Abstract
Bourdieu suggested that the habitus contains the ‘genetic information’ which both allows and disposes successive generations to reproduce the world they inherit from their parents’ generation. While his writings on habitus are concerned with embodied dispositions, biological processes are not a feature of the practical reason of habitus. Recent critiques of the separate worlds of biology and culture, and the rise in epigenetics, provide new opportunities for expanding theoretical concepts like habitus. Using obesity science as a case study we attempt to conceptualise the enfolding of biological and social processes (via a Deleuzian metaphor) to develop a concept of biohabitus – reconfiguring how social and biological environments interact across the life course, and may be transmitted and transformed intergenerationally. In conclusion we suggest that the enfolding and reproduction of social life that Bourdieu articulated as habitus is a useful theoretical frame that can be enhanced to critically develop epigenetic understandings of obesity, and vice versa.
Keywords
Introduction: Obesity as Fields of Struggle
It is undeniable that obesity is situated in a field of competing interests. Meanings of obesity are highly contested, and involve a ‘kaleidoscope of interest groups with different and sometimes diametrically opposed political leanings’ (Gard, 2011a: 38), even within their own disciplinary areas. Gard refers to the two broad camps competing for legitimacy on obesity studies as the ‘alarmists’ and ‘sceptics’ (2011a: 37, 2011b). Alarmists are represented by public health and medical specialists, who claim that a health crisis is upon us, and risks associated with a looming global obesity epidemic are imminent. In 2013 the American Medical Association moved to recognise obesity as a disease, rather than ‘a complex disorder’ or ‘risk factor’, although this is highly controversial even within the association.
Sceptics, on the other hand, and social scientists 1 who repudiate the very idea of obesity being a ‘risk factor’, let alone a disease, favour the term ‘critical fat studies’ as a way of distancing their research from the medicalisation and pathologisation of oversized bodies (Wann, 2009: x). In the field of critical fat studies, obesity research has been inspired by post-structuralism and deconstruction, including feminist scholarship, fat activism, Health at Every Size (HAES) advocates, critical dietetics, cultural studies, queer studies, anthropology/sociology, physical education and social geography. Again, there is no definitive standpoint within the sceptics group.
These contestations are classic examples of what Bourdieu refers to as ‘fields’ – the social spaces that encompass a set of objective, historically conditioned relations between agents. Different fields have different epistemic logics and different taken-for-granted structures, in which individuals and institutions vie for power through the acquisition of different forms of ‘capital’ (such as status and expert knowledge). Biomedical experts trained in disciplines such as physiology and endocrinology will come to know obesity as a disorder that has the potential to give rise to other co-morbidities, as well as intergenerational transmission of metabolic disease. Social scientists, particularly those trained in social constructionism, will come to know obesity as the product of medicalisation discourses, and be critical of the pathologisation and blaming of fat bodies.
There is a spectrum of social constructionist positionings, with extreme stances likening obesity science to a ‘state science’ (Holmes et al., 2006) in which ‘the fabrication of “evidence” … constitutes a good example of micro-fascism at play in the contemporary scientific arena’ (Rail et al., 2010: 259; see also Jette and Rail, 2013). Rail et al. (2010) suggest that obesity science relies ‘on a process that is saturated by ideology and intolerance of certain types of evidence, alternative discourses, and non-normative knowledge and ways of knowing (for example, qualitative research)’ (Rail et al., 2010: 262).
