Michael White - Why Our Molecular Make-Up Can’t Explain Who We Are

This is the fifth in a series of articles from Pacific Standard on Genes Are Us. These are not long articles, but they are interesting and useful for reframing our thinking about DNA and genetic inheritance.

Why Our Molecular Make-Up Can’t Explain Who We Are

By Michael White • August 29, 2014


(Photo: watchara/Shutterstock)

Our genes only tell a portion of the story.
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Every Friday this month we’ve taken a look at the relationship between the social and the biological—specifically, how and why the former becomes the latter. This is the the final installment.

Can the behavior of molecules and cells explain human behavior? The question of how the social becomes biological is, in one sense, about linking social effects with biological causes. Those causes are now more accessible than ever, thanks to new tools that researchers use to get under the hood in biology. But are we really connecting cause with effect? A close look at this research reveals a giant gap in our understanding of the relationship between molecular and human behavior. It’s a gap that we will rarely bridge.

At first glance, you would think we have ample reason to be optimistic. For much of the history of genetics, scientists couldn’t study our genes directly. Now, in the aftermath of the Human Genome Project, that’s no longer the case. We have the ability to directly analyze all human genes. We have a rapidly expanding catalog of genes and their molecular functions. And nearly every week, new studies report genetic differences between people that are correlated with differences in particular traits, including social ones such as personality, political orientation, and educational attainment.

But when you dig into the results, you’re quickly confronted with a major gap in our understanding. Even if you take the study results as given (which you shouldn’t), there is a lot left to explain. We may know the identity of a relevant gene, and we may even know how that gene functions inside the cell. But we usually have absolutely no idea how that function influences the behavior of a complete, living person—we don’t have an unbroken chain of cause and effect linking molecular behavior to human behavior. We don’t even come close; we’re not explaining the biological basis of something like educational attainment by merely listing associated genes like LRRN2, MDM4, and PIK3C2.

This problem isn’t limited to genetic studies of social traits in humans; it’s faced by all biologists interested in the molecular underpinnings of life, including those who study laboratory animals under highly controlled conditions. We have amassed a tremendous inventory of molecular parts, but in most cases, we’re unable to reason from molecules out to the traits of an entire organism. It’s a problem that we’re unlikely to solve. Aside from some exceptions—such as the molecular basis of blond hair in some Europeans—there is no reason to think that we’ll ever explain biology from molecules alone.

Why not? One way to see the problem is to compare biology with a science where we can explain large-scale behavior in terms of molecules: physics. Physical scientists can explain the properties of solids, liquids, and gases by writing down an equation that describes the quantum behavior of individual atoms. That equation then directly connects the function of the whole with the properties of its parts—the overall qualities of, say, a semi-conductor are explained by the features of trillions of individual silicon atoms. The reason biologists can’t do this is obvious: Biology is too complex. Living things are made up of too many different kinds of parts, organized in fantastically complex ways, all responding to each other and to the environment. And social behaviors in particular tend to involve many different parts. The gap between a molecular cause and a behavioral effect is too great. Outside of the most limited cases, we’ll never be able to span it with a complete chain of deductive reasoning.

Fifth in a Series

• How and Why Does the Social Become Biological?
• How Tiny Genetic Changes Have Massive Behavioral Effects
• How the Sexes Evolved
• Why ‘Nature Versus Nurture’ Often Doesn’t Matter

In other words, we shouldn’t expect a biological explanation of social traits to look like physics. We have to be more pragmatic in the kinds of explanations we look for. Sometimes the explanation will be an exercise in statistics, as in “genes explain 66 percent of the variation in reading ability.” In other cases, particularly pathological ones, a molecular explanation is more useful—knowing that a defective histidine decarboxylase enzyme causes Tourette syndrome, even if we can’t say why, opens up new options for treatment. Useful biological explanations will often bypass molecules and work instead on a higher level, such as the connection between alcohol abuse and the function of different regions of the brain. As the philosopher Philip Kitcher once put it, sometimes “it’s irrelevant whether the genes are made of nucleic acid or of Swiss cheese.”

Regardless of what kinds of biological explanations we resort to, we have to recognize that any answer to the question of how the social becomes biological will be a partial one. And that can be dangerous. When we’re unsatisfied with incomplete explanations, we may look to fill the gaps with facile answers supported by weak or no evidence. Genetic studies of social traits grab headlines, but they can mislead us into thinking that scientists are explaining more than is really the case. It’s hard to see how understanding the detailed workings of phosphatidylinositol-4-phosphate 3-kinase will ever tell us much about why some people succeed more than others at school, or how studying N(alpha)-acetyltransferase 15 will be of much help in understanding why people adopt a certain political orientation. How and why the social becomes biological is an important and fascinating question, but we shouldn’t expect genes to always be a useful answer.


Michael White is a systems biologist at the Department of Genetics and the Center for Genome Sciences and Systems Biology at the Washington University School of Medicine in St. Louis, where he studies how DNA encodes information for gene regulation. He co-founded the online science pub The Finch and Pea. Follow him on Twitter @genologos.

This is a brief and basic article, but the idea behind it, that we need to stop distinguishing between biological and social (especially as causes in dysfunctional behavior), is spot on - and I really like the term they mention, “neuropsychosocial.”

Why ‘Nature Versus Nurture’ Often Doesn’t Matter

By Michael White • August 22, 2014


(Photo: abstract/Shutterstock)
Sometimes it just doesn’t make any sense to try to separate the social and the biological.
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Every Friday this month we’re taking a look at the relationship between the social and the biological—specifically, how and why the former becomes the latter. Check back next week for the final installment.

When it comes to understanding ourselves, we tend to be splitters: mind and body, nature and nurture, or genes and environment. We take such a split for granted when we ask how the social becomes biological, but sometimes it’s not so useful to dichotomize the world into society and biology. Instead of looking for distinct social and biological influences (and believing that we can change one but not the other), we should recognize that the factors that drive our social behavior can, like a Zen koan, be two things at once.

Take the case of teen alcohol abuse. In a study published last week, an international team of researchers reported the “neuropsychosocial” factors that identify teens who are likely to abuse alcohol. The word “neuropsychosocial” does away with the common nature/nurture divide, and so did the researchers. Rather than asking whether teens abuse alcohol because of social influences or innate biology, the scientists looked at those variables that could be measured, regardless of whether the variables were social, biological, or a mix of both.

