalent normative implications. On the one hand, appreciation of the complex and influential role of the environment, broadly conceived, and blurred boundaries between the human body and our socio-material environment, could be seen as a necessary corrective to perspectives that place responsibility (and often, shame and guilt) solely at the feet of fat individuals. On the other hand, in actual scientific practice, these deterministic tendencies seem to risk reinforcing fatphobia and a distorted understanding of fatness, particularly when the environment is construed narrowly as food intake, or as the maternal environment. I suggest that the centrality of value-laden notions of biological normality lead to these distorting effects, drawing on the example of the creation of 'normal weight obesity' as an explanatory category. The existence of body diversity, combined with a sense of what is 'biologically normal' and deterministic hypotheses about the environment, can lead to a search for environmental interventions to restore 'normality', even in the face of conflicting evidence about their usefulness or what constitutes 'normal'.

The word "race" shows up frequently in daily interactions and on websites. It appears in legal documents and medical texts. In the United States President Obama wanted a national conversation that aimed to transform the understanding of race from charged to smarter and deeper. Donald Trump, on the other hand, spews racist language and comfortably receives the council of white supremacists. Race is undeniable important. But what, exactly, is race?

The USA had a national conversation about race, indeed it seems to always be having conversations about race, but we never did get to Obama's desired smarter and deeper understanding. As individuals and as a society it seems dazed and confused when it comes to race. It continues to experience a superficial racial conversation gridlock.  This situation is repeated across the globe. Some individuals fight against racism and others embrace racism as natural. Yet, few are focusing on the underlying question of what race is and its connections to racism. The confusion is deep but also something we can solve. If we ask and answer the right questions.  

Here I argue that those fighting again racism are fighting with their hands tied behind their back because most do not know the history of the idea of race and they especially do not know and understand the contemporary science of human variation. Not knowing history and science makes them incapable of answering many racist challenges and even confronting their own racial assumptions. Knowing the history and the science provides us the needed tools to fight racism. In this talk I provide an outline to better understand what race is and is not. I will address the shift in the biologic approach towards human difference resulting from advances in next generation sequencing technology. Finally, I will discuss how reconciling our understanding of the biological and socially defined race concepts is crucial for those committed to achieving social justice.

In seeking to understand the boundaries between the normal and the pathological, health and illness, French vitalist philosopher George Canguilhem (1991) argued we need to pay attention to the role of terrains, a term he uses to define an organism's resistance to pathogenic agents and predisposition to particular diseases. Recent research on the human microbiome suggests it may play a key role in shaping bodily terrains, but at the same time also begins to define the limits of these terrains by mapping out the spaces and sites deemed of greatest research interest. In this paper I want to propose three different ways in which the human microbiome (and its influence on bodily terrains) is mapped through an attention to (i) sites of microbial density and diversity within the human body; (ii) a focus on the domestic – and in particular the home and practices of child-rearing; and (iii) a focus on diet, especially where diet is seen as being shaped by distinctive regional (and often racialized) cultures of consumption. In conclusion, I offer some reflections on what might be at stake in these geographical imaginations and question how we might map human microbial terrains otherwise.

Our understanding of body–world relations is caught in a curious contradiction. On one side, it is well established that many concepts that describe influences of or interaction with the outer world – plasticity, metabolism, the same terms environment or milieu – appeared with rise of modern science. On the other side, although they lacked a unifying term for it, an anxious attentiveness to the power of environmental factors in shaping physical and moral traits held sway in nearly all medical systems before and alongside modern Europe.  In the light of this longer history, I build on a new historiography on the policing of bodies and environments in medieval times  (Rawcliffe, 2013; Geltner, 2019) to problematize Foucault's claim about the birth of biopolitics in the European eighteenth-century. I look in particular at tropes of environmental determinism (including proto-racialism) and manipulation of the milieu based on humoralist notions of corporeal permeability (Hippocrates, Galen, Ibn Sina) in the Islamicate and Latin Christendom between the 11th and the 15th century.  This has implications also for a richer genealogy of contemporary tropes of plasticity, permeability and environmental determinism that are discussed in contemporary postgenomics beyond usual genealogies that take as a starting point the making of the modern body and EuroAmerican biomedicine.