While some critical fat scholars do not deny the materiality of the body (Colls, Guthman and Mansfield, 2013), there is a clear disjuncture in the literature that pivots on a preoccupation as to whether obesity is real or constructed, nature or nurture, whether it is of consequence and, if so, whether the consequences are valued. It is rare to find critical fat scholars engaging with emerging scientific insights into obesity,
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and Bombak (2014) suggests that those who do rely on ‘outdated critiques of ever progressing, evolving/adapting [obesity sciences] discourses’. Gard similarly notes that: [the] vast majority of the social science that sought to critique mainstream obesity discourses paid scant attention to what mainstream obesity researchers actually said. For the most part, obesity science was simply added to the list of sexist, racist and classist scientific discourses that had for decades been the focus of academic critiques of science. (2013: 108)
The nature/nurture divide has undoubtedly been a useful theoretical device but, as Rose (2013: 4) recently argued: ‘no longer are social theories thought progressive by virtue of their distance from the biological’. Dichotomous positioning in obesity fields is no longer tenable, resting on what Fox-Keller (2010) calls a mirage, a space that has been constructed on a number of problematic assumptions. Theorising on bodies from the intersections of science and technology studies (Latour, 2004; Landecker, 2011; Martin, 2010a, 2010b; Pickersgill et al., 2013), social anthropology’s attention to relationality (Ingold and Palsson, 2013) and local and customary biologies (Gaines, 1992; Lock, 1993, 2013; Niewohner, 2011), relations between body, habit and affect (Blackman, 2013), developments in critical neuroscience (Fitzgerald and Callard, 2015; Pickersgill, 2013) and feminist materialist philosophy (Alaimo and Hekman, 2008; Grosz, 2004) critiques the separate worlds of biology and culture, and argues that it is impossible to reduce the lives of individuals that involve human relationships to either.
The ideas put forward in this article are situated in this post-Cartesian space. Using habitus and folding as metaphorical models, we suggest that epigenetic understandings of obesity provide an ‘excellent case study for thinking about the interaction of biological and social processes’ (Crossley, 2004: 222), demonstrating the ‘complex interplay of biology, agency and society’ (2004: 223). New developments in obesity science are challenging social scientists to think more deeply about the premises of past critiques – to reflect on the use of outdated and out of touch ‘folkbiology’ (Linquist et al., 2011; Meloni, 2014a, 2014b) – and to re-engage with postgenomic views of biology.
Epigenetics is a field of molecular biology that has grown prodigiously in the last decade. Broadly, it investigates the way the functioning of genes is modified by the environment. It looks beyond DNA to the course of one’s life and the socio-economic contexts in which lives take place and, at its most speculative and controversial, to intergenerational histories of exposures and experiences. This entails a constant interplay of biological and social bodies, of materiality, experience and representation. This is what Lock and Nguyen (2010) call a new approach to the human body, in which ‘the reality of the material is not denied for one moment, but equally, the biological body is not simply accepted as a universal entity that we are increasingly able to apprehend comprehensively by means of scientific investigation’ (Lock and Nguyen, 2010: 59).
We begin by outlining what epigenetics is (to the extent that it is definable) and its important role in current developments in obesity science. In particular, we focus on the use of epigenetic mechanisms to advance the developmental origins theory, a recent proposition to explain the intrauterine transmission of obesity and cardio-metabolic diseases, in order to recognise how bodies are embedded in recursive material, socio-economic and historical contexts across time and space. This is more than putting the biological and the social together – not a simple exteriority and interiority, but an exploration of the enfolding of processes and practices. We bring together Bourdieu’s habitus and Deleuze’s metaphor of folding to help us to think theoretically and empirically how bodies enfold molecular and social environments into their growth, thus allowing us to expand our understanding of habitus in light of epigenetics. We do not argue that it is necessary for social anthropologists to learn how to do molecular biology (or vice versa), but rather endorse entering into a ‘critical friendship’ (Rose, 2013: 13) with biological science, to think of it as ‘a mode of thought, a form of attention, or a resource with which to build hypotheses and models’ (Landecker and Panofsky, 2013: 346). In their own work on alliances between social science and neuroscience, Fitzgerald and Callard (2015) suggest that this space of interaction is speculative and experimental in its entanglements. Equally, the interaction of habitus and epigenetics is speculative, and we seek to contribute to a new vocabulary that can begin to allow social scientists who work in obesity studies to draw together the intimate entanglements of the social and biological.