The study is part of a long-term European project called IMAGEN, established to understand the “biological and environmental factors that might have an influence on mental health in teenagers.” The project enrolled 2,000 14-year-olds, from whom were collected several types of data, including personal histories, psychological assessments of behavior, brain images, and genetic data. The researchers asked theses teens about their alcohol consumption at the beginning of the study, and then again at age 16. Armed with this data and a relatively large sample size, the scientists set out to answer the question: What neuropsychosocial factors identify teens who abuse alcohol?

In one analysis, the researchers looked for the factors that identified “current” drinkers, 14-year-olds who were already abusing alcohol when the study data were collected. They compared “binge drinkers” (defined as having been drunk at least three times by age 14) to non-drinkers (teens who drank no more than twice before age 16). In a second analysis, they attempted to identify future alcohol abusers—teens who were not drinking at age 14, but went on to get drunk multiple times by age 16. For each of these analyses, they built a computer model that used the measured neuropsychosocial variables to classify teens as drinkers or non-drinkers. The first model correctly identified 82 percent of current binge-drinking teens and 89 percent of non-drinking teens. The second model, predicting future drinkers, didn’t fare quite as well: 66 percent of drinkers and 73 percent of non-drinkers were correctly classified.

The most important identifying factors of current and future alcohol abusers were an inseparable mix of the social and the biological. A look at those factors shows how teasing out distinct social and biological causes would be an analytical nightmare: the different genetic, neurological, and life history variables are linked together in a thicket of feedback connections. For example, a history of romantic or sexual relationships strongly predicted current and future binge drinking behavior. But teen sexual behavior is surely influenced by other variables the researchers measured, like personality (which has a substantial genetic component), and “reward anticipation” or “emotional reactivity,” which were measured using brain imaging. It’s important to keep in mind that the study was not designed to discover which factors cause teen drinking, a much more difficult task. Instead, the researchers focused on what they could measure—an approach that, while it has its limits, is one of science’s most successful strategies.

What are the neuropsychosocial factors that best identify current and future teen drinkers? Some predictive traits include the volume and activity level of certain brain areas: “Future binge drinkers had reduced grey matter volume but increased activity when receiving a reward in the superior frontal gyrus compared to controls.” A personality trait characterized by “searching for, and feeling rewarded by, novel experiences” predicts both current and future teen drinkers. Other factors, like disruptive family events and more developed pubertal status identify current (but not future) drinkers, while “anxiety sensitivity” predicts only future drinkers. Notably, one set of factors that are not very predictive are specific genetic variants associated with alcohol dependence. This isn’t surprising because the individual effect of any one gene on a behavior like alcohol abuse is likely to be small.

With these results, we can we say about the biological basis for the social phenomenon of teen alcohol abuse? Not much more than, “it’s complicated.” And anyway, framing the question like this is a mistake.

We often approach a social problem by splitting it into its social and biological root causes, and assuming that we can change the social ones while working around the supposedly irreversible biological ones. But when it comes to human behavior, this is often not very useful or informative. As the authors write, their data “speak to the multiple causal factors for alcohol misuse,” and, in fact, any one variable, taken in isolation, had a small influence in their study. The predictive power of their computer model came from combining variables that were measurable—regardless of whether they could be neatly categorized as social or biological—into a single risk profile. This profile offers clues for how to find and help at-risk teens, and the most effective interventions may turn out to have little to do with directly treating some key social or biological cause of alcohol abuse. As we think about the connection between our social behavior and our biology, we should, like good scientists, be pragmatic, and abandon the distinction between society and biology when it’s not useful.



Michael White is a systems biologist at the Department of Genetics and the Center for Genome Sciences and Systems Biology at the Washington University School of Medicine in St. Louis, where he studies how DNA encodes information for gene regulation. He co-founded the online science pub The Finch and Pea. Follow him on Twitter @genologos.

More From Michael White

• Why Our Molecular Make-Up Can't Explain Who We Are
• How the Sexes Evolved
• How Tiny Genetic Changes Have Massive Behavioral Effects

This is an interesting new research article from Frontiers in Human Neuroscience looks at the convergence of neuroscience, epigenetics, and sociobiology. This is certainly a big piece of the future of understanding the brain; of understanding what genes get turned on or off by trauma, diet, environment, and so on; and how all of this relates to human beings in relationship with each other.

Cool stuff, in my opinion, but also pretty geeky, so be warned.

Full Citation:
Meloni, M. (2014, May 21). The social brain meets the reactive genome: neuroscience, epigenetics and the new social biology. Frontiers in Human Neuroscience; 8:309. doi: 10.3389/fnhum.2014.00309

The social brain meets the reactive genome: Neuroscience, epigenetics and the new social biology

Maurizio Meloni

• School of Sociology and Social Policy, Institute for Science and Society, University of Nottingham, Nottingham, UK

Abstract

The rise of molecular epigenetics over the last few years promises to bring the discourse about the sociality and susceptibility to environmental influences of the brain to an entirely new level. Epigenetics deals with molecular mechanisms such as gene expression, which may embed in the organism “memories” of social experiences and environmental exposures. These changes in gene expression may be transmitted across generations without changes in the DNA sequence. Epigenetics is the most advanced example of the new postgenomic and context-dependent view of the gene that is making its way into contemporary biology. In my article I will use the current emergence of epigenetics and its link with neuroscience research as an example of the new, and in a way unprecedented, sociality of contemporary biology. After a review of the most important developments of epigenetic research, and some of its links with neuroscience, in the second part I reflect on the novel challenges that epigenetics presents for the social sciences for a re-conceptualization of the link between the biological and the social in a postgenomic age. Although epigenetics remains a contested, hyped, and often uncritical terrain, I claim that especially when conceptualized in broader non-genecentric frameworks, it has a genuine potential to reformulate the ossified biology/society debate.

After Gene-Centrism: the New Social Biology

Profound conceptual novelties have interested the life-sciences in the last three decades. In several disciplines, from neuroscience to genetics, we have witnessed a growing (and parallel) crisis of models that tended to sever biological factors from social/environmental ones. This possibility of disentangling neatly what seemed to belong to the “biological” from the “environmental” and to attribute a sort of causal primacy to biological factors (equated with genetic) in opposition to social or cultural ones (thought of as being more superficial, or appearing later in the ontology of development) was part and parcel of very vocal research-programs in the 1990s. These programs were all more or less heirs of the gene-centrism of sociobiology: from evolutionary psychology, to a powerful nativism that was very influential in psychology and cognitive neuroscience with its obsessive emphasis on hardwiring culture or morality into the brain.