In the last decade several research consortia devoted to the study environmentally induced pathologies have been created and funded (e.g., in Europe, LIFEPATH, EXPOsOMICS, DynaHEALTH, HELIX, etc.). All these projects use large cohorts to study the life-course risk of disease due to environmental exposure, and to identify the molecular changes mediating the effects of exposure on disease risk. Most of them are coordinated by researchers in epidemiology but also involve other disciplines (in particular, molecular epigenetics, in order to investigate the molecular, internal impact of environment; social sciences, to deal with health inequalities due to socioeconomic disadvantage). These research projects adopt an integrative approach. Still, integration is far from being accomplished because of the hegemony of biomedical on social sciences. Actually, researchers rely on the concept of "biological embodiment" (Krieger 2005) or of "biological embedding" (Hertzman 2012) to express the idea that social exposures "get under the skin". However, personal experiences and socio-economic and cultural environments are not studied on their own; rather, biography and milieu are

"miniaturized" (Niewöhner 2011) as they are reduced to the molecular changes they are correlated with (cf. also Landaecker & Panofsky 2013, Lock 2015, Meloni 2019). Thus, while these research projects can be seen as a first step towards an integrative study of environmentally induced pathologies, they are still far from the target.

That being said, I will focus on some other research projects with greater integrative and interdisciplinary scope that have been recently theorized and implemented in order to study environmentally induced diseases, in particular the relationship between environmental exposures and health disparities (e.g., Juarez et al 2014, Senier et al 2016). I will try to determine whether or not these projects represent a step further towards an effective interdisciplinary integration of biomedical and social sciences compared to the projects presented above. Actually, they are presented, on theory, as highly holistic projects aiming at integrating multi-level, multi-dimensional, and multi-modal analyses in one and the same study. I will thus focus on the question of whether they actually manage to be integrative in practice too, or they rather are explanatory ambitious projects from a theoretical point of view but empirically intractable, and so explanatory useless (cf. Longino 2013). As to integration, I will rely on the way it has been recently discussed in philosophy of biology in the context of the scientific pluralism debate (see Brigandt (eds.) 2013).

Environmental epigenetics explores how material exposures and social experiences affect gene expression. A key tenet of the field is that exposures that happen early in life can have health effects across the life course. Numerous labs today study the epigenetic effects of "early life adversity," prominently featuring research on the role of trauma and stress for long-term physical and mental health. In our previous work we argued that this research tends to focus on harm and lasting damage with little discussion of resilience and recovery. Consequently, while researchers often emphasize prevention, they offer few suggestions for how communities and individuals can find ways to live well with trauma and its effects on health and development. Seeking out alternative visions, we have been investigating initiatives in the fields of trauma-informed care and restorative justice that draw on insights from the epigenetics of early life adversity, but apply a framework that emphasizes the biosocial capacity for resilience – not as a way of erasing the experience of adversity, but to allow for learning, growth and well-being despite and with adversity. Drawing on our ongoing fieldwork in the Western U.S., we highlight novel practices designed to build "community resilience" in schools, juvenile corrections facilities, and beyond. We propose that these practices are not only important for responding well to trauma and early life adversity in social institutions and communities, but that they also offer a non-deterministic approach for applying postgenomic knowledge claims to advocate for biosocial change. 

This paper critically discusses the increasing trend in human microbiome research to draw on environmentalist narratives about race. This refers to the attempt to investigate the microbial profile of certain social and ethnic groups as environmentally induced and embodied racial traits. Here, race is treated as a necessary category that helps in identifying and solving health challenges, like obesity and type-2 diabetes, in 'western' or indigenous populations with particular microbial characteristics. We are skeptical of this emerging racialized view of human bodies due to two reasons: (i) These race studies repeat outdated historical narratives, which link especially nutrition and race in ways that are prone to stir deterministic, stereotypical and exclusionary views about indigenous groups. (ii) The concept of biological race used here is taxonomically problematic and conceptually inconsistent. It leads to a view in which human races are constituted by other non-human species. In addition, this approach cannot group biological individuals into human races and decouples races from ancestry. To support this critique, we draw on case studies of microbiome research on indigenous groups in Latin America.   