The Challenge of Epigenetics for Social Scientists
Meloni and Testa have highlighted the elusive, imprecise and multiple understandings of what constitute epigenetic phenomena, and the remarkable ambiguity of its defining terms, ‘with its apparent ability to accommodate … a rather diverse range of biological questions and epistemic stances’ (2014: 433). Although philosophers of science position epigenetics as an epistemic object with contested boundaries, a widely accepted understanding of epigenetics is that it refers to biochemical processes that ‘mark’ the genome (either directly or via its transcription factors and receptors), thereby modulating activities of genes (Singh, 2012: 313). The marks are not part of the DNA structure itself and, while some are ‘intrinsic’, others reflect environmental influences throughout the life course, and may even be inherited (2012: 313).
There are many different areas within epigenetics, which also draws on other disciplines such as epidemiology and physiology. As a heterogeneous field of research, epigenetics should be of deep interest to anthropologists as it is ‘the study of factors such as nutrition, pollution and stress in relation to gene regulation’ (Landecker and Panofsky, 2013: 334). This is not merely biological determinism (any more than the laws of physics might determine the outcome of a soccer match), but a direct engagement with ‘the social’ and how it alters, ‘dims’ or ‘switches’ genes on or off. Epigenetic change is continuous and dynamic within all individuals, but is of particular importance in critical periods of development during early life. In mammals, epigenetic changes have been shown to result from a range of prenatal exposures, including poor maternal diet (Burdge and Lillycrop, 2010), alcohol, pesticides and environmental pollutants (Kaur et al., 2013).
Epigenetics is deposing genetics as the ‘prime mover’ in explaining life processes (Landecker and Panofsky, 2013) and is concerned with the expression of genes (the creation of phenotypes) involving processes that are not locked away in cells, protected and untouched by the way one lives or what one does (as traditional thinking about genes suggested). It provides a new understanding of the ways in which social and biological experiences and processes intertwine across the life course and may even be inherited across generations, despite the fact that they do not involve changes in the DNA sequence (Fox-Keller, 2010: 5; Lane et al., 2014). This is not evolutionary time, but ‘life-in-the-making’ (Ramirez-Goicoechea, 2013); a Lamarckian temporality of change that can occur within a relatively short time space of decades.
In obesity science, one stream of epigenetics is concerned with how prenatal contexts impact on molecular processes of fetal growth, changing the susceptibility to chronic disease in later life, and creating a health legacy that will affect subsequent generations. This is a convergence of research on the developmental origins of adult disease (known previously as the Barker hypothesis or, more commonly, the fetal origins hypothesis), life course analysis and epigenetics. Epigenetics has been enthusiastically incorporated into these other areas to demonstrate how early life matters, ‘not only for early life itself but also for the whole life span’ (Hochberg et al., 2011, cited in Landecker and Panofsky, 2013: 340). What unites these approaches is a common concern in how ‘things outside of the body [such as food or stress] are transformed into the biology of the body’ (2011: 178) and transmitted across generations. The social is brought directly into the limelight, no longer a poor cousin of biological explanation (although possibly in danger of reductionism and ‘digitization’; see Meloni and Testa, 2014: 441). Thus, biology and the social are not mutually exclusive, or arranged hierarchically in order of importance as one might find in outmoded stratigraphic views of biology (Meloni, 2013) (such as the biopsychosocial model).
The Developmental Origins Theory – The Intrauterine Environment and the Fetus
Within medical science there is strong evidence to suggest that chronic diseases such as cardiovascular disease and diabetes can be transmitted across generations through two interconnected ‘environments’: 3 the intrauterine environment and the socio-economic environment. This work was inspired by Barker and his colleagues (Barker, 1991 , 2003 , 2004a, 2004b) who advanced the theory that chronic disease originated, at least in part, in the womb, with adverse intrauterine conditions capable of inducing permanent changes in fetal physiology and metabolism. This process was originally known as ‘fetal programming’, although better terms are ‘developmental plasticity’ or ‘phenotype induction’. The process is thought to be an adaptive response, whereby environmental cues produce a phenotype fitted to the predicted future environment. Poor maternal nutrition is thought to be a key determinant of developmental plasticity.