These programs have always received a barrage of criticisms from several intellectual traditions (Griffiths, 2009; Meloni, 2013a), particularly those with roots in ethology (Lehrman, 1953, 1970; Bateson, 1991; Bateson and Martin, 1999), and developmental biology (West and King, 1987; Griffiths and Gray, 1994; Gottlieb, 1997; Oyama, 2000a[1985],b; Oyama et al., 2001; Griffiths, 2002; Moore, 2003). However, never as in this last decade, we have had scientific evidence that the dichotomous view of biology vs. society and biology vs. culture is biologically fallacious (Meaney, 2001a).

Paradoxically, it was exactly the completion of the Human Genome Project that showed that the view of the gene as a discrete and autonomous agent powerfully leading traits and developmental processes is more of a fantasy than actually being founded on scientific evidence, as highlighted by the “missing heritability” case (Maher, 2008). The image of a distinct, particulate gene marked by “clearly defined boundaries” and performing just one job, i.e., coding for proteins, has been overturned in recent years (Griffiths and Stotz, 2013: 68; see also Barnes and Dupré, 2008; Keller, 2011). Although discussions are far from being settled, the work of the ENCODE consortium for instance has been crucial in showing the important regulatory functions of what, in a narrow “gene-centric view”, was supposed to be mere “junk DNA” (Encode, 2007, 2012; Pennisi, 2012). Not only does a very small percentage of the genome (less than 2%) act according to the classical definition of the gene as a protein-coding sequence, but most of the non-protein coding DNA in fact plays an important regulatory function. The genome is therefore today best described as a “vast reactive system” (Keller, 2011) embedded in a complex regulatory network with distributed specificity (Griffiths and Stotz, 2013). An important part of this regulatory network is involved in responding to environmental signals, which can cover a very broad range of phenomena, from the cellular environment around the DNA, to the entire organism and, in the case of human beings, their social and cultural dynamics.

To sum up a decade of empirical and conceptual novelties the conceptualization of the gene has become dynamic and “perspectival” (Moss, 2003), in what can be called the new “postgenomic view1”; it addresses genes as part of a broader regulative context, “embedded inside cells and their complex chemical environments” that are, in turn, embedded in organs, systems and societies (Lewkowicz, 2010). Genes are now seen as “catalysts” more than “codes” in development (Elman et al., 1996), “followers” rather than “leaders” in evolution (West-Eberhard, 2003; Robert, 2004). The more genetic research has gone forward, the more genomes are seen to “respond in a flexible manner to signals from a massive regulatory architecture that is, increasingly, the real focus of research in ‘genetics’” (Griffiths and Stotz, 2013: 2; see also Barnes and Dupré, 2008; Dupré, 2012).

As Michael Meaney (2001a: 52, 58) wrote more than a decade ago: “There are no genetic factors that can be studied independently of the environment, and there are no environmental factors that function independently of the genome… . At no point in life is the operation of the genome independent of the context in which it functions.” Moreover, “environmental events occurring at a later stage of development … can alter a developmental trajectory” making meaningless any linear regression studies of nature and nurture. Genes are always “genes in context”, “context-dependent catalysts of cellular changes, rather “controllers” of developmental progress and direction” (Nijhout, 1990: 444), susceptible to be reversed in their expression by individual’s experiences during development (Champagne and Mashoodh, 2009).

Epigenetics

The recent surge of interest in molecular epigenetics is probably the most visible example of these conceptual changes in contemporary biology. After a delay of almost fifty years from its coining, epigenetics has become a “buzzword” in XXI century biology (Jablonka and Raz, 2009: 131): the vertical growth of publications in the field in the last decade certifies this epidemic of epigenetics (Haig, 2012; Jirtle, 2012). It is far from my intention to oversell the conceptual and evidential strength of a discipline still as embryonic, multiple, and contested as molecular epigenetics. Many things in epigenetics remain highly controversial and debated, and cautiousness in dealing with its relevance, especially for humans, remains a good scientific policy (Feil and Fraga, 2012). Moreover, the notion of epigenetics is elusive and plastic, meaning different things for different research contexts (Morange, 2002; Bird, 2007; Ptashne, 2007; Dupré, 2012; Griffiths and Stotz, 2013). Despite (or, more likely, just because of) this semantic ambiguity epigenetics prospers as a scientific and social phenomenon in need of careful reflective scrutiny (Meloni and Testa, in press).

Also, the genealogy of epigenetics in biological thought is complex, and its current molecular “crystallization” is the result of a series of important conceptual shifts (Jablonka and Lamb, 2002; Haig, 2012; Griffiths and Stotz, 2013). The notion was firstly coined by embryologist and developmental biologist C. H. Waddington (1905–1975) in the 1940s as a neologism from epigenesis to define, in a broader non-molecular sense, the “whole complex of developmental processes” that connects genotype and phenotype (reprinted in Waddington, 2012). For Waddington epigenetics was “the branch of biology which studies the causal interactions between genes and their products which bring the phenotype into being” (Waddington, 1968 see Jablonka and Lamb, 2002).

A parallel origin of the concept is having probably a stronger influence on the present understanding of epigenetics. This latter tradition originates with Nanney’s (1958) paper in Epigenetic Control Systems, and refers more specifically to the existence of a second non-genetic system, at the cellular level, that regulates gene expression (Nanney, 1958; see, Haig, 2004; Griffiths and Stotz, 2013).

It is this second narrower molecular meaning that is becoming increasingly influential in the contemporary literature (Griffiths and Stotz, 2013). This is why it is probably more correct to call contemporary epigenetics “molecular epigenetics” to differentiate it from the broader Waddingtonian sense and the developmentalist-embryological tradition in which the term was firstly conceived, although it is true that the two meanings are not in principle irreconcilable as they both emphasize the context (molecular or at the level of the organism) where genetic functioning takes place (Hallgrímsson and Hall, 2011).

In the present mainstream molecular sense, a rather standard and very often quoted definition of “epigenetics” is “the study of mitotically and/or meiotically heritable changes in gene function that cannot be explained by changes in DNA sequence” (my italics, Russo et al., 1996, quoted in Bird, 2007: 396; see also Feng and Fan, 2009). This definition in a negative form is pretty typical even in less technical books, where we find epigenetics called as the study of all the “long-term alterations of DNA that don’t involve changes in the DNA sequence itself” (Francis, 2011: X, my italics).

In a broader but still negative form, epigenetics can be defined as any “phenotypic variation that is not attributable to genetic variation” (Haig, 2012: 15, my italics). If we search for an operationally positive definition (more rare), we can call molecular epigenetics “the active perpetuation of local chromatin states” (Bird and Macleod, 2004 quoted in Richards, 2006: 395) or the self-perpetuation of gene expression “in the absence of the original signal that caused them” (Dulac, 2010: 729). The preferred recourse to a negative definition not only reflects the uncertainty surrounding the range and stability of epigenetic mutations, but more importantly it makes evident the difficulties of conceptualizing epigenetics in a way that might finally go beyond a gene-centric view of heredity and phenotypic development2.