Contemporary research has suggested that the microbiome has substantial effects on the animal phenotype, affecting the expression of fundamental traits. Because of this, it has been argued that the microbiome and its host (i.e. holobiont) must have evolved as a single unit. A challenge for this hypothesis, however, is that the microbiome is not heritable. My aim in this talk will be to compare some recent research on how the microbiome affects the phenotype of animals and plants, with some research that studies microbiome heritability. I will show that these two types of research apply different research methods, and as a result look at different properties, which are hard to integrate with each other. Grounded on this difference, I will argue that while contemporary research on some causal effects of the microbiome on the host phenotype are empirically grounded, the type of research that extends this evidence to draw to deterministic hypothesis about host evolution is not. By deterministic hypotheses, I mean the belief that microbes shape host development and host phenotypic properties in a way that is disconnected from the environmental influences shaping its development and phenotype. In other words, that host development and phenotype is a consequence of the history of host-microbe evolutionary history, instead of a result of the environmental pressures that the host-microbe consortium experiences during its ontogeny.  I will argue that these deterministic hypotheses would need a different type of empirical evidence to be valid, and that the part of microbiome research dealing with heritable variation needs redirecting its focus. As far as our current evidence is available, the microbiome remains a problematic source of heritable variation. 

The genetic determinism of the second half of the 20th century is no longer taken as an epistemic cannon to create a deterministic framework to provide explanations directly based on genetic explanations (Baedke, 2018). Although initially seen as an escape route from epigenetics through the research programme of inherited non-genetic variation in the relatively mainstream biology perhaps most prominently by Jablonka and Lamb (2005), determinism based on the environmentally shapable inherited characteristics has became a concern within determinism debate (Waggoner and Uller, 2015).
I believe that most of the work so far resemble a nature-nurture looking dichotomy. The central characteristic of this dichotomy I claim, is the standardized model-based frameworks in which the individual organism is only seen as a token of a biological type. Against this strict explanatory model dichotomy, I believe that it is possible to construct an agent based non-deterministic approach to individual biology, based on individualized and localized approaches of explanation based on Cartwright’s ( 1999) understanding of how laws in science work in localized level and Barad’s (2007) agential realism when it comes to explain how the knowing subject creates the epistemic field under which she is explained in.
I believe that when the concerns of agential realism are considered, the epistemic status of the agent to be explained is changed from an object to a subject, in which the agent can have more autonomy to determine what can be known of her.

Research on soil microbiome had been very influential in the development of microbial ecology as a field and metagenomics as an approach. The role that biotic and abiotic environmental factors plays on microbial communities is emphasized by researchers and serves as a solution to the phenomenon known as the ‘great plate anomaly’. However, the environmental narratives found in soil microbiome research is mostly based on metagenomics approaches since late 1980s with the development of the first 16S rRNA sequencing technique. Consequently, the claimed access to microbial life in its natural habitat is granted from a genome-centered perspective. Therefore, the predictions about functions of naturally-occuring microbial communities, the ecological roles of certain microorganisms as well as the hypotheses regarding their physiology and cellular anatomy are mostly sequence-based as the factors such as dormancy, symbiotic interdependency, low abundance make it very difficult to cultivate microorganisms in laboratory conditions. In this poster, I aim to demonstrate how the efforts of emphasizing the role of environment on soil microbiome research became more genome-centered since the start of sequencing of environmental samples and accelerated with the next-generation platforms. Furthermore, explore the ways in which the indices for soil health are also dependent on these data. 

The transition from oviparity to viviparity ―which has occurred over 150 times in different vertebrate lineages (Blackburn, 2015)― is a particularly puzzling evolutionary innovation, which raises the question of whether the various independent origins (i.e. homoplasy) of viviparity respond to internal demands of the autonomous organism or they are rather conditioned by environmental factors. Here two arguments in favor of the former are reviewed. According to the first argument, the novelties involved in this transition encompass processes of internalization and separation from environmental influences, which would reflect a broader tendency in evolution towards an increase in autonomy understood as a “shift in the system-environment relationship such that the influences of the environment on the individual system are gradually reduced” (Rosslenbroich, 2014, p. 39). The second argument introduces a novel evolutionary model (SIEI, Stress-Induced Evolutionary Innovation model) of mammal viviparity, according to which this transition involves that a previous environmentally induced stress response occurring in the mother is internalized, giving rise to a physiologically regulated process that permits the implantation of the embryo (Wagner et al., 2019). Evolutionary developmental biology ought not to neglect the agency of the individual autonomous organism. Otherwise, the organism will “blend” into its environment (Baedke, 2019).