Early work foregrounded the gendered, socio-economic causes of maternal under-nutrition in pregnancy. Thus associations between fetal growth and chronic disease were seen to arise from broader inequalities in health. The initial research compared aggregate health outcomes for rich and poor regions and towns in the UK. Research throughout the 1990s focused more closely on the life course of individuals but continued to draw attention to socio-economic constraints on the health of women and their children.
The proposition that early life experiences have enduring consequences has a long history (Kuh and Davey Smith, 1993), but the specific theory of Barker and his colleagues generated heated debate for a decade. Critics disputed the interpretation of the statistical results, some arguing that the findings simply reflected persisting disadvantage and poor adult behaviour patterns (Baker, 1994; Elford et al., 1991), others focusing on the nature and standard of evidence required to demonstrate causation (Kramer and Joseph, 1996; Paneth and Susser, 1995), or suggesting that a common genetic factor was responsible for both low birth weight and later disease (Bradley, 1991; Hattersley and Tooke, 1999).
As findings from experiments in animals accumulated, the tide of opinion shifted, with consensus statements issued by 2000 (Grivetti et al., 1998; O’Brien et al., 1999) and mainstream acceptance further signalled by the First World Congress on the Fetal Origins of Adult Disease in 2001. Attention turned to the processes or mechanisms, with this agenda outlined by Barker (2003). These continue to be debated, along with the relative importance of early development compared with other determinants of chronic disease.
Yoshizawa argues that Barker’s work (and the numerous studies that tested and elaborated on his hypothesis) illustrates some important innovations, in suggesting that: responsibility for health and disease is found not only in biological pathways, but is diffused horizontally in the intersections of social, political and economic structures and patterns of human geography that affect maternal nutrition. (2012: 356)
Epigenetic Transmission of Obesity
In the developmental origins theory, the uterus is a social and relational space, not just a biological space. In critical periods of development (in utero, in early childhood and in adolescence) the body ‘goes through periods of plasticity and openness to the environment’ (Landecker, 2011: 174, our emphasis), in which nature and culture enfold upon each other. This is not the simple formula of a pregnant mother nourishing her child with the food she eats, but how food can affect the very systems that metabolise food (2011: 176) and become part of the body-in-time, not by building bones and tissues, but by leaving an imprint on a dynamic bodily process (2011: 177). Food is not just fuel. It becomes mutually constitutive of the nature and functioning of organs and systems through biological ‘being-in-each-other’ (Martin, 2010a, 2010b). In this context biology is constantly changing, and comprises of molecules that are in relation to one another, ‘within long chains or nets of causality across time and space that reach in and through the body’ (Landecker, 2011: 179).
Although the first focus of developmental origins research was on the effects of maternal under-nutrition, restricted fetal growth and low birth weight, the issue of maternal and hence fetal over-nutrition gained prominence in the context of the global obesity ‘epidemic’ (Oken and Gillman, 2003). Maternal obesity arguably alters the intrauterine milieu in a number of ways, through an excess of glucose, free fatty acids and amino acids (Whitaker and Dietz, 1998). Thus, in the early 2000s, the idea that prenatal over-nutrition might affect life-long risk of obesity was mobilised to explain a relationship between obese mothers, fat babies and the transmission of obesity through generations (Warin et al., 2012) with epigenetic mechanisms subsequently invoked (Rokholm et al., 2011).
Investigations began as to whether mothers who were obese or had elevated glucose levels during pregnancy ‘overfed’ their unborn children and in doing so may have set them on a pathway to greater adiposity throughout their lives. Furthermore, it was suggested that the increasing prevalence of obesity in women of reproductive age would potentially create transgenerational amplification of obesity and metabolic consequences in subsequent generations (Ebbeling et al., 2002).