DNA methylation, the addition of a methyl group to a DNA base that can silence gene expression, is the most well-known example of an epigenetic modification. Given its crucial function as regulator of gene expression, methylation has been defined as the “prima donna” of epigenetics (Santos, quoted in Sweatt, 2013). Other possible examples of epigenetic marks include histone modifications, alterations of chromatin structure, and gene regulation by non-coding RNA.

In evolutionary terms, epigenetic changes, far from being a biological anomaly, are fundamental for developmental plasticity, the “intermediate process” by which a “fixed genome” can respond in a dynamic way to the solicitations from a changing environment, and produce different phenotypes from a single genome (Meaney and Szyf, 2005; cfr. also Robert, 2004; Gluckman et al., 2009, 2011). Recent studies (Kucharski et al., 2008; Lyko et al., 2010) on the impact of DNA methylation on the development of different phenotypes between sterile worker and fertile queen honeybees (Apis mellifera) have shown the importance of epigenetic changes (via different nutrition in this case) on the mechanism underlying developmental plasticity.

Even more interestingly, these changes in gene expression (and the phenotypic alteration that results from it) have a twofold property whose importance in rethinking the nexus of biology and social factors cannot be underestimated: (1) some epigenetic modifications, like DNA methylation, can be maintained throughout life whereas others are susceptible to change even later in life being therefore reversible under certain circumstances; and (2) some epigenetic states, against established wisdom, appear to be transmissible inter-generationally.

Point 2 especially remains very controversial because received wisdom is that these epigenetic marks are reset at each generation and therefore incapable of offering the required stability to sustain transgenerational phenotypic changes. It is true that the issue of transgenerational epigenetic inheritance remains the source of more questions than answers so far (Daxinger and Whitelaw, 2010), but novel and interesting studies are challenging the established view of inheritance (Anway et al., 2005; Rassoulzadegan et al., 2006; Hitchins, 2007; Wagner et al., 2008; Franklin et al., 2010; Saavedra-Rodriguez and Feig, 2013) and pointing at the transgenerational effects on future generations (up to four) of environmental effects via epigenetic mechanisms in the two alternative forms of: (a) germline epigenetic inheritance (where the epigenetic mark is directly transmitted, see for instance Anway et al. (2005); and (b) experience-dependent non-germline epigenetic inheritance (where the epigenetic mark is recreated in each successive generation by the re-occurrence of the inducing behavior, or “niche recreation”: Champagne, 2008, 2013a, b; Champagne and Curley, 2008; Danchin et al., 2011; Gluckman et al., 2011).

Possible examples of these latter indirect or non germline epigenetic phenomena in humans include the often quoted research on transgenerational effects on chronic disease in individuals prenatally exposed to famine during the Dutch Hunger Winter in 1944–45 (Heijmans et al., 2008; Painter et al., 2008; Veenendaal et al., 2013). In the context of the growing interest in the developmental origins of chronic noncommunicable disease in humans (the so-called “developmental origins of health and disease”, DOHaD), epigenetic research is bringing to light how, during particularly plastic phases of development, environmental cues (for instance, in the above quoted example, levels of nutrition) set up stable epigenetic markers that shape (or “program”) the organism’s later susceptibility to disease (Gluckman et al., 2011).

In a broader evolutionary perspective, epigenetic marks, and DNA methylation in particular, are becoming recognized as “candidate mechanisms” (Kappeler and Meaney, 2010; see also Danchin et al., 2011) for parental effects, the phenomenon whereby exposures in one generation to certain environmental states (for instance in this case, famine) can affect the next generation’s phenotypes without affecting their genotypes (Badyaev and Uller, 2009; Danchin et al., 2011).

Consequences for Heredity

It appears evident even from this limited survey that the consequences of epigenetics for the notion of biological inheritance are profound. By challenging the idea that heredity is the mere transmission of nuclear DNA, epigenetics has opened the doors to a broader, extended view of heredity by which information is transferred from one generation to the next by many interacting inheritance systems (Jablonka and Lamb, 2005). Epigenetic variations act as a parallel inheritance system through which the organism can respond in a more flexible and rapid way to environmental cues and transmit to different cell lineages different “interpretations” of DNA information (ibid.).

It is no longer the mere DNA sequence that is transferred inter-generationally, but, expanding on the notions of “ontogenetic niche” coined in the 1980s (West and King, 1987), it is the whole “developmental niche” (Stotz, 2008), “the set of environmental and social legacies that make possible the regulated expression of the genome during the life cycle of the organism” (Griffiths and Stotz, 2013: 110). Taking seriously the idea of a developmental niche as the proper integrative framework for extended inheritance, as Griffiths and Stotz (2013) claim, means also understanding that environmental and social factors, not only merely “genetic” factors, “carry information in development” (ibid.: 179).

The environment is therefore now seen as directly inducing variations in evolution (Jablonka and Lamb, 2005), and its role as “initiator of evolutionary novelties” clearly recognized (see also Pigliucci, 2001; West-Eberhard, 2003; Pigliucci and Muller, 2010).

In sum, the narrow, gene-centric view of inheritance that was at the core of the Modern Synthesis in evolutionary thinking has been profoundly challenged and opened to a plurality of different non-genetic mechanisms (Bonduriansky, 2012; Bonduriansky and Day, 2009; Uller, 2013). By inviting one to think that “heredity involves more than genes”, and that “new inherited variations (…) arise as a direct, and sometimes directed, response to environmental challenge” epigenetic inheritance seems close to Lamarckian ideas of soft inheritance and inheritance of acquired features (Jablonka and Lamb, 1995: 1; see also Jablonka and Lamb, 2005; Gissis and Jablonka, 2011), although clearly the interpretation of epigenetics in such a broad and heterodox conceptual framework remains debated and controversial.

Where Epigenetics Meets Neuroscience

Some of the most influential studies that are behind the recent surge of interest in epigenetics originate from or directly cut-across neuroscience research. Epigenetic research offers a key missing link in the dynamic interplay between experience and the genome in sculpting neuronal circuits especially in critical period of plasticity (Fagiolini et al., 2009). It attempts to make visible the molecular pathway that explain how transient environmental factors can lead “long-lasting modifications of neural circuits and neuronal properties” (Guo et al., 2011).