Research regarding menstruation and its evolutionary meaning reached its peak in the 90’s with contributions by Profet, Strassmann and Finn. The odd phenomenon of cyclical bleeding, present only in three species aside from human beings, prompted the question on whether menstruation had been rewarded by natural selection thanks to an essential beneficial adaptive effect or if, in contrast, it was just a side-effect of the evolution of other traits. Profet endorsed an inherently adaptive definition of menstruation, describing its function as a defence mechanism against pathogens in sperm (Profet, 1993). This theory was challenged by accounts addressing menstruation as a side-effect of either energy-saving endometrial shutdown (Strassmann, 1996) or spontaneous decidualization (Finn, 1998) rather than a phenomenon on its own. The debate on whether menstruation is a subsidiary of reproductive evolution and, therefore, dispensable, determines how women embody and experience their menstruation. In this poster, these questions are considered in relation to recent medical trends promoting the suppression of the female menstrual cycle through birth control. I will challenge the idea that menstruation can be - and even whether it should be - safely suppressed. I will also underline how women’s menstrual narratives have been shaped by their socio-material environment, turning bodily phenomena into a process to be corrected with the support of questionable scientific arguments, and stigmatising the understanding women have of their own bodies. While highlighting the risks of menstrual suppression, I will point out its link to the recent rise of pathologies like CHD and osteoporosis among younger women as well as to the higher incidence of the diagnosis of hypothalamic amenorrhea in teenagers and young women.

Epigenetics and Ayurveda at first seem unlikely counterparts. The former is a budding field of science which explores how environmental influences create changes in gene expression. The latter is an ancient Indian science and traditional medical system with associations to the Hindu religion. However, when it comes to their social and behavioural implications, the two areas are finding common ground particularly around notions and practices of regulation of the maternal body. Although there have been recent attempts to bring together history of science and postcolonialism there is a gap in the literature, particularly in historical epistemology. The ways in which biomedicine and health knowledges of the Global South interact plays an important role in assessing colonial legacies and postcolonial modernity. The many facets of modern Ayurveda allow for the examination of both local Indian and global relationships between biomedicine and Global South health knowledge and practices in the postgenomic era. By focusing on preconception this project aims to discover how the scientific knowledge of epigenetics is being acted on and challenging discourse in the reproductive arena.

In the wake of recent discoveries in emerging disciplines such as epigenetics or eco-devo, the genocentric concept of inheritance proper to the Modern Synthesis has been subjected to intense analysis and revision. The poster has two central objectives. First, to outline the basic features and shortcomings of the genocentric view of inheritance. Second, to highlight the idea that inheritance, and adaptive evolution itself, does not rely on a particular channel of inheritance –genetic transmission–, but on all those mechanisms that contribute to the construction and stability of intergenerational similarity of lineages. Based on recent discoveries in epigenetics, I will show that, in order to constitute an evolutionarily relevant channel of inheritance, hereditary phenomena need not be gametic or stable at the transgenerational level. I will also outline the important role played by the environment (biotic and abiotic) in the construction and stabilization of the phenotypes of organisms. I will show how the environment can cause targeted epigenetic changes that can have a profound impact on the fitness of organisms –by mediating disease-associated phenotypes, for example– and on evolutionary dynamics itself. This last fact calls into question the causal sufficiency of genes and opens up the problem of determining the degree of causal influence of the environment. I will conclude by affirming that it is a conceptual error to take genetic transmission as the minimum causal model, sensu Weisberg, and that only by adopting an inclusive and pluralistic model of inheritance is it possible to overcome the organism-environment dichotomy imposed by the genocentric concept, being able to integrate the results obtained by disciplines such as eco-devo or niche construction.