In relation to this, various scholars (McNaughton, 2011; Meloni and Testa, 2014; Richardson, 2015; Warin et al., 2011, 2012; Warin, 2014) draw attention to the hyper-responsibility invoked for mothers and a new scope for somatic reductionism, in which women become targeted as entirely responsible for passing obesity on to their children. This opens the door for intense surveillance and governmentality, as a result of which women potentially will bear the burden and blame for their children’s obesity, arguably heightened by the epigenetic turn. At the same time, epigenetics may help us to understand the increased incidence of large bodies in the last 40 years, and how experiences of profound social change ushered in by a post-industrial society (and in particular in market-liberal welfare regimes; Offer et al., 2010) have affected our bodies.
The developmental origins of obesity concept is now firmly part of the child obesity lexicon, extending the understanding of obesity ‘back to the future’, and locating the origins and potentiality of obesity in the maternal and fetal environment. Epigenetic explanations are considered promising, but ahead of the available evidence, which is largely confined to studies in laboratory animals (Lawlor, 2013).
There are few social scientists critically engaged in the implications of obesity science beyond the ‘nurture fortress’ (with Yoshizawa one exception). McNaughton (2011) understands Barker’s hypothesis from a mode of Cartesian body/mind critique, in which maternal nutrition and its effects on the fetus are constructed negatively in a biological determinist discourse, with nature separated from nurture. This separation positions birth as a clear marker of before and after, as a clear line in the sand. Fox-Keller suggests that there is in fact nothing special about birth as a cut-off point (2010: 75), and many of the early origins researchers do not see birth as a clear divide. Yet many social science scholars continue to use this as an epistemological framing of inner and outer environments, in which bodies and environments are separate entities bound by skin, open only through physical means of childbirth.
The Opening of Simultaneous Spaces – Biohabitus
Bourdieu’s life work was aimed at transcending the subjectivist/objectivist divide in social sciences, and his theory of practice was a way of explaining the recursive relationship between bodies and worlds. Habitus is the major link between social structure and practice, for social structures become internalised and embodied as dispositions, which, in turn, reproduce social structures (Bourdieu, 1977, 1990a). The habitus is thus both an embodied structure and is structuring: a product and producer of social worlds. It captures both the ‘embodied-performative aspect of social structures, and the mechanism whereby they are transmitted across generations and through historical time’ (Crossley, 2003: 43). As the taken-for-granted practices of everyday life are learned, modified and passed on, successive generations reproduce and transform a world inherited from their parents’ generation (Bourdieu and Passeron, 1996). Moreover, class-based cultural advantages are passed from parents to children through the habitus, reproducing social stratification (Crossley, 2003: 43).
In Reproduction (Bourdieu and Passeron, 1996), Bourdieu uses the analogy of genes to explain habitus, suggesting that habitus contains the genetic information for the reproduction of the social body (Bourdieu and Passeron, 1996, cited in Crossley, 2003). Habitus does have a key reproductive function, but the analogy with genes invokes a determinist flavour. A number of critics have argued that habitus is a ‘theoretical deus ex machina’ (DiMaggio, 1979: 1464) and Bourdieu’s theory of habitus has repeatedly been charged with determinism (Akram, 2013: 55; Downey, 2014). However, habitus is not a determinist account of culture that ‘erases history and freezes practice in the endless replication of structure’ (Wacquant, 2014: 5). Wacquant reminds critics that Bourdieu introduced habitus in his Algerian work in order to account for the colonial politics of ‘cultural disjuncture and social transformation’ (Wacquant, 2014: 5). Habitus never dictates reproduction of the same practice, as it is the meeting between a ‘skilled agent and [a] pregnant world … acquired over time in diverse circumstances [and] social space … that may itself undergo swift and sweeping change’ (Wacquant, 2014: 5). Habitus is not static or deterministic, but flexible, open and adaptable to change.