The porousness of the brain to social signals has been at the core of social neuroscience since its beginning in the 1990s. I will focus here on three streams of research that have played a crucial role in taking this openness and plasticity of the social brain to a new level. Epigenetics in this sense can be seen as the climax of that very visible process of the “socialization” of biological and neurobiological concepts that we have witnessed in action in evolutionary thinking since at least the 1990s (Meloni, 2014).

Molecular Pathways of Maternal Care in the Brain

In current epigenetic studies the story of how Michael Meaney, a neuroscientist and clinical psychologist at McGill, and Moshe Szyf, a molecular biologist and professor of pharmacology at the same McGill, met in a bar during a conference in Spain, has been told many times (Buchen, 2010; Hoag, 2011) to show the almost serendipitous encounter of a neurobiological perspective with a genetic one that is behind social epigenetic research. This interdisciplinary approach lies at the very core of Meaney’s group’s maternal care studies on the intergenerational transmission of stress and inadequate mothering in rodents (Meaney, 2001b), amongst the most known in all the epigenetic literature (along with Waterland and Jirtle’s studies on agouti mice: Waterland and Jirtle, 2003, 2004). Also the story of how this study was first rejected by Science and Nature is told to illustrate the impervious terrain that marked the beginning of epigenetic research.

Meaney et al.’s study, finally published as Epigenetic programming by maternal behavior in Nature Neuroscience (Weaver et al., 2004) has become a massively quoted article (with more than 2500 citations), almost an icon of the new linkage between behavioral exposures (in this case: maternal care and neonatal handling) and genetic expression/development in the brain.

The basic findings of the study are that increased licking and nursing activity by rat mothers altered the offspring DNA methylation patterns in the hippocampus, thus affecting “the development of hypothalamic-pituitary-adrenal responses to stress through tissue-specific effects on gene expression” (Weaver et al., 2004: 847). Even more interestingly, cross-fostering pups of non-caring mothers to affective ones, the DNA methylation phenotype reflected that of the foster mother and was maintained stably into adulthood thus shaping life-long behavioral trajectories.

This direct linkage between maternal care and neurological development (via DNA methylation) was conceptualized in terms of environmental (or epigenetic) programming that is a stable non-sequence based modification (Francis et al., 1999) of gene expression that proceeds without germline transmission. Another take-home message of Meaney’s group study is the emphasis on a critical period, the first week of life, for the effects of early experience on methylation patterns in the hippocampus. Epigenetic modifications are stably encoded during early life experiences becoming therefore the critical factor in “mediating the relationship between these experiences and long-term outcomes” (Fagiolini et al., 2009). The sustained effects of these cellular modifications “appear to form the basis for the developmental origins of vulnerability to chronic disease” (Meaney et al., 2007).

Stigmas of Trauma in the Brain

But what about epigenetic research involving more specifically humans? In 2009, another study appeared with a significant impact on the field of social epigenetic. The research, originating again from Meaney’s lab, focused on the level of DNA methylation in postmortem hippocampal tissue from two groups of suicide victims (using samples from the Quebec Suicide Brain Bank), one of which with a history of abuse (McGowan et al., 2009).

The study found higher levels of DNA methylation of the regulatory region of the glucocorticoid receptor (resulting in decreased levels of glucocorticoid receptor mRNA) in the abused group compared to the nonabused and the control group. Early life adversities therefore (childhood abuse), not suicide per se, are the key factors to explain the alteration of DNA methylation in crucial genomic regions (neuron-specific glucocorticoid receptor gene, NR3C1) in the brain.

This work, which translates Meaney’s research into human studies for the first time, is consistent with the findings of the studies on rodents and has been welcomed as biological evidence of how traumatic life experiences become embedded in the “memory” of the organism, getting “under the skin” (Hyman, 2009).

The findings of this research, along with others of McGowan et al. (2008), are consistent with the non-human animal studies of Meaney’s group about the emphasis on early life events as a critical period for the establishment of stable DNA methylation patterns, and therefore different pathways of neural development. As the study claims: “early life events can alter the epigenetic state of relevant genomic regions, the expression of which may contribute to individual differences in the risk for psychopathology” (McGowan et al., 2009: 346).

Like in Meaney’s group previous studies, the emphasis is on the effects of disruption of parental care on methylation levels in critical areas of the brain implicated in the regulation of responses to stress and anxiety disorders. More importantly, the study aims to open up important connections between variations in DNA methylation in the hippocampus and the emergence of psychiatric disorders, a topic that is becoming increasingly relevant in epigenetic research (see for instance Tsankova et al., 2007; Nestler, 2009), as it can be seen from the third and final cluster of what can be named “epigenetic neuroscience” research.

Neuroepigenetics: Mechanisms of Plasticity for the Adult Brain

A final and parallel development at the crossroads of epigenetics and neuroscience comes from the newborn sub-field of (cognitive) neuroepigenetics (Day and Sweatt, 2011; Sweatt, 2013) that focuses on how epigenetic mechanisms impact the adult brain and the central nervous system.

Neuroepigenetics aims to investigate changes in epigenetic marks that accompany neuronal plasticity and the processes of learning and memory formation/maintenance in the brain (see also Levenson and Sweatt, 2005; Borrelli et al., 2008). In a sense, epigenetic marking itself can be seen as a “persistent form of cellular memory” by which memories of past environmental events are fixed on the genome. This would explain, it has been claimed, the fact that the nervous system has co-opted this mechanism “to subserve induction of synaptic plasticity, formation of memory and cognition in general” (Levenson and Sweatt, 2006). Another task of neuroepigenetics is the understanding how epigenetic mechanisms may vary depending on the different neural circuits and behavioral tasks involved (Day and Sweatt, 2011). The main difference compared to the other studies highlighted in this section is the emphasis on the adult brain. Here, given the non-divisibility of adult neuron cells, epigenetic tags although long-lasting are non-heritable, thus setting “the roles of epigenetic mechanisms in adult neurons apart from their roles in developmental biology” (Sweatt, 2013: 627). The term neuroepigenetics is what distinguishes therefore this specific aspect of epigenetic research from other areas of developmental biology (Day and Sweatt, 2011). A new wave of publications on the epigenetics of the adult brain illustrates well the high expectations surrounding epigenetic knowledge to explain the molecular mechanisms of plasticity. In a recent article, for instance, Woldemichael et al. (2014) look at the way epigenetic processes may subserve brain plasticity in relation to, amongst other things, drug addiction and cognitive dysfunctions (age-associated cognitive decline, Alzheimer’s disease, etc.). Moreover, they do so always with an eye to the potential of epigenetic therapies to reverse neurodegenerative disorders (see also Gapp et al., 2014). Other recent publications in the field examine the epigenetics of stress vulnerability and resilience (see also Stankiewicz et al., 2013; Zannas and West, 2014), neuropsychiatric disorders (Hsieh and Heisch, 2010), major psychosis (Labrie et al., 2012), autism spectrum disorders (Ptak and Petronis, 2010), mood disorders (Fass et al., 2014); again, with an eye to the development of novel therapeutics.