As habitus is concerned with the ways in which bodies learn, hold and practise socially shared dispositions, habitus is firmly centred on how ‘culture’ is embodied (and ingrained cognitively); for example, on how everyday eating practices and food preferences are taken-for-granted dispositions that relate to one’s social class, gender and identity. Bourdieu’s habitus does not include the materiality of the body, and he did not engage with biology beyond his analogy between genes and habitus. However, as Crossley notes, habitus is ‘a question-begging concept’ (2013: 137) that is inventive and invites extension.
What if we extended Bourdieu’s habitus to engage with the epigenetic transmission of obesity? If we imagine the epigenetic transmission of obesity as a biohabitus, of the molecular and structural processes of food and eating incorporating each other, we can understand how the social and biological environments interact and respond to each other across the life course, and could be transmitted intergenerationally. As Barker’s earlier work highlighted, socio-economic environments are key to nutrition and health and people experiencing socio-economic disadvantage are at increased risk of obesity (Abbott et al., 2012: 855). This pattern is particularly pronounced among women (Warin et al., 2011). The developmental origins theory potentially offers a way to understand these health inequalities by giving attention to the living conditions, health, and nutrition of young women, pregnant mothers, and their children. In his analysis of the transmission of obesity, Wells (2010) notes that poor maternal diets, fetal exposure to maternal work during pregnancy, and gender bias through preferential feeding of male children means that obesity is structurally embedded in socio-cultural contexts (2010: 296). Education, social independence and economic independence (as well as the role of fathers in intergenerational obesity; Cole et al., 2008) are all important factors in understanding obesity.
These interactions between habitus and molecular processes in women’s bodies are all examples of what Bourdieu refers to as embodied capital. For Bourdieu (1986: 245), cultural capital declined and died with its bearer (‘with his [sic] biological capacity, his [sic] memory’) but Wells suggests that many components of the phenotype can be regarded generically as ‘capital’, which can then be transferred from one generation to another. Like Bourdieu, Wells distinguishes different forms of capital – ‘somatic capital’ (the mother’s body) or ‘liquid capital’ (energy stores) – which have different consequences for the genome and development. Extending Bourdieu further, maternal capital is subject to competition, best encapsulated in the notion of differential social status. Thus, the potentiality for reproductive processes to be adversely affected by socio-economic environments is dependent on the embodied capital of one’s habitus.
Biohabitus invites us to think of nature and culture not as different Cartesian concepts but rather as simultaneous ingredients, in which difference can dwell within the same space rather than between. Like a Russian doll or chimera, biohabitus entails the mutual constitution and interchange of different bodies and persons through history (see also Martin, 2010a). And literally like a Russian doll, the egg that became us was in our mother’s ovary when she was in the womb of her mother, being exposed to and modified epigenetically by historical experiences. Hence, we are in part directly affected by the events in our grandmother’s pregnancy, and the events that influenced her reproductive capacity. As in early origins theorising, habitus is embodied and is a constant interplay between individuals and entire collective histories (Bourdieu, 1990b: 91). For Bourdieu, it is learned from early childhood, but spans the past and present. Biohabitus suggests that social practice is embodied much earlier, in utero and in the memory traces of molecular and cellular lives. And, like epigenetic processes, biohabitus is conceptually permeable and responsive to what is going on in the social environment. Its permeability is thus distinct from earlier sociobiology accounts that studied the evolutionary significance of behaviours and saw social behaviours as genetically fixed.
Fox-Keller (2010) and Ingold and Palsson (2013) identify a peculiar difficulty in trying to overcome the impasse of Cartesian dualism – in that new concepts, like biosocial or indeed biohabitus, are trapped by the same dualistic language that they aim to critique, and as concepts are thus prone to the very kinds of entrapment they are trying to escape. It might be argued that a concept of biohabitus simply drifts back into the core categories of nature and culture in which nature (fetal conditions) and culture (everything outside the body) are simply put together. It is extraordinarily difficult to conceptualise a dynamic, multi-directional and multi-dimensional process that spans intracellular and social environments across time and space. We propose that the molecular process of protein folding provides a Deleuzian metaphor to overcome the simple joining of two distinct parts.