Although many of these publications reflect very early attempts to use epigenetic knowledge to explain the molecular mechanisms of brain plasticity, and although in much of this literature the supposed distinctiveness of epigenetic changes in the brain rather than in other organs is never really problematized, it is still helpful to survey this emerging literature as an illustration of the current process of rewriting, in epigenetic terms, of many themes from the last decade of research about the social brain, particularly its plasticity and permeability to environmental signals. Epigenetics in this sense can be seen as the last frontier in the construction of the narrative about the sociality of the brain, the discovery of a possible crucial mechanism mediating between environmental exposures, gene expression and neuronal development, that is likely to validate and give further strength, at the molecular level, to many of the intuitions that have been at the core of social neuroscience research since the 1990s.

Implications for Social Theory

In the last two decades of research in cognitive science, mind and cognition have been understood increasingly as an extended, enacted and embodied phenomena (Clark and Chalmers, 1998; Thompson, 2007; Clark, 2008; Noë, 2009; Menary, 2010). Neuroscience has joined this trend: the brain has ceased to be represented as an isolated organ and instead become a multiply connected device profoundly shaped by environmental influences. One of the membranes demarcating the biological from the social, the skull (Hurley in Noë, 2009), has been made increasingly permeable to a two-way interaction.

The brain is increasingly thought of as a tool specifically designed to create social relationships, to reach out for human relationships and company, literally made sick by loneliness and social isolation (Cacioppo and Patrick, 2008; Hawkley and Cacioppo, 2010). The emergence of this novel language certifies to the success of a discipline like social neuroscience (Matusall et al., 2011), with its landscape populated by empathic brains and moral molecules, mirror neurons and plastic synapses.

However, in the context of this trend toward an increasing openness of the biological to social signals, the rise of molecular epigenetics promises to bring this discourse to an entirely new and more powerful level. Undoubtedly, this promissory vocabulary, which has always been part of the rhetoric of the life-sciences (as highlighted by a consistent body of scholarship in Science and Technology Studies), has not to be taken at face value. The “economy of hope” that surrounds epigenetics as a possible relaunch of the genomics discourse is in particular something that deserves critical scrutiny (Meloni and Testa, in press). However, the appreciation of this more critical moment, cannot become a reason to deny the potential contained in the epigenetic discourse, especially when conceptualized in more sophisticated non gene-centric frameworks (Griffiths and Stotz, 2013).

When compared with recent arguments about the sociality of the brain, epigenetics seems to play a twofold function. Epigenetics not only supplements social neuroscience by highlighting the molecular mechanisms that orchestrate brain plasticity and memory formation, but also seeks to blur any residual distinction between biology and social/ecological contexts. If the first model of the cognitive brain was that of a computing machine, entirely severed from environmental influences, and the brain of social neuroscience still oscillated between plastic change and hardwiring metaphors, with the rise of what can be named the “epigenetic brain” or neuroepigenetics research the reciprocal penetration of the social and the biological reaches a point where trying to establish any residual distinction seems increasingly a meaningless effort.

Particularly when conceptualized within theoretical frameworks like Developmental Systems Theory (Oyama, 2000a[1985], b; Oyama et al., 2001) and other postgenomics approaches, epigenetic research illustrates exemplarily how we are moving toward a post-dichotomous view of biosocial processes that research in social neuroscience was only partially able to anticipate. With the rise of molecular epigenetics, the biological is opened to environmental influences, to social factors, and to the marks of personal experience like never before. The sovereign role of the gene has been decentralized (Van Speybroeck, 2002) and the genome made a “reactive genome” (a term first coined by Gilbert, 2003, and expanded on more recently by Keller, 2011; Griffiths and Stotz, 2013).

At the same time the notion of vitality has been expanded to a new range of actors and “democratized” (Landecker and Panofsky, 2013). In epigenetic research, the “social” seems to assume a causative role in human biology to a degree unseen before (Landecker and Panofsky, 2013). The same emergence of a new terminology of “social and environmental programming” reflects this unprecedented prominence of the social level. Such a discourse was quite unimaginable under the Weismannian’s conception of an impenetrable barrier between soma and germ-line, as well in what can be seen as the molecular translation of Weismann’s argument (Griesemer, 2002) in the so-called Central Dogma of Molecular biology (Crick, 1958) which stated the strict one-side flow of information from DNA to RNA. In reversing the informational asymmetry between genotype and phenotype, in stressing the relevance of context (interpretation) upon the level of DNA information (Jablonka and Lamb, 2005; Jablonka and Raz, 2009) and finally in giving a life-span to genetic process, making them radically dependent on temporal factors (Landecker and Panofsky, 2013), epigenetics displays unique features that promise to radically change the language of biology and, as a consequence, the system of rules that have so far regulated the biology/society boundary.

On one level, this unprecedented porousness of the biological to the social comes as a good news for social scientists with an interest in notions of embodiment and in exploring the pathways through which the social shapes and is literally inscribed into the body. The investigation of the ways in which social structures and socio-economic differences literally get under the skin (and in the brain), affecting the deep recesses of human physiology, has always been an important concern of sociological theory, from the French doctor and economist René Villermé and Friedrich Engels in the 1800s (see Krieger and Davey Smith, 2004), to social epidemiologists (Krieger, 2001, 2004, 2011; Shaw et al., 2003; Krieger and Davey Smith, 2004) and neuroscientists (Lupien et al., 2000; Noble et al., 2005, 2007, 2012; Farah et al., 2006; Kishiyama et al., 2009; Hackman et al., 2010; Rao et al., 2010) in the early twenty-first.

However, given the epistemological and political implications of gene-centrism and the mainstream view of biology as an unchangeable form of secular destiny in the twentieth-century, these more plastic biosocial approaches have remained so far exceptions (Boas, 1910 research on the changing bodily form of immigrants and their descendants in the USA, being one of these exceptions). Under these unfavourable epistemic circumstances, the possibility of sophisticated and enriching biosocial explorations has been profoundly limited and mostly faced with skepticism by social theorists. To import the biological into the social, across the twentieth century, meant almost exclusively refer to unacceptable class, race or gender biased explanations. Facing this view of biology, disembodied social constructionist explanations that rejected biology entirely seemed (almost) the only way out for social scientists.

However, in the present scenario marked by the rise of epigenetics and the new social biology, this marginalization no longer seems compulsory for social scientists. Undoubtedly, epigenetics is likely to revitalize a social science approach interested in how “phenomena of the outside (….) undergo transformations and are incorporated to re-appear or be reproduced on the inside” (Beck and Niewöhner, 2006: 224; Niewöhner, 2011; Guthman and Mansfield, 2012). It may supplement various findings from medicine, neuroscience, and various animal studies on the way in which social phenomena (social position, socio-economic status (SES), social isolation, rank, stress, etc.) are translated into the body and affect human health. On these novel bases, a fresh dialog between social and biological disciplines in which epigenetics can penetrate the “sometimes obdurate wall between the life and social sciences” (Landecker and Panofsky, 2013: 2) seems more realistic than in the past (Rose, 2013; Meloni, 2013b, 2014).

On the other level, however, a recognition of the great potential of epigenetic research to reframe and go beyond the sterile nature/nurture opposition, is no reason to deny the ambiguities and contradictory claims aligning in the field, and the difficult methodological and epistemic questions still awaiting to be answered before any major biosocial synthesis may be proposed.

Even leaving aside hypes and controversies surrounding epigenetics, social scientists and theorists need to be aware that an entire new array of problems is emerging in the postgenomic scenario. This new complex of social problems does not derive from the dichotomous separation of biological and social causes in which the biological is supposed to have a causal primacy (as in the hostile post 1970 debates on sociobiology, genetic reductionism, or evolutionary psychology). Rather they arise for the exact opposite reason, that is, because of the inextricable mixture of social and biological factors typical of the epigenetics and postgenomic conceptual landscape.

There is a specific and in a way unprecedented profile of problems in the postgenomic age (Meloni, 2013b, 2014; Meloni and Testa, in press) that without any ambition to be conclusive I will try to sketch below. Rather than as consolidated analyses of what is likely to happen in the epigenetic era, though, these different clusters of problems can be read as preliminary questions for a possible agenda of the social studies of the life-sciences in the future years.

Postgenomic Epistemology: Molecularizing Nurture?

Epigenetic research undermines the nature/nurture opposition on both sides of the dichotomy. To the extent that genes are now “defined by their broader context”, our understanding of nature becomes less essentialist and “more epigenetic” (Griffiths and Stotz, 2013: 228), that is, always entangled with social and environmental factors. However the epistemic conditions for environmental, social or experiential factors to become readable in the epigenetic paradigm is their translation into signals at the molecular level (Landecker, 2011). This trend finds confirmation in the fact that different social categories (from race to class), and environmental factors (from maternal care, to food and toxins) are being increasingly conceptualized today in molecular terms (Landecker, 2011; Niewöhner, 2011).

Only to the extent that our understanding of nurture becomes more “mechanistic” (Griffiths and Stotz, 2013: 5) can we therefore find a solution to the nature/nurture conundrum in the postgenomic era. It is important to notice here that mechanisms are understood by Griffiths, Stotz and other philosophers of biology not as a vulgar reductionist concept but as a more sophisticated, multilevel, and emergentist notion which includes looking “upward to higher levels” (Bechtel, 2008: 21) as well as making room for the active, autonomous role of human agency.

This new version of mechanism, as Griffiths and Stotz again claim, is producing an unexpected rapprochement with themes from the holistic tradition, or as they prefer “integrationist” (ibid.: 103).

Nonetheless, although social scientists will recognize in this anti-reductionist rethinking of the notion of mechanism an appealing theoretical move, two sources of skepticism remain to be addressed: (1) that in spite of the many sophistications of philosophers of science and biology, the bulk of epigenetic research will much more naively try to do business as usual, inscribing the effects of complex social phenomena at the digitalized level of methylation marks (Meloni and Testa, in press), with serious risk of over-simplification as well as attributing causal relevance to random biological processes; and (2) that mainstream social theory will remain not convinced by any idea of the tractability of social and cultural phenomena, given the legacy of traditions (from Weberian neo-Kantism to Durkheim, from Western Marxism to Boasian anthropology: Benton, 1991; Meloni, 2011, 2014) that made anti-naturalism and the incommensurable nature of social and cultural processes the hallmark of social research.

Given these opposite limitations, complex biosocial and biocultural approaches are likely to remain a minority strategy, caught between persisting reductionist tendencies in bioscience and the continuing legacy of bio-phobia in social theory.

Postgenomic Biopolitics: “Upgrade Yourself” or Born Damaged for Ever?

The epigenome is caught in a curious dialectic of stability and modifiability (Meloni and Testa, in press). Whereas genetic sequences are fixed and unchangeable, epigenetic marks are at the same time “long lasting” but “potentially reversible” (Weaver et al., 2005; McGowan and Szyf, 2010). In its social dimension, the plasticity of the epigenome, just like the plastic brain which Catherine Malabou (2008) has written about, can be understood in two alternative ways: (i) passively, as a capacity to receive form: the epigenome, in contrast to genes, is vulnerable to environmental insults; (ii) actively, as a capacity to give form: the epigenome can change and upgrade, through diet, exercise, therapeutic and social manipulations.

In the wider society, this dialectic within the language of epigenetics is likely to become even more amplified as an oscillation between determinism and hopes of individual/social amelioration: (i) determinism, because of the concerns that social and environmental insults can leave indelible scars on the body and brain (“Babies born into poverty are damaged forever before birth” titled the UK newspaper The Scotsman (Mclaughlin, 2012), to comment on a research on levels of methylation amongst different social groups in Glasgow, of which more below); (ii) amelioration, because the upgradable epigenome may become the basis for a new motivation to intervene, control and improve it through pharmacological agents or social interventions.

On the first dimension, political theorists and bioethicists have already started to reflect upon the “collective responsibility” to protect the vulnerable epigenome (Dupras et al., 2012; Hedlund, 2012) while legal theorists are speculating on the “number of novel challenges and issues” that epigenetic transgenerational effects may represent as a new possible “source of litigation and liability” (Rothstein et al., 2009: 37). The transmissibility via the epigenome of the insults of the past into the bodies of present or future generations raises therefore novel issues of intergenerational equity. This possible moralization of behaviors around the vulnerable epigenome is having a particularly visible example on the overwhelmingly centrality of the maternal body as a target of responsibility for harmful epigenetic consequences on the child’s health (Richardson, in press).