Conceptualising Biohabitus
Central to epigenetics are the ways in which proteins change shape and configuration. Proteins are long chain-like molecules and, under appropriate conditions, most proteins that are active in biological systems coil up and rearrange lengths of the chains so as to assume a characteristic shape. This process is called protein folding. Brown (2003) writes that protein folding is more than simply a name for a molecular process; it is a three-dimensional reconfiguration that takes place over time. It invites us to probe the cross-domain mapping between the literal, everyday act of folding and consider what constitutes folding in a metaphorical sense.
Just as scientists use metaphors (often unknowingly) to understand and communicate their findings (Stelmach and Nerlich, 2015), social scientists need metaphors to translate differing processes of embodiment. Grosz (1994) famously used the Moebius strip as a metaphor to conceptualise the non-binary interplay of embodiment; the interconnecting and dynamic flow between outsides and insides, and minds and bodies. We use folding to conceptualise the continual ‘interpenetration’ (Ingold and Palsson, 2013: 11) of food, eating and bodies across time, space and generations at both molecular and structural levels.
Deleuze’s visceral philosophy of folding (1991) is a model that provides rethinking of bodies outside of the binary polarisations of ‘the mind/body, nature/culture, subject/object, and interior/exterior oppositions’ (Grosz, cited in Bristow, 1997: 35), and is valuable for conceptualising the folding of environments that biohabitus entails. Deleuze’s concept of the fold is a critique of typical Cartesian accounts of subjectivity that presume a simple interiority and exteriority (appearance and essence, or surface and depth). In Deleuzian folding, everything folds, unfolds and refolds, and we can observe other folds between inside and outside, depending upon how perception occurs. There is no inside or outside. Similarly, there is no one model to describe how proteins fold, as ‘no single representation captures the elusive behaviors of a polypeptide chain as it wriggles its way through a range of conformations in search of its “active” or “native” state’ (Myers, 2009: 176).
Conceiving biohabitus as a series of Deleuzian folds resonates with an epigenetic understanding of an ‘embedded body’, that is, a body that is heavily impregnated by its own past and by the social and material environment within which it dwells. It is a body, as Niewohner (2011) argues ‘that is imprinted by evolutionary and transgenerational time, by “early-life” and a body that is highly susceptible to changes in its social and material environment’ (Niewohner, 2011: 290). These are open and emergent bodies, in which agency is expressed through a series of loops, organs, flows, energies, corporeal substances, incorporeal events, intensities, and durations.
Conclusions and Implications of Biohabitus
Lock and Nguyen observe that within the field of epigenetics ‘networks involving social scientists, social epidemiologists, and basic scientists – formations that might well incite radical change and insights – remain very rare indeed’ (2010: 338). Rose (2013: 3) argues that new relations with the life sciences are required, beyond commentary and critique, if the social and life sciences are to revitalize themselves for the 21st century. To deem something biological is not to assert destiny or fatalism, but (cautious) opportunity (2013: 5). As we have suggested in this article, there is, for example, an opportunity to think how obesity science might challenge social scientists to reconceptualise obesity, and to challenge our conceptual categories that up until this point have only provided critique (Warin, 2014). More broadly, this is an opportunity to conceptualise the role that the social sciences might play in their relations with life sciences, and vice versa (Rose, 2013: 13).
Moving beyond critique doesn’t mean suddenly abandoning the lessons we have learned from social constructionism and post-structuralism, but to recognise the limits of these positions with respect to a reappraisal of ‘disciplinary defense systems’ (Singh, 2012: 315). Through the lens of the developmental origins of disease and epigenetic mechanisms, our task is to reach beyond the individual life course and engage with the societal processes that shape it. This means presenting obesity not so much as the ‘corporeal manifestation of accumulated poor choices of individuals or their mothers, but rather a materialisation of our social and material situatedness in space and time, indicating diffuse biosocial responsibility that transcends the individual and the present time’ (Yoshizawa, 2012: 359).