The second pole of this dialectic of plasticity, is instead represented by the many injunctions (it is enough to surf the web for some minutes to find many examples) to “upgrade”, “improve”, “train” or “change your epigenome”. The possibility of influencing the epigenome through diet, lifestyle, physical activity, stress, tobacco, alcohol, and pharmacological intervention becomes the likely basis for new forms of “therapeutic manipulations” (McGowan and Szyf, 2010). In David Shenk’s recent The Genius in All of Us one can see iconically the mobilization of epigenetics, celebrated as a “new paradigm” and “the most important discovery in the science of heredity since the gene” (Shenk, 2010: 129), at the service of a view of unlimited plasticity and constant struggle to enhance our capacity to reach talent and brilliance (see for a comment, Papadopoulos, 2011).

Which of the two poles of this dialectic of plasticity is going to prevail in the representation of epigenetics in the wider society, and in the shaping of epigenetic science itself, remains an open question. Science and society are constantly co-produced: this two-way interaction seems particularly visible in epigenetic research, thus representing a great opportunity to make of this newly emerging discipline a theoretical spyglass to observe the vivid emergence of the tensions and complexities of the postgenomic age.

Postgenomic Social Policies?

The increasing emphasis on the biological embedding of life’s adversities at the genomic level is bringing to public attention what has been called a new “biology of social adversity” (Boyce et al., 2012). Epigenetic mechanisms are a major part of this novel approach. Epigenetics has already been used in the service of explaining the persistent nature, within specific groups, of “connections that have previously been hard to explain” (Landecker, 2011), particularly the perpetuation of health disparities between the rich and the poor, between and within countries (Vineis et al., 2013). An important trend is the use of epigenetic and developmental findings in the so-called early-intervention programmes (Shonkoff et al., 2009).

Over the last few years, a new array of studies has started to look at the way in which social influences can become embodied via epigenetic mechanisms and have lifelong and even inter-generational effects (Miller et al., 2009; Wells, 2010; Borghol et al., 2012). Kuzawa and Sweet (2009) study on racial disparities in cardiovascular health in the USA is a major example of the reconfiguration of the relationship between biological and social factors brought about by epigenetics. This work has focused on epigenetic and other developmental mechanisms as the missing link between early life environmental factors (e.g., maternal stress during pregnancy) and adult race-based health disparities in “hypertension, diabetes, stroke, and coronary heart disease”. It is an important attempt to rethink race along a different, somatic and socio-cultural together, line of thought.

In the UK, the study of McGuinness et al. (2012) on the correlation between SES and epigenetic status (variations in the level of methylation) between socio-economically deprived and more affluent groups in Glasgow (but also between manual and non-manual workers) points more empirically to an association between social neglect, poverty, and “aberrant” levels of methylation. “Global DNA hypomethylation” the study claims “was associated with the most deprived group of participants, when compared with the least deprived”. Epigenetic markers are used in this and other studies as a “bio-dosimeter” (ibid., 157) to measure the impact of social adversity on lifestyle and disease susceptibility (see also: Landecker and Panofsky, 2013).

Looking at the past two decades of attempts to use genetics and neuroscience in the public arena as the ultimate bastion of evidence for social deprivations and inequalities, it is possible that epigenetic findings will become increasingly relevant in social policy strategies. How these findings will help convince policy-makers of the “non-ethereal” nature of environmental influences in order to make “more effective arguments” about the biological impact of social forces (Miller, 2010), and influence specific political agendas (as seen in the notion of neuropolicy, see Racine et al., 2005) is difficult to foresee at this stage. It is clear however that the seductive appeal of neurobiological explanations (Wastell and White, 2012) is likely to be amplified further when combined with the seductive appeal of epigenetics, where social differences and environmental insults are expected now to be seen literally “imprinted on DNA”.

It is important however to remember the huge gap existing between public sensationalism, especially in its public health implication, and the cautious takes of the experts (Feil and Fraga, 2012; Meloni and Testa, in press). Even more ambiguously, the emergence of a possible discourse that identifies, at the local level, subgroups with abnormal epigenetic marks (reflecting the perpetuation of historically disadvantageous conditions) may create a whole new set of social and public policy questions. The legacy of soft or Lamarckian inheritance in social policy discourses has not always been particularly progressive (Bowler, 1984), and its possible returning appeal today should become a matter of reflection for social scientists (Meloni and Testa, in press). Moreover, there is increasing concern among social scientists that constructs rather widespread in epigenetics and DOHaD literature, from “maternal capital” (Wells, 2010) to the growing emphasis on maternal behaviors and the maternal body as the “vector” through which epigenetic patterns are established in early life (as highlighted by Richardson, in press), could have problematic effects on public health strategies and moral reasoning about families, parenting, and women in particular.

Conclusion

In spite of my emphasis on some ambiguities of epigenetic research, the most important lesson for social scientists and theorists at this stage is probably that the future and therefore the social meaning of postgenomics and epigenetics is not already written. As Michel Morange (2006: 356) has claimed some years ago: “the very fashionable post-genomic programs can have very different stakes, some reductionist and other holistic, depending upon who is supporting them. The current state of biological research is very contrasted, because biology is hesitating at a crossroads between reductionism and holism”. It is therefore too early to say if molecular epigenetics will become mired in another form of reductionism (Lock, 2005) or will join new exciting theoretical collaborations capable to “transcend the divide between ‘nature’ and ‘nurture’ intellectually and methodologically” (Singh, 2012). Epigenetics is not set in stone, but an open field where theoretical debates and critiques are vital (Landecker and Panofsky, 2013). Given the multiple and plastic nature of its same concept, at the crossroads of different traditions and research-styles, epigenetics will likely be a terrain for conceptual battle between different stakeholders and intellectual agendas. This is probably one further reason for social scientists to be part of this debate from its very beginning.

Conflict of Interest Statement

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

I thank Tobias Uller and Frances A. Champagne for kindly commenting on the first section of this article (of course, I am solely responsible for any possible inaccuracy there), and Andrew Turner for his help with the English language in the text. Thanks to the two referees for their extremely helpful remarks, many of which are reflected in the final iteration. I acknowledge the contribution of a Marie Curie ERG grant, FP7-PEOPLE-2010-RG (research titled “The Seductive Power of the Neurosciences: An Intellectual Genealogy”).

Footnotes

1. ^ Here postgenomics has to be understood in a twofold meaning: chronologically it refers to what has happened after the deciphering of the Human Genome in 2003; epistemologically it illustrates the emergence of a number of gaps in knowledge and unforeseen complexities surrounding the gene that has led to the current contextual conceptualization of the genome as affected by environmental signals and part of a broader regulative architecture (Dupré, 2012; Griffiths and Stotz, 2013). It is particularly this latter meaning that is central here.
2. ^ I thank one of the two anonymous reviewers for bringing this to my attention.

References are available at the Frontiers site