Developmental origins theory, enhanced by knowledge of epigenetics, offers a real opportunity for studying social environments – and this is squarely in the domain of anthropology and the social sciences more broadly. In epigenetics the environment so far has been construed in a fairly limited way (e.g. chemical) and only extreme social disruptors have been considered (e.g. trauma, famine) – not the everyday environment of social networks, social experiences, group dynamics or complex social interactions (Singh, 2012: 318). This is where social scientists (such as Elizabeth Roberts’ [2015] bio-ethnographic methodological experiment) can contribute methodological, theoretical, conceptual and pragmatic understanding.
Social sciences and life sciences thus could be considered as historically and socially constructed folds – these are embedded bodies that are enfolded into what Niewohner (2011) calls customary biology. Anthropology further develops its ‘interliteracy’ capacity (Franklin and Roberts, 2006) as a consequence of new understandings of the complex folds of social and biological worlds, and of how ‘food consumption, long term health and reproductive potential – the very notion of kinship and the pathways of reproduction – are transformed’ (Yates-Doerr, 2011: 305).
In reading Bourdieu’s theory of practice in light of epigenetics, it is clear that bodies are embedded in temporo-spatial landscapes of materiality and history. The habitus creates a system of dispositions – ‘a past which survives the present and tends to perpetuate itself into the future by making itself present in practices’ (Bourdieu, 1977: 82). Extending habitus into biohabitus allows us to understand the situated and contingent nature of bodies across time.
Epigenetic theories bring to the fore what anthropologists have known for decades: ‘bodies, and the cultural technologies and artefacts around which they coalesce, are not just individually performed, but are built up over time in individuals, families and communities’ (Yates-Doerr, 2011: 304). Cells and methylation processes have intentionality and agency, and are enmeshed in a biohabitus and network of biosocial relations. Epigenetics does raise significant questions for social scientists and, as Lock (2013: 303) suggests, is ‘signalling a trend that should not go unattended by anthropologists’. Whether epigenetics is, as Meloni and Testa (2014: 431) state, a ‘new critical frontier’ in the social study of life sciences remains to be seen, but we should be responsive to the field’s claims.
The danger, however, in the enchantment of epigenetics, is that popular discourses of developmental origin theories burden people – overwhelmingly women – with the impossible responsibility for preventing illness in themselves and others (Richardson, 2015; Warin, 2014). There is a continuing role for social scientists to point to slippages, for example, in how the developmental origins of obesity may be misrepresented in scientific and public discourse. Authors of this article have already written about the ways in which the Australian print media have used developmental origins research to blame mothers for producing obese children, and the serious implications of maternal blame and individualised responsibilisation for maternal health (Warin et al., 2012). Epigenetics does recognise environments, but it is easy for environments to be collapsed into the in utero environment, not acknowledging multiple environments or the collective responsibility for health. As mentioned, anthropologists are pointing to the potential molecularisation of life, and as a consequence the potential for intensified biopolitics and targeting of particular bodies and populations (Lock, 2013; Meloni and Testa, 2014; Pickersgill et al., 2013; Warin, 2014).
These dangers provide even more reason for social scientists to make connections with life scientists, to renew conversations (Downey, 2014) and to recognise what opportunities and constraints different fields contain. For Bourdieu, however, fields are never equal and include a wide array of actors who hold different forms of power: not just researchers but also industry, funders, reviewers, advocates, policy makers, among others. Epigenetics will always operate in Bourdieusian fields, and social scientists are familiar with the challenges that working in fields that hold a monopoly over the rules of the game can bring (see, for example, Fitzgerald and Callard, 2015; Pickersgill, 2013). There is much uncertainty about where epigenetics will lead, but the possibilities for ‘reconfiguring the boundaries between taken-for-granted ontological distinctions regarding “biology” and “society”’ (Pickersgill, 2013: 325) provide a rich space for conceptual and methodological thinking in obesity studies.
